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CARDIOLOGY

ANATOMY of the
HEARTYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

R ATRIUM (Tricuspid valve) R VENTRICLE


L ATRIUM (Mitral Valve) L VENTRICLE
The MITRAL and TRICUSPID (atrioventricular
valves).
Valves prevented being everted during systole
(into atria) by chordae tendinae and papillary
muscles that contract in systole.
Pulmonary semilunar valve- Pulmonary artery.
Aortic semilunar valve Aorta (passively close
at the end of systole- ventricular pressure now
less than in arteries).
Atria and ventricles separated by ANNULUS
FIBROSUS
A band of fibrous connective tissue- provides
skeleton for attachment of muscle and insertion of
the valves.
Prevents conduction between atria and ventricles
except at AV NODE.
AV node near the inetratrial septum and mouth of
the coronary sinus.
During diastole, ventricles fill.
At initiation of systole, atria contract and complete
ventricular filling.
As ventricles contract, pressure rises sharply, and
AV valves close.
When ventricular pressure exceeds
pulmonary/aortic pressure, semilunar valves open,
and ejection occurs.
Semilunar valves closed by backflow from aretries.
Force of contraction generated by MYOCARDIUM.
Ventricles have thicker myocardium than atria.
Inside of heart lined with ENDOCARDIUM (thin
cell layer)- Thin, slick sheet of connective tissue
located on the inner surface of the myocardium. It
is continuous with the blood vessels.
Outer surface of myocardium lined with
EPICARDIUM (Visceral layer of serous
pericardium)
Heart enclosed in PERICARDIUM (sac)
o Fibrous Pericardium
o Serous pericardium (visceral and
parietal layer, in-between is the pericardial
cavity)
PERICARDIAL CAVITY, enclosed in the serous
pericardium, contains interstitial fluid as lubricant.
Myocardium made of cardiac myocytes (muscle
cells)
Connected together by network of intercalated
disks
The disks provide a structural attachment (glue
together at dermosomes) and electrical
connection through GAP JUNCTIONS.
Myocardium acts as a FUNCTIONAL

CIRCULATIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

SUPERIOR and INFERIOR VENA CAVA.


PULMONARY TRUNK
R. and L. PULMONARY ARTERIES
L. and R. PULMONARY VEINS
AORTA
o BRACHIOCEPHALIC ARTERY
o COMMON CAROTID ARTERY
o LEFT SUBCLAVIAN ARTERY
o DESCENDING AORTA
Blood supply from LEFT and RIGHT CORONARY ARTERIES
BOTH have descending and marginal just the left also has a circumflex.
Arise from the aortic sinus, at the base of the aorta.
Remain patent throughout cardiac cycle, and not blocked by cusps of aortic semilunar valve.
RIGHT CORONARY- runs between pulmonary trunk and R. Atrium, to AV sulcus.
Then descends to lower heart, dividing into posterior descending and right marginal
LEFT CORONARY, runs behind pulmonary trunk and forward between it and L. Atrium, divides into
the 3 further trunks.
Anastamosis between L and R Marginal branches.
Anastamosis between anterior and posterior descending branches.
Blood returns via coronary sinus and anterior coronary veins
LEFT CORONARY ARTERY
o Left Atrium
o Left ventricle
o Interventricular septum
o Anterior wall of right ventricle
RIGHT coronary artery
o Right Atrium
o Right Ventricle
o (in most people) supplies AV and SA NODE
o Arterial disease here can cause AV block or slow HR.
Coronary perfusion pressure: difference between the diastolic pressure in aorta and diastolic
pressure in RA, which creates the perfusion pressure (coronary arteries fill in diastole)
In tachycardia, less time spent in diastole- inc risk of ischemia

CIRCULATIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
LEFT CORONARY ARTERY

The left main coronary artery (LMCA) arises from the left aortic sinus,

It quickly divides into the anterior interventricular branch also known as the left anterior
descending (LAD) artery and the circumflex artery.

The LAD runs along the anterior interventricular sulcus, (groove in the anterior surface of the heart
that separates the left and right ventricle) down towards the apex.

LAD runs around to the posterior surface of the heart in another groove called the posterior
interventicular sulcus.

The LAD artery supplies blood to the walls of both the left and right ventricles.

The circumflex, follows a different course to the LAD. It runs along the atrioventricular groove, which
seperates the atria from the ventricles, giving rise to the left marginal branch in the process.

The circumflex then continues around the heart, terminating on its posteroinferior aspect, to supply blood
to both the left and right atrium.

RIGHT CORONARY ARTERY

The right coronary artery (RCA) arises from the right aortic sinus, and along the right
atrioventricular groove.

From here, it curls around towards the inferior surface of the heart, forming the posterior
interventricular branch, more commonly known as the posterior descending artery (PDA).

The PDA runs along the posterior interventiculas sulcus, to supply blood to the walls of both the left
and right ventricle.

However, before turning towards the diaphragmatic surface of the heart the RCA gives rise to the right
marginal branch, that runs along the right margin, to supply the wall of the right ventricle.

Important branches from the RCA include, the conus branch and the sino-atrial node artery.

As an aside, compared to the left ventricle the right ventricle has a greater ratio of muscle fibres to
capillaries: it is more likely to suffer toxic damage but less likely to suffer ischaemic damage.

CORONARY BLOOD FLOW

Small arteries and arterioles are key players in altering vascular resistance and thus regulating
myocardial blood flow.

Myocardial blood flow is closely linked with oxygen demand, with an increase in cardiac activity resulting
in an increase in demand for oxygen.

This is achieved by an increase in myocardial blood flow, involving autoregulation.

Whenever there is a change in coronary perfusion pressure, through changes in aortic pressure, the
process of autoregulation ensures that myocardial blood flow is always maintained.

Adenosine and nitric oxide (NO) are important mediators in the regulation of coronary blood flow as
well as the involvement of the sympathetic and parasympathetic nervous system.

QUICK RELATION TO EGC

ISCHEMIA: ST depression and T-wave inversion

INJURY: ST elevation

INFARCTION: ST elevation

PREV INFARCTION: Q waves


SEPTAL:
ANTERIOR:

V!, V2
V3, V4

LATERAL:

V5, V6, V1,

INFERIOR:

II, III, aVF

aVL

THE CARDIAC CYCLE- VENTRICLE AP


YYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

What is an action potential? It is when a cell transiently depolarizes, due to ion channels.
CARDAC ACTION POTENTIAL is a lot longer than those in nerves or skeletal muscle.
Because of a PLATEAU PHASE in cardiac muscle, lasting 200-300ms.

I
aVL
II
V2
V5

V1

V4

VENTRICULAR MUSCLE ACTION POTENTIAL

(4) -90 RESTING POTENTIAL

The membrane at rest is most permeable to K+ ions, so the RESTING POTENTIAL is


most dependent on the K+ gradient. (K+ out)

There is transmission from an adjacent cell through intercalated disks.

An action potential is initiated when the membrane is depolarized to a THRESHOLD


POTENTIAL.
o
(0) RAPID DEPOLERISATION:

Rapid Na+ channels are stimulated to open, flooding the cell with positive Na+ ions.

Transmembrane potential is the is the difference in voltage inside, compared to outside


the cell. Positive change.

The Na+ going in is large enough to overcome the outward current through K+
channels.

This causes further depolarization, and activates more Na+ channels.

Depolarization becomes self-generating, so has a rapid upstroke.


ARTERIAL OCCLUSIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

Depolarisation of one cell triggers the Na+ channels in surrounding cells to open as
well, causing the depolarizing wavefront to propagate cell by cell throughout the heart.

Very fast conduction velocity- ie. The slope of 0 is very steep.


LAD: the LEFT
ANTERIOR
from left coronary

After
this, theDESCENDING,
cell begins to repolarize
and return to the resting state, as it cant
o
V1
(septal) again until its in its resting state.
depolarize
V2Initial(septal)
o o (1)
phase of repolarization.
o
V3
(anterior)
Rapid
inactivation of Na+ channels.
V4PLATEAU
(anterior)
o o (2)
STAGE
o
V5
(lateral)
The
membrane potential goes down slowly, followed by a more rapid repolarization
o
V6
(lateral)
phase.

Rate of repolarization is slowed by the INFLUX OF Ca2+ ions into the cell.
L. Circumflex

They activate relatively slowly, when the membrane potential starts getting more
o
1
(all lateral)
positive
(over 35).
o
aVL

Ca2+ ions enter the cell slower than the Na+ ions, and help prevent the cell
o
V5 andrepolarizing
V6 (maybe)too quickly- extending the REFRACTORY PERIOD (cant respond to a new
stimulus)
R. Coronary
Artery
The refractory period and length of AP, means that the cardiac muscle cannot be
o
II
(inferior)
tetanized.
o
III
(inferior)
The
length of the plateau is related to slow inactivation of Ca+ channels.
o
aVF
(inferior)

Ca2+
entry in the plateau is vital for contraction (calcium channel blockers reduce
force)
o
(3)

Critical period where a strong signal may trigger depolarization and cause VT or VF

Its the later stages of repolarization.


o
(4)
o
Repolarization is complete.
o
K+ outward current becomes dominant
o

III
aVF
V6
V3

HYPERKALAEMIA (K+)
o
Plasma K+ can be increased in

RENAL FAILURE

TISSUE DAMAGE
o
Can cause dangerous arrhythmias eg. VF, as the membrane depolarizes (positive) and
becomes closer to threshold potential.
o
MORE K+ outside cell, so less wants to move out, so resting potential is more positive.
o
Also slows and weakens the upstroke of the action potential, as it partially inactivates the
Na+ channels, and slows conduction.
o
Above 8, this leads to complete cessation of conduction- and heart block.
HYPOKALAEMIA
o
Hyperpolarises the membrane, making it difficult to reach threshold.

THE CARDIAC CYCLE SA NODE Action


PotentialYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

SA NODE INITIATING THE HEART BEAT


o
SA node is primary heart pacemaker.
o
Innervated by

Parasympathetic VAGUS CNX (dec Heart rate, not contraction)

Sympathetic T1- T4 Spinal nerves (innervate atria and


ventricles too so can increase contraction force as well as HR)
o
The SA node cells have no resting potential- regular spontaneous
Action Potentials are generated.
o
SA node cells are special, as slow Ca2+ channels carry the current,
rather than the fast Na+ channels.
o
Relies on CALCIUM influx, rather than SODIUM.
o
In terms of how fast they depolarize, the action potentials are much
slower than in eg. Skeletal muscle or cardiac muscle.
o
Can be referred to as slow-response action potentials- the curve
doesnt go up sharp.
o
Conduction velocity is slow- slower conduction cell to cell.
o
An action potential in the SA node is generated at -40- (rather than -60
in cardiac myocytes)- ie the cell has to get even more positive before
an action potential is created- its harder.
o
The Ca2+ channels activate in a more positive environment than the
Na+ ones.
o
The rate of decay of the resting potential, (to make an action potential)
determines the heart rate.
o
Initially, an outward K+ current, slows over time, so more positive.

SA nodal action potentials are divided into:

Phase 4
o

The spontaneous depolarization (pacemaker potential) that triggers the action potential once
the membrane potential reaches threshold between -40 and -30 mV).

(K+ out slower and slower, Na+ in) slow decline in the outward movement of K + as the K+
channels close- that were open in phase 3.

At the end of repolarization, when the membrane potential is very negative (about -60 mV), ion
channels open that conduct slow, inward (depolarizing) Na + currents.

These currents are called "funny" currents and abbreviated as "If".

These depolarizing currents cause the membrane potential to begin to spontaneously


depolarize- initiating Phase 4.

As the membrane potential reaches about -50 mV, another type of channel opens (transient or
T-type Ca++ channel)

As Ca++ enters the cell through these channels down its electrochemical gradient, the inward
directed Ca++ currents further depolarize the cell.

When the membrane depolarizes to -40 mV, a second type of Ca ++ channel opens (long-lasting
L-type Ca++ channels)

Opening of these channels causes more Ca ++ to enter the cell and to further depolarize the cell
until an action potential threshold is reached (usually between -40 and -30 mV).

Phase 0 is the depolarization phase of the action potential. Action potential threshold has been reached!

Phase 3 repolarization. (calcium channels close)


o

A hyperpolarized (very negative) state is necessary for pacemaker channels to become


activated again

THE CARDIAC CYCLE CARDIAC MUSCLE


CONTRACTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

Between the ends of adjacent cardiac muscle cells are specialised intercellular junctions called
INTERCALATED DISCS.

These are irregular transverse thickenings of the sarcolemma that contain structures called
DESMOSOMES.

Desmosomes are like spot-rivets, that hold adjacent cardiac muscle fibres together.

The intercalated discs act as points of anchorage for the contractile proteins, and they contain channels
called GAP JUNCTIONS.

These connect the cytoplasm of adjacent cardiac muscle fibres and permit the extremely rapid lowresistance spread of action potentials from one cell to another.

Adjacent fibres are caused to contract almost simultaneously

Three types of cardiocytes are found in the myocardium.

1. AUTORHYTHMIC CELLS: Cells found at the junction of the great veins and the right atrium
have the fastest intrinsic rhythm (this is the sinoatrial (SA) node or 'pacemaker' of the heart).

Spontaneously discharge about 100 times per minute.

Nervous and hormonal input can alter the rate of this automatic discharge so that the normal
heart rate is about 70 beats per minute.

2. PURKINJE FIBRES (conduction fibres) allow fast conduction of action potentials around the
heart.

3. MYOCYTES (contractile cells)

CONTRACTION- depends on CALCIUM!


o
Remember: calcium induced calcium release. In the absence of external Ca2+, there can be no
contraction.
o
Cardiac muscle contraction occurs by utilising the sliding filament model already described for
skeletal muscle.
o
The action potential spreads from the cell membrane into the T tubules.
o
Calcium enters the cell from the ECF (this doesn't happen in skeletal muscle).
o
This triggers the release of even more calcium from the SR. (the amount released depends on
the amount previously stored and on the size of the inward current from the ECF)
o
Intracelllular calcium increases.
o
Calcium binds to the troponin/tropomysin complex, and tropomysin moves out of the way of the
active site on the actin filament.
o
Actin and myosin bind, and the thick and thin filaments slide past each other
o
The myocyte contracts.
o
Relaxation occurs when calcium is actively transported back into the SR (by calcium-ATPase
pump) or out of the cell into the ECF.
IONTROPES- Iron- iron man- strong contraction
o
Alter the CONTRACTILITY of cardiac muscle
o
POSITIVE IONOTROPE: Increases contractility
o
E.g. high plasma Ca2+ increases contractility, as calcium entry is increased during the action
potential.
o
NORADRENALINE and ADRENALINE

Physiological positive ionotrope.

(from sympathetic nerve endings)

Also positive chronotropes (increase HR)- Chrone- clock HR

Bascially, the noradrenaline binds to beta1-adrenoceptors on the sarcolemma, and


inreases cAMP, this causes more calcium channels to be phosphorylated, which

THE CARDIAC CYCLE THE ACTUAL


CYCLEYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

The sequence of mechanical events that occur during a heart beat

Ie. Diastole, Systole, and the Pause.

Cycle begins when SA node initiates a heart beat

Its the end of diastole

Atrium and ventricles are relaxed

Mitral and Tricuspid (atrioventricular valves) are open

Pulmonary and Aortic (semilunar valves) are closed- as the arterial pressure- both pulmonary
and aortic pressure is greater than the relaxed ventricular.

1. ATRIAL SYSTOLE (ATRIAL contraction)


o

Blood from Atrium - Ventricles

Fills the ventricles and completes ventricular filling

AV valves open

Semilunar valves closed

Ventricles are already partially filled from when the whole heart was relaxed.

Ventricles receive the last 30% blood- final vol of approx. 130ml.

2. ISOVOLUMETRIC CONTRACTION (VENTRICLES CONTRACT)


o

Ventricles filled with blood contract

Tricuspid and Mitral valves close as pressure now high in ventricles

Ventricular volume unchanged, but the pressure rockets.

Semilunar valves still closed.

3. VENTRICULAR EJECTION
o

Pressure in ventricles now higher than in pulmonary arteries and aorta, so semilunar (arterial)
valves open.

Blood into arteries

Pressure in aorta is 80mmHg, and pulmonary artery 10mmHg- ventricular pressure is above
this.

Ejection is rapid, and slows down as systole progresses

THE CARDIAC CYCLE SOUNDS and


CONDUCTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY
Heart Sounds HS I-II+0
o

S1: Closure of AV Valves


o

Lub

Normally close together, if split- might indicate delayed conduction

In L or R bundle of HIS.

AV valves close during ventricular contraction, so ie. A ventricle is contracting a bit


late

S2: Pulmonary/aortic valve closure


o

Splits in young people due to inspiration of exercise- longer ejection period in right
ventricle.

Lungs are lower pressure, want to keep blood, less returns to Left ventricle

Increase in blood into Right ventricle from vena cava, as sucked into Right Atrium, and
wants to go into the lungs.

Takes longer to empty Right ventricle as more blood, pulmonary valve stays open a bit
longer than aortic.

Aortic closes slightly earlier, as less blood.

S3: Rapid refilling, S4: atrial systole (S3 and S4 togther produce a gallop rhythem)- HF.

Electrical conduction pathways

CARDIAC MUSCLE
o

Muscle cells connected by intercalated discs

On the intercalated disc connections are GAP JUNCTIONS, where membranes of cells are very
close, consist of low resistance proteins: CONNEXONS

Allow transfer of small ions, therefore ELECTRICAL CURRENT.

Cardiac muscle is a FUNCTIONAL SYNCTIUM: as its electrically connected.

If Action Potential is initiated in one cell, local currents via gap junctions will cause adjacent
cells to depolarize, initiating their own action potential.

A wave of depolarization, will conduct cell-cell throughout the myocardium.

(Rate of conduction is related to gap junction resistance and size of depolarizing currentrelated to upstroke of action potential).

Drugs that slow this phase (0).. slow conduction

THE CARDIAC CYCLE THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

HEART BLOCK
o

Complete heart block (third degree) occurs when conduction between atria and ventricles
abolished.

Ischemic damage to nodal tissue/ Bundle His.

AVN and Bundle of His then generate HR of around 40bpm

Abnormally slow conduction through AV Node- causes incomplete (1 st degree) Heart Block- delay
is greater than normal- extended P-R interval on ECG.

2nd degree heart block when only a fraction of impulses from atria are conducted- eg. Ventricular
contraction only initiated every 2nd or 3rd atrial contraction (2:1 or 3:1 block)

Wencheback (Mobitz2) is another type of 2nd degree block- P-R interval progressively lengthens,
until no transmission from atria to ventricles, and a QRS is missed.

BUNDLE BRANCH BLOCK


o

When one branch of bundle of His doesnt conduct.

The part of the ventricle it serves will still be stimulated by conduction through the myocardium
from unaffected areas.

Conduction is slower, activation is delayed and QRS broadened (ventricular systole takes longer)

ARRYTHMIAS
o

Caused, promoted, potentiated by defects in conduction system/ ischemia/ damage

WOLF-PARKINSON WHITE SYNDROME


o

AV NODE normal, but a separate extra congenital conduction pathway (bundle of Kent) between
atrium and ventricle.

Atrial impulses conducted to ventricles by AV NODE and Bundle of Kent.

