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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: V!, V2
ANTERIOR: V3, V4
LATERAL: V5, V6, V1,
aVL
INFERIOR: II, III, aVF
THE CARDIAC CYCLE- VENTRICLE AP

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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 V1 V4

VENTRICULAR MUSCLE ACTION POTENTIAL


aVL
II
V2
V5

o (4) -90 RESTING POTENTIAL


The membrane at rest is most permeable to K+ ions, so the RESTING POTENTIAL is
III
aVF
V6
V3 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
After this, theDESCENDING, from left coronary
cell begins to repolarize and return to the resting state, as it cant
o V1 (septal) again until its in its resting state.
depolarize
o o (1)V2Initial(septal)
phase of repolarization.
o V3 (anterior)
Rapid inactivation of Na+ channels.
o o (2)V4PLATEAU (anterior)
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

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).

o (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.

o 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.

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

o These depolarizing currents cause the membrane potential to begin to spontaneously


depolarize- initiating Phase 4.

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

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

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

o 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 low-
resistance 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.

o 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).

o Spontaneously discharge about 100 times per minute.

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

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

o 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

o Its the end of diastole

o Atrium and ventricles are relaxed

o Mitral and Tricuspid (atrioventricular valves) are open

o 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

o Fills the ventricles and completes ventricular filling

o AV valves open

o Semilunar valves closed

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

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

2. ISOVOLUMETRIC CONTRACTION (VENTRICLES CONTRACT)

o Ventricles filled with blood contract

o Tricuspid and Mitral valves close as pressure now high in ventricles

o Ventricular volume unchanged, but the pressure rockets.

o Semilunar valves still closed.

3. VENTRICULAR EJECTION

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

o Blood into arteries

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

o 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

o Normally close together, if split- might indicate delayed conduction

o In L or R bundle of HIS.

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


late

o S2: Pulmonary/aortic valve closure

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

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

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

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

o Aortic closes slightly earlier, as less blood.

o 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

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

o Allow transfer of small ions, therefore ELECTRICAL CURRENT.

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

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

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

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

o 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.

o Ischemic damage to nodal tissue/ Bundle His.

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

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

o 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)

o 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.

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

o 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.

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

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

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

HAEMODYNAMICS

DARCYS LAW:

Pump Pressure
Flow =
resistance

Mean Arterial BPCentra l Venous Blood Pressure(0)


CARDIAC OUTPUT =
Total Peripheral Resistance
THE CARDIAC CYCLE THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

BLOOD VISCOSITY

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

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

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

o 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.

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

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

o Occurs in the microcirculation.

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

o Reduces the viscisoty of the blood in the microcirculation, reducing the resistance (Fahraeus-
Lindqvist effect)

WALL TENSION (TRANSMURAL PRESSURE)

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

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

o This is the FRANK/LAPLACE LAW

vessel rad ius


Wall Tension = Transmural Pressure
wallThickness

o 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.

o 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.

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

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

o The end systolic volume is larger than the beat before.

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

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

o 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

o So very important in controlling BP.

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

Positive IONOTROPE, and CHRONOTROPE

o The ventricular function curve is shifted upwards

o Nor-adrenaline inc this too.

o Negative ionotropes decrease force

o Acidity

CVP and Autonomic NS are prime determinants of CO.

Heart
Rate Stroke Vol
END DIASTOLIC VOLUME
- Compliance
Positive Chronotropes, eg. SYMPATHETIC NS
- CVP (pessure pushing it) and so EDP (how much fills with
blood before contracts)
END SYSTOLIC VOLUME
- Arterial pressure
Negative Chronotropes, e.g. PARASYMPATHETIC NS - 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.

o There are autonomic reflexes and local mechanisms.

o Intrinsic reflexes (respond to stimuli in CV system)

Baroreceptor

Cardiopulmonary

Chemoreceptor

o Extrinsic reflexes- Cardiac responding to stimuli elsewhere.

o Eg. Pain/temp changes

o Cardiovascular reflexes involve

o RECEPTORS: Afferent nerves- sense change, communicate to brain

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

o EFFERENT NERVES: control cardiac, vascular and renal function- homeostasis-


reverse change.

THE BARORECEPTOR REFLEX

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

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

o They are MECHANORECEPTORS

o Sense alterations in wall stretch caused by pressure changes.

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

o 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

o Stimulated by brainstem hypoxia.

o During severe hypotension

o Helps maintain bloodflow to brain in shock

o 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.

o Severe pain has opposite effect.

o 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.

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

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

o 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.

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

o 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.

o Homeostatic adjustment to postural changes.

o Change in heammorhage and blood gases.

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

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

o 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.

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

o Alterations in blood vol affect venous return, and CO.

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

o Volume of blood affected by changes in total body contents of

o Water

o Na

o These are both controlled by kidneys.

o 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

o Changes the plasma osmolarity

o Any deviation from normal sensed by HYPOTHALAMIC OSMORECEPTORS

o Activate thist

o Release ADH from pituitary

o ADH is a peptide that suppresses renal water excretion

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

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

o THEREFORE PLASMA VOLUME mainly controlled by Na+ content of EXTRAVELLULAR


FLUID (in blood).

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

o 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.

o Response to Volume Overload.

o 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

o Measured intermittently using automated sphygmomanometer

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

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

- CENTRAL VENOUS PRESSURE (CVP)

o Reflects RIGHT ATRIAL PRESSURE

o Measured with internal jugular/ subclavian vein catheters

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

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

o CVP isnt as important as the response to a fluid challenge

o 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/GTN-


reproducible.

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

Cardia ischemia, and pericarditis-


retrosternal pain.

BASIC CHEST PAIN DIFFERENTIALSiix


Ischemia- pain tight and crushing- radiates
to neck, back, jaw, arms
PLEURITIC
Pericarditis is pleuritic, relieved sitting
o Sharp pain forwards, worse laying flat.

o Worse on deep inspiration, Dissecting AA: tearing pain radiating


coughing, movement through the back

o Pneumothorax Pulmonary disease- unilateral pain that the


patient can locate specifically
o Pneumonia
Oesophageal disease- retrosternal pain- may
mimic cardiac pain
o PE

Referred pain from vertebral collapse/


o Pericarditis: Retrosternal
shingles- dermatomal pattern

CENTRAL
ASSOCIATED SYMPTOMS

o Angina (crushing, tightness)


DYSPNOEA:
RISK FACTORSiix

IHD
o smoking, family, hypercholesterol,
hypertension, diabetes.
o (SF C HD Sausage Fest Causes HD!)
PE

otravel history, immobility, surgery,


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

LOOK FOR?

abnormal lipids:
o xantholasma
o tendon xanthoma
CHEST
Tar PAIN
stained INVESTIGATIONS
fingers (IHD) ix CHEST PAIN INVESTIGATIONSix
Hot, oedematous calf: DVT
GP,Hypertension
(non-acute chest (IHD)
pain) ECG (ACS)
Marfans syndrome
Diabetes (IHD)
FBC (to exclude anaemia). o New onset LBBB

Renal function tests and electrolytes. o T wave changes

TFTs. (arrhythmia from hyper T) o ST depression/elevation

CRP. ECG (PE)

Fasting lipids and glucose. o Sinus Tachycardia

Resting ECG. Note: a resting ECG is normal in o AF


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

o R. Axis deviation
Additional tests if a non-cardiac cause is
suspected - eg,
o RBBB

o CXR,
o S1Q3T3 (deep S wave in 1, Q
wave in 3, T-wave inversion in
o LFTs and amylase, 3)

o abdominal ultrasound. ECG (pericarditis)


PRESENTING WITH PALPITATATIONSx

Palpitation
s
PALPITATIONS HISTORY kkkkkmmmmm
REGULAR CAUSES ooo
REGULAR IRREGULAR
IRREGULAR
Non- Cardiac causes TACYCARDIA:
What the patient means by palpitations.
It should mean an awareness SLOW
SLOW
of the heart beating.
FAST
FAST
It may really be a pulsatile tinnitus or a carotid bruit. FAST PACE!!!!
Ask the patient
o how often it happens, PERSISTANT
PERSISTANT OCCASIONAL
how long it lasts and
o VT OCCASIONAL
VT SINUS
SINUS BRADY
BRADY Fever
o any precipitating or relieving factors.
Sometimes people are only aware of it whilst lying down
at night. AF
AF ECTOPIC
ECTOPIC
AF- Anaemia
Determine whether the rate is regular AF- degree
degree of block
of block
or irregular.
TACHYCARDIA
TACHYCARDIA
Ask the patient to tap out the beat.
This may be regular or irregular. It may be a normal rate ECTOPIC AF
COMPLETE HEART ECTOPIC
Sympathomimetic
S drugs AF
(paroxysmal)
or fast.
AF COMPLETE HEART S (paroxysmal)
Try toAFestimate the rate. BLOCK
BLOCK
Establish whether there are any symptoms that ATRIAL
ATRIAL
Thyrotoxicosis
accompany the palpitations, such as sweating or FLUTTER (with
FLUTTER (with
SVT
breathlessness.
SVT block)
These may be organic or psychosomatic in origin.
block)
Associated chest pain?.sinister significance! Pregnancy
Enquire about consumption of caffeine. Palpitations may
be related in time to consumption but assess daily intake
too Anxiety (pain) Arteriovenous
Ask about alcohol consumption. fistulae
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:

o Does the patient look well?

o Does the patient look anxious?

o Is there exophthalmos to suggest thyrotoxicosis?

