Diseases of Heart Muscle

Diseases of heart muscle
Causes;
o Viruses coxsacckie, polio, HIV, Lassa fever
o Bacteria Clostridia, diphtheria, Meningococcus Mycoplasma, Psittacosis
o Spirochaetes Leptospirosis, syphilis, Lyme disease
o Protoszoa Chagas disease
o Drugs
o Toxins
o Vasculitis

* Signs/symptoms
o Fatigue, dyspnoea, chest pain, palpitations, tachycardia, soft S1, S4 gallop

* Test
o ECG ST segment elevation/depression, T wave inversion, atrial arrhythmias,
transient AV block
o Serology may be helpful

* Management
o Treat underlying cause
o Patient may recover or get retractable heart failure

Dilated cardiomyopathy
* Associated with;
o Alcohol
o Hypertension
o Haemochromatosis
o Viral infection
o Autoimmune
o Peri or postpartum
o Thyrotoxicosis
o Congenital

* Presentation
o Fatigue, dyspnoea, pulmonary oedema, RVF, emboli, AF, VT

* Signs
o Raised pulse, lowered BP, raised JVP, displaced apex beat, S3 gallop, mitral or
tricuspid regurgitation, pleural effusion, oedema, jaundice, hepatomegaly,
ascites

* Tests
o CXR cardiomegaly, pulmonary oedema
o ECG tachycardia, non-specific T wave changes
o Echo globally hypokinetic heart with low ejection fraction

* Management
o Bed rest, diuretics, digoxin, ACEI, anticoagulation, consider heart transplant
o Mortality
o Variable 40% in 2 years

Hypertrophic cardiomyopathy
* This is LV outflow tract obstruction from an asymmetric septal hypertrophy
* Prevalence
o 0.2% autosomal dominant inheritance by 50% are sporadic (genes include
?-myosin, ?-tropomyosin)

* Symptoms and signs
o Angina, dyspnoea, palpitaions, syncope, sudden death, a wave in JVP, harsh
ejection systolic murmur

* Tests
o ECG LVH, progressive T wave inversion, deep Q waves, AF, WPW,
ventricular ectopics and VT
o Echo asymmetrical septal hypertrophy, small LV cavity with
hypercontractile posterior wall

* Management
o ?-blockers and verapamil for symptoms
o Amiodarone for arrhythmia
o Anticoagulate for paroxysmal AF of systemic emboli
o Dual chamber pacing
o Septal myomectomy

Restrictive cardiomyopathy
* Causes;
o Amyloidosis
o Haemochromatosis
o Sarcoidosis
o Scleroderma
o Lofflers eosinophilic endocarditis
o Endomyocardial fibrosis

* Presentation
o Like constrictive pericarditis
o Features of RVF predominate, raised JVP with prominent x and Y decents,
hepatomegaly, oedema, ascites

Cardiac myxoma
* Rare benign cardiac tumour
* Usually sporadic but may be familial (autosomal dominant)
* May mimic IE (fever, weight loss, clubbing, raised ESR) or mitral stenosis (left
atrial obstruction, systemic emboli, AF)
* A tumour plop may be heard

* Test
o ECHO
o Treatment
o Excision Acute myocarditis

* Causes;
o Viruses coxsacckie, polio, HIV, Lassa fever
o Bacteria Clostridia, diphtheria, Meningococcus Mycoplasma, Psittacosis
o Spirochaetes Leptospirosis, syphilis, Lyme disease
o Protoszoa Chagas disease
o Drugs
o Toxins
o Vasculitis

* Signs/symptoms
o Fatigue, dyspnoea, chest pain, palpitations, tachycardia, soft S1, S4 gallop

* Test
o ECG ST segment elevation/depression, T wave inversion, atrial arrhythmias,
transient AV block
o Serology may be helpful
* Management
o Treat underlying cause
o Patient may recover or get retractable heart failure