Bundle of Kent faster, so part of ventricle stimulated before the rest- wide QRS COMPLEX. (preexcitation).

A premature impulse can set up a re-entry circuit and bad and fast arrhythmia.

HAEMODYNAMICS
DARCYS LAW:

Flow =

Pump Pressure
resistance

CARDIAC OUTPUT =

Mean Arterial BPCentra l Venous Blood Pressure(0)


Total Peripheral Resistance

THE CARDIAC CYCLE THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

BLOOD VISCOSITY
o

Viscosity is caused by frictional forces in a fluid that resist flow.

Blood is 4x as viscous as water because of erythrocytes.

ANAEMIA: haematocrit (cell concentration) is low, viscosity and vascular resistance decrease,
Cardiac Output rises.

POLYCYTHEMIA: vascular resistance and blood pressure are increased.

LAMINAR FLOW
o

As liquid flows through a tube, frictional forces are exerted by the tube wall.

These, and viscous forces in the tube, set up a velocity gradient across the tube.

Flow velocity is greatest at tube centre. (LAMINAR FLOW)

Occurs in the microcirculation.

Erythrocytes move away from vessel wall, and sit in the middle flow, aligned.

Reduces the viscisoty of the blood in the microcirculation, reducing the resistance (FahraeusLindqvist effect)

WALL TENSION (TRANSMURAL PRESSURE)


o

The wall has a pressure exerted on it: Pressure inside the vessel, minus the interstitial pressure.

This distends the blood vessel wall (ie, the pressure of the blood pushes it out)

This is the FRANK/LAPLACE LAW

Wall Tension = Transmural Pressure

vessel rad ius


wallThickness

In the aorta, where the transmural pressure (blood pushing wall out) is high, atherosclerosis may
cause thinning of the blood vessel wall, and the development of a bulge/anyeurysm.

This increases the vassel radius, and decreases wall thickness, which sets up a viscious cycle of
increasing wall tension, which if not treated may lead to rupture.

CARDIAC OUTPUT LAWS

What is the cardiac output?

CARDIAC OUTPUT = (STROKE VOLUME) x (HEART RATE)

I.e. is the Vol blood pumped through heart per minute

In a normal 70kg man, about 5 L.min, exercise can be 25L/min.

THE CARDIAC CYCLE THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

WHAT IF THE AFTERLOAD (BP) IS HIGH? WILL SV DECREASE?


o

Starlings law means that even if the afterload (blood pressure) increases, the stroke volume can
be maintained.

The resistance to outflow increases, the left ventricle has to pump against a higher resistance,
and the amount of blood ejected is reduced.

This means the EJECTION FRACTION has decreased, and the proportion of the END DIASTOLIC
VOLUME pumped out falls.

The end systolic volume is larger than the beat before.

So when the ventricle is being filled again in diastole, there is already more blood than usual in
the ventricle.

The end diastolic volume is now larger! Ventricle wall is stretched more, so STROKE VOLUME
INCREASES.

When BP increases, the ENP and EDV increase too, so CO can remain the same, despite pushing
against greater force.

AUTONOMIC NS
o

Externally regulates CO

So very important in controlling BP.

Sympathetic stimulation (adrenaline) causes an increase in HR and contractile force.

Positive IONOTROPE, and CHRONOTROPE

The ventricular function curve is shifted upwards

Nor-adrenaline inc this too.

Negative ionotropes decrease force


o

Acidity

CVP and Autonomic NS are prime determinants of CO.

Heart
Rate

Stroke Vol

Positive Chronotropes, eg. SYMPATHETIC NS

END DIASTOLIC VOLUME


- Compliance
- CVP (pessure pushing it) and so EDP (how much fills with
blood before contracts)

Negative Chronotropes, e.g. PARASYMPATHETIC NS

END SYSTOLIC VOLUME


- Arterial pressure
- Contractility
(both of which affected by symp stimulation and tissue
health - o2, pH etc

CARDIAC REFLEXESYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

REFLEXES
o

Fluctuations in MABP (Mean arterial BP) and volume need to be minimized, to maintain
adequate cerebral and cardiac perfusion.

There are autonomic reflexes and local mechanisms.

Intrinsic reflexes (respond to stimuli in CV system)

Baroreceptor

Cardiopulmonary

Chemoreceptor

Extrinsic reflexes- Cardiac responding to stimuli elsewhere.

Eg. Pain/temp changes

Cardiovascular reflexes involve

RECEPTORS: Afferent nerves- sense change, communicate to brain

BRAIN: Processes and responds to info, so later activity of efferent nerves

EFFERENT NERVES: control cardiac, vascular and renal function- homeostasisreverse change.

THE BARORECEPTOR REFLEX


o

Minimizes fluctuations in moment-moment MEAN ARTERIAL BLOOD PRESSURE (MABP)

Afferent (sensory) nerve endings in CAROTID SINUS (dilations at the origin of the carotid
arteries and aortic arch).

They are MECHANORECEPTORS

Sense alterations in wall stretch caused by pressure changes.

Change the frequency they send action potentials- more pressure, more frequent.

MABP decreasesBaroreceptors fire less,

Brain reduces vagal supply to SA node TACHYCARDIA.

Brain inc sympathetic supply to heart and blood vessels.. CONSTRICTION


VEINS+ARTERIES, INC CONTRACTILITY.

Brain increases stimulation of renal sympathetic nerves RENIN is released.. so


angiotensin II production inc, and aldosterone Fluid retention.

BP increased by fluid retention, tachycardia, vasoconstriction, and contractility.

CARDIAC REFLEXESYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

CNS ISCHAEMIC RESPONSE


o

Generalized peripheral vasoconstriction

Stimulated by brainstem hypoxia.

During severe hypotension

Helps maintain bloodflow to brain in shock

Also causes the CUSHING REFLEX: Brainstem hypoxia due to a tumor which is causing
increased CSF pressure: vasoconstriction and hypertension develop.

EXTRINSIC REFLEXES
o

Moderate pain causes increased MABP and tachycardia.

Severe pain has opposite effect.

Cold causes cutaneous and coronary vasoconstriction- can precipitate angina.

HOW IS THIS ALL CENTRALLY REGULATED!?


o

Cardiovascular autonomic control arises when areas of the brainstem, hypothalamus, cortex and
cerebellum interact.

Afferent nerves carrying the stimulus from the receptors terminate in the NTS (NUCLEUS
TRACTUS SOLITARIUS) of the medulla.

Neurones from here (NTS) project to areas of the brainstem which control parasympathetic and
sympathetic outflow.

The nucleus ambiguous and dorsal motor nucleus contain the cell bodies of the pre-ganglionic
vagal parasympathetic neurons- slow the heart when NTS says theres an increased BP.

Neurons from NTS project to areas of ventro-lateral medulla.. blah blah its complicated.

Higher centres eg. Limbic system in cortex modify the action of the brainstem centres, integrated
and appropriate responses are generated.

AUTONOMIC CONTROL OF THE CV SYSTEM


o

Help maintain appropriate MABP in response to the reflexes and receptors.

Homeostatic adjustment to postural changes.

Change in heammorhage and blood gases.

Can override local vascular control- serves body as a whole.

Regulated by brain signals to- so reacts to EMOTIONAL STRESS/ENVORONMENT

Brain can selectively override /modify the CV reflexes, behavioral responses and CV adjustments

CONTROL OF BLOOD VOLUMEYYxxxxxxxxxxxxxxYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

BLOOD VOL CONTROL


o

Baroreceptors measure short term fluctuations in BP.

Long term, body needs constant blood volume, to sustain constant BP.

Alterations in blood vol affect venous return, and CO.

Changes in CO lead to adaptive effects of the vasculature that : Increase peripheral resistance
and therefore BP.

Volume of blood affected by changes in total body contents of


o

Water

Na

These are both controlled by kidneys.

Maintain a stable BP relies on adjusting renal excretion of Na and Water.

PLASMA VOLUME: Na and Osmoregulation


o

Water content in body altered by sweating/ fluid intake

Changes the plasma osmolarity

Any deviation from normal sensed by HYPOTHALAMIC OSMORECEPTORS


o

Activate thist

Release ADH from pituitary

ADH is a peptide that suppresses renal water excretion

ADH acts on DISTAL NEPHRON- to increase its reabsorption of water: reducing loss water in
urine.

Opposite happens if less osmolarity- more water excreted and less ADH.

THEREFORE PLASMA VOLUME mainly controlled by Na+ content of EXTRAVELLULAR


FLUID (in blood).

95% of the osmotic solute in the ECF is Na+ with Cl- and HCO-

After eg. Eating a salty meal, the plasma osmolarity is changed and the body will adjust the water
content (plasma vol)

CONTROL OF TOTAL BODY Na CONTENT

CONTROL OF BLOOD VOLUMEYYxxxxxxxxxxxxxxYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

ANP: ATRIAL NATRIURETIC PEPTIDE


o

Released from atrial myocytes when stretched by INCREASED ATRIAL VOL.

Response to Volume Overload.

Causes DISURESIS and NATIURESIS by

INCREASING GFR

Decreasing Renin and Aldostreone Secretion

Reducing Na+ reabsorption throughout nephron- loose Na+ and therefore water.

Dilates arterioles

Increases capillary permeability

CARDIAC MONITORING
-

Trends more important than single readings

Non invasive techniques better (less risks eg. Pneumothorax/ line infection)

BLOOD PRESSURE

Measured intermittently using automated sphygmomanometer

BP doesnt reflect CO.. BP can be high, but CO low if peripheral vasoconstriction raises
peripheral vascular resistance (SVR)

Vasodilated septic patients, with low SVR may have a high CO, but still be hypotensive.

CENTRAL VENOUS PRESSURE (CVP)


o

Reflects RIGHT ATRIAL PRESSURE

Measured with internal jugular/ subclavian vein catheters

Useful means of assessing circulating blood volume- determine rate to administer fluid.

Increased venous tone can act to maintain CVP, and mask volume depletion during
hypovoluemia/heamorrhage.

CVP isnt as important as the response to a fluid challenge

High CVP indicates

Fluid overload

BASIC CHEST PAIN HISTORYiix


ONSET and PROGRESSION

Cardiac ischemia builds up over few mins

Brought on exercise, exertion, cold weather,


emotion

Angina- resolves with rest/GTNreproducible.

Unstable angina- pain at rest/ inc severity/


inc frequency

MI- severe, nausea, vomiting, sweating, lasts


at least 30mins, not fully relieved by GTN

Spontaneous pneumothorax or PE cause


sudden onset pleuritic pain and dyspnoea
(patient usually remembers exactly what
doing at time)

SITE & RADIATION

BASIC CHEST PAIN DIFFERENTIALSiix

Cardia ischemia, and pericarditisretrosternal pain.

Ischemia- pain tight and crushing- radiates


to neck, back, jaw, arms

Pericarditis is pleuritic, relieved sitting


forwards, worse laying flat.

PLEURITIC
o

Sharp pain

Worse on deep inspiration,


coughing, movement

Dissecting AA: tearing pain radiating


through the back

Pneumothorax

Pulmonary disease- unilateral pain that the


patient can locate specifically

Pneumonia

Oesophageal disease- retrosternal pain- may


mimic cardiac pain

Referred pain from vertebral collapse/


shingles- dermatomal pattern

PE

Pericarditis: Retrosternal

CENTRAL
o

Angina (crushing, tightness)

ASSOCIATED SYMPTOMS

DYSPNOEA:

RISK FACTORSiix

IHD
o
o

smoking, family, hypercholesterol,


hypertension, diabetes.
(SF C HD Sausage Fest Causes HD!)

PE
travel history, immobility, surgery,
fam hist, pregnancy, malignancy
o
wells score (Pist FM )
Pneumothorax
o
spontaneous- (young, thin men),
trauma, emphysema, asthma,
malignancy
o

LOOK FOR?
abnormal lipids:
o
xantholasma
o
tendon xanthoma
CHEST
PAIN
INVESTIGATIONS
ix
Tar
stained
fingers
(IHD)
Hot, oedematous calf: DVT
(IHD)
GP,Hypertension
(non-acute chest
pain)
Marfans syndrome
Diabetes (IHD)

CHEST PAIN INVESTIGATIONSix

ECG (ACS)

FBC (to exclude anaemia).

New onset LBBB

Renal function tests and electrolytes.

T wave changes

TFTs. (arrhythmia from hyper T)

ST depression/elevation

CRP.

Fasting lipids and glucose.

Sinus Tachycardia

Resting ECG. Note: a resting ECG is normal in


over 90% patients with recent symptoms of
angina. If an urgent ECG is considered
necessary on clinical grounds, admission to
hospital is usually required.

AF

R. heart strain

R. Axis deviation

RBBB

S1Q3T3 (deep S wave in 1, Q


wave in 3, T-wave inversion in
3)

Additional tests if a non-cardiac cause is


suspected - eg,

ECG (PE)

CXR,

LFTs and amylase,

abdominal ultrasound.

ECG (pericarditis)

PRESENTING WITH PALPITATATIONSx

Palpitation
s
PALPITATIONS
HISTORY kkkkkmmmmm
REGULAR
REGULAR

CAUSES ooo
IRREGULAR
IRREGULAR

Non- Cardiac causes TACYCARDIA:


What the patient means by palpitations.
SLOW
It should mean
an awareness
of the heart beating.
SLOW
FAST
FAST
It may really be
a pulsatile tinnitus or a carotid bruit.
FAST PACE!!!!
Ask the patient
PERSISTANT
o how often it happens,
PERSISTANT
OCCASIONAL
OCCASIONAL
o VT
how long it lasts and
SINUS
BRADY

Fever
VT
SINUS
BRADY
o any precipitating or relieving factors.
Sometimes people are only aware of it whilst lying down
AF
ECTOPIC
at night.
AF
ECTOPIC

Anaemia
AFof block
block
Determine whether the rate is regular
or irregular.
AF- degree
degree
of
TACHYCARDIA
TACHYCARDIA
Ask
the patient to tap out the beat.
ECTOPIC
AF
This may be regular or irregular. It may be a normal rate
AF
ECTOPIC
Sympathomimetic
drugs
COMPLETE
HEART
S
(paroxysmal)
or fast.
COMPLETE
HEART
S
(paroxysmal)
AF
BLOCK
BLOCK
Try toAF
estimate the rate.
ATRIAL
Establish whether there are any symptoms that
ATRIAL

Thyrotoxicosis
accompany the palpitations, such as sweating or
FLUTTER
(with
FLUTTER (with
breathlessness.
SVT
SVT
block)
block)
These may be organic or psychosomatic in origin.

Pregnancy
Associated chest pain?.sinister significance!
Enquire about consumption of caffeine. Palpitations may
be related in time to consumption but assess daily intake

Anxiety (pain) Arteriovenous


too
fistulae
Ask about alcohol consumption.
Ask about smoking. The level of nicotine in cigars tends to
be rather higher than in cigarettes.
In young people ask about use of illicit substances,

Cigrettes, alcohol, caffeine


especially cocaine, 'ecstasy' methylenedioxymethamfetamine (MDMA) - and
amfetamines.

Exercise
OTC and prescribed meds!
High levels of anxiety can also result from withdrawal of
sedatives such as benzodiazepines.
Causes of Bradycardia
Ask about general health and well-being. There may be
great anxiety in the individual's life at present.
There may be shortness of breath on exertion, loss of

Athletes
weight or gain in weight, with ankle oedema.
Symptoms of thyrotoxicosis- can cause sinus tachycardia,
AF / Atrial flutter.

Hypothyroidism
History of:

PALPITATIONS- EXAMINATIONx

If the patient currently has the palpitations then it is easy to assess the rate and regularity of the
pulse and to get an ECG to confirm the diagnosis.

Consider the following:

Does the patient look well?

Does the patient look anxious?

Is there exophthalmos to suggest thyrotoxicosis?

Are the fingers stained with nicotine?

PALPITATIONS- WORKING OUT DIFFERENTIALSx

Anxiety: diagnosis of exclusion: It may be part of a panic attack.


There may be an occasional 'missed beat'. This is really a misnomer, as what happens is a premature
beat, usually from an ectopic source and this leads to a weak beat followed by a prolonged refractory
period during which the ventricles fill more than usual and, when ejection occurs, it is more forceful
than usual and so is noticed. Occasional ectopics are fairly common and usually of no sinister
significance. They are more likely with a slow pulse.
AF or atrial flutter is often paroxysmal before AF becomes established.
It is often quite fast but can be slow. T
he crucial feature is the random irregularity but this is more difficult to discern with a faster rate.
AF is often associated with shortness of breath on exertion, as it tends to reduce cardiac output by
about 20%.
As a general rule,
o
ventricular tachycardia (VT) has a rate of 120 to 160 BPM
o
supraventricular tachycardia (SVT) a rate of 160 to 200 BPM.
Paroxysmal tachycardia can result from a junctional re-entry phenomenon.
This tends to produce a very fast rate, often in a young person: Wolff-Parkinson-White (WPW)
syndrome is well documented.
A hyperdynamic pulse may occur with anaemia and thyrotoxicosis.
Thyrotoxicosis may produce AF, especially in the elderly where that may be the only feature.
Drugs that reduce the resistance in the circulation may also be responsible. These can include
nitrates and calcium-channel blockers. Excessive use of a beta agonist inhaler will cause palpitations.
Irregularities of rhythm may occur with cardiomyopathy.
Bradycardia may produce palpitations, as a high stroke volume is required to meet the necessary

PALPITATIONS- INVESTIGATIONSx

The gold standard is a full 12-lead ECG taken at the time of palpitations. It should, however, be
performed even if the palpitations have resolved. Shows
o
irregular rate and it is easy to deduce the type.
o
abnormalities suggestive of ischaemia, hypertrophy or cardiomyopathy.
o
occasional ectopics that are not currently causing symptoms.
o
incomplete heart block.
o
short PR interval in WPW syndrome.

Basic
blood
tests
HEART MURMURS
x
HEART MURMURS Hx
x
o
FBC,
o
U&Es
EJECTION oSYSTOLIC

No real symptoms- so need to find out


TFTs. (A and P area)
cause/
consequences.

A 24-hour ECG should be arranged (many GPs now have direct


access
to this).
(a Rheumatic
feverwhich
(mitral
Originate
either is
ventricle
tractsofor 24 hours
o
Thein
patient
given a outflow
device to
wear
Holter monitor)
is valve)
returned to the
either hospital
around the
or the

IHD (mitral regurg)


for pulmonary
analysis thearteries
following
day.
aorta
o
The time that palpitations start and finish shouldbe noted
so this
can disease
be correlated with the
Congenital
heart
Theyre
either
before the valves (in the
ECG
recording.

Hypertension (flow murmus)


heart),
in athe
valves, oran
in the
arteries.
o
As
refinement,
event
recorder can be used for
patients
IVDU whose palpitation frequency is
Reach less
a crescendo
mid-systole, die down
than daily.

Family Hx hypertrophic cardiomyopathybefore


second
heart
sound (semilunar
o
For
added
convenience,
leadless monitors have beenautosomal
developed.
dominant.
shutting)

If the
problem is related to exercise then a treadmill ECG
is AORTIC
required.
Sometimes
there is with)
an

REGURG
(associated
- irregularity
Causes in
AORTIC
AREA..
either
valvular
/
at rest that is suppressed on exercise. These tend to be
ofRheumatoid
rather less sinister
significance
o
arthritis
supravalvular / subvalvular
o
Seronegative arthropathies
o
Coactation of aorta
HEARToMURMURS
x
(ankloysing spondylitis, reiters
Supra-aortic stenosis
syndrome, psoriatitic arthritis
o
Aortic sclerosis
o
Coarctation of aorta
o
Hypertrophic
obstructive

Murmurs are vibrations due t turbulent blood flow in heart.