o 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
HEART MURMURS tests x HEART MURMURS Hx x
o FBC,
o U&Es
EJECTION oSYSTOLIC
TFTs. (A and P area) No real symptoms- so need to find out
A 24-hour ECG should be arranged (many GPs now have direct cause/ consequences.
access to this).
- Originate
o Thein either is
patient ventricle
given a outflow
device totract-
wear (a Rheumatic
sofor 24 hours feverwhich
Holter monitor) (mitral
is valve)
returned to the
either hospital
around the for pulmonary
analysis thearteries or the
following day. IHD (mitral regurg)
aorta
o The time that palpitations start and finish shouldbe noted so this
Congenital can disease
heart be correlated with the
- TheyreECGeither before the valves (in the
recording. Hypertension (flow murmus)
heart),Asin athe valves, oran
refinement, in the arteries.
event recorder can be used for
o patients
IVDU whose palpitation frequency is
- Reach less
a crescendo
than daily.mid-systole, die down
before second heart sound (semilunar Family Hx hypertrophic cardiomyopathy-
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
- irregularity
Causes in AORTIC AREA.. either valvular / REGURG (associated
at rest that is suppressed on exercise. These tend to be o ofRheumatoid
rather less sinister significance
arthritis
supravalvular / subvalvular
o Coactation of aorta o Seronegative arthropathies
HEARToMURMURS Supra-aortic stenosis x (ankloysing spondylitis, reiters
o Aortic sclerosis syndrome, psoriatitic arthritis
o Hypertrophic obstructive o Coarctation of aorta
Murmurs are vibrations due t turbulent blood flow in heart.
cardiomyopathy (subvalvular) MiTRAL REGURG
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,
left-Right shunts (ASD)- left side o Osteogenesis imperfect.
EJECTIONbigger-SYSTOLIC
remember Consequences
PANSYSTOLIC o Aortic valve disease and mitral

PANSYSTOLIC DIASTOLIC
MURMURS (T and M area) regurg may be asymptomatic.
CONTINUOUS o LOW CO- fatigue and weakness
- Same intensity o Paliptations- AF
- Heard throughout the whole of systole and o Angina (aortic stenosis)
merge with the 2nd heart sound (semilunar o Symptoms of RV failure
valves shutting) Anorexia
- Causes at APEX (mitral) Ankle and leg oedema
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
DIASTOLIC MURMURS *always pathological, stenosis)
always hard to hear. Orthopnoea
Paroxysmal nocturnal
- When blood ejected from the ventricles dyspnoea
and the heart relaxes, Atria are filling. o Syncope (poor CO)- eg, severe
- Causes at PULMONARY area aortic stenosis.
o Aortic regurg (early diastolic) o Emboli- TIA/Stroke- mitral stenosis
o Pulmonary regurg (early diastolic) o Infective endocarditis
- Causes at APEX (MITRAL) area o Symptoms of enlarged LA,
o Mitral stenosis- think in pressing on other structures,
isovolumentic relaxation- ventricles especially in mitral stenosis
are filling through here. Recurrant laryngeal nerve-
o Carey Combs murmus (acute horseness- Ortners
rheumatic fever, mitral valves syndrome
MITRAL STENOSIS x

MITRAL REGURGITATION
x

-
Narrowing of the mitral valve (when LA-
LV)
Backpressure builds up behind the
narrowed valve
Reduced amount of blood ejected from LV.
Backpressure into lungs.
Most caused by past Rheumatic fever-
Mitral valve doesnt close properly follows a bacterial infection with
Blood leaks back into LA when LV streptococcus- body makes autoantibodies
contracts, instead of going into the to clear infection, but also attack mitral
body. valve- inflammation, damage and
Due to infective endocarditis, Ehlers thickening.
Danlos, Marfans, SLE, scleroderma, Can also be calcification, congenital,
acute rheumatic fever endocarditis.
SYMPTOMS More effort form LA to pump into LV- get a
o If acute, you get rapid hypertrophy of the LA.
backpressure into lungs and SYMPTOMS
acute pulmonary oedema- o SOB during exercise
emergency valve repair! o Fainting, dizzy
o Chronic- eventually, dilation of o Tired
Left ventricle, HF. o Chest pains (reduced flow
EXAMINATION
o
OF A MURMUR
Progressive exertional coronary arteries)
x
dyspnoea o Chest infections- due to bronchial
o (Systemic emboli/stroke, chest vein ruptures, congention,
pain
Inspection, AF, less common
palpation, than
auscultation pulmonary infarction.
stenosis)note when maximum
Time a murmur, o Coughing up bloody sputum.
o
intensity. and radiation COMPICATIONS
COMPICATIONS
SYSTOLIC o AF- due to faulty LA
o o AF- due to faulty LA
Pansystolic? o HF: orthopnoea, PND
o o HF: orthopnoea,
Ejection PND
systolic? o Stroke/emboli- due to AF
o
DIASTOLICStroke/emboli- due to AF o Fatigue and cold hands- low CO
o o Fatigue and cold (start
Early diastolic? hands-from
low CO SIGNS
SIGNS 2nd sound) o Malar flush
oo Bibasal crackles- pulmonary
Mid diastolic? o Pulse: small vol/ AF
oedema o Evidence emboli- ischaemic
o LA enlargement- parasternal bowel/ leg etc
heave o JVP raised
o LV dilation- thrill at apex o Swollen liver
o Look for things eg. Rheumatoid MURMUR
arthritis, EhlersDanlos, o MID DIASTOLIC (blood from A
oesteogenesis imperfect (blue to V, before V contract- blood fills
sclera) ventricles in diastole, as in
MURMUR systole, pumps to body.)
o PANSYSTOLIC MURMUR at o At APEX (M area)
AORTIC STENOSIS x AORTIC REGURG x

- -

Aortic Sclerosis is the precursor of Usually asymptomatic, until ventricle fails!


calcified, degenerative aortic stenosis Ventricles make up and make up to pump
Congenital or calcified from aging. the body, loosing a bit every time, then
Blood harder to pump into body at can enlarge and keep up no more.
ventricular systole. After rheumatic fever, infective
SYMPTOMS endocarditis, collogen vascular diseases,
o Usually none until late SLE, lupus, marfans, ehlers-danlos,
o Angina ankylosing spondylitis, reiters, bechets.
o Exertional dyspnnoea SYMPTOMS
o Syncope o Heart failure when ventricle fails
o . Triad- chest pain, HF, syncope SIGNS
COMPICATIONS o Low diastolic BP
o Sudden death- ventricular o Wide pulse pressure- large
dysrrythmia. difference between systolic and
SIGNS diastolic, as diastolic is even
o BP- narrow pulse pressure (less lower.
difference between systolic and o Collapsing pulse- sharp rise and
diastolic, as systolic lower. fall (historical)
o LV hypertrophy as more force o Head bobbing with each pulse
needed to pass valve- small (hist)- de mussets sign
decrease in radius, massively o Corrigans sign: visible pulsation
more resistance. arterial in neck
o Small volume, slow rising o Traubes sign- pistol shot femoral
pulse. artery
o Ventricular heave. MURMUR
MURMUR o DIASTOLIC
o EJECTION SYSTOLIC o (T) Lower L sternal edge-
o at AORTIC area (A) EXPIRATION, LEAN
o RADIATES TO carotids FORWARDS AND HOLD
o Loudest at expiration BREATH
o no radiation
Investigations
o CXR: enlarged heart / Investigations
TRICUSPID REGURG x