Infective endocarditis
A fever plus new murmur is endocarditis unless proved otherwise
Classification
50% of all endocarditis occurs on normal valves, this follows an acute
course and presents with acute heart failure
Endocarditis on abnormal valves tends to run a more subacute course
Causes
Bacteria
Any cause of bacteraemia can expose the valves to risk of
colonisation
Strep viridans in the most common cause
Other enterococci, Staph aureus or epidermidis
Rarely HACEK group of Gram negs, Haemophilus,
Actinobacillus, Cardiobacterium, Eikenella, Kingella and
Coxiella burnetti and Chlamydia
Fungi
Candida, aspergillus and histoplasma
Other causes;
SLE (Libman-Sacks endocarditis), malignancy
Clinical features
Septic signs
Fever, rigors, night sweats, weight loss, anaemia, splenomegaly,
clubbing
Cardiac lesions
Any new murmur or change in pre-existing murmur
Vegetations may cause valve destruction, severe regurgitation or
valve obstruction
An aortic root abscess may prolong the P-R interval or lead to
complete heart block
Immune complex deposition
Vasculitis may affect any vessel
Glomerulonephritis and acute renal failure
Splinter haemorrhages
Roth spots (boat shaped retinal haemorrhages with pale centre)
Oslers nodes (painful pulp infacts in fingers and toes)
Janeway lesions (painless palmar or plantar macules)
Embolic phenomenon
Emboli may cause abscesses in the relevant organ (brain, heart,
kidney, spleen, GI tract)
In right sided IE pulmonary abscesses are common
Tests
Blood cultures 3 sets at different times and from different places at
peak fever
10% are negative
Bloods normocytic normochromic anaemia, neutrophilic leukocytosis,
high ESR/CRP, also check U&Es, Mg+ and LFTs
Urinalysis haematuria
ECG prolonged P-R interval
ECHO may show vegetations if >2mm
Diagnosis
Duke criteria
Need to have 2 major or 1 major and 3 minor or all 5 minor
criteria for diagnosis
Major criteria
Positive blood culture
Endocardium involved positive ECHO (vegetation, abscess,
dishiscence of prosthetic valve) or new murmur
Minor criteria
Predisposition cardiac lesion or IV drug abuse
Fever >38C
Vascular/immunological signs
Positive blood cultures that dont meet diagnostic criteria
Positive ECHO that doesnt meet major criteria
Management
Antibiotics empirical benzylpenicillin, gentamycin +/- flucloxacillin
if acute
Consider surgery if heart failure, valvular obstruction, repeated
emboli, fungal endocarditis, persistent bacteraemia, myocardial abscess,
unstable infected prosthetic valve
Prognosis
30% mortality with staphylococci
15% with bowel organisms
6% with sensitive streptococci

Right heart valve disease
Causes;
Functional (pulmonary hypertension)
Rheumatic fever
Infective endocarditis (IV drug users)
Carcinoid syndrome
Congenital
Symptoms
Fatigue
Hepatic pain on exertion
Ascites
Signs
Murmur best heard at the lower sternal edge in inspiration
Giant V waves and prominent y decent in JVP
RV heave
Pulsatile hepatomegaly
Jaundice
Ascites
Management
Treat underlying cause
Drugs diuretics, digoxin, ACEI, valve replacement (20%
operative mortality)
Tricuspid stenosis
Causes
Rheumatic fever (almost always with mitral or aortic valve
disease)
Symptoms
Fatigue
Ascites
Oedema
Signs
Giant a wave and slow y decent in JVP
Opening snap
Diastolic murmur best heard at the left sternal edge during
inspiration
Diagnosis
ECHO
Treatment
Diuretics and surgical repair
Pulmonary stenosis
Usually congenital;
Turners syndrome
Noonans syndrome
Williams syndomre
Fallots tetralogy
Rubella
Acquired causes;
Rheumatic fever
Carcinoid syndrome
Symptoms
Dyspnoea
Fatigue
Oedema
Ascites
Signs
Dysmorphic facies (congenital causes)
Prominent a wave on JVP
RV heave
Ejection systolic murmur that radiates to the left shoulder
Tests
ECG RAD, P-pulmonale, RBBB
CXR post-stenotic dilation of pulmonary artery, oligaemic
lung fields, RV hypertrophy and right atrial hypertrophy
Treatment
Pulmonary valvuloplasty or valvotomy
Pulmonary regurgitation
Causes by any cause of pulmonary hypertension
A decrescendo murmur is heard in early diastole at left sternal edge
(Graham Steell murmur)
Cardiac surgery
Valve replacements
Mechanical valves can be;
Ball-cage (Starr-Edwards)
Tilting disc (Bjork-Shiley)
Double tilting disc (St Jude)
Patients require lifetime coagulation
Xenografts are made from porcine valves or pericardium and
dont last as long but dont require thromboembolism
Complications of prosthetic valves;
Systemic embolism
Haemolysis
Structural valve failure
Arrhythmias

Aortic Valve Disease
Aortic stenosis
Causes;
Senile calcification (commonest)
Congenital bicuspid valve, Williams syndrome
Presentation;
Angina
Dyspnoea
Dizziness
Faints
Systemic emboli if infective endocarditis
CCF
Sudden death
Signs
Slow rising pulse with narrow pulse pressure
Heaving, non-displaced apex beat
LV heave
Aortic thrill
Ejection systolic murmur which radiates to the carotids
Tests
ECG P-mitrale, LVH with strain pattern, LAD, LBBB or
complete AV block (calcified rings)
CXR LVH, calcified aortic valve, post-stenotic dilation of the
ascending aorta
ECHO diagnostic, severe stenosis if gradient >50mmHg and
valve area <0.5cm
Differential diagnosis
HOCM
Management
If symptomatic then prognosis is poor 2-3yr survival if
angina/syncope, 1-2yr if cardiac failure
Prompt valve replacement is recommended if symptomatic or if
not symptomatic but with severe AS and deteriorating ECG