MiTRAL
REGURG
cardiomyopathy (subvalvular)

Non valvular causes


o
Lupus
o
Hyperkinetic Cardiac Output states
o
Innocent flow murmurs in children
o
Rheumatoid arthritis
Causes in PULMONARY AREA
o
High CO: fever, thyrotoxicosis, pregnancy.
o
Ankylosing spondylitis
o
Pulmonary arterial stenosis
o
Congenital heart diseases: ASD, VSD, PDA, Coarctation ofoaorta.
Marfans
o
Pulmonary valve stenosis
CLASSIFICATION
o
Ehlers-Danlos
o
Flow murmurs, hyperkinetic states,
o
Osteogenesis imperfect.
left-Right shunts (ASD)- left side

EJECTION
SYSTOLIC
biggerremember

Consequences

PANSYSTOLIC
o
Aortic valve disease and mitral

DIASTOLIC
regurg may be asymptomatic.
PANSYSTOLIC
MURMURS (T and M area)

CONTINUOUS
o
LOW CO- fatigue and weakness
o
Paliptations- AF
Same intensity
o
Angina (aortic stenosis)
Heard throughout the whole of systole and
o
Symptoms of RV failure
merge with the 2nd heart sound (semilunar

Anorexia
valves shutting)

Ankle and leg oedema


Causes at APEX (mitral)
o
Mitral Regurg

Hepatic pain
o
Mitral valve prolapse

Intestinal mucosal
Causes at TRICUSPID area
congestion
o
Tricuspid regurg
o
Symptoms of LV failure
o
VSDs- left side bigger/louder
Breathlessness exertion
remember

Cough

Haemoptysis (mitral
stenosis)
DIASTOLIC MURMURS *always pathological,

Orthopnoea
always hard to hear.

Paroxysmal nocturnal
dyspnoea
When blood ejected from the ventricles
o
Syncope (poor CO)- eg, severe
and the heart relaxes, Atria are filling.
aortic stenosis.
Causes at PULMONARY area
o
Emboli- TIA/Stroke- mitral stenosis
o
Aortic regurg (early diastolic)
o
Infective endocarditis
o
Pulmonary regurg (early diastolic)
o
Symptoms of enlarged LA,
Causes at APEX (MITRAL) area
o
Mitral stenosis- think in
pressing on other structures,
especially in mitral stenosis
isovolumentic relaxation- ventricles

Recurrant laryngeal nerveare filling through here.


o
Carey Combs murmus (acute
horseness- Ortners
syndrome
rheumatic fever, mitral valves

MITRAL STENOSIS

MITRAL REGURGITATION

x
-

Mitral valve doesnt close properly


Blood leaks back into LA when LV
contracts, instead of going into the
body.

Due to infective endocarditis, Ehlers


Danlos, Marfans, SLE, scleroderma,
acute rheumatic fever

SYMPTOMS
o
If acute, you get rapid
backpressure into lungs and
acute pulmonary oedemaemergency valve repair!
o
Chronic- eventually, dilation of
Left ventricle, HF.
EXAMINATION
OF A MURMUR
o
Progressive exertional
dyspnoea
o
(Systemic emboli/stroke, chest
pain
AF, less common
than

Inspection,
palpation,
auscultation
stenosis)note when maximum

Time a murmur,
o
. and radiation
intensity
COMPICATIONS
SYSTOLIC
o o AFdue to faulty LA
Pansystolic?
o o HF:
orthopnoea,
PND
Ejection
systolic?
o
Stroke/emboli- due to AF

DIASTOLIC
o o Fatigue
and cold (start
hands-from
low CO
Early diastolic?

SIGNS
2nd sound)
oo Bibasal
crackles- pulmonary
Mid diastolic?
oedema
o
LA enlargement- parasternal
heave
o
LV dilation- thrill at apex
o
Look for things eg. Rheumatoid
arthritis, EhlersDanlos,
oesteogenesis imperfect (blue
sclera)

MURMUR
o
PANSYSTOLIC MURMUR at

Narrowing of the mitral valve (when LALV)


Backpressure builds up behind the
narrowed valve
Reduced amount of blood ejected from LV.
Backpressure into lungs.
Most caused by past Rheumatic feverfollows a bacterial infection with
streptococcus- body makes autoantibodies
to clear infection, but also attack mitral
valve- inflammation, damage and
thickening.
Can also be calcification, congenital,
endocarditis.
More effort form LA to pump into LV- get a
hypertrophy of the LA.
SYMPTOMS
o
SOB during exercise
o
Fainting, dizzy
o
Tired
o
Chest pains (reduced flow
coronary arteries)
o
Chest infections- due to bronchial
vein ruptures, congention,
pulmonary infarction.
o
Coughing up bloody sputum.
COMPICATIONS
o
AF- due to faulty LA
o
HF: orthopnoea, PND
o
Stroke/emboli- due to AF
o
Fatigue and cold hands- low CO
SIGNS
o
Malar flush
o
Pulse: small vol/ AF
o
Evidence emboli- ischaemic
bowel/ leg etc
o
JVP raised
o
Swollen liver
MURMUR
o
MID DIASTOLIC (blood from A
to V, before V contract- blood fills
ventricles in diastole, as in
systole, pumps to body.)
o
At APEX (M area)

AORTIC STENOSIS

AORTIC REGURG

Aortic Sclerosis is the precursor of


calcified, degenerative aortic stenosis

Congenital or calcified from aging.

Blood harder to pump into body at


ventricular systole.

SYMPTOMS
o
Usually none until late
o
Angina
o
Exertional dyspnnoea
o
Syncope
o
. Triad- chest pain, HF, syncope

COMPICATIONS
o
Sudden death- ventricular
dysrrythmia.

SIGNS
o
BP- narrow pulse pressure (less
difference between systolic and
diastolic, as systolic lower.
o
LV hypertrophy as more force
needed to pass valve- small
decrease in radius, massively
more resistance.
o
Small volume, slow rising
pulse.
o
Ventricular heave.

MURMUR
o
EJECTION SYSTOLIC
o
at AORTIC area (A)
o
RADIATES TO carotids
o
Loudest at expiration

Investigations
o
CXR: enlarged heart /

Usually asymptomatic, until ventricle fails!


Ventricles make up and make up to pump
the body, loosing a bit every time, then
can enlarge and keep up no more.
After rheumatic fever, infective
endocarditis, collogen vascular diseases,
SLE, lupus, marfans, ehlers-danlos,
ankylosing spondylitis, reiters, bechets.
SYMPTOMS
o
Heart failure when ventricle fails
SIGNS
o
Low diastolic BP
o
Wide pulse pressure- large
difference between systolic and
diastolic, as diastolic is even
lower.
o
Collapsing pulse- sharp rise and
fall (historical)
o
Head bobbing with each pulse
(hist)- de mussets sign
o
Corrigans sign: visible pulsation
arterial in neck
o
Traubes sign- pistol shot femoral
artery
MURMUR
o
DIASTOLIC
o
(T) Lower L sternal edgeEXPIRATION, LEAN
FORWARDS AND HOLD
BREATH
o
no radiation
Investigations

TRICUSPID REGURG
-

Mitral Stenosis, can cause pulmonary hypertension, which can cause Tricuspid regurgitation
Trauma or infective endocarditis
Rheumatic fever
Blood goes from RA to RV, but in systole, RV is meant to squeeze it into the lungs and it goes
back into RA, pressure on venous system of body- portal hypertension.
-ISCHAEMIC
IVDU? Infective
endocarditis?
HEART
DISEASE- Basics
x

SYMPTOMS
o
Fatigue

Result of
imbalance
Myocardial oxygen supply and demand
o anOedema
andbetween
ascites (peripheral)

Term covers
o
Hepatic pain- liver capsule stretched.
o
Angina

MURMUR
o
ACS
o
PANSYSTOLIC MURMUR
o
Anything
that reduces
blood edge
supplyintoinspiration
heart!
o
Loudest
at L sternal
(T)

Due too
No radiation
o
Atherosclerosis
of coronary arteries (COMMON)
o
Investigations
o
Coronary artery spasm
o
Emboli
o
Aortic stenosis (supplies coronary arteries)
o
Hypertrophic obstructive cardiomyopathy
o
Arrythmias- cause dec coronary perfusion.
o
Anaemia
o
Syndrome X- normal coronary arteries- but abnormal small vessels.

Risk Factors
o
Age- Raised cholesterol, hypertension, cigarettes over time.
o
Male / post-menopausal women
o
Family Hx- below 50 / hypercholesterolemia.
o
Cigarettes (x3)- after 10 years same as non-smoker
o
Blood lipids- HDL protective, LDL and Triglycerides inc risk
o
Hypertension- (also a risk of stroke and renal failure)- drugs decrease risk heart disease by 16%
o
DM (2x risk major ISH event)
o
Race- Asian- more DM.
o
Weight: overweight 2x risk IHD. (increased BP, total cholesterol, insulin resistance, decreased HDL,
dec exercise)

IHD Investigations
o
EGC- ACS
o
Exercise ECG- look for 1mm ST depression
o
ECHO: assess ventricular function- an exercise stress echo can be used to look at areas of
hibernating myocardium- where reduced bloodflow in exercise, as decreased coronary reserve
in a territory- if improve at rest- good for intervention.
o
Nuclear Imaging- Radioactive isotope (thallium) injected during exercise and image after.
Isotope taken up by healthy myocardium- infarction are cold spots. Adenosine can give
pharmatological stress instead.

PATHOLOGY OF ATHEROSCLEROSIS- Basic


TREATING IHD (Basic)
x

Slowly progressive, focal proliferation of connective tissue in arterial intima. Begins in early life. High lipid
GENERAL
levels.
o
Inc exercise, (better collaterial circulation heart, and for VD) smoking stop, diet,
LDL main athrogenic lipid
weightloss
Plaques- mostly made of COLLOGEN synthesized by smooth muscle cells.
oDRUGS
1. ENDOTHELIAL DYSFUNCTION- associated with high cholesteriol, inflammation, and shear forces.
2. MACROPHAGES enter arterial wall, between endothelial cells, take up lipids and become FOAM
- oANTIPLATELET
CELLS.
o
All patients ASPIRIN 75mg Daily- lowers risk subsequent MI and death
o
3.o FOAM
ACCUMULATE
subendothelial
zone- forms FATTY STREAKS
RiskCELLS
of GI bleedmelena,intake
with food, PPI
o
4.o FOAM
CELLS/MACROPHAGES
release toxic productslead to aggregation)PLATELET ADHESION,
MUSCLE
CLOPIDOGREL
if aspirin contraindicated
(inhibits platelet
mostly used
postCELL
PROLIFERATION,
THROMBUS FORMATION
NSTMI/angioplasty.
5. Becomes organized- ATHEROSCLEROTIC CAP with FIBROUS CAP.
- oBETA-BLOCKERS
o
6.o Progressive
enlargement,
and narrowing of lumen- exertional angina.
Reduce Sympathetic
tone.
o
7.o RUPTUREsudden(reduce
thrombus
Negativecause
ionotropes
contractility)- reduce oxygen demand
o
Neg Chronotripoc (HR)- reduce oxygen demand
o is
Increase
of ischaemic
area- decreasing
HR, increases
time
Atherosclerosis
initiatedperfusion
by inflammatory
processes
in the endothelial
cells of diastolethe vessel
wallfor
in coronary
response to
retained (LDL) blood flow.
o
Contraindications? Asthma, PVD with skin ulceration, 2 nd and 3rd degree heart block.
Lipoproteinsoin the
blood survival
vary in size.
Some data suggests that small dense LDL particles are more prone to
Improve
post-MI
pass between
endothelial
cells,
going
behind
the cellular
monolayer
of endothelium.
o the
Good
in chronic
heart
failureshouldnt
be given
in acute.
NITRATES
LDL particles and their content are susceptible to oxidation by free radicals- risk is higher while in the wall than
o
Cause peripheral vasodilation- especially in veins
while in the bloodstream.
o
Reduces venous return, and ventricular pre-load.
o
Reduction
in a
heart
wallof
distensiondecreases
o2and
demand
of heart(LDL
wall-particles
angina relief.
However, LDL particles
have
half-life
only a couple
of days,
their content
typically carry
o fat
Nitrates
are converted
NO- which phospholipids,
results in an increased
intracellular
cyclic guanosine
3,000 to 6,000
molecules,
including:to
cholesterol,
cholesteryl
esters, tryglycerides
& all other
in smooth
This stimulates
calcium
processes
and LDL
fats in the watermonophosphate
outside cells, to cGMP
the tissues
of themuscle.
body) changes
with time.
Oncebinding
inside the
vessel wall,
free calcium
vaaliable
to trigger muscle contraction is reduced.
particles can become
more prone
to oxidation.
o
Nitrates and rest relieve angina in minutes.
Endothelial cells
respond
by attracting
monocyte
white for
blood
cells,
causing them
to leave
the blood by
stream,
o
Longer
acting
nitrates can
be effective
hours.
(isosorbide
dinitrate,
metabolized
penetrate into the
arterial
walls and
transform into
liver
to isosorbide
mononitratethemacrophages.
main active metabolite- helps avoid bad 1 st pass
metabolism.
o
Adverse effects due to arterial dilation- headaches, flushing, hypotension, fainting
CALCIUM CHANNEL BLOCKERS
o
Calcium antagonists inhibit influx of calcium into myocyte during action potential and relax
peripheral smooth muscle.
o
Reduced afterload (so less myocardial oxygen demand), reduce HR, increase coronary
vasodilation.
o
Therefore reduce angina
o
Useful in coronary artery spasm
o
Dihydropyridines (Nifedipine) may be combined with a beta blocker, as they cause
peripheral vasodilation and reflex tachycardia.
o
Diltiazem has slight neg iontropic and chronotropic effect- if on betablocker- needs
monitoring for bradycardia
o
Al CCB are net iotrope to a degree- be careful in impaired LV function (even through
amilodipine good in HF)
o
Headache, dizziness, flushing, constipation, gravitational oedema.
K CHANNEL ACTIVATORS
o
Nicrorandil- has arterial and venous vasodilating properties
o
Useful if refractory to other anti-anginal agents.
STATINS
o
HMG-CoA REDUCTASE INHIBITORS
o
Lipid lowering therapy
o
Help stabilize plaques- reduce freq of acute coronary events.
o
If IHD, and cholesterol normal, still should be on statin.

DIAGNOSING ACSx
-

After acute MI
o
Up to 18hrs: No macroscopic or microscopic changes
o
24-48hrs (2 days): Pale oedematus muscle (macro), (micro) oedema, acute inflammatory
cell infiltration, necrosis of myocytes.
o
3-4 days: yellow rubbery centre with haemorrhagic border (macro), (micro) Obvious
necrosis and inflammation, early granulation tissue.
o
3-6 weeks: Silvery scar becoming rough and white, (micro) dense fibrosis.
Cardiac Enzymes
o
Intracellular enzymes that leak out of infarcted myocardium into bloodstream
o
CREATININE KINASE (peak 1 day)

Peaks in 24hrs

Cardiac enzyme, also produced by skeletal muscle and brain.

CK-MB can be requested if in doubt- a myocardium-bound isoenzyme, specific heart


muscle damage.

Site of infarct related to serum level of enzyme.

Used to assess reinfarction in patients who have elevated troponin from a previous
MI
o
ASPARTATE AMINOTRANSFERASE (peak day 1-2)
o
LACTATE DEHYDROGENASE (peak day 1-2)
o
TROPONIN I or T (8-12hrs)

Good markers of cardiac damage

Proteins involved in myocyte contraction

8-12hrs post MI most reliable

MANAGEMENT HYPERTENSION- Basic

THIAZIDE DIURETICS
o
Lower body sodium stores- BP falls as dec in blood vol, venous return and CO.
o
Gradually the CO returns to normal, but the hypotensive effect remains as peripheral
resistance decreases
o
Side effects: GOUT, impaired glucose tolerance.
o
Low doses (2.5mg bendrofluthiazide) cause little biochemical disturbance without loss of
anti-hypertensive effect. High doses not usually needed.

POTASSIUM-SPARING DIURETICS
o
Diuretic induced hypokalaemia.

BETA-BLOCKERS
o
Decrease CO, so initially cause fall in BP
o
CO returns to normal, but peripheral resistance is set to a new lower level so BP remains
low.
o
Renin levels are reduced.
o
Side-effects: Provokes asthma, and heart block. Neg ionotrope. Cold hands and fatigue.

CALCIUM CHANNEL BLOCKERS


o
Calcium antagonists.
ACUTE CORONARY
SYNDROMES: (Nifedipine)- good vasodilating drugs that can cause reflex tachycardia.
o
Dihydropyridines
Pathophysiology
o
Diltiazem- neg ionotrope, and chronotrope- contraindicated in HF
o
Amlodipine- safe in HF
ACUTE CORONARY SYNDROMES:
o
Flusing, headache, oedema, constipation

Affects 7% population
Pathophysiology
o
Dont use verapamil with beta-blocker.

Increases with age, males, post-menopause

ACE INHIBITORS

RF: smoking,
hypertension,
diabetes,
o
Inhibit
renin-angiotensin-aldosterone
axis
Affects 7% population
cholesterol,
family.
o
Increase in vasodilating bradykiin

Increases with age, males, post-menopause

About 20%
all deaths
in UK
o ofMore
effective
in yonger patients with higher
levels- best
in young white
renin
RF: smoking,
hypertension,
diabetes, cholesterol,

After MI-o30-60%
hospital,
10%
Gooddeath
in HF,before
proteinurig
nephropathy,
diabetes family.
in hospital,
years (HF to
or bradykinin),
MI)
o 20%
Dry within
cough 2
(secondary
Hyperkalaemia,
Transient
worsening
in serum

About 20%
of all deaths
in UK

Variant Angina?
Vasospasm
creatinine
(GFR)- as intraglomerular pressure
falls,
Acute
renal
failure
(if
sepsis,

After MI- 30-60% death before hospital, 10% in

Stable angina?
Fixed Plaque renal artery stenosis)
hypovolumeia,
hospital, 20% within 2 years (HF or MI)

ACS: thrombosis
overelectrolytes
ruptured complex
o
Monitor
until dose titrated.