- 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
HEART endocarditis?
DISEASE- Basics x
SYMPTOMS
o Fatigue
Result of
o anOedema
imbalanceandbetween Myocardial oxygen supply and demand
ascites (peripheral)
Term covers
o Hepatic pain- liver capsule stretched.
o Angina
MURMUR
o ACS
o PANSYSTOLIC MURMUR
o Anything
o that reduces
Loudest blood edge
at L sternal supplyintoinspiration
heart! (T)
Due too No radiation
o Atherosclerosis
o of coronary arteries (COMMON)
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 x
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.
- 1. ENDOTHELIAL DYSFUNCTION- associated with high cholesteriol, inflammation, and shear forces.
oDRUGS
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
RiskCELLS ACCUMULATE
of GI bleed- melena,intakesubendothelial zone- forms FATTY STREAKS
with food, PPI
o 4.o FOAM CELLS/MACROPHAGES
CLOPIDOGREL release toxic products-
if aspirin contraindicated lead to aggregation)-
(inhibits platelet PLATELET ADHESION, MUSCLE
mostly used postCELL
PROLIFERATION, THROMBUS FORMATION
NSTMI/angioplasty.
5. Becomes organized- ATHEROSCLEROTIC CAP with FIBROUS CAP.
- oBETA-BLOCKERS
o 6.o Progressive enlargement,
Reduce Sympathetic and narrowing of lumen- exertional angina.
tone.
o 7.o RUPTURE-
Negativecause sudden(reduce
ionotropes thrombuscontractility)- reduce oxygen demand
o Neg Chronotripoc (HR)- reduce oxygen demand
Atherosclerosis
o is Increase
initiatedperfusion of ischaemic
by inflammatory area- decreasing
processes HR, increases
in the endothelial cells of diastole-
the vesseltime
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
Improve vary in size. Some data suggests that small dense LDL particles are more prone to
post-MI
pass between o the Goodendothelial cells,
in chronic going
heart behind
failure- the cellular
shouldnt monolayer
be given in acute. of endothelium.
- 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
However, LDL particles in a
have heart wallof
half-life distension- decreases
only a couple of days,o2and
demand of heart(LDL
their content wall-particles
angina relief.
typically carry
o fat
3,000 to 6,000 Nitrates are converted
molecules, including:to NO- which phospholipids,
cholesterol, results in an increased intracellular
cholesteryl cyclic guanosine
esters, tryglycerides & all other
fats in the watermonophosphate
outside cells, to cGMP in smooth
the tissues of themuscle. This stimulates
body) changes calcium
with time. Oncebinding processes
inside the and LDL
vessel wall,
free calcium
particles can become vaaliable
more prone to trigger muscle contraction is reduced.
to oxidation.
o Nitrates and rest relieve angina in minutes.
Endothelial cells
o respond
Longer by attracting
acting monocyte
nitrates can white for
be effective blood cells,
hours. causing them
(isosorbide to leave
dinitrate, the blood by
metabolized stream,
penetrate into the arterial
liver walls and
to isosorbide transform into
mononitrate- themacrophages.
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 o SYNDROMES: (Nifedipine)- good vasodilating drugs that can cause reflex tachycardia.
Dihydropyridines
Pathophysiologyo Diltiazem- neg ionotrope, and chronotrope- contraindicated in HF
o Amlodipine- safe in HF
ACUTE CORONARY SYNDROMES:
o Flusing, headache, oedema, constipation
Affects 7% population
o Dont use verapamil with beta-blocker.
Pathophysiology
Increases with age, males, post-menopause
ACE INHIBITORS
RF: smoking, hypertension,
Inhibit diabetes,
renin-angiotensin-aldosterone axis
o Affects 7% population
cholesterol, family.
Increase in vasodilating bradykiin
o Increases with age, males, post-menopause
About 20%o ofMore
all deaths in UK
effective in yonger patients with higher renin levels- best
RF: smoking, in young white
hypertension, diabetes, cholesterol,
After MI-o30-60%
Gooddeath
in HF,before hospital,
proteinurig 10%
nephropathy, diabetes family.
in hospital,
o 20%Dry within
cough 2 years (HF to
(secondary or bradykinin),
MI) 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
o overelectrolytes
Monitor ruptured complex
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
Good if chronic OCCLUSION
cough on ACE- dont effect bradykinin production
o CV protective effect
CONSEQUENCES OF CORONARY ARTERY OCCLUSION
o
LEFT CORONARY ARTERY
MINOXIDIIL
Supplies
o Potent vasodilator,
LAD and dec Major
Circumflex: PVR- can cause reflex tachycardia- use beta-blocker
Fluid retention o LEFT CORONARY ARTERY
contribution
o to LV and (use diuretic)
RV perfusion
o RIGHT CORONARY
o Hirsutism ARTERY Supplies LAD and Circumflex: Major
Occlusion causes inferior MI. contribution to LV and RV perfusion
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

FACTORS LIMITING OXYGEN SUPPLY


Artery NARROWING: Vasospasm and complex
plaque thrombosis
Reduced FLOW: Hypotension, tachycardia- Artery NARROWING: Vasospasm and complex
reduces diastolic time, inc LV end-diastolic plaque thrombosis
pressure, LV hypertrophy. Reduced FLOW: Hypotension, tachycardia- reduces
Reduced OXYGEN CARRYING capacity: diastolic time, inc LV end-diastolic pressure, LV
Anaemia, hypoxaemia. hypertrophy.
Reduced OXYGEN CARRYING capacity: Anaemia,
hypoxaemia.
FACTORS LIMITING OXYGEN DEMAND

FACTORS LIMITING OXYGEN DEMAND


Increased HR: (anxiety/ exercise)
Inc LV AFTERLOAD / MASS: (increases
myocardial wall stress eg. Hypertension and 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?
Autonomic manifestations eg. Nausea and 1st you need to differentiate ACS form other
sweating? Radiation to new sites eg. Jaw? life threatening conditions e.g. Aortic
Indicate increasing coronary artery dissection and benign things e.g. Reflux,
ACUTE CORONARY occlusion SYNDROME
and NSTEMI(ACS) CHRONIC STABLE (exertional)
musculoskeletal.
o Typically: Crescendo angina: inc freq ANGINA
INVESTIGATIONS
Spectrumperiods of prolonged,
of increasingly freq angina.
life-threatening Angina in which
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
Initiated by STRESSon ECG.
INDUCED RUPTURE (hypertension) of small o Site and Size infarct.
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
plaques, with and cores
lipid-rich deathand(in 4-6
thinweeks)
fibrous plaques. revascularization)
exercise.
Plaque 8% hospitalized
o rupture die in 30 days, 8% re-
stimulates o ST Depression and T inversion: NSTEMI
Stenosis are caused by
o infarction. formation
Thrombus doesnt benefit from thrombolysis.
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 STEMI- even though early to
o Arterial Occlusion thick fibrous caps: unlikely
o Elevated troponin
Length of time and extent of the occlusion determine severity of mortality higher in STEMI.
rupture.
o Recurrent angina o Serial ECGS
toThick
diagnose.
fibrous cap, small lipid
ischemia: defines the syndrome, ECG changes, symptoms, degree of
o
myocardial Diabetes
necrosis (cardiac enzyme release). o INFERIOR: RCA, II, III, aVF
core.
o
UNSTABLE Previous
ANGINASTEMI o ANTERIOR: LAD, l, aVL, often
Ischemia V2, V3,
sub-V4, V5
Impaired artery
oo Coronary LV occlusion of limited extent/duration. o INTEROSEPTAL: LAD, V2, V3,
endocardial, as V4
systolic
HF
oo Ischemia, not necrosis o ANTEROLATERAL: LAD, V3,greater
compression V4, V5 than
NSTEMI High for
o (send risk!? Early cardiac angiography.
PCI!) o APICAL: LAD, endocardial
II, III, aVF, V5, V6 epicardial
than
No risk factors-
oo Occlusion may be Exercise ECG incomplete/ alleviated by
temporary/ o LATERAL: Circumflex/diagonal,
aretries. I, aVL, V6
MI collateral vessels o POSTERIOR: VARIANT- PRINZMETALS
Right/Circumflex, R wave in
NSTEMI and
oo Ischemia andSTEMI (cardiac
necrosis limitedenzyme
to SUBENDOCARDIUM V1,-2 with ST ANGINA:
depression. uncommon, caused
o positive)
Myocardial damage: cardiac enzymes. ENZYMES by transient coronary artery
STEMI Thrombolytic
o (send for PCI!) therapy is only beneficial on o vasospasm
A twofold increase in plasma due enzymes
to over- in
o STEMI
Occlusion causes transmural ischemia reactivity (to noradrenaline)/
myocardial damage.
o MI: abrupt onset severe, prolongued pain, o impaised
Cardiac Troponins flow-mediated
at 12hours are
o Q-waves
unrelieved by nitrates. sensitive and vasodilation. Often near
specific for necrosis- can
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 Ascultation may show 3rd and 4th heart o Failure of BP and HR appropriate
sound (gallop rhythem) and systolic responses.
murmur. o EST= Bruce protocol
o EARLY COMPLICATIONS MI (1 week) st MYOCARDIAL PERFUSION SCANS
Arrythmias o Detects reduced isotope uptake in poorly
Pericarditis perfused myocardium using a gamma
Papillary muscle/ free wall rupture camera.
o Alternative to exercise stress test in bed-
VSD
ACS GENERAL MANAGEMENT

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/
MANAGEMENT OF STABLE ANGINA drugs (Statins)
ACENSTEMI
inhibitors- reduce atherosclerosis-

NITROVASODILATORS Thrombolytic therapy not


o Efective, but tolerance develops beneficial.
BETA-BLOCKERS Nitrates, Beta blocker, CCA and
o First line therapy ANTIPLATELET THERAPY
o Improve prognosis o All patients 300mg Aspirin
o Increase myocardial perfusion in diastole- slow HR immediately
and reduce pre-load and afterload so reduce LV o 75mg a day
tension. o Irreversible cyclo-oxygenase
CALCIUM CHANNEL ANTAGONISTS inhibition prevents platelet
o Useful when beta-blockers contraindicated. aggregation within 15mins
o Relive coronary vasospasm. chewing aspirin- preventing
o Nifedipine, can cause reflex tachycardia, and MI/sudden death by 50%
exercerbate HD (neg ionotrope) o Clopidogrel inhibits its ADP-
REVASCULARISATION Stimulated platelet aggregation,
o Needed if symptoms deteriorate. reduces mortality when combined
o Needed if positive exercise stress test with aspirin after 30days.
o Needed if angiography revelas over 70% stenosis GLYCOPROTEIN IIb/IIIa
in all 3 main, left main or proximal LAD arteries. ANTAGONISTS
o Most effective platelet inhibitors-
Used 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
o Monitoring
CONTRAINDICATION TO THROMBOLYTIC
o Oxygen Therapy 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
NITRATES Previous CVA/TIA
o Under 24hrs Recent CPR
o Reduce pain, infarct size, HF Systemic Hypertension
ACE INHIBITORS Recent Central lines
o Over 24hrs, improve LV remodeling Intracardiac thrombus
o Reduce HF in high risk patients. AAA
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
STREPTOKINASE (SK) or tPA TISSUE PLASMINOGEN ARRYTHMIAS
ACTIVATOR
o Main TT agents
Abnormalities of thegiven
HeartbyRate/Rhythem
infusion
o SK cheap but allergenic
Due to Aberrant impulse generation(single use)
/ 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 SINUS TACHYCARDIA