Aortic regurgitation
Causes;
Congenital
Rheumatic fever
IE
RA, SLE
Aortic root disease;
Hypertension
Trauma
Aortic dissection
Seronegative arthropathies AS, Reiters syndrome, psoriatic
arthropathy
Marfans syndrome
Osterogenesis imperfecta
Syphilitic aortitis
Symptoms
Dyspnoea
Palpitations
Cardiac failure
Signs
Water hammer pulse
Wide pulse pressure
Displaced hyperdynamic apex beat
High pitched early diastolic murmur best heard in expiration
with patient sitting forward
Corrigans sign carotid pulsation
De Mussets sign head nodding
Quinckes sign capillary pulsation in nail beds
Duroziezs sign femoral diastolic murmur as blood flows
backward in diastole
Traubes sign pistol shot femorals
In severe AF an Austin flint murmur may be heard
Tests
ECG LVH
CXR cardiomegaly, dilated ascending aorta, pulmonary
oedema
ECHO
Cardiac catheterisation
Management
Indications for surgery
Increasing symptoms
Enlarging heart on CXR/Echo
ECG deterioration (T wave inversion)
Infective endocarditis refractive to surgery
Aim to replace the valve before significant dysfunction occurs

Mitral Valve Disease
Causes;
Rheumatic
Congenital
Mucopolysaccharidoses
Presentation
Dyspnoea
Fatigue
Palpitations
Chest pain
Systemic emboli
Haemoptysis
Signs
Malar flash
Low volume pulse
AF common
Tapping non displaced apex beat (palpable S1)
On auscultation loud S1, opening snap, rumbling mid-diastolic
murmur (best heard in expiration on the patients left side)
The more severe the stenosis the longer the diastolic murmur
Tests
ECG AF, P-mitrale if in sinus, RVH, progressive RAD
CXR left atrial enlargement, pulmonary oedema, mitral valve
calcification
ECHO diagnostic
Management
If in AF rate control
Anticoagulate with warfarin
Diuretics decrease preload and pulmonary venous congestion
Balloon valvuloplasty, open mitral valvotomy or valve
replacement
Complications;
Pulmonary hypertension
Emboli
Pressure of large LA on other structures e.g. recurrent laryngeal
nerve (hoarseness), oesophagus (dysphagia), bronchial
obstruction
Mitral regurgitation
Causes;
Function (LV dilatation)
Annular calcification
Rheumatic fever
Mitral valve prolapse
Papillary muscle dysfunction/rupture
CT disorders Ehlers-Danlos, Marfans syndrome
Cardiomyopathy
Congenital
Symptoms
Dyspnoea
Fatigue
Palpitations
Signs
AF
Displaced hyperdynamic apex
RV heave
Soft S1, split S2, loud P2 (pulmonary hypertension)
Pansystolic murmur at apex radiating to the axilla
Tests
ECG AF, P-mitrale if in sinus, LVH
CXR big LA and LV, mitral valve calcification and pulmonary
oedema
ECHO diagnostic
Management
Control rate if in AF
Anticoagulate if - history of AF, history of embolism, prosthetic
valve, additional mitral stenosis
Diuretics improves function
Surgery for deteriorating symptoms aim to repair or replace
valve before LV is irreversibly impaired

Mitral valve Prolapse
Prevalence 5%
Occurs alone or with ASD, PDA, cardiomyopathy, Turners syndrome,
Marfans syndrome and osteogenesis imperfecta
Symptoms
Asymptomatic or atypical chest pain and palpitations
Signs
Mid-systolic click and or late systolic murmur
Complications
Cerebral emboli
Arrhythmias
Sudden death
Tests
ECHO is diagnostic
ECG may show inferior T wave inversion
Treatment
?-blockers may help palpitations and chest pain

Congenital heart disease
Bicuspid aortic valve
Function well at birth and go undetected
Eventually develop AS and or AR
Atrial septal defect
Ostium secundum defects are the most common
Ostium primum defects are associated with AV valve anomalies
Secundum ASDs may not present until adulthood
Left to right shunting may precipitate heart failure
There may be pulmonary hypertension, cyanosis, arrhythmia,
haemoptysis and chest pain
Signs;
AF
Raised JVP
Fixed split S2
Pulmonary ejection systolic murmur
Pulmonary hypertension may cause pulmonary or tricuspid
regurgitation
Complications
Reversal of the left to right shunt (Eisenmengers complex)
Paradoxical embolisation
VSD
Can be congenital (2 in 1000 births) or post-MI
May present with severe heart failure in infancy or remain
asymptomatic until detected in later life
Signs
Harsh pansystolic murmur heard over the left sternal edge with
a systolic thrill and left parasternal heave
Larger holes may be associated with pulmonary hypertension
Coartation of the aorta
Congenital narrowing of the aorta usually occurring just distal to the
origin of the left subclavian artery
Associated with biscuspid aortic valve and Turners syndrome
Signs
Radio-femoral delay, weak femoral pulse, raised BP, scapular
bruit, systolic murmur best heard over left scapula
Complications
Heart failure
Tests
ECG shows rib notching