Variant Angina? Vasospasm


plaque

ANGIOTENSIN II RECEPTOR BLOCKERS

Stable angina? Fixed Plaque


o
Block rein angiotensin system- similar to ACE

ACS: thrombosis over ruptured complex plaque


CONSEQUENCES oOF CORONARY
ARTERY
OCCLUSION
Good if chronic
cough
on ACE- dont effect bradykinin production
o
CV protective effect
CONSEQUENCES OF CORONARY ARTERY OCCLUSION
o
LEFT
CORONARY ARTERY

MINOXIDIIL
o
Potent
vasodilator,
dec Major
PVR- can cause reflex tachycardia- use beta-blocker

Supplies
LAD and
Circumflex:
o
LEFT CORONARY ARTERY
o
Fluid retention
diuretic)
contribution
to LV and (use
RV perfusion

Supplies LAD and Circumflex: Major


o
RIGHT CORONARY
ARTERY
o
Hirsutism
contribution to LV and RV perfusion

Occlusion causes inferior MI.


o
RIGHT CORONARY ARTERY

Main Supply to RV and AV node

Occlusion causes inferior MI.


o
LAD ARTERY

Main Supply to RV and AV node

Occlusion causes Anterior MI


o
LAD ARTERY

Supplies LV, Septum and RV

Occlusion causes Anterior MI


o
CIRCUMFLEX ARTERY

Supplies LV, Septum and RV

Causes lateral MI
o
CIRCUMFLEX ARTERY

Causes lateral MI
FACTORS LIMITING OXYGEN SUPPLY

Artery NARROWING: Vasospasm and complex


plaque thrombosis
Reduced FLOW: Hypotension, tachycardiareduces diastolic time, inc LV end-diastolic
pressure, LV hypertrophy.
Reduced OXYGEN CARRYING capacity:
Anaemia, hypoxaemia.

FACTORS LIMITING OXYGEN SUPPLY

FACTORS LIMITING OXYGEN DEMAND

Increased HR: (anxiety/ exercise)


Inc LV AFTERLOAD / MASS: (increases
myocardial wall stress eg. Hypertension and

Artery NARROWING: Vasospasm and complex


plaque thrombosis
Reduced FLOW: Hypotension, tachycardia- reduces
diastolic time, inc LV end-diastolic pressure, LV
hypertrophy.
Reduced OXYGEN CARRYING capacity: Anaemia,
hypoxaemia.

FACTORS LIMITING OXYGEN DEMAND

Increased HR: (anxiety/ exercise)

CLINICAL FEATURES OF MI
Crushing/ heavy retrosternal pain
Radiates to
o
Neck
o
Medial L arm
o
Right chest or shoulder blades

Atypical: Burning, localized eg. Only jaw,


absent.

STABLE ANGINA
o
Precipitated by exercise/anxiety
o
Relieved in 5 mins by rest/sublingual
nitrates.

UNSTABLE ANGINA and NSTEMI


o
Frequent, unpredictable, over 15mins
ACS INVESTIGATION
o
Respond less to nitrates
o
New pain? Pain with less exertion?

1st you need to differentiate ACS form other


Autonomic manifestations eg. Nausea and
life threatening conditions e.g. Aortic
sweating? Radiation to new sites eg. Jaw?
dissection and benign things e.g. Reflux,
Indicate increasing coronary artery
musculoskeletal.
ACUTE CORONARY
SYNDROME
CHRONIC STABLE (exertional)
occlusion
and NSTEMI(ACS)
ANGINA
o
Typically: Crescendo angina: inc freq
INVESTIGATIONS
of prolonged,
freq angina.
Angina in which

Spectrumperiods
of increasingly
life-threatening
conditions
ischemia
at rest/minimal exertion
(and myonecrosis) follows sudden artery occlusion due to thrombosis

Fixed stable coronary artery


o
Both have ST depression and T wave

ECG
(and vasoconstriction).
occlusions limit blood flow
inversion
ECG.
o
Site and Size infarct.

Initiated by
STRESSon
INDUCED
RUPTURE (hypertension) of small
causing predictable, reversible
o
NSTEMI- high risk of coronary artery
o
ST Elevation (immediate
eccentric (non-circumferential), non-occluded (under 50%) COMPLEX
cardiac ischemia during
occlusion
and cores
deathand
(in 4-6
revascularization)
plaques, with
lipid-rich
thinweeks)
fibrous plaques.
exercise.
o rupture
8% hospitalized
die in 30 days, 8% reo
ST Depression
and T inversion:
NSTEMI

Plaque
stimulates

Stenosis
are caused
by
infarction. formation
doesnt benefit
from thrombolysis.
o
Thrombus
smooth
circumferential

INCREASED RISK OF FUTURE EVENTS


o
Survival at 6 months
is similar
for a with
o
Vasospasm
atherosclerotic
plaques
o
ST depression
NSTEMI, and STEMIeven though
early to
o
Arterial Occlusion
thick fibrous
caps: unlikely
o
Elevated troponin
in STEMI.
rupture.

Length of time and extent of the occlusion determine severity of mortality higher
o
Recurrent angina
o
Serial
ECGS
diagnose.
toThick
fibrous cap, small lipid
ischemia: defines the syndrome, ECG changes, symptoms, degree
of
o
Diabetes
o
INFERIOR: RCA,
II, III, aVF
core.
myocardial
necrosis (cardiac enzyme release).
o
Previous
o
ANTERIOR:
l, aVL, often
V2, V3,
V4, V5
LAD,
Ischemia
sub
UNSTABLE
ANGINASTEMI
Impaired artery
LV
INTEROSEPTAL:
LAD, V2, V3,
endocardial,
as V4
systolic
oo Coronary
occlusion of limited extent/duration. o
HF
o
ANTEROLATERAL:
LAD, V3,greater
V4, V5 than
compression
oo Ischemia,
not necrosis
o (send
High for
risk!?
Early cardiac angiography.
o
APICAL: LAD, endocardial
II, III, aVF, V5,
V6 epicardial
than

NSTEMI
PCI!)
No risk factorsExercise
ECG incomplete/ alleviated by
o
LATERAL: Circumflex/diagonal,
I, aVL, V6
aretries.
oo Occlusion
may be
temporary/

MI collateral vessels
Right/Circumflex,
VARIANT- PRINZMETALS
o
POSTERIOR:
R wave in
NSTEMI and
(cardiac
enzyme
uncommon, caused
V1,-2 with ST ANGINA:
depression.
oo Ischemia
andSTEMI
necrosis
limited
to SUBENDOCARDIUM
positive)
by transient coronary artery

ENZYMES
o
Myocardial damage: cardiac enzymes.
o (send
Thrombolytic
vasospasm
due enzymes
to over- in
o
A twofold increase
in plasma

STEMI
for PCI!) therapy is only beneficial on
reactivity (to noradrenaline)/
STEMI
myocardial damage.
o
Occlusion causes transmural ischemia
impaised
flow-mediated
o
MI: abrupt onset severe, prolongued pain,
o
Cardiac Troponins
at 12hours
are
o
Q-waves
Often near
unrelieved by nitrates.
sensitive and vasodilation.
specific for necrosiscan
o
Autonomic symptoms: Cold, clammy,
detect MI after surgery, and when ECG
sweating, nausea, vomiting.
non-specific eg. LBBB.
o
Dyspnea, anxiety

CXR
o
Only 25% have preceding unstable
o
Heart Failure
angina.
o
Aortic disssection
o
Pain might not occur in elderly/diabetic

ECHOCARDIOGRAPHY
patients presenting with collapse,
o
Assesses contractility.
confusion, HF, metabolic dysfunction.
o
Reveals dyskinesia
o
TACHYCARDIA: Anterior MI
o
Mural thrombus
o
BRADYCARDIA + HEART BLOCK: Inferior MI
o
Septal defects
(conducting tissue damage)
o
Papillary muscle rupture.
o
Hypotension (systolic under 90): indicates

INCREMENTAL EXERCISE STRESS TESTS


a large MI, ie over 40% LV damage and
o
Reveal cardiac ischemia as angina.
heralds cardiogenic shock.
o
Failure of BP and HR appropriate
o
Ascultation may show 3rd and 4th heart
responses.
sound (gallop rhythem) and systolic
o
EST= Bruce protocol
murmur.
st

MYOCARDIAL
PERFUSION SCANS
o
EARLY COMPLICATIONS MI (1 week)
o
Detects reduced isotope uptake in poorly

Arrythmias
perfused myocardium using a gamma

Pericarditis
camera.

Papillary muscle/ free wall rupture


o
Alternative to exercise stress test in bed
VSD

ACS GENERAL MANAGEMENT

MANAGEMENT OF STABLE ANGINA

NITROVASODILATORS
o
Efective, but tolerance develops
BETA-BLOCKERS
o
First line therapy
o
Improve prognosis
o
Increase myocardial perfusion in diastole- slow HR
and reduce pre-load and afterload so reduce LV
tension.
CALCIUM CHANNEL ANTAGONISTS
o
Useful when beta-blockers contraindicated.
o
Relive coronary vasospasm.
o
Nifedipine, can cause reflex tachycardia, and
exercerbate HD (neg ionotrope)
REVASCULARISATION
o
Needed if symptoms deteriorate.
o
Needed if positive exercise stress test
o
Needed if angiography revelas over 70% stenosis
in all 3 main, left main or proximal LAD arteries.

Treatment aims to reduce MYOCARDIAL


OXYGEN CONSUPMPTION, whilst
increasing supply.
By DECREASING
o
HR (beta-blockers)
o
AFTERLOAD: (antihypertensives)
Risk Factor Reduction
o
Smoking, diet, weightloss, treating
hypertension and DM.
Antiplatelet (aspirin) and lipid lowering
MANAGEMENT UNSTABLE ANGINA/
drugs (Statins)
NSTEMI
ACE
inhibitors- reduce atherosclerosis

Thrombolytic therapy not


beneficial.
Nitrates, Beta blocker, CCA and
ANTIPLATELET THERAPY
o
All patients 300mg Aspirin
immediately
o
75mg a day
o
Irreversible cyclo-oxygenase
inhibition prevents platelet
aggregation within 15mins
chewing aspirin- preventing
MI/sudden death by 50%
o
Clopidogrel inhibits its ADPStimulated platelet aggregation,
reduces mortality when combined
with aspirin after 30days.
GLYCOPROTEIN IIb/IIIa
ANTAGONISTS
o
Most effective platelet inhibitorsUsed after PCI to prevent stent
thrombosis.
ANTICOAGULANT THERAPY
o
IV unfractunated heparin.

MANAGEMENT OF INFARCTION/STEMI

Early reperfusion after MI limits infact size and


mortality.
IMMEDIATELY
o
Pain relief
CONTRAINDICATION TO THROMBOLYTIC
o
Monitoring
THERAPY
o
Oxygen Therapy
o
Aspirin
o
Beta-Blockers
Absolute
o
Clopidogrel
o
(Heparin)

Active Bleeding (GI heamorrhage)


o
Revascularisation with PCI/TT

Aortic Dissection
OPIATES

Neurosurgery/ head injury


o
Morphine

Recent CNS disease (tumor) under


o
Pain, reduces pre-load, lower myocardial oxygen
6months
consumption, lower anxiety induced catachlomine

CVA in last 2 months


release.

Recent operation (under 4 weeks)


ASPIRIN

Recent Trauma (under 4 weeks)


o
Reduces 35-day mortality by 23% when with TT.

Diastolic Hypertension
BETA-BLOCKADES

Coagulopathy (less platelets)


o
Reduces size of Infarct
o
Reduces arrhythmias
Relative
o
Reduces Mortality- espesh if tachy/ Hypertensive
o
CONTRAINSICATED: Asthma, HF, Bradycardia

Previous CVA/TIA
NITRATES

Recent CPR
o
Under 24hrs

Systemic Hypertension
o
Reduce pain, infarct size, HF

Recent Central lines


ACE INHIBITORS

Intracardiac thrombus
o
Over 24hrs, improve LV remodeling

AAA
o
Reduce HF in high risk patients.
IONOTROPIC SUPPORT
o
In cardiogenic shock
PCI
o
If under 90mins, is the preferred method of
revascularization.
o
Primary PCI- under 6hrs, re-opens over 90%
occluded arteries
o
Significant mortality of unsuccessful.
THROMBOLYTIC THERAPY (TT)
o
Dissipates thrombus
o
Reverses Ischemia
o
Limits myocardial injury
o
Limits complications (HF)
o
Most effective under 2hrs of symptom onset- until
12hrs
ARRYTHMIAS
STREPTOKINASE (SK) or tPA TISSUE PLASMINOGEN
ACTIVATOR
o
Main TT agents
byRate/Rhythem
infusion
Abnormalities
of thegiven
Heart
o
SK
cheap
but
allergenic
(single
use)
Due to Aberrant impulse generation
/ conduction (eg. Re-entry circuits)
AF affects 10% of over 75s
Arrythmias (VF/VT) cause 40% deaths in IHD
Asymptomatic/stable rhythems can be just observed, while cause corrected eg. Hypokalaemia.
Prevention
o
Early correction hypoxaemia
o
Electrolyte disturbances (hypokalaemia)
o
Acid-base imbalance
o
Cardiac ischemia
o
Vagal stimulation (pain)
o
Drugs (theophylline)
o
Cardiac irritants (intra-cardiac catheters)
Antiarrythmic drugs
o
Selected due to rhythem and underlaying pathophysiology
o
Therapy often doesnt work and can cause new arrhythmias.
Other Therapy? DC Cardioversion, Implantable defibrillators, radiofrequency catheter ablation (destroys
accessory pathways)/ ectopic pacemakers.

TACHYARRYTHMIAS

Tachy is over 100bpm

Physiological (exercise)
Either Supra-ventricular or ventricular

Pathological (thyrotoxicosis/ HF)


Detrimental if cause symptoms:- terminate immediately

Stimuli which inc sympathetic tone,


with cardioversion/ drugs!
accelerates SA node paceing.
o
Hypotension
TREAT? Remove case.
o
Pulmonary oedema
o
Reduce tissue perfusion
ATRIAL FLUTTER
Caused by
o
INCREASED PACEMAKER ACTIVITY
BRADYARRYTHMIAS
o
RE-ENTRY CIRCUITS

An anticlockwise atrial re-entry circuit.


Increased pacemaker: faster spontaneous membrane

Causes rapid, co-ordinated

Under
60bpm
depolarization, lower thresholds and oscillations during
redepolarization.

Due
to
Delayed
conduction.
polarisation trigger early APs.

300bpm

If symptomatic treat with


Re-entry circuits:A depolarization wave travels around
a

Ventricular rate depends on AV Node


ATROPINE
circle of myocardial tissue. If the tissue is not refactory o
refractoriness, with conduction of
o
BETA AGONISTS
when the impulse returns, it will depolarize again producing
every 2nd, 3rd or 4th depolarization.
a recurring circuit (paroxysmal tachys).
o
PACING
(2:1, 3:1, 4:1 block)

BP and CO fall if stroke volume cant increase due to

Tachycardia with rate of exactly


DIAGNOSIS
reduced compliance / contractility.
150bpm suggests Atrial Flutter.
o
NARROW QRS TACHYCARDIAS

SINUS BRADYCARDIA

Treat?

Adenosine bolus

HEART BLOCK
o
Class 1a, 2, 3, 4 drugs /

To assess/ terminate
o
FIRST
digoxin.

Usually SVT.
o
SECOND: MOBITZ 1+2
o
Class 1a may cause VT, so
o
WIDE COMPLEX TACHYCARDIAS
o
COMPLETE

Usually VT
AF

Hard to tell if its unusal conduction of SVC


SINUS BRADYCARDIA

Exclude AV node block.

Spontaneous, chaotic, atrial

If haemodynamically unstable, treat as VT


Normal ECG p waves, and Av node conduction
depolarization.

DC Cardioversion

Treated by addressing
causes eg. Vagal reflexes
Over 300bpm

Doesnt work? Probably SVT- use adenosine


(pain), Drug
Toxicity
(beta-blockers),
Atropine.

Refractory AVN conductions


limits

Ongoing treatment amiodarone.


ventricles
to
under
200bpm.

VAGAL STIMULATION (eg. Carotid sinus massage)


HEART BLOCK

Ineffective atrial contraction


slows HR and may cardiovert some SVT
predisposes to atrial thrombus and
Due to AV node
or Conducting tissue ischemia.
thromboembolism.
SUPRAVENTRICULAR TACHYARRYTHMIAS (SVT)

Treat?!

Common after
inferior MI (RCA supplies the AV node)
o
Originate above the AV Node
o anterior
Anticoagulation
(stroke)

Heart Block after an


MI suggests
a large
o
Dizziness, palpitations, breathlessness
o
Digoxin
(controls
resting HR)
infarct
requires
early
pacemaker
insertion.
o
Rarely life-threatening. Can be sudden death.
o
Beta-blockers (control exercise

SINUS TACHYCARDIA
st
HR)
1 DEGREE HEART BLOCK

ATRIAL FLUTTER

AF
VENTRICULAR FIBRILLATION

AVN RE-ENTRANT TACHYCARDIA

Slows AV node conduction

PRE-EXCITATION SYNDROMES
Prolongued P-R (over 0.2 secs)

Chaotic
ventricular
rhythm

An early warning
of worse
heart block
later.
VENTRICULAR TACHYARRYTHMIAS

Follows Acute MI
VENTRICULAR
TACHYCARDIA
o
Arise in ventricles,
in patients with IHD, 2nd DEGREE HEARTBLOCK
Treat?! Immediate DC cardioversion!
cardiomyopathy, congenital disease.
o Class 2/3 drugs/ implant defib
Seriouscircuits eg. Scar tissue from
Due oto re-enry
(recurs)

Some Atrial beats are not


conducted to the ventricles
VF
MI, with uniform QRS

MOBITZ1: WENKEBACH
Or focal ectopic automaticity (drugs or
o
Progressive P-R lengthening, then failure of
metabolic) with irregular or phasic
impulse (dont really treat)
TORSADE DE POINTES QRS (polymorphic

MOBITZ2:
VT)- unstable and may progress to VF.
o
Below the AVN in the His Purkinje system
Ventricular rate 150 250
o
Eveny 2nd or 3rd artrial impulse initiates
Treat!? Terminate with cardioversion
ventricular contraction (2:1 block etc)
Or class 1a/1b drugs
o
(need pacemaker, as complete heart block
Use class 2 or 3 to prevent initial
often follows)
reoccurance

AV RE-ENTRANT TACHYCARDIAS

SINUS TACHYCARDIA

PAROXYSMAL SVT!
Re-enrant circuits between atria and
ventricles.
Or between atria and AV Node- ie in the AV
NODE
Treat!? Vagal Stimulation
Drugs slowing Av node conduction
(Adenosine), class 2, class 4

3rd DEGREE COMPLETE HEART BLOCK

Conduction between atrium and ventricles ceases


AV Node pacemaker action produces nonconducting junctional escape rhythems
(asymptomatic)
Infranodal WC pacemaker escape rhythms are
unstable, slower (30 bpm), symptomatic.
Essentail to insert pacemaker.

PRE-EXCITATION SYNDROMES
An Accessory AV Pathway: BUNDLE OF
KENT in Wolf Parkinson White Syndrome.
Bypasses the AV node, depolarizing an
area of the ventricle early, shortening the
P-R interval (time for atria then ventricles
to contract)
Slow transmission from the pre-excited
area- no conducting tissue, creates a delta
wave on ECG.
Treat!? Class 1a, 1c, III IV drugs
And ADENOSINE

ATRIAL TACHYCARDIA
Automaticity in ectopic atrial pacemakers
Treat!?
o
ADENOSINE to terminate
o
Class 1c or 3 drugs
o
Correct underlying metabolic
defect
o Radiofrequency catheter ablation.

PATHOPHYSIOLOGY OF HEART FAILURE


SYSTOLIC FAILURE

HEART FAILURE AND PULMONARY OEDEMA

When CO insufficient to meet the


metabolic needs of the body.
Or can only do so with ELEVATED FILLING
PRESSURES. (pre-load)
Initially compensatory mechanisms maintain
CO at rest
But as HF and CO deteriorates, exercise
tolerance falls, and downstream hydrostatic
pressures increase
Common causes: IHD and Hypertension.
Volume overload can cause pulmonary
oedema, despite cgood heart function.
5 year survival under 50%.