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
Caused by ATRIAL FLUTTER
o INCREASED PACEMAKER ACTIVITY BRADYARRYTHMIAS
o RE-ENTRY CIRCUITS
An anticlockwise atrial re-entry circuit.
Increased pacemaker: faster spontaneous membrane
Under 60bpm Causes rapid, co-ordinated
depolarization, lower thresholds and oscillations during re-
Due to Delayed depolarization.
conduction.
polarisation trigger early APs.
300bpm
Re-entry circuits:A depolarization wave travels around If symptomatic treat with
a
Ventricular rate depends on AV Node
circle of myocardial tissue. If the tissue is not refactory o ATROPINE
refractoriness, with conduction of
BETA AGONISTS
when the impulse returns, it will depolarize again producing o
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 WIDE COMPLEX TACHYCARDIAS o COMPLETE
o Class 1a may cause VT, so
Usually VT AF
Hard to tell if its unusal conduction of SVCSINUS BRADYCARDIA
Exclude AV node block.
If haemodynamically unstable, treat as VT Spontaneous, chaotic, atrial
Normal ECG p waves, and Av node conduction
DC Cardioversion depolarization.
Treated by addressing causes eg. Vagal reflexes
Over 300bpm
Doesnt work? Probably SVT- use adenosine (pain), Drug Toxicity (beta-blockers), Atropine.
Ongoing treatment amiodarone. Refractory AVN conductions limits
VAGAL STIMULATION (eg. Carotid sinus massage) ventricles to under 200bpm.
HEART BLOCK Ineffective atrial contraction
slows HR and may cardiovert some SVT
predisposes to atrial thrombus and
SUPRAVENTRICULAR TACHYARRYTHMIAS (SVT) Due to AV node or Conducting tissue ischemia.
thromboembolism.
o Originate above the AV Node Common after Treat?!
inferior MI (RCA supplies the AV node)
o Dizziness, palpitations, breathlessness Heart Block after an Anticoagulation
o anterior MI suggests(stroke)
a large
o Rarely life-threatening. Can be sudden death. infarct requires o
earlyDigoxin (controls
pacemaker resting HR)
insertion.
SINUS TACHYCARDIA o Beta-blockers (control exercise
ATRIAL FLUTTER 1 DEGREE HEART BLOCK
st HR)
AF
VENTRICULAR FIBRILLATION
AVN RE-ENTRANT TACHYCARDIA Slows AV node conduction
PRE-EXCITATION SYNDROMES Prolongued P-R (over 0.2 secs)
An early warning
Chaotic ventricular
of worse rhythm
heart block later.
VENTRICULAR TACHYARRYTHMIAS Follows Acute MI
VENTRICULAR
o TACHYCARDIA
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
MI, with uniform QRS VF
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
3rd DEGREE COMPLETE HEART BLOCK
AV RE-ENTRANT TACHYCARDIAS
Conduction between atrium and ventricles ceases
PAROXYSMAL SVT! AV Node pacemaker action produces non-
Re-enrant circuits between atria and conducting junctional escape rhythems
ventricles. (asymptomatic)
Or between atria and AV Node- ie in the AV Infranodal WC pacemaker escape rhythms are
NODE unstable, slower (30 bpm), symptomatic.
Treat!? Vagal Stimulation Essentail to insert pacemaker.
Drugs slowing Av node conduction
(Adenosine), class 2, class 4
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

Reduced Myocardial contractility and


Ejection Fraction (under 50%) accounts
HEART FAILURE AND PULMONARY OEDEMA
for most of HF.
o Due to
When CO insufficient to meet the o IHD
metabolic needs of the body. o Cardiomyopathy
Or can only do so with ELEVATED FILLING o Metabolic toxicity
PRESSURES. (pre-load) o Valve defects
Initially compensatory mechanisms maintain o Arrhythmias
CO at rest Initially CO maintained by compensatory
But as HF and CO deteriorates, exercise mechanisms
tolerance falls, and downstream hydrostatic o Inc. sympathetic drive
pressures increase o Raised circulating volume (renin)
Common causes: IHD and Hypertension. o Raised Filling pressures
Volume overload can cause pulmonary These mechanisms have detrimental effects
oedema, despite cgood heart function. Failing heart responds poorly to preload
5 year survival under 50%. Subsequent pulmonary and peripheral
congestion
LV FAILURE Large ventricular volumes increase cardiac
work and impair function
Most common In pressure overload (aortic stenosis),
Downstream pulmonary capillary wedge compensatory hypertrophy initially improves
pressure (PCWP) rises to 25 ish. ventricular Ejection Fraction.
Fluid filters into the alveoli and interstitial Reduced compliance and capillary density
spaces, causing pulmonary oedema, and eventually decreases blood supply and
breathlessness. contractility.
Low plasma oncotic pressure
(hypoalbuminaemia) or increased membrane DIASTOLIC DYSFUNCTION
permeability (inflammation) can cause
pulmonary oedema at lower PCWP. When LV relaxation/filling (an energy
dependent process) is impaired due to
RV FAILURE o myocardial ischemia
o Fibrosis
Causes SYSTEMIC CONGESTION (e.g. ankle o LV hypertrophy (hypertension)
swelling, hepatomegaly) Poor diastolic LV perfusion
Usually associated with LV failure. Reduced LV compliance inc PWCP, and
Biventricular failure: CONGESTIVE CARDIAC precipitates pulmonary oedema- even if
FAILURE normal Ejection Fraction and contractility.
MANAGE HF

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
CLINICAL FEATURES treatment.

Presentation depends on ACUTE LEFT VENTRICULAR FAILURE


o Onset speed
o Underlaying Priority: Immediate relief of breathlessness of
o Ventricular involvement pulmonary oedema.
DIAGNOSTIC
Sitting position INVESTIGATIONS
most comfortable.
HF precipitated/ aggravated by
o Stress Supplemental OXYGEN (60%) corrects hypoxaemia.
o Acute illnesses Loop
DIURETICS
Cardiac Enzymes(furosemide IV) initially reduce LV
o Drugs preload,
ECGand relieve dyspneoa by pulmonary venous
o Pregnancy dilation.
CXR
Reduced CO causes fatigue, anorexia, exercise Subsequent
Serum diuresis
BNP (b-typelowers fluid loadpeptide)
natrieuritic and cardiac
limitation. filling increased
pressures.by myocardial wall stress: sensitive
LVF NITRATES (IV/sublingual)
and specific for HF. inc venous capacitance,
CAUSES
o HF AND PULMONARY
Breathlessness and dilate
ECHO:coronary arteries in ventricular
wall hypokinesia, IHD.
o OEDEMA
Hypoxaemia DIAMORPHONE
enlargement. decreases preload- potent
o Orthopnoea venodilator
effects,
Ejection andreduced
fraction: V02, by in relieving
HF anxiety.
o PND BRONCHODILATORS
CO and BP may be (salbutamol)
normal reduce
MYOCARDIAL DYSFUNCTION bronchospasm (but aminophylline precipitates
o Cough- frothy pink sputum
GALLOP RHYTHEM (S3, S4 added arrhythmias).
o NEW YORK
CPAP reduces HEARTand
hypoxaemia, ASSOCIATION
work of breathing-
IHD
o sounds)
o CARDIOMYOPATHIES used more CLASSIFICCATION
often in HF HF
o COURSE CREPS LUNG BASES
RVF o PREGNANCY ARRYTHMIA CONTROL essential.
MYOCARDIAL
o o Systemic DISEASE
congestion, raised JVP CLASS 1: (mild): no activity limitation, no
o (amyloidosis)
Hepatomegaly LOW-OUTPUTsymptoms
LEFT VENTRICUAR
from ordinary FAILURE
activity. E.g. Fatigue,
If you
o o Ankle have an inferior MI,
oedema dyspnoea, palpitations
o you can have RV failure
Ascites When
CLASS 2: (mild):
pulmonary oedema Slight limitation
controlled, physicalaims
treatment
o isolated,
Onset as blood
may be acute supply
(MI) with activity.LV
to IMPROVE Comfortable
FUNCTION, at Diastolic
rest, symptoms with
Dysfunction
from RCA. ordinary activity.
D, PROGNOSIS.
cardiogenic shock/ acute pulmonary
PRESSURE OVERLOAD ACE CLASS 3: (moderate):
INHIBITORS: Marked limitation
Reduce afterload, increase CO,
o LEFT: hypertension, aortic reducephysical
symptomsactivity, only and
(fatigue) comfortable
lengthenat rest-
survival.
stenosis (mitral stenosis Benefit minimal
most HF activity
patientscauses
unless symptoms.
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
effusion, cardiac But detrimental if high RV filling pressures remain to
tamponade). maintain CO
ARRYTHMIA Afterload reduction with pulmonary vasodilators
o Impair ventricular filling: (CCB) usually limited by hypotension.
hypotension OXYGEN THERAPY relieves cor pulmonale
TACHYCARDIA
o Cause myocardial ischemia- CARDIOGENIC SHOCK
Reduced
Reduced CO
CO Reduced CO
Reduced CO
Reduced CO
Reduced CO
(digoxin)
(digoxin)

ALPHA
ALPHA RENIN-ANGIOTENSIN
RENIN-ANGIOTENSIN
SYMPATHETIC
SYMPATHETIC ACTIVATION
ACTIVATION
ACTIVATION
ACTIVATION
BETA
BETA
SYMPATHETIC
SYMPATHETIC
ACTIVATION
ACTIVATION
(Betablockers) ALDOSTERONE:
ALDOSTERONE:
(Betablockers) (spironolactone)
(spironolactone)
Fluid retention
Fluid retention
ARTERIAL
ARTERIAL (diurteics)....... PRELOAD
VASOCONSTRICTIO (diurteics)....... PRELOAD
VASOCONSTRICTIO INCREASED!
INCREASED!
N
N (venodilators)
(venodilators)
(arterial
(arterial
INCREASES
INCREASES vasodilators)
vasodilators)
CONTRACTILITY
CONTRACTILITY
and HR ANGIOTENSIN
ANGIOTENSIN II:II:
and HR (angiotensinII receptor
(angiotensinII receptor
blockers)
blockers)
ARTERIAL
ARTERIAL
INC
INC AFTERLOAD
AFTERLOAD VASOCONSTRICTION......
VASOCONSTRICTION......
AFTERLOAD
AFTERLOAD INCREASED!
INCREASED!
Renal artery...
Renal FLUID
artery... FLUID
RETENTION
RETENTION
heart- More Work
heart- More Work PRELOAD
PRELOAD INCRESED
INCRESED
and
and oxygen
oxygen
consumption
consumption
heart-
heart- More Work
More Work
and oxygen
and oxygen
consumption
consumption
heart-
heart- More Work and
More Work and
INC
INC Myocardial
Myocardial oxygen consumption
oxygen consumption
Damage
Damage
INC Ca2+ Overload
INC Ca2+ Overload
INC
INC Myocardial
Myocardial
INC energy deficit
INC energy deficit Damage
Cardiac Damage
Cardiac INC Ca2+ Overload
INC Ca2+ Overload
Remodelling
Remodelling INC energy
INC energy deficit
deficit INC Myocardial
INC Damage
Myocardial Damage
INC Ca2+
INC Overload
Ca2+ Overload
Cardiac
Cardiac INC energy deficit
INC energy deficit
Remodelling
Remodelling Cardiac Remodelling
Cardiac Remodelling

Reduced
Reduced CO
CO
Reduced
Reduced CO
CO Reduced CO
Reduced CO

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

HF.