LV FAILURE

Most common
Downstream pulmonary capillary wedge
pressure (PCWP) rises to 25 ish.
Fluid filters into the alveoli and interstitial
spaces, causing pulmonary oedema, and
breathlessness.
Low plasma oncotic pressure
(hypoalbuminaemia) or increased membrane
permeability (inflammation) can cause
pulmonary oedema at lower PCWP.

DIASTOLIC DYSFUNCTION

RV FAILURE

Causes SYSTEMIC CONGESTION (e.g. ankle


swelling, hepatomegaly)
Usually associated with LV failure.
Biventricular failure: CONGESTIVE CARDIAC
FAILURE

Reduced Myocardial contractility and


Ejection Fraction (under 50%) accounts
for most of HF.
o
Due to
o
IHD
o
Cardiomyopathy
o
Metabolic toxicity
o
Valve defects
o
Arrhythmias
Initially CO maintained by compensatory
mechanisms
o
Inc. sympathetic drive
o
Raised circulating volume (renin)
o
Raised Filling pressures
These mechanisms have detrimental effects
Failing heart responds poorly to preload
Subsequent pulmonary and peripheral
congestion
Large ventricular volumes increase cardiac
work and impair function
In pressure overload (aortic stenosis),
compensatory hypertrophy initially improves
ventricular Ejection Fraction.
Reduced compliance and capillary density
eventually decreases blood supply and
contractility.

When LV relaxation/filling (an energy


dependent process) is impaired due to
o
myocardial ischemia
o
Fibrosis
o
LV hypertrophy (hypertension)
Poor diastolic LV perfusion
Reduced LV compliance inc PWCP, and
precipitates pulmonary oedema- even if
normal Ejection Fraction and contractility.

MANAGE HF

CLINICAL FEATURES

Treat the
o
CAUSE (IHD/valve)
o
Pathophysiology (DD)
o
Precipitating events (arrhythmias)
AFTERLOAD REDUCTION rapidly improves LV function
and CO in the failing heart.
But may cause Hypotension.
PRELOAD REDUCTION: relieves symptoms (eg.
Pulmonary oedema), but CO is not increased.
Non-invasive monitoring and less frequently pulmonary
artery catheterization- may be required to measure
filling pressures, CO, vascular resistance.to optimize HF
treatment.

ACUTE LEFT VENTRICULAR FAILURE


Presentation depends on
o
Onset speed

Priority: Immediate relief of breathlessness of


o
Underlaying
pulmonary oedema.
o
Ventricular involvement
DIAGNOSTIC
INVESTIGATIONS

Sitting position
most comfortable.
HF precipitated/ aggravated by

Supplemental OXYGEN (60%) corrects hypoxaemia.


o
Stress

Loop
(furosemide IV) initially reduce LV
DIURETICS
Cardiac Enzymes
o
Acute illnesses
preload,
and relieve dyspneoa by pulmonary venous

ECG
o
Drugs
dilation.

CXR
o
Pregnancy
Subsequent
lowers
fluid loadpeptide)
and cardiac
Reduced CO causes fatigue, anorexia, exercise

Serum diuresis
BNP (b-type
natrieuritic
filling increased
pressures.by myocardial wall stress: sensitive
limitation.

NITRATES
(IV/sublingual)
LVF
and specific
for HF. inc venous capacitance,
and
coronary
arteries in ventricular
IHD.
CAUSES
HF AND PULMONARY
dilate
ECHO:
wall hypokinesia,
o
Breathlessness

DIAMORPHONE
decreases preload- potent
OEDEMA
enlargement.
o
Hypoxaemia
venodilator
effects,
andreduced
V02, by in
relieving
anxiety.

Ejection
fraction:
HF
o
Orthopnoea

BRONCHODILATORS
(salbutamol)
reduce

CO and BP may be
normal
o
PND

MYOCARDIAL DYSFUNCTION
bronchospasm (but aminophylline precipitates
o
Cough- frothy pink sputum
arrhythmias).
o
GALLOP RHYTHEM (S3, S4 added
NEW YORK
HEARTand
ASSOCIATION

CPAP reduces
hypoxaemia,
work of breathingo sounds)
IHD
CLASSIFICCATION
HF
used
more
often
in
HF
o
CARDIOMYOPATHIES
o
COURSE CREPS LUNG BASES

ARRYTHMIA
CONTROL
essential.
PREGNANCY
RVF o
MYOCARDIAL
DISEASE

CLASS 1: (mild): no activity limitation, no


o o Systemic
congestion,
raised JVP
(amyloidosis)
LOW-OUTPUTsymptoms
LEFT VENTRICUAR
FAILURE
from ordinary
activity. E.g. Fatigue,
o
Hepatomegaly
If you
have an inferior MI,
dyspnoea, palpitations
o o Ankle
oedema
you can have RV failure

CLASS
2: (mild):
Slight
limitation
physicalaims

When
pulmonary
oedema
controlled,
treatment
o
Ascites
isolated,
as blood
activity.LV
Comfortable
at Diastolic
rest, symptoms
with
to IMPROVE
FUNCTION,
Dysfunction
o
Onset
may be
acute supply
(MI) with
from RCA.
ordinary activity.
D, PROGNOSIS.
cardiogenic shock/ acute pulmonary

PRESSURE OVERLOAD
INHIBITORS:
CLASS 3: (moderate):
Marked limitation

ACE
Reduce afterload,
increase CO,
o
LEFT: hypertension, aortic
activity,
only and
comfortable
restreducephysical
symptoms
(fatigue)
lengthenat
survival.
stenosis (mitral stenosis
minimal
activity
causes
symptoms.

Benefit
most HF
patients
unless
contraindicated
doesnt cause LV failure)
(renal artery stenosis), or side effects (cough)
o
RIGHT: Pulmonary

Selectove BETA-BLOCKERS BISOPROLOL improve


hypertension due to chronic
prognosis by reducing myocardial ischemia and
lung disease (cor
arrhythmias. May precipitate pulmonary oedema,
pulmonale), pulmonary
bronchospasm, heart block.
stenosis.

CALCIUM CHANNEL BLOCKERS: alleviate diastolic

VOLUME OVERLOAD
dysfunction by reducing hypotension and coronary
o
Excessive fluid
vasospasm
administration

Tachycardia and impaired contractility limit use.


o
Retention (renal failure)

DIGOXIN: no ionotropic effects, useful in HF with AF


o
Aortic/ mitral valve regurg

PROPHYLACTIC ANTICOAGULANTS: reduce


causes LVF
associated thromboembolic events.
o
Tricuspid regurg causes RVF.

IMPAIRED FILLING
RIGHT VENTRICULAR FAILURE
o
Constrictive pericarditis
(TB, rheumatic heart

Diuresis reduces peripheral oedema


disease, pericardial

But detrimental if high RV filling pressures remain to


effusion, cardiac
maintain CO
tamponade).

Afterload reduction with pulmonary vasodilators

ARRYTHMIA
(CCB) usually limited by hypotension.
o
Impair ventricular filling:

OXYGEN THERAPY relieves cor pulmonale


hypotension

TACHYCARDIA
o
Cause myocardial ischemia-

CARDIOGENIC SHOCK

Reduced
Reduced CO
CO
(digoxin)
(digoxin)

BETA
BETA
SYMPATHETIC
SYMPATHETIC
ACTIVATION
ACTIVATION
(Betablockers)
(Betablockers)

INCREASES
INCREASES
CONTRACTILITY
CONTRACTILITY
and
HR
and HR

Reduced
CO
Reduced CO

Reduced
CO
Reduced CO

ALPHA
ALPHA
SYMPATHETIC
SYMPATHETIC
ACTIVATION
ACTIVATION

ARTERIAL
ARTERIAL
VASOCONSTRICTIO
VASOCONSTRICTIO
N
N
(arterial
(arterial
vasodilators)
vasodilators)

INC
INC AFTERLOAD
AFTERLOAD

heartMore Work
Work
heart- More
and
and oxygen
oxygen
consumption
consumption

INC
INC Myocardial
Myocardial
Damage
Damage
INC
Ca2+ Overload
Overload
INC Ca2+
INC
energy deficit
deficit
INC energy
Cardiac
Cardiac
Remodelling
Remodelling

heartWork
heart- More
More Work
and
oxygen
and oxygen
consumption
consumption

RENIN-ANGIOTENSIN
RENIN-ANGIOTENSIN
ACTIVATION
ACTIVATION

ALDOSTERONE:
ALDOSTERONE:
(spironolactone)
(spironolactone)
Fluid retention
retention
Fluid
(diurteics).......
PRELOAD
(diurteics)....... PRELOAD
INCREASED!
INCREASED!
(venodilators)
(venodilators)

ANGIOTENSIN
II:
ANGIOTENSIN II:
(angiotensinII
receptor
(angiotensinII receptor
blockers)
blockers)
ARTERIAL
ARTERIAL
VASOCONSTRICTION......
VASOCONSTRICTION......
AFTERLOAD
AFTERLOAD INCREASED!
INCREASED!
Renal artery...
FLUID
Renal
artery... FLUID
RETENTION
RETENTION
PRELOAD
PRELOAD INCRESED
INCRESED

heartWork and
and
heart- More
More Work
oxygen
consumption
oxygen consumption

INC
INC Myocardial
Myocardial
Damage
Damage
INC
Ca2+ Overload
INC Ca2+
Overload
INC energy
energy deficit
deficit
INC
Cardiac
Cardiac
Remodelling
Remodelling

INC Myocardial
Damage
INC
Myocardial Damage
INC Ca2+
Overload
INC
Ca2+ Overload
INC
energy deficit
deficit
INC energy
Cardiac Remodelling
Remodelling
Cardiac

Reduced
Reduced CO
CO

Reduced
CO
Reduced CO

Reduced
Reduced CO
CO

Cardiovascular compensatory mechanisms and the detrimental positive feedback effects they exert in
HF.

CARDIAC EMERGENCIES: HYPERTENSIVE


EMERGENCY

Severe hypertension is
o
Systolic 220-240
o
Diastolic 120-140
Used to be called accelerated/malignant
hypertension, now based on presence/absence
LIFE-THREATENING END ORGAN DAMAGE.
(LTOD)- e.g. aortic dissection
This determines treatment urgency.
If organ damage, needs to be reduced to safe
levels (diastolic 100) within 2 hrs.
Caution: rapid fall in BP can cause strokes,
accelerated renal failure, cardiac ischemia.
If NO end organ damage. Gradual reduction
over 6-72hrs preferred.
Most common cause
o
Inadequate/discontinued therapy for
benign essential HT.

In under 30s or blacks, over 50% have a


secondary cause
o
Renovascular disease
o
Phaeochromocytoma
o
Endocrine
o
Drug induced catachlomine
release (cocaine)
o
Pregnancy related

Most end organ damage due to ARTERIOLAR


NECROTIZING VASCULITIS

And LOSS OF VASCULAR AUTOREGULATION

HYPERTENSIVE EMERGENCY

o
o
o

o
o
o

Clinical features of end organ damage (HTN)


ENCEPHELOPATHY
Decreased vascular auroregulation- cerebral oedema
Headache, nausea, vomiting, blurred vision,
confusion.
Later: Focal neurological deficits, seizures,
papilloedema, coma
PULMONARY OEDEMA
Due to Increased LV afterload (not fluid overload):
treat by reducing afterload.
PROGRESSIVE RENAL IMPAIRMENT
Increased urea and creatinine, dec GFR.
Haematuria, proteinuria
HTN can be secondary to glomerulonephritis and
renal artery stenosis- bruit?
STROKE SYNDROMES
o
Cerebral infarctions
o
Cerebral Heamorrhage
o
SAH
RETINOPATHY
o
Grade3: exudates and hemorrhage
o
Grade4: Papilloedema.
AORTIC DISSECTION
o
Tearing chest/back pain
o
Arm/leg BP difference
o
Absent peripheral pulses
ANGINA + MI
o
Due to inc LV afterload, inc wall stress, dec
myocardial perfusion
PREGNANCY RELATED

HYPERTENSIVE EMERGENCY: MANAGEMENT

Severe HTN with end organ failure:


REQUIRES ADMISSION!
Rarely, immediate BP reduction needed (eg.
Dissecting AA)
Potent, titratable, vasodilator infusions.
Arterial BP monitoring Mandarory!
IV Therapies:
o
SODIUM NITROPRUSSIDE (rapidly
reversible arterio-venous dilator)administered by infusion pump to avoid
hypotensive episodes.
o
GTN (arteriovenous dilator)- effective
when Myocardial ischemia and
pulmonary oedema there.
o
LABETALOL: alpha and beta blockergood for hypertensive encephalopathy.
May exacerbate asthma, HF, heart
block.
Severe hypertension with no end organ
damage
o
Use oral regimes when possible
o
Lower over 24-72 hrs
o
NIFEDIPINE (sublingual) rapid onset,
short half-life, titratable.

ACUTE PERICARDITIS
Infection (most viral), MI, Uremia,
Connective tissue disease, Trauma, TB,
Neoplasia. Dresslers syndrome.
DRESSLERS SYNDROME
o
2 weeks after an MI
o
Immulogically-mediated febrile
pleuropericarditis
Clinical features
o
Severe positional (relieved by sitting
forward)
o
Retrosternal chest pain
o
Pericardial rub on Ascultation
Investigations
o
ECG: CONCAVE ST-SEGMENT ELEVATION
IN ALL LEADS
o
Cardiac enzymes may be elevated
Manage
o
Antiinflammatory drugs (ASPIRIN)

INFECTIVE ENDOCARDITIS

PERICARDIAL EFFUSION

Infection, (TB), Uremia, MI, Aortic


dissection, myxedema, neoplasia,
radiotherapy.
Clinical features
o
Due to cardiac tamponade- when
pericardial effusion impairs ventricular
filling, reducing CO.
o
Breathlessness
o
Pericarditic pain
o
Acute cardiovascular collapse
Examination
o
Raised JVP- increases on inspiration.
o
Distant heart sounds
ECG
o
Reduced voltage
o
CXR (globular cardiomegaly)
o
ECHO- (pericardial fluid and cardiac
tamponade induced RV diastolic
collapse)- diagnostic.
Manage

Usually subacute
Infection of heart valves / endocardium
Causes a chronic illness when organism is nonvirulant (streptococcus viridans)
Can be ACUTE with virulent:
STAPHYLOCOCCUS
Common in
o
Elderly with degenerative aortic and mitral
valve
o
Prosthetic valves
o
Rheumatic fever
o
Congenital heart disease
Abnormal valves more susceptible to infection
after dental procedures.
Normal valves occasionally infected by virulent
organisms. (staphylococcal valve infection after IV
drug use)
CNS FEATURES
o
Embolic infarction
o
Abscesses
o
Meningitis
GENERAL INFECTION
o
Low grade fever
o
Lethargy, malaise
o
Anaemia, weightloss
CARDIAC
o
Murmurs
o
HF
o
Mycotic aneurysms
LATE SIGNS
o
Clubbing
o
Splenomegaly
JOINTS
o
Arthralgia
o
Septic Arthritis
SKIN
o
Vasculitis rash
SOLES OF FEET
o
Janeway lesion
IMMUNE COMPLEX DEPOSITION
o
RETINAL HEAMORRHAGES (Roth spots)
o
SUBCONJUNCTIVAL HEAMORRHAGE
o
SPINTER HEAMORAGES, NAILBED INFARCTS
o
JANEWAY LESIONS (small, red macular)
o
OSLERS NODES (subcut swellings in finger/toe
pulps, pain.
o
MICROSCOPIC HAEMATURIA
o
GLOMERULONEPHRITIS
o
LUNG: R. SIDED EMBOLIC INFARCT
o
LOSS PERIPHERAL PULSES
o
RENAL/CEREBRAL EMBOLIC INFARCTS
Diagnosis initially clinical
Suspected in fever, anaemia, high ESR or CRP,
microscopic haematuria, new heart murmurs, flulike symptoms, weightloss.
Confirmed by repeatedly positive blood cultures,
and ECHO confirm diagnosis.
Transthoracic ECHO detects under 50%
vegetations- transoesophageal studies better.

Manage
-

Look for and treat underlaying infection


(dental abscess?)
BENZYLPENICILLIN (empirical antibiotic
therapy)
Adjusted when know cultures.
Treat 3-6 weeks

WHAT TO DO IN CHEST PAIN EMERGENCY

AIRWAY
(patent, manouvres, adjuncts)
BREATHING
(no resp effort.. ARREST
TEAM)
CIRCULATION
(no pulse.. ARREST TEAM)
CALL FOR SENIOR HELP:
(unewell/
deteriorating)
SIT UP
15L/min OXYGEN
(sats under 94% / sob)
MONITOR
(pulse oximiter, BP, ECG,
Defib)
OBS:
(BP both arms,
ECG)
BRIEF Hx, /NOTES/ STAFF
EXAMINE:
(chest, Rx, Abdo)
ESTABLISH LIKELY CAUSES
RULE OUT SERIOUS CAUSES
CONSIDER
o
PCI / THROMBOLYSIS
o
ASPIRIN 300mg PO STAT
o
NEEDLE DECOMPRESSION
INITIATE FURTHER TREATMENT
(analegesia)
VENOUS ACCESS
o
FBC, U&E, LFT, CRP, gluc, cardiac
marker, D-dimer
o
CXR
Call senior help- worsening/ no improvement
No improvement? REPEAT ECG after 20MINS
REASSESS A, B, C
LIFE THREATENING CAUSES

NOTES ON EMERGENCY CHEST PAIN

MYOCARDIAL INFARCTION
TENSION PNEUMOTHORAX

Stable Angina
Musculoskeletal

Exertion pain
Lifting
Radiates to L arm/ Jaw
injury
-Impact
Under
20mins
May
be
pleuritic
STEMI
Breathlessness
Pneumonia
onwhen rest/GTN
-Worse
Dec
Sudden
onset pain
palpation/movement
Productive
sputum
- - Radiates
to L cough,
arm/ jaw
- Pleuritic
Dyspnoea
pain
- - Over
20mins
-- - -Resp
exam
normal
Tachycardia
Feels
unwell
Breathless,
nausea,
Tender
-sweating
Non-tender
Normal after pain goes
- - Febrile
-- - Normal
CXR
Asymmetrical
air entry
Dyspnoea
ECG
-Normal
Transient
changes
Corse
creps ECG
(unilateral?)
-- - Arrythmia
Troponin
not elevated
Dull
to percussion
- - -Sweating
-Non-tender
Positive stress ECG
CORONARY
ANGIOGRAPHY
- - INC
WCC
up
- - STCRP
elevation
CXR
- consolidation
New LBBB
- Increase cardiac Markers

WORRYING FEATURES
o
Inc/dec HR
o
Dec BP
o
Inc RR
o
Dec GCS
o
Sudden onset
o
Sweating
o
Nausea & vomiting
o
Pain to jaw/ L. Arm / Back
o
ECG Changes
THINK ABOUT COMMON
o
MI / ACS / ANGINA
o
PE
o
MUSCULOSKELETAL
o
PNEUMONIA
o
PNEUMOTHORAX (simple / tension)
o
PERICARDITIS
o
REFLUX, PEPTIC ULCER
UNCOMMON
o
AORTIC DISSECTION
o
CARDIAC TAMPONADE
o
SICKLE CELL CRISIS.
ASK ABOUT: Site, onset, radiation, quality (heavy/
aching/ sharp), intensity (1-10), time onset, duration,
associated symptoms (sweating, nausea,
palpitations, breathless), exacerbating or relieving
factors (breathing, position, exertion, eating), recent
trauma/exertion, previous episodes
PMHx: cardiac/ Resp problems / DM / GORD
DRUGS: Cardiac / respiratory meds, antacids
FHx: IHD / premature cardiac death
SH: Smoking / Exercise tolerance
INVESTIGATIONS
o
ECG
o
FBC, U&E, LFT, D-dimer, Cardiac markers, ABG
o
CXR- portable? Standard?
o
ECHO/ CT if large proximal PE/ aortic root
dissection.
TREAT:
o
15L OXYGEN
o
IV OPIOID
o
ANTI-EMETIC
Diagnosis to exclude
o
CARDIAC ISCHEMIA (ECG, Hx, Cardiac
markers)
o
PE (dec sats, ECG, risk, D-Dimer, CT-PA)
o
PNEUMOTHORAX (Mediastinal shift, dec
breath sounds)

Pericarditis
Pulmonary Embolism
----------

Hx viral-like illness
Breathlessness
Pleuritic pain
PE risk
factors
Increased
NSTEMI
on lying
Pleuritic
chest
painforwards
Decreased
sitting
Sudden
onset pain
Haemoptysis
Radiates to L arm/ jaw
Pericardial
Rub
Over 20mins
Oesophageal
Normal
exam
Otherwise
normal
CVS and
Breathless, nausea,
Spasm/reflux
May
Hx DVT (swollen red
RS
exams
sweating
Previous indigestion/reflux
leg)
Hiatus herniadyspnoea
Tachycardia/
Dyspnoea
Saddle-shaped
by antacids ST
Dec
BP
Arrythmia on most ECG
segments
Sweating
leads
Upperoxygen
abdo tender
ABG:
Dec
Non-tender
Inc
CRP & ESR
Normal
CV and RS
Clear CXR
Positive D-dimer
ST
DEPRESSON
Sinus
Tachycardia
ECGexclude
cardiac
S1Q3T3
CXR
normal
T-WAVE
INVERSION
Echo:
Thrombus
Antacids
trial
INC TROPONIN

AORTIC DISSECTION
-

Sudden onset
Severe inetrscapular pain
Tearing in nature
Breathlessness
Pneumothorax
Limb weakness /
ACS /numbness.
Unstable Angina
Sudden onset pleuritic
Anginal
pain at rest
chest
pain
Tachycardia
Inc
severity / freq /
Trauma
Decreased
BP
duration
Tall
and Thin
Difference
in brachial
COPD
pulses
and pressures
Dyspnoea
Increased
RR
Tachycardia
Mediastinal
shift
Limb
weakness
/
Non-Tender
Unequal
airway and
paraesthesia
Normal after pain resolves
expansion
Hyper-resonance
-CXR
WIDENED
ST depression
MEDIASTINUM
T waveseparated
Inversion from ribs
Pleura
-ECHO/
CT: Aortic
Troponin
on
CXR not elevated.
dilation
ANGIOGRAM: aortic

ACUTE CORONARY SYNDROME


-

General term- presentations of varying levels of myocardial


ischemia.
Management and outcome better if you know whats going on
exactly.
Typical sounding chest pain lasting over 20 mins?
o
New LBBB / ST elevation on ECG? 12hr Troponin will be
raised, but not needed for diagnosis: STEMI
o
Ischemia other than ST elevation on ECG?

NSTEMI:

(TropT: over 0.1) or

(TropI over 1)

ACS SERUM CARDIAC MARKERS


TROPONINS (I or T)

A protein: If theyre in the


blood- very likely myocardial
injury

Can be raised in PE, renal


failure, septicemia, after
tachyarrythmias

But CK not usually raised as


well in these conditions.

Detection can be 6hrs after


injury

Levels elevated for 14days

Troponins used as prognostic


indicator in UNSTABLE
ANGINA / NSTEMI
CK CREATININE KINASE

Enzyme found in all muscle


and released in muscle cell
lysis.

Not specific for cardiac


muscle

Peaks 24HRS post MI

Returns to normal, 48-72


hrs post-MI

Useful in detecting further


infarction in patients with
pain 3-14 days post MI.
CK-MB

Cardiac isomer of
CREATININE KINASE enzyme

More specific than total CK.

ST ELEVATION MI

WORRYING SIGNS: LV failure and cardiac dysrrythmia.


Central crushing heavy chest pain, (over 20mins)
Radiating to L arm/jaw
SOB, nausea, sweating, vomiting, palpitations, anxiety
RISK
o
Smoking, obesity, DM, Hypertension, cholesterol,
family, previous IHD.
SIGNS
o
ST Elevation (over 1mm in 2 leads, or 2mm in 1 lead)
o
New LBBB: subsequent Q waves, and T wave
inversion
o
CXR: Cardiomegaly, LV failure
o
Cardiac markers raised.
ACUTE TREATMENT (MONAC)
o
Rapid re-perfusion by percutaneous coronary
intervention (PCI) in those UNDER 12HRS SYMPTOMS.
o
IE: seek senior help

M: DIAMORPHINE 2.5-5mg IV

O: OXYGEN 15l/min

N: NITRATES: GTN: 2 puffs every 5 mins until no


pain- if still pain, give IV unless hypotensive.

A: ASPIRIN 300mg

C: CLOPIDOGREL 300mg

(ANTIEMETIC)
WHEN PCI NOT AVAILABLE WITHIN 3 HRS?
o
Fibrinolysis
o
Beta blocker: Bisoprolol 10mg/PO- limits mortality
and decreases infarct size- avoid in COPD,
hypotension, failure.
SECONDARY PROHHYLAXIS (BAN SCAR)
o
B: BETA BLOCKERS
o
A: ACEi
o
N: Nitrates (symptoms)
o
S: STATIN
o
C: Clopidogrel 1yr
o
A: aspirin lifetime
o
R: Risk factors (smoking, DM, obesity, BP, cholesterol)
COMPLICATIONS
o
Dysrhythmias

AV Block, Bradycardia, VF/VT

LVF

Valve prolapse

Ventricular septal rupture

Ventricular aneurysm formation

Pericarditis, Dresslers syndrome (pericarditis- fever,


pleuritic pain after heart injury)

Recurrent Pain
CARE AFTER MI
o
Bed rest 48hrs with continuous ECG
o
Daily 12lead ECG, and clinical examination
o
Thromboembolism prophylaxis
o
Beta blocker (unless contraindicated), ACEi, Statin
o
Discussion over modifiable risk factors, arrange cardiac
rehab
o
PRIMARY PCI: patients at lower risk of complications,

RISK STRATIFICATION IN ACS


o
o
o

Estimation of death allows


individualused assessment of risks
and benefits interventions
Careful targeting of resources to
those patients who stand to
benefit the most.
Validated scoring algorithms
o
TIMI: THROMBOLYSIS IN
MI RISK SCORE
GRACE: ACS RISK MODEL
Data from GLOBAL REGISTRY OF
ACUTE CORONARY EVENTS- huge
amount of info from many
countries.
o
Risk scores calculated on
admission
o
Predict in hospital and
6month mortality.
o
On discharge: to predict
6month mortality.
High risk?
o
Patients need a coronary care
unit bed.
o
Consider for glycoprotein
llb/llla inhibitors and urgent
catheterization
Low/intermediate risk?
o
Observation to ensure pain
free
o
Futher stratification using
exercise ECG, coronary
calcium scoring/ stress

NSTEMI

WORRYING SIGNS: LV failure and cardiac dysrrythmia.


Central crushing heavy chest pain, (over 20mins)
Radiating to L arm/jaw
SOB, nausea, sweating, vomiting, palpitations, anxiety
RISK
o
Smoking, obesity, DM, Hypertension, cholesterol,
family, previous IHD.
SIGNS
o
Same as STEMI
o
Patients tend to be older with more co-morbidities
than STEMI
o
ST DEPRESSION, INVERTED T WAVES
o
CARDIOMEGALY , FAILURE (CXR)
o
ELEVATEED TROPONIN (12hrs after worst pain)
ACUTE TREATMENT (MONAC)

M: DIAMORPHINE 2.5-5mg IV

O: OXYGEN 15l/min

N: NITRATES: GTN: 2 puffs every 5 mins until no


pain- if still pain, give IV unless hypotensive.

A: ASPIRIN 300mg

C: CLOPIDOGREL 300mg

FONDAPARINUX (anticoagulate)
Beta-blocker- Bisoprolol 10mg STAT- beware in
COPD, hypotension, failure

RISK STRATIFY: for ones needing bed in CCU,


catheterization or glycoprotein inhibotors.
SECONDARY PROHHYLAXIS (BAN SCAR)- same as
STEMI
o
B: BETA BLOCKERS
o
A: ACEi
o
N: Nitrates (symptoms)
o
S: STATIN
o
C: Clopidogrel 1yr
o
A: aspirin lifetime
o
R: Risk factors (smoking, DM, obesity, BP,
cholesterol)
COMPLICATIONS- same as STEMI, but less common
o
Dysrhythmias

AV Block, Bradycardia, VF/VT

LVF

Valve prolapse

Ventricular septal rupture

Ventricular aneurysm formation

Pericarditis, Dresslers syndrome (pericarditis-

STABLE ANGINA

UNSTABLE ANGINA

Retrosternal chest discomfort occurring predictably upon


exertion
Relieved by rest and nitrates.
SYMPTOMS
o
Central, heavy chest pain
o
Lasting under 20mins- radiating to L.arm and jaw
o
Precipitated by exertion, relieved by rest, or GTN in
under 5 mins
o
SOB, nausea, sweating, palpitations.
o
Tachycardia, cool, sweaty, clammy, pallor- normal after
episode.
ECG
o
Transient ST-depression during pain
o
Flat or inverted T-waves
o
Signs of previous MI
Cardiac markers not elevated!
PRIMARY PROPHYLAXIS- kind of the same.
o
B: BETA BLOCKERS
o
A: ACEi
o
N: Nitrates (symptoms)
o
S: STATIN

WORRYING SIGNS: LV failure and cardiac


dysrrythmia.
Central crushing heavy chest pain, (over
20mins)
Radiating to L arm/jaw
SOB, nausea, sweating, vomiting,
palpitations, anxiety
Typically, episodes of angina, occurring
at rest or minimal provocation, with poor
response to GTN.
More frequent and painful than usual.
RISK
o
Smoking, obesity, DM,
Hypertension, cholesterol,
family, previous IHD.
SIGNS
o
ST DEPRESSION, INVERTED T
WAVES
o
Dynamic ECG changes over
time
o
Signs of previous MI?
o
Troponin not elevated.
ACUTE TREATMENT (MONAC)

M: DIAMORPHINE 2.5-5mg IV

O: OXYGEN 15l/min

N: NITRATES: GTN: 2 puffs


every 5 mins until no pain- if still
pain, give IV unless hypotensive.

A: ASPIRIN 300mg

C: CLOPIDOGREL 300mg
PLUS! BETA-BLOCKERS to limit
ischemia
FONDAPARINUX (disrupt thrombus)
o

Same further management as


NSTEMI

SECONDARY PROHHYLAXIS (BAN SCAR)same as STEMI

PERICARDITIS

Pleuritic chest pain


Worse on laying flat and deep inspiration
Relieved by sitting forward, recent viral
illness
SIGNS?
o
May be none
o
Pericardial rub
ECG
o
Saddle shaped ST segments in
most leads
BLOODS
o
High WCC
Inflammatory markers
ECHO
o
Pericardial Effusion
TREAT
o
Acutely- reassurance and
anaelgesia
o
Paracetamol, NSAIDS
o
Should settle 2-4 weeks

AORTIC DISSECTION

Aortic dissection occurs when a tear in the inner wall of the aorta causes blood to flow between the
layers of the wall of the aorta, forcing the layers apart.
Severe characteristic chest or abdominal pain- "tearing" with other symptoms from decreased blood
supply to organs.
Aortic dissection is a medical emergency and can quickly lead to death, even with optimal treatment, as
a result of decreased blood supply to other organs, cardiac failure, and sometimes rupture of the aorta.
More common: high blood pressure, known thoracic aortic aneurysm, Marfan syndrome, EhlersDanlos
syndrome.
The treatment of aortic dissection depends on the part of the aorta involved.
Surgery in dissections that involve the aortic arch, while dissections further away from the heart treated
with blood lowering BP (systolic under 100)
SYMPTOMS
o
Sudden onset, severe chest pain
o
Anterior or interscapular
o
Tearing in nature
o
Dizziness, breathlessness, sweating, neurological deficits
RISK FACTORS
o
Smoking
o
Obesity
o
DM
o
High BP
o
Increased Cholesterol
o
Family history
o
IHD
SIGNS
o
Unequal radial pulses
o
Tachycardia
o
Hypertension/ Hypotension
o
Difference in brachial pressures of over 15mmHg
o
Aortic regurg
o
Pleural Effusion (left more than right)
o
Neurological defects from carotid artery dissection
INVESTIGATIONS
o
ECG normal/ show LV strain or ischemia.
o
CXR widened mediastinum over 8cm (rare)
o
Blood can track down and cause irregularity of aortic knuckle and small left pleural effusion
o
ECHO: shows aortic root leak, aortic valve regurg, pericardial effusion
o
Consider MRI/CT
ACUTE TREATMENT (HYPOTENSIVE? Treat as shock)
o
Senior help!!!
o
OXYGEN (15/min)
o
CANNULA (2 large bore)
o
BLOOD: X-MATCH 6units
o
OPIDOIDs (anaelgesia)
TREATMENT
o
Surgery: for type A (Ascending aorta)

TACHYARRYTHMIAS EMERGENCY!!!

AIRWAY: (patent, manouvres,


adjuncts)
BREATHING (no resp effort- crash
team)
CIRCULATION (no pulse, crash team)
SENIOR HELP! If patient unstable
o
Reduced GCS
o
Systolic under 90
o
Chest pain
o
HF
SIT UP (if hypotensive, lay flat, legs
up)
OXYGEN (15l/min- non rebreather)
MONITOR
o
Pulse oximiter
o
Defib paddles
o
BP
o
ECG leads
Request full set obs and ECG
Hx- BRIEF, CHECK NOTES, MEDS, ASK
STAFF
EXAMINE- CV, resp, Abdo
LIKELY CAUSES and SERIOUS CAUSESestablish
INITIATE FURTHER TREATMENT
VENOUS ACCESS
o
Bloods
o
FBC
o
U+E
o
D-Dimer
o
Cardiac Markers
o
TFT
Consider requesting urgent CXRportable
Reassess ABC

LIFE THREATENING CAUSES

VT
VF

ADULT TACHYCATRDIA WITH PULSE ALGORHYTHM


UNI! unstable? narrow? Irregular?
1.

2.
3.

4.

FIRST
Assess ABCDE
Oxygen and IV access
Monitor: EGC, BP, Sp02, 12-lead ECG
Identify and treat reversible causes.. electrolytes?
ADVERSE FEAUURES?
Myocardial Ischemia, HF, Shock, Syncope.
(My hearts So Speedy)
YES UNSTABLE!!! (adverse features)
o
SYNCHRONISED DC SHOCK
o
Up to 3 attempts
o
AMIODARONE 300mg IV (10-20mins)
o
Repeat shock followed by
o
AMIODARONE 900mg over 24hrs.
NO STABLE
o
IS QRS NARROW OR BROAD??

BROAD QRS

5. REGULAR / IRREGULAR?

NARROW QRS

5. REGULAR /
IRREGULAR?

Regular
Regular

VT (AMIODARONE)
o
300mg Over 20mins
o
900mg over 24hrs
SVT with BBB
(ADENOSINE)

Irregular

AF with BBB
Pre-Excited AF
(AMIODARONE)
POLYMORPHIC VT eg.

Use vagal manouvres


ADENOSINE (6mg rapid
IV bolus, then give 12 if
needed , then 12)
SINUS RHYTHEM
BACK??
If now sinus rhythem,
was probably REENTRY PAROXSMAL
SVT
NO SINUS RHYTHEM?
ATRIAL FLUTTER:
beta blocker.

Irregular

IRREGULAR, NARROW
COMPLEX TACHCARDIA
Probably AF
o
Beta blocker
o
Diltazem

TACHYARRYTHMIAS
TACHYARRYTHMIAS
SINUS TACHYCARDIA
Worrying Features

Decreased GCS
Dec BP (systolic under 90)
Chest Pain
HF

Causes

FAST AF

Common
o
Sinus Tachycardia
o
Fast ventricular rate in AF
o
SVT
o
Atrial Flutter
o
Physiological: shock, sepsis
Uncommon
SVT
o
VT
o
Re-entrant tachycardia (Wolf-Parkinson)

Ask about

Onset
Associated Symptoms (chest, SOB, dizziness,
palpitations, facial flushing, headchaes)
VT (pulseless/pulse)
Previous
PMHx: Cardiac (IHD, valve lesions, HTN), Thyroid, DM
Drugs: Cradiac, Levothyroxine, salbutamol,
anticholinergics, caffeine, nicotine
Smoking, Alcohol, Drugs

Observations: UNSTABLE?

VFBP, Cap-refill, RR, oxygen sats, GCS, temp


Pulse,
Look for worrying/ unstable features (My hearts so
speedy)

ECG:

SINUS.. 100, P before QRS


AF..100, Irregular QRS with no p (new
Torsades de pointes
onset?)
ATRIAL FLUTTER. Sawtooth baseline
SVT. 140, Narrow (help, get drugs ready)
VT.150, Broad Complex- check for pulse
(arrest team if none)
FBC, U&E, TFT, CRP, (D-DIMER, Cardiac Markers,
X-match)

WOLF-PARKINSON WHITE SYNDROME

A re-entrant tachycardia
Due to accessory conduction pathway (bundle of kent) between atria and ventricles.
SHORT P-R INTERVAL and DELTA WAVE
Avoid Digoxin and verapamil
Refer to cardiologist for ablation

ATRIAL FIBRILLATION
WARNING SIGNS
o
HF
o
Hypotension
o
Decreased GCS
o
Chest pain
SYMPTOMS
o
SOB
o
Palpitations
o
Dizziness
o
Chest Pains
RISK FACTORS
o
Previous AF
o
BP
o
IHD
o
Valvular heart disease
o
PE
o
Pneumonia
o
Thyrotoxicosis
o
Alcohol (acute excess, chronic
misuse, withdrawal)
o
Dilated cardiomyopathy
o
Age
o
Acute illness
COMPLICATIONS
o
Thromboembolic disease (ischaemic
stroke)
o
Drug side effects (amiodarone, warfarin,
beta blockers, digoxin)
SIGNS
o
Irregularly irregular pulse
SVT
o
Hypotension
(CV compromise)
o
Signs of disease (thyrotoxicosis,
pneumonia)
WARNING
SIGNS
Investigate
o
HF
o
Absent
p waves
o
Hypotension
o
Irregularly
irregular QRS
o
Decreased GCS
o
WCC
highbloods?
Infection?
o
Chest pain
o
U&E
SYMPTOMS
o
o TFT?
SOB
o
o Alcohol
Palpitations
o
o D-Dimer
Dizziness(PE?)
o
(if ischemic episode
o Troponin
Chest Pains
responsible?)
RISK FACTORS
o
Previous SVT
o
Structural cardiac anomaly
o
Alcohol
o
Increased T4 (thyroid)
COMPLICATIONS
o
Hypotension,
o
Ischemia,
o
HF,
o Deterioration into more sinister
arrhythmia.