CARDIAC EMERGENCIES: HYPERTENSIVE HYPERTENSIVE EMERGENCY


EMERGENCY
Clinical features of end organ damage (HTN)
Severe hypertension is ENCEPHELOPATHY
o Systolic 220-240 o Decreased vascular auroregulation- cerebral oedema
o Diastolic 120-140 o Headache, nausea, vomiting, blurred vision,
Used to be called accelerated/malignant confusion.
hypertension, now based on presence/absence o Later: Focal neurological deficits, seizures,
LIFE-THREATENING END ORGAN DAMAGE. papilloedema, coma
(LTOD)- e.g. aortic dissection PULMONARY OEDEMA
This determines treatment urgency. o Due to Increased LV afterload (not fluid overload):
If organ damage, needs to be reduced to safe treat by reducing afterload.
levels (diastolic 100) within 2 hrs. PROGRESSIVE RENAL IMPAIRMENT
Caution: rapid fall in BP can cause strokes, o Increased urea and creatinine, dec GFR.
accelerated renal failure, cardiac ischemia. o Haematuria, proteinuria
If NO end organ damage. Gradual reduction o HTN can be secondary to glomerulonephritis and
over 6-72hrs preferred. renal artery stenosis- bruit?
Most common cause STROKE SYNDROMES
o Inadequate/discontinued therapy for o Cerebral infarctions
benign essential HT. o Cerebral Heamorrhage
In under 30s or blacks, over 50% have a o SAH
secondary cause RETINOPATHY
o Renovascular disease o Grade3: exudates and hemorrhage
o Phaeochromocytoma o Grade4: Papilloedema.
o Endocrine AORTIC DISSECTION
o Drug induced catachlomine o Tearing chest/back pain
release (cocaine) o Arm/leg BP difference
o Pregnancy related o Absent peripheral pulses
Most end organ damage due to ARTERIOLAR ANGINA + MI
NECROTIZING VASCULITIS o Due to inc LV afterload, inc wall stress, dec
And LOSS OF VASCULAR AUTOREGULATION myocardial perfusion
PREGNANCY RELATED
HYPERTENSIVE EMERGENCY: MANAGEMENT INFECTIVE ENDOCARDITIS

Severe HTN with end organ failure: Usually subacute


REQUIRES ADMISSION! Infection of heart valves / endocardium
Rarely, immediate BP reduction needed (eg. Causes a chronic illness when organism is non-
Dissecting AA) virulant (streptococcus viridans)
Potent, titratable, vasodilator infusions. Can be ACUTE with virulent:
Arterial BP monitoring Mandarory! STAPHYLOCOCCUS
IV Therapies: Common in
o SODIUM NITROPRUSSIDE (rapidly o Elderly with degenerative aortic and mitral
reversible arterio-venous dilator)- valve
administered by infusion pump to avoid o Prosthetic valves
hypotensive episodes. o Rheumatic fever
o GTN (arteriovenous dilator)- effective o Congenital heart disease
when Myocardial ischemia and Abnormal valves more susceptible to infection
pulmonary oedema there. after dental procedures.
o LABETALOL: alpha and beta blocker- Normal valves occasionally infected by virulent
good for hypertensive encephalopathy. organisms. (staphylococcal valve infection after IV
May exacerbate asthma, HF, heart drug use)
block. CNS FEATURES
Severe hypertension with no end organ o Embolic infarction
damage o Abscesses
o Use oral regimes when possible o Meningitis
o Lower over 24-72 hrs GENERAL INFECTION
o NIFEDIPINE (sublingual) rapid onset, o Low grade fever
short half-life, titratable. o Lethargy, malaise
o Anaemia, weightloss
ACUTE PERICARDITIS CARDIAC
o Murmurs
o HF
o Infection (most viral), MI, Uremia, o Mycotic aneurysms
Connective tissue disease, Trauma, TB, LATE SIGNS
Neoplasia. Dresslers syndrome. o Clubbing
DRESSLERS SYNDROME o Splenomegaly
o 2 weeks after an MI JOINTS
o Immulogically-mediated febrile o Arthralgia
pleuropericarditis o Septic Arthritis
Clinical features
SKIN
o Severe positional (relieved by sitting
o Vasculitis rash
forward)
SOLES OF FEET
o Retrosternal chest pain
o Janeway lesion
o Pericardial rub on Ascultation
IMMUNE COMPLEX DEPOSITION
Investigations
o RETINAL HEAMORRHAGES (Roth spots)
o ECG: CONCAVE ST-SEGMENT ELEVATION
o SUBCONJUNCTIVAL HEAMORRHAGE
IN ALL LEADS
o SPINTER HEAMORAGES, NAILBED INFARCTS
o Cardiac enzymes may be elevated
o JANEWAY LESIONS (small, red macular)
Manage
o OSLERS NODES (subcut swellings in finger/toe
o Antiinflammatory drugs (ASPIRIN)
pulps, pain.
o MICROSCOPIC HAEMATURIA
PERICARDIAL EFFUSION o GLOMERULONEPHRITIS
o LUNG: R. SIDED EMBOLIC INFARCT
Infection, (TB), Uremia, MI, Aortic o LOSS PERIPHERAL PULSES
dissection, myxedema, neoplasia, o RENAL/CEREBRAL EMBOLIC INFARCTS
radiotherapy.
Clinical features Diagnosis initially clinical
o Due to cardiac tamponade- when Suspected in fever, anaemia, high ESR or CRP,
pericardial effusion impairs ventricular microscopic haematuria, new heart murmurs, flu-
filling, reducing CO. like symptoms, weightloss.
o Breathlessness Confirmed by repeatedly positive blood cultures,
o Pericarditic pain and ECHO confirm diagnosis.
o Acute cardiovascular collapse Transthoracic ECHO detects under 50%
Examination vegetations- transoesophageal studies better.
o Raised JVP- increases on inspiration.
o Distant heart sounds Manage
ECG
o Reduced voltage - Look for and treat underlaying infection
o CXR (globular cardiomegaly) (dental abscess?)
o ECHO- (pericardial fluid and cardiac - BENZYLPENICILLIN (empirical antibiotic
tamponade induced RV diastolic therapy)
collapse)- diagnostic. - Adjusted when know cultures.
Manage - Treat 3-6 weeks
WHAT TO DO IN CHEST PAIN EMERGENCY NOTES ON EMERGENCY CHEST PAIN

AIRWAY (patent, manouvres, adjuncts) WORRYING FEATURES


BREATHING (no resp effort.. ARREST o Inc/dec HR
TEAM) o Dec BP
CIRCULATION (no pulse.. ARREST TEAM) o Inc RR
o Dec GCS
CALL FOR SENIOR HELP: (unewell/ o Sudden onset
deteriorating) o Sweating
SIT UP o Nausea & vomiting
15L/min OXYGEN (sats under 94% / sob) o Pain to jaw/ L. Arm / Back
MONITOR (pulse oximiter, BP, ECG, o ECG Changes
Defib) THINK ABOUT COMMON
OBS: (BP both arms, o MI / ACS / ANGINA
ECG) o PE
BRIEF Hx, /NOTES/ STAFF o MUSCULOSKELETAL
EXAMINE: (chest, Rx, Abdo) o PNEUMONIA
ESTABLISH LIKELY CAUSES o PNEUMOTHORAX (simple / tension)
RULE OUT SERIOUS CAUSES o PERICARDITIS
CONSIDER o REFLUX, PEPTIC ULCER
o PCI / THROMBOLYSIS UNCOMMON
o ASPIRIN 300mg PO STAT o AORTIC DISSECTION
o NEEDLE DECOMPRESSION o CARDIAC TAMPONADE
INITIATE FURTHER TREATMENT o SICKLE CELL CRISIS.
(analegesia) ASK ABOUT: Site, onset, radiation, quality (heavy/
VENOUS ACCESS aching/ sharp), intensity (1-10), time onset, duration,
o FBC, U&E, LFT, CRP, gluc, cardiac associated symptoms (sweating, nausea,
marker, D-dimer palpitations, breathless), exacerbating or relieving
o CXR factors (breathing, position, exertion, eating), recent
Call senior help- worsening/ no improvement trauma/exertion, previous episodes
No improvement? REPEAT ECG after 20MINS PMHx: cardiac/ Resp problems / DM / GORD
REASSESS A, B, C DRUGS: Cardiac / respiratory meds, antacids
FHx: IHD / premature cardiac death
LIFE THREATENING CAUSES SH: Smoking / Exercise tolerance
INVESTIGATIONS
MYOCARDIAL INFARCTION o ECG
TENSION PNEUMOTHORAX 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)