ATRIAL FIBRILLATION- treat


TREAT:
-

Haemodynamically compromised?
Help, shock?, oxygen, iv access,
cardioversion (AMIODARONE)

CONSERVATIVE

Treat the precipitant (sepsis?) if new


onset and this is obvious

RATE CONTROL

Control Tachycardia to reduce


myocardial metabolic demand BETA
BLOCKER / DILTIAZEM or
VERAPAMIL (a rate limiting CCB)
DIGOXIN (added in when the
previous were insufficient- not 1st line)

RHYTHEM CONTROL

Younger patients/ those with new AFsuitable for attempted cardioversion


FLECAINIDE: (if doesnt have IHD)
AMIODARONE (IV through central line
if has IHD)
DC CARDIOVERSION (under sedationanother option)
Maintain sinus rhythm if successful,
SVT
with beta-blocker

ANTICOAGULATION
SIGNS
o
Tachycardia
Anxiety
oIn all
patients where a rate control
ostrategy
Hypotension
(compromise)
is adopted
(rather than
rhythem).
Investigate
oCanNarrow
use aspirin
75mg tachycardia
evey day.. or
complex
other
drugs-have
basedBBB
on stroke
(unless
too) risk
oassessment.
P waves merge into the QRS
Anticoagulation
be achieved
can be hardmust
to see
before
any planned
o4weeks
Regular
QRS
o
Rate over 140
Acute Treatment
o
Oxygen
o
2 large bore cannula
o
Monitor rhythem on defib
o
Vagal manouvres
o
cardioversion
o
If recurrent, cardio might need to
test conduction pathways.

VENTRICULAR TACHYCARDIA
WORRYING SIGNS
o
HF
o
Hypotension
o
Decreased GCS
o
Chest pain
o
PULSELESS!!!!!!!!
SYMPTOMS
o
SOB
o
Palpitations
o
Dizziness
o
Chest Pains
o
ARREST!!!
RISK FACTORS
o
IHD
o
Trauma
o
Hypoxia
o
Acidosis
o
Long QT
COMPLICATIONS
o
May deteriorate into VF or other
dysrhythmia
SIGNS
o
Tachycardia
o
Anxiety
o
Pallor
o
Hypotension
o
Decreased GCS/ shock
Investigate
o
ECG: Broad complex tachycardia
o
Absence of p waves
o
Rate over 150
o
Check U&E urgent! Especially K! and
MG2+!
o
Cardioversion the main priority
Acute Treatment
o
Pulseless VT? Call arrest team, commence
ALS after precordial thump
o
Pulse? Oxygen, large bore cannula
o
Drugs: SOTALOL, AMIODARONE
o
DC CARDIOVERSION
o
Possible SVT with bundle branch block? Or
VF? Treat as VT
Chronic Treatment
o
Implantable cardiovertor/ defib
*** NB: Torsades de pointes looks like FB but with a

BRADYARRYTHMIAS
EMERGENCY!!!

AIRWAY: (patent, manouvres,


adjuncts)
BREATHING (no resp effort- crash
team)
CIRCULATION (no pulse, crash
team)
SENIOR HELP! If patient unstable
o
Reduced GCS
o
Systolic under 90
o
Chest pain
o
HF
SIT UP (if hypotensive, lay flat, legs
up)
OXYGEN (15l/min- non rebreather)
MONITOR
o
Pulse oximiter
o
Defib paddles
o
BP
o
ECG leads
Request full set obs and ECG
Hx- BRIEF, CHECK NOTES, MEDS,
ASK STAFF
EXAMINE- CV, resp, Abdo
LIKELY CAUSES and SERIOUS
CAUSES- establish
CONSIDER
o
IV ATROPINE
500micrograms
o
Repeat every 2-3 mins
o
Max 3mg (6x)
BRADYARRYTHMIAS
EMERGENCY!!!
INITIATE
FURTHER TREATMENT
o
Transcutaneous pacing
VENOUS
ACCESS
THINK ABOUT
Bloods
o o SINUS
BRADYCARDIA
o
FBC
After an inferior MI (gets the SA
o
U+E
node)
o
D-Dimer

Drugs (digoxin toxicity)


o
Cardiac
Markers
Vasovagal
o
TFT
Low thyroxine
Consider requesting
urgent CXR
Hypothermia
portable

Cushings reflex (bradycardia


Reassess ABC
and hypertension secondary to

increased ICP)
Sleep
Anorexia nervosa
Physical fitness

ASK ABOUT
o
Dizziness
o
Postural dizziness
o
Fits/faints
o
Weight change
o
Visual disturbance
o
Nausea and vomiting

PMHx: Cardiac Disease (IHD/AF), Thyroid surgery,


DM, Intercranial pathology/ head injury, glaucoma,
eating disorder.
Drug Hx: Cardiac meds, (Beta blockers, Ca2+
antagonists, amiodarone, digoxin)
Social Hx: Exercise tolerance, IHD risk factors
OBS

LOOK

HR,
BP,
Postural BP
RR
Sats
FOR
Pulse rate/rhythem
Volume
Pallor
SOB
Dec GCS
Drowsy
Inc JVP (cannon waves in 3rd degree AV
block)
Signs of cardiac failure (increased JVP,
pulmonary oedema, swollen ankles)

Investigate Bradyarrythmia
o
ECG:

Sinus bradycardia/ complete


heart block

Evidence ischemia/infarction

Evidence digoxin toxicity


o
Bloods

FBC

U&E

Glucose

Ca2+

Mg2+

TFT

Cardiac markers

Digoxin level

Coagulation (if considering


pacing wire)
o
CXR

Not really helpful, but may reveal


heart size or pulmonary oedema.
o
HEAD CT

If suspect raised ICP- but would be


in extremis ie. About to coneneed neurosurgeon

BRADYARRYTHMIAS ON AN ECG

VASOVAGAL ATTACKS

Sudden reflex bradycardia from unopposed


parasympathetic nervous inhibition is
common.
Light-headedness, visual disturbance,
nausea and sweating, then brief LOC,
Prompt recovery of consciousness
Precipitants:
o
FEAR
o
PAIN
o
POST-MICTURITION
o
NAUSEA AND VOMITING
o
DILATION ANAL SPHINCTER AND CERVIX
o
PULLING OF EXTRA-OCULAR MUSCLES
o RAISED ICP (straining etc)

SINUS BRADYCARDIA
o
P before every QRS
1st DEGREE AV BLOCK
o
P-R interval over 0.2 secs (5 small squares)
MOBITZ 1 (WENKEBACH)
o
P-R intervals lengthen from beat to beat
o
Until failure of AV conduction, then pattern
restarts
MOBITZII
o
Intermittent P waves fail to conduct to
ventricles
o
But P-R does not lengthen (unlike MOBITZ1)
o
Typically 2:1
o
3:1 and above are considered high grade AV
block
DIGOXIN EFFECT TOXICITY
o
Down sloping ST segment- often present
even when drug at non-toxic levels
RATE CONTROLLED AF

SINUS BRADYCARDIA
DRUGS PRECEEDING BRADYCARDIA

Worrying: HF, Hypotension, decreased GCS


BETA
BLOCKERS (even in eye drops)

Symptoms:
DIGOXIN
(if patients in AF revert to sinus)
o
None?
Ca2+oANTAGONISTS
that slow on
HRstanding
Dizziness, especially
o
VERAPAMIL
o
Recurrent falls
o
DILTIAZEM
o
Palpitations
AMIODARONE
o
SOB can cause bradycardia
A-AGONISTS:
PNENYLEPHERINE
o
Symptoms
of raised ICP used by
anaethatistsincreased decreased
PVR so causes
o
Hypothermia/
T4 reflex
brady.
ECG
o
QRS preceeded by a P-wave
SICK
SINUS
SYNDROME
o
Rate
under
60
o
QRS narrow unless BBB
o
Exclude ischemia and infarction
Dysfunction of the SA Node

BLOODS
Precipitated by ischemia/fibrosis
o
FBC
Results in bradycardia/ arrest
o
U&E
SA block/ SVT with alternating
o
Ca2+
bradycardia/asystole
o
Mg2+
Tachy-brady syndrome
o
TFT
Needs opacing
if symptomatic.
Cardiac
markers
o
Coagulation (if considering pacing wire)

OTHER TYPES OF BLOCK

1st Degree and MOBITZ1


o
no treatment unless symptomatic or
reversible cause.

MOBITZ2 and HIGH GRADE AV BLOCK


o
Can deteriorate into complete heart
block
o
May need temp/permanent pacing
o
Espesh when associated with ACS/

COMPLETE 3rd DEGREE HEART BLOCK

ACUTE
If symptomatic or dizzy (GCS under 15)
Or systolic under 90bpm
Monitor HR on defib
Lay flat with legs elevated, as long as
ICP not raised.
o
OXYGEN, ACCESS, BLOODS,
worrying signs? ARREST
Titrate 500micrograms ATROPINE
Every 2-3 mins, up to 5mg
Followed by large flush, until HR improves
Identify correct precipitant
Consider pacing wire via central line/ external
pacing
A precordial thump (percussion pacing) can
be used in extremis, when an external pacing
machine not immediately available.
o
o
o
o

CHRONIC
o
o
o

Consider 24hr tape


Frequent symptomatic episodes of
bradycardia/pauses are a sign of SICK
SINUS SYNDROME
May need a permanent pacemaker.

COMPLICATIONS

Severe bradycardia and high vagal tone can

Worrying?
o
HF, Hypotension, Decreased GCS
Symptoms
o
None? Dizzy? Palpitations? SOB? Chest
pain?
Causes
o
Underlying ischemic damage (inferior MI)
o
Post cardiac surgery
o
Drug induced (beta blockers, Ca2+
blockers)
o
Amyloid, Sarcoid, Myeloma, Infective
(Lyme)
Signs
o
Decreased BP / GCS
o
Cannon waves in increased JVP (due to
asynchronous of right atria against
closed tricuspid valve
o
HF signs/ underlaying disease
Investigations
o
ECG: complete dissociation of p waves
from QRS
o
Narrow QRS implies proximal lesion
(responds to atropine)
o
Broad implies distal lesion (less likely to
respond to atropine)
o
Look for evidence MI
o
FBC, U&E, Ca2+, Mg2+ TFT, markers,
coagulation
ACUTE: ATROPINE / external pacing
CHRONIC: pacemaker/ correct precipitant
COMPLICATIONS
o
Severe bradycardia and high vagal tone
can deteriorate into asystole- prompt
treatment required
o
Talk contunially

HYPERTENSION EMERGECNY

AIRWAY:
Patent? Manouvres?
Adjuncts?
BREATHING:
No resp effort? ARREST
CIRCULATION:
No pulse? ARREST
DISABILITY: GCS under 8? Anesthetist
o
o
o
o

o
o
o
o
o
o
o

o
o
o

IF SYSTOLIC OVER 200, DIASTOLIC 120


Sit up
OXYGEN (15l)- if SOB/ sats under 94%
MONITOR

Pulse oximiter

BP

Defib leads- if unwell


Request full set OBS and ECG
Bried HX / NOTES/ Ask staff
Examine

RS, CVS, abdo, EYE


Rule out serious causes, establish likely
causes- is it new??
DO NOT GIVE STAT DOSE ANTIHYPERTENSIVE WITHOUT SENIOR REVIEW
Further treatment
ACCESS

FBC, U&E, markers, TFT, glucose,


cortisol
Consider urgent CXR
Urinalysis and bHCG (if childbearing age)
Senior advice reassess, ABC

Life threatening causes

PRE-ECLAMPSIA/ ECLAMPSIA
MALIGNANT HYPERTENSION (200/120)
HYPERTENSIVE ENCEPHALOPATHY
PHAEOCHROMOCYTOMA

HYPERTENSION EMERGECNY

AIRWAY:
Patent? Manouvres?
Adjuncts?
BREATHING:
No resp effort? ARREST
CIRCULATION:
No pulse? ARREST
DISABILITY: GCS under 8? Anesthetist
o
o
o
o

o
o
o
o
o
o
o

o
o
o

IF SYSTOLIC OVER 200, DIASTOLIC 120


Sit up
OXYGEN (15l)- if SOB/ sats under 94%
MONITOR

Pulse oximiter

BP

Defib leads- if unwell


Request full set OBS and ECG
Bried HX / NOTES/ Ask staff
Examine

RS, CVS, abdo, EYE


Rule out serious causes, establish likely causesis it new??
DO NOT GIVE STAT DOSE ANTI-HYPERTENSIVE
WITHOUT SENIOR REVIEW
Further treatment
ACCESS

FBC, U&E, markers, TFT, glucose,


cortisol
Consider urgent CXR
Urinalysis and bHCG (if childbearing age)
Senior advice reassess, ABC

Life threatening causes

PRE-ECLAMPSIA/ ECLAMPSIA
MALIGNANT HYPERTENSION (200/120)
HYPERTENSIVE ENCEPHALOPATHY
PHAEOCHROMOCYTOMA

HYPERTENSION: 140/90

SYSTIOLIC over 140


DIASTOLIC over 90
Worrying: Altered mental state, seizures, retinal hemorrhages, acute renal failure, chest pain
CRISIS!??!?? Over 200 or over 120!
Think about
o
Is it a hypertensive crisis? 200/120, or pre-eclampsia?
o
Other: anxiety, pain, primary (essential) or secondary (thyroid storm, pheochromocytoma).

PHMx of, and signs of disease


o
Previous hypertension
o
Phaeochromocytoma
o
Coarctation aorta,
(Radiofemoral delay)
o
renal artery stenosis
(renal bruits)
o
Thyroid disease,
(Tremor, exopthalmus)
o
DM,
o
Conns syndrome,
o
Cushings,
(Straie, central obesity)
o
Acromegaly
(large hands, feet, face)
o
Pregnancy
(gravid uterus)

Drugs
o
Cardiac meds and Antihypertensives
o
Steroids, Contraceptive pill, Levothyroxine/carbimazole, MAOI, antipsychotics
o
Coke and amphetamines

Family
HYPERTENSIVE CRISIS
o
Hypertension, endocrine disease, polycystic kidney disease

Social: exercise tolerance and smoking.

Elevation of BP iver 200 is a

END ORGAN DAMAGE?


HYPERTENSION:
140/90 hypertensive retinopathy)
hypertensive emergency
o
Fundoscopy
(papilloedema,
When accompanied by end-organ
o
LV hypertrophy: displaced apex beat of S4
damage INVESTIGATIONS
o
Haematuria
KEY SECONDARY CAUSES

Hypertensive urgency when no end


o
RENAL ARTERY DISEASE/STENOSIS
organ damage

Renal failure

BP:

Abnormal urine dipstick


o
Confirm with ambulatory
END ORGAN DAMAGE

Renal bruit
measuring

Family history may be relevant

ECG:

CNS
o
LV hypertrophy?

Urine Microscopy
o
Decreased GCS, confusion

Bloods:

Renal Doppler USS


o
Headache
o
FBC,
U&E, Glucose,

Autoantibodies
o
Vomiting
cholesterol,
TFT

Renal biopsy
o
New motor weakness

Urine o
o
PHAEOCHROMOCYTOMA
Seizures, coma

Sweating
TREATMENT
o
CT
may show a SAH, ICH,

Labile
hypertensive encephalopathy

Hypertension
occurs with cerebral oedema

Smoking cessation

Palpitations
following loss of vascular

Regular exercise
auto-regulation.

Plasma metanephrines

Reduce
alcohol and caffeine intake
EYES

24hr urine catachlomines and VMA

Balanced
diet
o low-salt
Headache
(norepinephrine becomes

Modifiable
risk factors:
DM, lipids
vanillylmandelic acid)
o
Visual
Disturbance
o
THYROID DYSFUNCTION
o
Fundoscopy
shows retinal

PHARMACOLOGICAL
THERAPY

Cold
hemorrhage, and

Heat intolerance, sweating


Complications papilloedema.
are end organ damage and
malignant
HEARThypertension

Lack of energy
o
Chest pain

TFTs
o
Orthopnea
o
ACROMEGALY
o
ECG changes,

Headache
o
Elevated cardiac markers

Visual Field disturbance


o
Pulmonary oedema on CXR

Change in facial features

AORTA

IGF-1
o
Sudden, tearing chest pain

Pituitary hormone levels


radiating to back
o
CUSHINGS SYNDROME
o
Collapse

Centripetal obesity
o
Echo/CT may reveal oertic

Skin thinning, weakness


dissection

Urinary free cortisol

PHARMACOLOGICAL TREATMENT

Everyone
o
HYPERTENSIVE 160/100 (aim for 140/90)
or (150/90 if over 80)
o
TYPE2 DIABETES: if end organ damage aim
for under 130/80- microalbuminuria, or eGFR
under 60, retinopathy, Hx TIA/stroke
o
TYPE1 DIABETES:
o
HYPERTENSIVE PATIENTS: with existing
cardiovascular disease/end-organ damage,
or predicted 10year risk CV disease over
20%
Under
55
Under 55

Over
Over
55/Black
55/Black

A&C

A&C

A, C, D

A, C, D

CARDIAC HISTORY AND EXAMINATION

A: ACEi / Angiotensin receptor blockers (RAMIPRIL)

C: Calcium Channel Blockers (AMLODIPINE,


INSPECTION
OVERALL:
o
ECG monitor suggestive? Pain? Cannula? Malar flush? (mitral stenosis), tachypnea (HF),
Cyanosis (HF), Forceful neck pulsations eg. Carotid (aortic regurg), ankle oedema (HF)
HANDS:
Splinter haemorrhages
HYPERTENSIVE
(IE)
CRISIS- Treat ACUTELY
Clubbing (IE or congenital cyanotic heart disease- caused by supperative disease ie that can
lead to pus filled cavities- Chrohns, UC, empyema, bronchiectasis, CF, fibrosis).
NO end organ damage
o
Pallor,
o
Peripheral cyanosis,

Calcium
or ACEi (A or C)
o Channel
nicotineBlocker
staining
o
cap refill (Over 2 secs dehydration or PVD)
END ORGAN
o DAMAGE
Asterixis- flap sign of CO2 retention (dont confuse with tremor from b2 agonist salbutamol, or
parkinsonian)
NECK:
Admit
to HDU or ICU
JVP

Close omonitoring
of BP, ECG, neurological state, Fluid balance
FACE:line, central line, catheterization)
(arterial
Malar flush

Rapid oreduction
in BP can be dangerous due to cerebral hypoperfusion
o
Anaemia
conjunctiva

Only necessary
in ACUTE
MI / AORTIC DISSECTION
o
Central

Otherwise,
aim to Cyanosis
reduce diastolic to 100 or by 25% (the higher one), over 24hrs
o
Hypercholersterolemia:
Xantholasma

More severe
end organ damage needs
IV therapy, otherwise oral is okay
o
Breathing
difficulty

No evidence LV failure? LABETALOL


VLCHEST:
Failure? HYDRALAZINE (vasodilator) and FUROSEMIDE
o
Hands on hips to expose lateral chest walls. Look at back too.

ACEi helps to counteract high circulating renin


o
Scars: Midline sternotomy- valve replacement or bypass? If bypass, scar on leg from where artery
In CVA (acute
stroke),
thecerebral
auroregulation
be backimpaired
and aggressive
lowering
of BP
taken.ischemic
Thoracotomy
scar:
Scar left axilla
diagonallycan
down
previous
mitral stenosis
(or line
causes hypoperfusion
and
poor outcome
from L breast to
axilla)
o
Deformities: sternal depression, scoliosis, kyphosis- can displace apex beat and cause ejection
systolic murmur.
o
Apex- look for cardiac pulsation
o
o

PALPATION

ARMS:
o
Radial pulse: rate, rhythm, character

Brady (under 60), Beta-blockers, heart block, hypothyroidism, young


Tachy (over 100), anxiety, exercise, pyrexia, hyperthyroidism, beta2 agonists (salbutamol),
hypovolemic shock, arrhythmia.

Radio-radial delay

Aortic dissection

Proximal arterial disease (atherosclerosis of axillary artery)


Radio-femoral delay

Co-arctation of the aorta (stricture of the aortic arch, distal to the L. Subclavian artery)

Delayed and weak femoral pulse

Other things pointing to co-arctation? Raised BP, continuous murmur over scapula, systolic
murmur L sternal edge (P/T)
Collapsing pulse

Aortic regurgitation

Ask if pain in shoulder


BP

Sitting and standing

Hypertrophic obstructive cardiomyopathy.

NECK:
o
Carotid pulse (edge of adams apple and move back)

Pulse character- valvular lesions cause it to be abnormal


Slow rising, then plateau (aortic stenosis)
Fastrising (watrehammer) and fast falling (collapsing) : (arotic regurg)
Bissfiriens Pulse (double impulse): Mixed aortic valve disease- both stenosis and regurg
Other- character abnormalities are usually due to aortic valve problems, or things like
hypertrophic obstructive cardiomyopathy.
Comment on pulse volume, and how quickly it rises and falls
o
JVP
45deg, look to left, look just above clavicle at 2 heads sternocleidomastoid
JVP is an approximate measure of pressure in RA (as right internal jugular vein
communicates directly with RA)
Lay at 45deg, - should be visible at level of clavicle between 2 heads of
sternocleidomastoid. If elevated- pulsation seen further up neck.
Carotid vs jugular: JVP cant be palpated and has a double wave waveform.
Hepatojugular reflex: pressing on R Hypochondrium (liver) to try and inc visibility
(JVP: Internal jugular lays between 2 heads- sternal and clavicular of SCM, external is more
superficial, and lateral to 2 heads)
Causes of raised JVP

Right HF: common. Secondary to LHF.

Fluid overload: kidney failure, excessive intake.

Tricuspid regurg: Massive V wave on JVP waveform.

Common heart block: Atrioventricular dissociation, and A and V contractions not


co-ordinated. Giant wave produced when atria contracts when tricuspid valve
closed so huge atrial pressure.

SVC onstruction: elevated without pulsation. Distended. Hepatojugular reflex


neg- due to mediastinal lymphadenopathy- lung cancer.

AF: no atrial systole, - JVP has no A wave.

CHEST:
o
Palpate Apex beat (placement and character)

Mitral Stenosis: Tapping, not displaced- you feel the normal apex beat plus the closure of
the valve- on auscultation sounds like a loud 1st heart sound. Apex more abrupt and feels
like tapping.

Aortic stenosis and Hypertension: Both obstruct cardiac output. Extra strain and
hypertrophy. Apex sustained and heavy, displaced down and out.

Mitral and aortic regurgitation: Backflow of blood causes large L ventricle. Apex displaced
down and out. Character unchanged as outflow of ventricle the same.

LV dilation: heart failure, apex displaced down and out

Cant palpate apex?

Emphysema (overinflation)

Pericardial effusion

Dextrocardia
Heaves and Thrills

Thrills: murmur producing a palpable sensation. Aortic stenosis produces a thrill in aortic
area

Feel with palm of hand over 4 valve areas

Parasternal Heave: 4th intercostal space, lateral to sternum LHS

Mitral: 5th intercostal space, midclavicular line LHS

ASCULTATION
o
o

A, P, T, M
Roll to axilla, mital area for mitral stenosis (diastolic)

Places to Listen

Altered Heart sounds

Mitral regurgitation and aortic stenosis


Both Pan-systolic (aortic stenosis also classed as ejection systolic)

Aortic stenosis

Splitting of Heart sounds (LUB SPLAT):


Extra sound after S2 is called P2, Normal finding in
inspiration
Loud S1 (LUUBB!dub)
Mitral stenosis- narrowed valve, shuts quicker, louder sound
Soft S1 (lubDUB)
Mitral regurg, valve not completely closed
Soft S2
Aortic stenosis (reduced valve movement)
Wide fixed splitting of S2
ASD
Prosthetic heart sounds
Metallic clicking sound

Brief systolic murmurs

Aortic: 2nd intercostal space, midclavicular line RHS


Pulmonary: 2nd inercostal space, lateral to sternum LHS
Tricuspid: 4th intercostal space, lateral to sternum LHS
Mitral: 5th intercostal space, midclavicular line LHS

More clinically severe than mitral regurg


Can cause
o
Hypotension
o
LV enlargement
o
Congestive heart failure
o
Cold peripheries
Heard over Aortic area, radiates to carotids
(murmur in carotids but not atrial area probs a carotid bruit)
Shorter than mitral regurg, crescendo-decrescendo sound

Mitral Regurg (lubb swoosh-dub)

A bit quiteter
Heard in apex, radiates to axilla
Causes
o
Rheumatic heart disease, IE, IHD, Post-MI, Cardiomyopathy, AF, Congenital

DIASTOLIC MURMURS

Aortic
Mitral
o
o
o
o
Aortic
o
o
o

regurgitation
stenosis
Mid diastolic murmur (click whoosh)
Associated with AF
Lay on LHS, listen to mitral area
Caused by rheumatic fever
regurg
Early diastolic murmur
High pitched, starts loud and lets quitter
Heard sitting up and forwards at L sternal edge, patient holding breath at end of expiration.

Extra heart sounds

Third heart sound (S3)


o
Low pitched
o
Heard with bell in mitral area
o
Comes right after S2 sounds like lub- dubdub
o
Fit and young, or pregnant (high SV)
o
Left ventricular failure
o
Mitral and aortic regurg (stroke vol high to compensate for regurg)
4th heart sound (S4)
o
low pitched, heard with bell in mitral area
o
Just before S1, lublub-dub
o
NEVER normal
o
Very non complient ventricle- atrium is having to push out the last little bit of blood

Aortic stenosis

Hypertension

CF

NOISES

Opening snap
o
Mitral stenosis
o
High pitched snap after S2
Ejection click
o
Aortic valve opening
o
Aortic stenosis
o
Heard in aortic area after 1st heart sound
Mid-systolic click
o
Mitral valve prolapsing
o
Halfway through systole, pressure in ventricles risen to such a level to prolapse the mitral
valve
Pericardial friction rub
o
Acute pericarditis
o
Scratching sound in systole or diastole
o
Can vary hr to hr
o
When inflamed, vicsceral and parietal pericardium rub together
o
Heard sitting forwards, expiration and hold breath.

Remember
o
lEEEft sided noises- heard in expiration

READING AN ECG
1.
2.
3.

Check NAME, DATE, TIME


Examine ECG in relation to previous ECGs (St changes can be fixed or dynamic)
Always interpret it in CONTEXT to the clinical situation.

ABOUT THE ECG

The ECG represents electrical activity, primarily from the L.Ventricle, as it has more muscle mass than
the RV.
The ECG therefore tells you little about the RV.
This is important as RV infarcts can occur, and can be missed if you dont request specific RHS leads.
They have a high rate of death, so important not to miss them.
Suspect RV INFARCTS in patients who are VERY HYPOTENSIVE with little in the way of ST
CHANGES in the ECG, or minor ST CHANGES in the inferior leads.
The ECG electrodes are place primarily across the anterior chest wall.
The ECG is therefore very good at detecting ischemia originating from the LAD and RCA territories, as
they supply they supply areas of the heart well covered by the ECG electrodes.
However, they may miss ischemia originating from the Circumflex artery, which is poorly represented
by ECG electrodes.
Leads 1 and AVL that look at the lateral wall of the LV may give some indication but changes are
subtle.
For this reason, posterior infarcts are missed on ECG
If you see ST DEPRESSION across V1-V3, ask for posterior leads, ST elevation in V4, V5, V5 will
become evident.
Ie. While a normal ECG in the setting of chest pain is reassuring, its NOT a definitive indication that
ischemia and infarction are absent.
If the history and context fit, then treat patients as if they do have ischemia- you can repeat the ECG
every 20mins
Remember: we often see NSTEMIS with NORMAL LOOKING ECGs.

THE QRS COMPLEX

QRS Width represents speed of conduction through AV node and ventricle.


HEIGHT represents ventricular mass (high), and impedance to conduction (low)
(Impedance is the effective resistance of an electrical circuit)
TALL COMPLEXES either (low impedance)
o
LV Hypertrophy- high ventricular mass
o
A thin person
SMALL COMPLEXES represent a (high impedance)
o
Fat person, or pericardial fluid
WIDTH
o
Any impulse that is generated from within the atrium, can only access the ventricle via the
AVN
o
The atria and ventricles are electrically insulated from each other.
o
The AVN slows conduction momentarily, to allow atrial conduction to finish.
o
The bundles of His then speed up the conduction, to allow the ventricles to contract.
o
Therefore any QRS complex, that travels through the normal intact conduction system by
definition is NARROW (UNDER 3 SMALL SQUARES)
The causes of a broad complex rhythm are (2 things going on, fast rate, and slow conduction)
ACCESSORY, BBB, VENTRICULAR!
o
1. An atrial rhythm that is conducted in the presence of a BBB (bundle branch slows
conduction through the bundles, and hence the ventricles- making the QRS broad)- SVT with
BBB
o
2. An atrial rhythm that bypasses the AV node, so enters the ventricles outside the
high-speed bundles (ventricular conduction slowed, making the QRS broad)- SVT conducted
via accessory pathway
o
3. A rhythm that is generated outside of the normal conducting system (any
ventricular rhythm/paced rhythem)- VT
If you remember this, then you will have no problems dealing with any broad complex tachycardia
that you come across on-call.
A broad complex tachcardya can only be due to
o
SVT with BBB
o
SVT conducted via an accessory pathway
o
VT
You dont need to know whats going wrong you just need to know the ONE drug that treats them..
AMIODARONE!

READING AN ECG

If you were to treat fast AF that was broad with DIGOXIN or BETA-BLOCKER, you can make AF worse.
They act on AV NODE ONLY!
If you block the AVNODE in the presence of an accessory pathway, the only way the beat can get to
the ventricles is the accessory pathway.

BUNDLE BRANCH BLOCKS

Impulse travels down the bundle of His, and divides into


o
RIGHT BUNDLE BRANCH (one fascicle)
o
LEFT BUNDLE BRANCH (two fascicles)

Left anterior fascicle

Left posterior fasicle


SIMPLE! You would PRICK YOUR FINGER ON A RBBB, but not a LBBB.
RIGHT can be ALRIGHT ie a normal finding.
LBBB associated with Coronary artery disease, and is an indication for THROMBOLYSIS.
Since the electrical impulse can no longer use the path it wants (heart disease/MI), it moves instead
through muscle fibres, which slows movement, and changes the direction of the propagation of the
impulses.
Loss of ventricular synchrony, ventricular depolarization is prolonged, and may be a drop in CO

DIAGNOSED ON ECG, WHEN DURATION OF QRS IS over 120ms


LBBB broadens the entire QRS (and may shift axis to the left)- look in V1 for a BROAD QRS!

WHAT???!??!
HEART BLOCK

The first sign to look for is a p wave, they doesnt have a QRS complex following
Then decide what type
If no impulse arrives in the ventricle, after a period of time, a ventricular escape response takes over,
and this is ALWAYS REGULAR.
Therefore, complete heart block always has a regular ventricular rhythm.
1st DEGREE
o
Prolonged P-R
o
Over 0.2secs
o
Fibrosis of the AVN, increases risk of further block in 20% cases
o
Every p wave followed by a QRS complex.
2nd DEGREE
o
MOBITZ 1 (WENKEBACH)

PR progressively lengthens, until one P wave fails to conduct

The cycling of lengthening and dropping is irregular

Irregular conduction through the AV node, so ventricular rhythm irregular too.

If you look at the rhythm strip, and see the ventricular rhythm is irregular, it has to be
Wenkebach, after youve realized it must be a block because there are p waves
without a QRS.
o
BOBITZ 2 (2:1)

Regular pattern to non-conducted p-waves.

P-R interval in conducted beat is always the same.

Regular conduction through the AV node.

Regular ventricular rhythem


COMPLETE HEART BLOCK
o
Lack of any relationship between p and QRS
o
REGULAR VENTRICULAR RHYTHM
In 2:1 block and Complete block are treated the same.- They are paced.

ECG and TERRATORIES


I

AVR

V1

V4

II

AVL

V2

V5

III

AVF

V3

V6

INFERIOR:
SEPTAL:
ANTERIOR:
LATERAL:

II, III, AVF (the bottom L) RIGHT CORONARY


Proximal LAD
V3, V4
LAD
V5, V6, I, AVL
Circumflex
V1, V2

An occlusion of the LAD at the beginning (ie proximal) is a lot worse, as the territory is septal,
then also a lot of the ventricles too- so more likely to lead to HF. V1 and V2 is bad.
Occlusion distally results in a small loss of territory- so low risk of HF.

ST CHANGES
Can be transient or permanent.

ST ELEVATION
o
MI, Pericarditis, Scarring, aneurysm.
ST DEPRESSION
o
Ischemia strain (LVH)
o
Repolarisation abnormalities (BBB)
o
Digitalis effect
T WAVE INVERSION
o
Ischemia
o
Repolarization abnormalities (BBB)
o
Changes in posture normal.

DEFINITIONS

MI: ST elevation or new onset LBBB


NSTEMI: Biochemical evidence of infarction (troponin) in the absence of ST elevation or LBBB.
ECG may look normal!

QUICK CHECK

1.
2.
3.
4.

Name, Date, time


Rate and Rhythem (strip at bottom)
Check leads 1 and 3 for axis (Left alone, Right-alright)
V1 check
o
P-R interval (0.12 sec to 0.2 sec)
o
If LBBB present, you CANT INTERPRET THE ECG ANY FURTHER!!!
o
If RBBB, you can, but any QRS and t changes might be due to BBB.
5. If no LBBB, check each lead looking for morphological abnormalities in the QRS
and T waves.
(LVhypertrophy defined as deepest S wave V1 or V2 added to the tallest R wave in
V5 or V6. If over 25mm LVH)

BASIC INTERPRETATION AND REGIGNITION ECG


RATE
RHYTHEM
AXIS
P WAVES
P-R INTERVAL
QRS COMPLEX
ST
Q-T interval
T WAVES

RATE

Check paper speed is 25mm/sec


Tiny square is 0.04 secs
5 small squares = 0.2 seconds.
The ventricular rate is calculated by looking at distance between R-R
NUMBER OF LARGE SQUARES BETWEEN R-R. DIVIDED BY 300.
If really fast, number of small squares between R-R, counted divided by 1500.

RHYTHEM

SINUS
o
P before every QRS and at fixed interval from it.

P BEFORE EVERY QRS

P-R NORMAL

P-R CONSTANT
ATRIAL FIBRILLATION
o
No P waves, irregular QRS
ATRIAL FLUTTER
o
ECG shows presence of flutter waves
o
Baseline adopts a saw-tooth appearance
o
AV flutter may occur with a fixed degree of block (3:1 block)- ie for every 3 flutter
waves, a QRS
o
May have variable block
HEART BLOCK
o
1st: prolongued P-R interval (over more than 5 small squares), constant P-R interval
o
2nd WENKE: P-R lengthens, then drops a QRS
o
2nd MOB2: P-R might be normal, but every 2 or so, theres a p with no QRS.
o
3rd p waves and QRS totally dissociated. Mark the p waves, then try to line up with
QRS

CARDIAC AXIS

Describes the average direction of electrical activity in the heart.


I and lll away.. LEFT (alone). I and III towards (RIGHT.. alright)
Normal is little up, little up, little up I II III

P WAVES

P wave should be 2.5 SMALL SQUARES UP AND 3 ACROSS


Tall P waves? P PULMONALE (enlarged right atrium)- p are peaked

BASIC INTERPRETATION AND REGIGNITION ECG


Q WAVES

Should be 2 SMALL SQUARES DOWN and ONE ACROSS


In the lateral leads, its fine for them to be big (V5, V6, AVL, 1)
If theyre BIG ANYWHRE ELSE
o
Abnormal: scar tissue in heart after a MI

R, and S WAVES

Used to predict LV HYPERTROPHY


Add together the height (mm) of
o
R in V6
o
S in V1
If greater than 35mm- LVH present.
Echo to confirm
Causes of small complexes? Pericarditis, pericardial effusion, emphysematous lungs.

QRS DURATION

LESS THAN 3 SMALL SQUARES WIDE


Wide- abnormal conduction through ventricles.
Ie. Not through bundle of His etc.. but more slowly through non-specialized cardiac tissue.
o
RBBB

2 R-WAVES (upward deflections) seen in the QRS in V1 (RSR PATTERN)

And a deep S-WAVE in V6


o
LBBB

Looks BIZARRE

RSR may be seen in V6

STOP interpretation after establishing


o
RATE
RHYTHEM
o
AXIS
o
PRESENCE OF LBBB

ST SEGMENT

ST ELEVATION: MI, pericarditis (saddle shaped- droopy in pericarditis)


ST DEPRESSION: Cardiac ischemia
Strain pattern: ST depression in lateral chest leads, and features of LVHypertrophy- this
means marked LV hypertrophy.
Down-sloping ST-depression seen on patients on DIGOXIN.

QT INTERVAL

Long Q-T predispose to cardiac dysrrythmias


Shouldnt be more than 2 BIG SQUARES
Usually varies with HR- ie QT increases as HR slows
Corrected QT should be less than 0.45 SECS.

T WAVE

Shouldnt be more than 2 SQUARES TALL


Inversion Normal if in
o
V1 and V2 together (but not V2 alone)
o
aVR
o
aVL
Tall tented: HYPERKALAEMIA
Flat, broad: HYPOKALAEMIA

Hyperkalaemia: TallTentedTwaves, no P waves, broad QRS, Sine waves, ARREST RHYTHEMS


Hyperkalaemia: FlatBroadTwaves, STdepression, LongQT, Ventricular dysrrythmias.

BASIC INTERPRETATION AND REGIGNITION ECG


CARDIAC ARREST RHYTHEMS

SHOCKABLE
o
VF
o
VT
NON-SHOCKABLE- need to reverse the cause of the arrest, and start CPR
o
PEA
o
ASYSTOLE
o
P wave ASYSTOLE: only p waves, can respond to cardiac pacing

ATRIAL FLUTTER

WENKEBACH

1st DEGREE BLOCK

3rd DEGREE BLOCK

LBBB

RBBB

VT

VF