Stable Angina Pericarditis AORTIC DISSECTION


Musculoskeletal Pulmonary Embolism
- Exertion pain - Hx viral-like illness - Sudden onset
- Lifting
- Radiates to L arm/ Jaw - Breathlessness
Pleuritic pain - Severe inetrscapular pain
- -Impact injury
Under 20mins - NSTEMI
PE risk factors
Increased on lying - Tearing in nature
- May
- STEMI
be pleuritic
Breathlessness - Pleuritic
Decreased chest painforwards
sitting - Breathlessness
- -Worse Pneumonia
Deconwhen rest/GTN -- Sudden onset pain
Haemoptysis - Pneumothorax
Limb weakness /
- Sudden onset pain
palpation/movement - Radiates to L arm/ jaw ACS /numbness.
Unstable Angina
- - Radiates Productive
to L cough,
arm/ jaw sputum -- Pericardial
Oesophageal
Over 20mins Rub - Sudden onset pleuritic
- - Over - Pleuritic
Dyspnoea
20minspain -- Normal
Otherwiseexamnormal
Breathless, nausea, CVS and - Anginal
chest pain at rest
pain
-- - -Resp exam normal
Tachycardia
Feels unwell - Spasm/reflux
May
RS Hx DVT (swollen red
exams - Tachycardia
Inc severity / freq /
Trauma
Breathless, nausea, sweating
- Tender
-sweating
Non-tender - Previous indigestion/reflux
leg) - Decreased
duration
Tall and Thin BP
- Hiatus herniadyspnoea
Tachycardia/ - Difference in brachial
- - Febrile Normal after pain goes
-- Dyspnoea
Saddle-shaped
by antacids ST
COPD
-- - Normal CXR Dec BP pulses and pressures
Asymmetrical
Dyspnoea air entry - Arrythmia on most ECG
segments - Dyspnoea
- Increased RR
-- - Arrythmia
-Normal
Corse ECG
Transient
creps ECG changes
(unilateral?) - Sweating
leads - Tachycardia
Mediastinal shift
- Upperoxygen
ABG: abdo tender
Dec - Limb weakness /
- - -Sweating Troponin
Dull not elevated
to percussion - Non-tender
Inc CRP & ESR - Non-Tender
Unequal airway and
-Non-tender
Positive stress ECG - Normal
Clear CXRCV and RS - paraesthesia
Normal after pain resolves
- expansion
- Positive D-dimer
- - INC CORONARY
WCC ANGIOGRAPHY
--- ST DEPRESSON
- Hyper-resonance
Sinus
ECG- Tachycardia
exclude cardiac -- CXR WIDENED
- - STCRP up
elevation ST depression
--- S1Q3T3
CXR
T-WAVEnormal
INVERSION MEDIASTINUM
CXR
- consolidation
New LBBB - T waveseparated
Pleura Inversion from ribs
-- Echo: Thrombus
Antacids trial -- ECHO/ CT: Aortic
- Increase cardiac Markers - INC TROPONIN Troponin
on CXR not elevated.
dilation
- ANGIOGRAM: aortic
ACUTE CORONARY SYNDROME ACS SERUM CARDIAC MARKERS

- General term- presentations of varying levels of myocardial o TROPONINS (I or T)


ischemia. A protein: If theyre in the
- Management and outcome better if you know whats going on blood- very likely myocardial
exactly. injury
- Typical sounding chest pain lasting over 20 mins? Can be raised in PE, renal
o New LBBB / ST elevation on ECG? 12hr Troponin will be failure, septicemia, after
raised, but not needed for diagnosis: STEMI tachyarrythmias
o Ischemia other than ST elevation on ECG? But CK not usually raised as
NSTEMI: well in these conditions.
(TropT: over 0.1) or Detection can be 6hrs after
(TropI over 1) injury
Levels elevated for 14days
ST ELEVATION MI
Troponins used as prognostic
indicator in UNSTABLE
WORRYING SIGNS: LV failure and cardiac dysrrythmia. ANGINA / NSTEMI
Central crushing heavy chest pain, (over 20mins) o CK CREATININE KINASE
Radiating to L arm/jaw Enzyme found in all muscle
SOB, nausea, sweating, vomiting, palpitations, anxiety and released in muscle cell
RISK lysis.
o Smoking, obesity, DM, Hypertension, cholesterol, Not specific for cardiac
family, previous IHD. muscle
SIGNS Peaks 24HRS post MI
o ST Elevation (over 1mm in 2 leads, or 2mm in 1 lead) Returns to normal, 48-72
o New LBBB: subsequent Q waves, and T wave hrs post-MI
inversion Useful in detecting further
o CXR: Cardiomegaly, LV failure infarction in patients with
o Cardiac markers raised. pain 3-14 days post MI.
ACUTE TREATMENT (MONAC) o CK-MB
o Rapid re-perfusion by percutaneous coronary Cardiac isomer of
intervention (PCI) in those UNDER 12HRS SYMPTOMS. CREATININE KINASE enzyme
o IE: seek senior help More specific than total CK.
M: DIAMORPHINE 2.5-5mg IV RISK STRATIFICATION IN ACS
O: OXYGEN 15l/min
N: NITRATES: GTN: 2 puffs every 5 mins until no
pain- if still pain, give IV unless hypotensive. o Estimation of death allows
A: ASPIRIN 300mg individualused assessment of risks
C: CLOPIDOGREL 300mg and benefits interventions
(ANTIEMETIC) o Careful targeting of resources to
o WHEN PCI NOT AVAILABLE WITHIN 3 HRS? those patients who stand to
o Fibrinolysis benefit the most.
o Beta blocker: Bisoprolol 10mg/PO- limits mortality o Validated scoring algorithms
o TIMI: THROMBOLYSIS IN
and decreases infarct size- avoid in COPD,
hypotension, failure. MI RISK SCORE
SECONDARY PROHHYLAXIS (BAN SCAR) GRACE: ACS RISK MODEL
o B: BETA BLOCKERS Data from GLOBAL REGISTRY OF
o A: ACEi ACUTE CORONARY EVENTS- huge
o N: Nitrates (symptoms) amount of info from many
countries.
o S: STATIN
o Risk scores calculated on
o C: Clopidogrel 1yr
admission
o A: aspirin lifetime
o Predict in hospital and
o R: Risk factors (smoking, DM, obesity, BP, cholesterol)
6month mortality.
COMPLICATIONS o On discharge: to predict
o Dysrhythmias 6month mortality.
AV Block, Bradycardia, VF/VT High risk?
LVF o Patients need a coronary care
Valve prolapse unit bed.
Ventricular septal rupture o Consider for glycoprotein
Ventricular aneurysm formation llb/llla inhibitors and urgent
Pericarditis, Dresslers syndrome (pericarditis- fever, catheterization
pleuritic pain after heart injury) Low/intermediate risk?
Recurrent Pain o Observation to ensure pain
o CARE AFTER MI free
o Bed rest 48hrs with continuous ECG o Futher stratification using
o Daily 12lead ECG, and clinical examination exercise ECG, coronary
o Thromboembolism prophylaxis calcium scoring/ stress
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,
NSTEMI UNSTABLE ANGINA

WORRYING SIGNS: LV failure and cardiac dysrrythmia. WORRYING SIGNS: LV failure and cardiac
Central crushing heavy chest pain, (over 20mins) dysrrythmia.
Radiating to L arm/jaw Central crushing heavy chest pain, (over
SOB, nausea, sweating, vomiting, palpitations, anxiety 20mins)
RISK Radiating to L arm/jaw
o Smoking, obesity, DM, Hypertension, cholesterol, SOB, nausea, sweating, vomiting,
family, previous IHD. palpitations, anxiety
SIGNS Typically, episodes of angina, occurring
o Same as STEMI at rest or minimal provocation, with poor
o Patients tend to be older with more co-morbidities response to GTN.
than STEMI More frequent and painful than usual.
o ST DEPRESSION, INVERTED T WAVES RISK
o CARDIOMEGALY , FAILURE (CXR) o Smoking, obesity, DM,
o ELEVATEED TROPONIN (12hrs after worst pain) Hypertension, cholesterol,
ACUTE TREATMENT (MONAC) family, previous IHD.
M: DIAMORPHINE 2.5-5mg IV SIGNS
O: OXYGEN 15l/min o ST DEPRESSION, INVERTED T
N: NITRATES: GTN: 2 puffs every 5 mins until no WAVES
pain- if still pain, give IV unless hypotensive. o Dynamic ECG changes over
A: ASPIRIN 300mg time
C: CLOPIDOGREL 300mg o Signs of previous MI?
o Troponin not elevated.
FONDAPARINUX (anticoagulate) ACUTE TREATMENT (MONAC)
Beta-blocker- Bisoprolol 10mg STAT- beware in M: DIAMORPHINE 2.5-5mg IV
COPD, hypotension, failure O: OXYGEN 15l/min
RISK STRATIFY: for ones needing bed in CCU, N: NITRATES: GTN: 2 puffs
catheterization or glycoprotein inhibotors. every 5 mins until no pain- if still
SECONDARY PROHHYLAXIS (BAN SCAR)- same as pain, give IV unless hypotensive.
STEMI A: ASPIRIN 300mg
o B: BETA BLOCKERS C: CLOPIDOGREL 300mg
o A: ACEi - PLUS! BETA-BLOCKERS to limit
o N: Nitrates (symptoms) ischemia
o S: STATIN - FONDAPARINUX (disrupt thrombus)
o C: Clopidogrel 1yr
o Same further management as
o A: aspirin lifetime
NSTEMI
o R: Risk factors (smoking, DM, obesity, BP,
cholesterol)
COMPLICATIONS- same as STEMI, but less common SECONDARY PROHHYLAXIS (BAN SCAR)-
o Dysrhythmias same as STEMI
AV Block, Bradycardia, VF/VT PERICARDITIS
LVF
Valve prolapse Pleuritic chest pain
Ventricular septal rupture Worse on laying flat and deep inspiration
Ventricular aneurysm formation Relieved by sitting forward, recent viral
Pericarditis, Dresslers syndrome (pericarditis- illness
STABLE ANGINA
SIGNS?
o May be none
Retrosternal chest discomfort occurring predictably upon o Pericardial rub
exertion ECG
Relieved by rest and nitrates. o Saddle shaped ST segments in
SYMPTOMS most leads
o Central, heavy chest pain BLOODS
o Lasting under 20mins- radiating to L.arm and jaw o
o Precipitated by exertion, relieved by rest, or GTN in High WCC
under 5 mins Inflammatory markers
o SOB, nausea, sweating, palpitations. ECHO
o Tachycardia, cool, sweaty, clammy, pallor- normal after o Pericardial Effusion
episode. TREAT
ECG o Acutely- reassurance and
o Transient ST-depression during pain anaelgesia
o Flat or inverted T-waves o Paracetamol, NSAIDS
o Signs of previous MI o Should settle 2-4 weeks
Cardiac markers not elevated!
PRIMARY PROPHYLAXIS- kind of the same.
o B: BETA BLOCKERS
o A: ACEi
o N: Nitrates (symptoms)
o S: STATIN
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!!! ADULT TACHYCATRDIA WITH PULSE ALGORHYTHM

AIRWAY: (patent, manouvres, UNI! unstable? narrow? Irregular?


adjuncts)
BREATHING (no resp effort- crash
1. FIRST
team)
- Assess ABCDE
CIRCULATION (no pulse, crash team)
- Oxygen and IV access
SENIOR HELP! If patient unstable - Monitor: EGC, BP, Sp02, 12-lead ECG
o Reduced GCS - Identify and treat reversible causes.. electrolytes?
o Systolic under 90 2. ADVERSE FEAUURES?
o Chest pain - Myocardial Ischemia, HF, Shock, Syncope.
o HF - (My hearts So Speedy)
3. YES UNSTABLE!!! (adverse features)
SIT UP (if hypotensive, lay flat, legs o SYNCHRONISED DC SHOCK
up) o Up to 3 attempts
OXYGEN (15l/min- non rebreather) o AMIODARONE 300mg IV (10-20mins)
MONITOR o Repeat shock followed by
o Pulse oximiter o AMIODARONE 900mg over 24hrs.
o Defib paddles
o BP 4. NO STABLE
o ECG leads o IS QRS NARROW OR BROAD??
Request full set obs and ECG
Hx- BRIEF, CHECK NOTES, MEDS, ASK
STAFF
BROAD QRS NARROW QRS
EXAMINE- CV, resp, Abdo
LIKELY CAUSES and SERIOUS CAUSES-
establish
INITIATE FURTHER TREATMENT 5. REGULAR / IRREGULAR? 5. REGULAR /
IRREGULAR?
VENOUS ACCESS
o Bloods Regular
o FBC Regular
o U+E VT (AMIODARONE)
o D-Dimer o 300mg Over 20mins Use vagal manouvres
o Cardiac Markers o 900mg over 24hrs ADENOSINE (6mg rapid
o TFT SVT with BBB IV bolus, then give 12 if
Consider requesting urgent CXR- (ADENOSINE) needed , then 12)
portable SINUS RHYTHEM
Reassess ABC Irregular BACK??
If now sinus rhythem,
LIFE THREATENING CAUSES AF with BBB was probably RE-
ENTRY PAROXSMAL
Pre-Excited AF
SVT
VT (AMIODARONE)
NO SINUS RHYTHEM?
VF POLYMORPHIC VT eg.
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
o SVT
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 ATRIAL FIBRILLATION- treat

WARNING SIGNS TREAT:


o HF
o Hypotension - Haemodynamically compromised?
o Decreased GCS - Help, shock?, oxygen, iv access,
o Chest pain cardioversion (AMIODARONE)
SYMPTOMS
o SOB CONSERVATIVE
o Palpitations
o Dizziness Treat the precipitant (sepsis?) if new
o Chest Pains onset and this is obvious
RISK FACTORS
o Previous AF RATE CONTROL
o BP
o IHD Control Tachycardia to reduce
o Valvular heart disease myocardial metabolic demand BETA
o PE BLOCKER / DILTIAZEM or
o Pneumonia VERAPAMIL (a rate limiting CCB)
o Thyrotoxicosis DIGOXIN (added in when the
o Alcohol (acute excess, chronic previous were insufficient- not 1st line)
misuse, withdrawal)
o Dilated cardiomyopathy RHYTHEM CONTROL
o Age
o Acute illness Younger patients/ those with new AF-
COMPLICATIONS suitable for attempted cardioversion
o Thromboembolic disease (ischaemic FLECAINIDE: (if doesnt have IHD)
stroke) AMIODARONE (IV through central line
o Drug side effects (amiodarone, warfarin, if has IHD)
beta blockers, digoxin) DC CARDIOVERSION (under sedation-
SIGNS another option)
o Irregularly irregular pulse Maintain sinus rhythm if successful,
o Hypotension SVT(CV compromise) SVT
with beta-blocker
o Signs of disease (thyrotoxicosis,
WARNING pneumonia)
SIGNS ANTICOAGULATION
SIGNS
Investigate
o HF o Tachycardia
o
o Absent p waves
Hypotension Anxiety
oIn all patients where a rate control
o
o Irregularly
Decreased GCSirregular QRS Hypotension
ostrategy is adopted(compromise)
(rather than
o
o WCC high-
Chest pain bloods? Infection? rhythem).
Investigate
o
SYMPTOMSU&E oCanNarrow
use aspirin 75mg tachycardia
complex evey day.. or
o TFT?
o SOB other drugs-have
(unless basedBBB
on stroke
too) risk
o Alcohol
o Palpitations oassessment.
P waves merge into the QRS-
o D-Dimer
o Dizziness(PE?) Anticoagulation
can be hardmust be achieved
to see
o Troponin
o (if ischemic episode
Chest Pains o4weeks before
Regular QRSany planned
responsible?) o Rate over 140
RISK FACTORS
o Previous SVT Acute Treatment
o Structural cardiac anomaly o Oxygen
o Alcohol o 2 large bore cannula
o Increased T4 (thyroid) o Monitor rhythem on defib
COMPLICATIONS o Vagal manouvres
o Hypotension, o cardioversion
o Ischemia, o If recurrent, cardio might need to
o HF, test conduction pathways.
o Deterioration into more sinister
arrhythmia.
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
INITIATE FURTHER TREATMENT EMERGENCY!!! PMHx: Cardiac Disease (IHD/AF), Thyroid surgery,
o Transcutaneous pacing DM, Intercranial pathology/ head injury, glaucoma,
VENOUS ACCESS eating disorder.
THINK ABOUT Drug Hx: Cardiac meds, (Beta blockers, Ca2+
Bloods
o o SINUS BRADYCARDIA antagonists, amiodarone, digoxin)
o FBC After an inferior MI (gets the SA Social Hx: Exercise tolerance, IHD risk factors
o U+E node)
o D-Dimer Drugs (digoxin toxicity) o OBS
o Cardiac Markers
Vasovagal HR,
o TFT Low thyroxine BP,
Consider requesting
urgent CXR-
Hypothermia Postural BP
portable Cushings reflex (bradycardia RR
Reassess ABC and hypertension secondary to Sats
increased ICP) o LOOK FOR
Sleep Pulse rate/rhythem
Anorexia nervosa Volume
Physical fitness Pallor
ASK ABOUT SOB
o Dizziness Dec GCS
o Postural dizziness Drowsy
o Fits/faints Inc JVP (cannon waves in 3rd degree AV
o Weight change block)
o Visual disturbance Signs of cardiac failure (increased JVP,
o Nausea and vomiting pulmonary oedema, swollen ankles)
Investigate Bradyarrythmia
o ECG:
Sinus bradycardia/ complete
heart block
Evidence ischemia/infarction
Evidence digoxin toxicity
o Bloods
FBC
U&E
BRADYARRYTHMIAS ON AN ECG
Glucose
Ca2+ SINUS BRADYCARDIA
Mg2+ o P before every QRS
TFT 1st DEGREE AV BLOCK
Cardiac markers o P-R interval over 0.2 secs (5 small squares)
Digoxin level MOBITZ 1 (WENKEBACH)
Coagulation (if considering o P-R intervals lengthen from beat to beat
pacing wire) o Until failure of AV conduction, then pattern
o CXR restarts
Not really helpful, but may reveal MOBITZII
heart size or pulmonary oedema. o Intermittent P waves fail to conduct to
o HEAD CT ventricles
o But P-R does not lengthen (unlike MOBITZ1)
If suspect raised ICP- but would be
o Typically 2:1
in extremis ie. About to cone-
need neurosurgeon 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

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
DRUGS PRECEEDING BRADYCARDIA
Worrying: HF, Hypotension, decreased GCS
BETA
BLOCKERS (even in eye drops)
Symptoms:
DIGOXIN
o (if patients in AF revert to sinus)
None?
OTHER TYPES OF BLOCK
Ca2+oANTAGONISTS that slow on
Dizziness, especially HRstanding
o VERAPAMIL
o Recurrent falls 1st Degree and MOBITZ1
o DILTIAZEM
o Palpitations o no treatment unless symptomatic or
AMIODARONE
o SOB can cause bradycardia reversible cause.
A-AGONISTS:
o PNENYLEPHERINE
Symptoms of raised ICP used by
anaethatists-
o increased decreased
Hypothermia/ PVR so causes
T4 reflex MOBITZ2 and HIGH GRADE AV BLOCK
brady.
ECG o Can deteriorate into complete heart
o QRS preceeded by a P-wave block
SICK
o SINUS
Rate SYNDROME
under 60 o May need temp/permanent pacing
o QRS narrow unless BBB o Espesh when associated with ACS/
o Exclude ischemia and infarction
Dysfunction of the SA Node
BLOODS
Precipitated by ischemia/fibrosis COMPLETE 3rd DEGREE HEART BLOCK
o FBC
Results in bradycardia/ arrest
o U&E
SA block/ SVT with alternating
o Ca2+ Worrying?
bradycardia/asystole
o Mg2+ o HF, Hypotension, Decreased GCS
Tachy-brady syndrome
o TFT Symptoms
Needs opacing if symptomatic.
Cardiac markers o None? Dizzy? Palpitations? SOB? Chest
o Coagulation (if considering pacing wire) pain?
Causes
ACUTE o Underlying ischemic damage (inferior MI)
o Post cardiac surgery
o If symptomatic or dizzy (GCS under 15) o Drug induced (beta blockers, Ca2+
o Or systolic under 90bpm blockers)
o Monitor HR on defib o Amyloid, Sarcoid, Myeloma, Infective
o Lay flat with legs elevated, as long as (Lyme)
ICP not raised. Signs
o OXYGEN, ACCESS, BLOODS, o Decreased BP / GCS
worrying signs? ARREST o Cannon waves in increased JVP (due to
Titrate 500micrograms ATROPINE asynchronous of right atria against
Every 2-3 mins, up to 5mg closed tricuspid valve
Followed by large flush, until HR improves o HF signs/ underlaying disease
Identify correct precipitant Investigations
Consider pacing wire via central line/ external o ECG: complete dissociation of p waves
pacing from QRS
A precordial thump (percussion pacing) can o Narrow QRS implies proximal lesion
be used in extremis, when an external pacing (responds to atropine)
machine not immediately available. o Broad implies distal lesion (less likely to
respond to atropine)
CHRONIC o Look for evidence MI
o FBC, U&E, Ca2+, Mg2+ TFT, markers,
coagulation
o Consider 24hr tape
o Frequent symptomatic episodes of
ACUTE: ATROPINE / external pacing
bradycardia/pauses are a sign of SICK
CHRONIC: pacemaker/ correct precipitant
SINUS SYNDROME

o May need a permanent pacemaker.
COMPLICATIONS
o Severe bradycardia and high vagal tone
COMPLICATIONS
can deteriorate into asystole- prompt
treatment required
Severe bradycardia and high vagal tone can o Talk contunially
HYPERTENSION EMERGECNY HYPERTENSION EMERGECNY

AIRWAY: Patent? Manouvres? AIRWAY: Patent? Manouvres?


Adjuncts? Adjuncts?
BREATHING: No resp effort? ARREST BREATHING: No resp effort? ARREST
CIRCULATION: No pulse? ARREST CIRCULATION: No pulse? ARREST
DISABILITY: GCS under 8? Anesthetist DISABILITY: GCS under 8? Anesthetist

o IF SYSTOLIC OVER 200, DIASTOLIC 120 o IF SYSTOLIC OVER 200, DIASTOLIC 120
o Sit up o Sit up
o OXYGEN (15l)- if SOB/ sats under 94% o OXYGEN (15l)- if SOB/ sats under 94%
o MONITOR o MONITOR
Pulse oximiter Pulse oximiter
BP BP
Defib leads- if unwell Defib leads- if unwell
o Request full set OBS and ECG o Request full set OBS and ECG
o Bried HX / NOTES/ Ask staff o Bried HX / NOTES/ Ask staff
o Examine o Examine
RS, CVS, abdo, EYE RS, CVS, abdo, EYE
o Rule out serious causes, establish likely o Rule out serious causes, establish likely causes-
causes- is it new?? is it new??
o DO NOT GIVE STAT DOSE ANTI- o DO NOT GIVE STAT DOSE ANTI-HYPERTENSIVE
HYPERTENSIVE WITHOUT SENIOR REVIEW WITHOUT SENIOR REVIEW
o Further treatment o Further treatment
o ACCESS o ACCESS
FBC, U&E, markers, TFT, glucose, FBC, U&E, markers, TFT, glucose,
cortisol cortisol
o Consider urgent CXR o Consider urgent CXR
o Urinalysis and bHCG (if childbearing age) o Urinalysis and bHCG (if childbearing age)
o Senior advice reassess, ABC o Senior advice reassess, ABC

Life threatening causes Life threatening causes

PRE-ECLAMPSIA/ ECLAMPSIA PRE-ECLAMPSIA/ ECLAMPSIA


MALIGNANT HYPERTENSION (200/120) MALIGNANT HYPERTENSION (200/120)
HYPERTENSIVE ENCEPHALOPATHY HYPERTENSIVE ENCEPHALOPATHY
PHAEOCHROMOCYTOMA 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.
END ORGAN DAMAGE? Elevation of BP iver 200 is a
o HYPERTENSION:
Fundoscopy 140/90 hypertensive retinopathy)
(papilloedema, hypertensive emergency
o LV hypertrophy: displaced apex beat of S4 When accompanied by end-organ
o Haematuria damage INVESTIGATIONS
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
Urine Microscopy o LV hypertrophy?
o Decreased GCS, confusion
Renal Doppler USS Bloods:
o Headache
Autoantibodies o
o FBC, U&E, Glucose,
Vomiting
Renal biopsy o cholesterol, TFT
New motor weakness
o PHAEOCHROMOCYTOMA Urine o Seizures, coma
Sweating o CTTREATMENT
may show a SAH, ICH,
Labile hypertensive encephalopathy
Hypertension occurs with cerebral oedema
Palpitations Smoking cessation
following loss of vascular
Plasma metanephrines Regular exercise
auto-regulation.
24hr urine catachlomines and VMA Reduce
EYES alcohol and caffeine intake
(norepinephrine becomes Balanced
o low-salt
Headache diet
vanillylmandelic acid) Modifiable
o risk factors:
Visual DM, lipids
Disturbance
o THYROID DYSFUNCTION Fundoscopy
PHARMACOLOGICAL
o shows retinal
THERAPY
Cold hemorrhage, and
Heat intolerance, sweating Complications papilloedema.
are end organ damage and
Lack of energy malignant
HEARThypertension
TFTs o Chest pain
o ACROMEGALY o Orthopnea
Headache o ECG changes,
Visual Field disturbance o Elevated cardiac markers
Change in facial features o Pulmonary oedema on CXR
IGF-1 AORTA
Pituitary hormone levels o Sudden, tearing chest pain
o CUSHINGS SYNDROME radiating to back
Centripetal obesity o Collapse
Skin thinning, weakness o Echo/CT may reveal oertic
Urinary free cortisol dissection
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%

Over
Over
Under 55
Under 55 55/Black
55/Black
A C

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:

o Splinter haemorrhages HYPERTENSIVE


(IE) CRISIS- Treat ACUTELY
o 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
o Channel
nicotineBlocker
stainingor ACEi (A or C)
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)
Admit
NECK:
to HDU or ICU
JVP
Close omonitoring of BP, ECG, neurological state, Fluid balance
(arterial
FACE:line, central line, catheterization)
Malar flush
Rapid oreduction in BP can be dangerous due to cerebral hypoperfusion
o Anaemia
Only necessary conjunctiva
in ACUTE MI / AORTIC DISSECTION
o
Otherwise, Central
aim to Cyanosis
reduce diastolic to 100 or by 25% (the higher one), over 24hrs
o
More severeHypercholersterolemia:
end organ damage needs Xantholasma
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
taken.ischemic
Thoracotomystroke), thecerebral
scar: auroregulation
Scar left axilla diagonallycan be back-
down impaired and aggressive
previous lowering
mitral stenosis of BP
(or line
causes hypoperfusion
from L breast to and poor outcome
axilla)
o Deformities: sternal depression, scoliosis, kyphosis- can displace apex beat and cause ejection
systolic murmur.
o Apex- look for cardiac pulsation

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.
o Radio-radial delay
Aortic dissection
Proximal arterial disease (atherosclerosis of axillary artery)
o 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)
o Collapsing pulse
Aortic regurgitation
Ask if pain in shoulder
o 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

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

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

Altered Heart sounds

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

Mitral regurgitation and aortic stenosis


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

Aortic stenosis

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 regurgitation
Mitral stenosis
o Mid diastolic murmur (click whoosh)
o Associated with AF
o Lay on LHS, listen to mitral area
o Caused by rheumatic fever
Aortic regurg
o Early diastolic murmur
o High pitched, starts loud and lets quitter
o 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. Check NAME, DATE, TIME


2. Examine ECG in relation to previous ECGs (St changes can be fixed or dynamic)
3. 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: II, III, AVF (the bottom L) RIGHT CORONARY


SEPTAL: V1, V2 Proximal LAD
ANTERIOR: V3, V4 LAD
LATERAL: V5, V6, I, AVL Circumflex

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. Name, Date, time


2. Rate and Rhythem (strip at bottom)
3. Check leads 1 and 3 for axis (Left alone, Right-alright)
4. 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