Pericardial disease
Acute pericarditis
Inflammation of the pericardium which may be primary of secondary to
systemic disease
Causes;
Viruses coxackie, flu, EBV, mumps, varicella, HIV
Bacteria pneumonia, rheumatic fever, TB
Fungi
MI, Dresslers syndrome
Others uraemia, RA, SLE, myxoedema, trauma, surgery,
malignancy, radiotherapy
Clinical features;
Chest pain, worse on inspiration and releived by leaning forward
May be a pericardial rub
May be fever
Tests
ECG classically shows saddled shaped ST segment
Bloods FBC, ESR, U&Es, cardiac enzymes (troponin may be
raised), viral serology, blood cultures and if indicated
autoantibiodies, fungal precipitans, TFTs
CXR cardiomegaly
Echo if suspected pericardial effusion
Treatment
Analgesia
Treat cause
Consider colchicines before steroids or immunosuppressants if
relapse or continuing symptoms occur (15-40% do recur)
Pericardial effusion
Accumulation of fluid in the pericardial sac
Causes;
Any of the causes of pericarditis
Clinical features;
Dyspnoea, raised JVP
Bronchial breathing at the left base (Ewarts sign large
effusion pressing on the left lower lobe)
May be signs of cardiac tamponade
Diagnosis
CXR shows enlarged globular heart
ECG shows low voltage QRS complexes and alternating QRS
morphologies (electrical alterans)
Echo shows an echo-free zone around the heart
Management
Address the cause
Pericardiocentesis may be diagnostic or therapeutic
Send pericardial fluid for ZN stain/TB culture and cytology
Constrictive pericarditis
The heart if encased in a rigid pericardium
Causes often unknown or any cause of pericarditis
Clinical features
Mainly RHF with raised JVP, Kussmauls sign (JVP rising with
inspiration), soft diffuse apex meat and quite heart sounds, S3,
diastolic pericardial knock, hepatomegaly, ascites
Tests
CXR small heart +/- pericardial calcification
CT/MRI
Echo
Cardiac catheterization
Management
Surgical excision
Cardiac tamponade
Accumulation of pericardial fluid raises intra-pericardial pressure,
hence poor ventricular filling and reduced cardiac output
Causes
Any cause of pericarditis, aortic dissection, haemodialysis,
warfarin, trans-septal puncture at cardiac catheterization, post
cardiac biopsy
Signs
Raised pulse, lowered BP, pulsus paradoxus, raised JVP,
Kussmaul/s sign, muffled heart sounds
Diagnosis
Becks triad falling BP, rising JVP, small quite heart
CXR big globular heart (if >250ml of fluid)
ECG low voltage QRS +/- electrical alterans
Echo diagnostic echo free zone >2cm, >1cm if acute around
the heart, +/- diastolic collapse of the RA and RV
Management
Urgent drainage, send fluid off for cytology and culture as before

Hypertension
Treat all patients with malignant hypertension or a sustained pressure
>160/100mmHg
For those with pressures >140/90 the decision depends upon the risk of
coronary and stroke events, diabetes or end-organ damage
Examples of end organ damage are; LVH, past MI or angina, past stroke
or TIA, peripheral vascular disease or renal failure
For diabetics aim for <130/90 and 125/75 if proteinuria
Evidence from the Framingham and MrFIT studies indicates that
systolic is more important that diastolic in determining risk in the over
50s
Isolated systolic hypertension
Most common form in the UK (>50% of over 60)
Results from stiffening of the large arteries (arteriosclerosis)
Not benign doubles risk of MI, triples risk of CVA
Malignant hypertension
Systole >200, diastolic >130mmHg in conjunction with bilateral
haemorrhages and exudates (papilloedeam may or may not be
present)
Symptoms are headache and visual disturbance
May precipitate renal failure, heart failure and encephalopathy
Untreated 90% die within a year, if treated 70% survive 5 years
Pathological hallmark is fibrinoid necrosis
Causes of hypertension;
Primary hypertension 95%, of unknown cause
Secondary hypertension;
Renal disease
Intrinsic renal disease (75%);
Glomerulonephritis
Polyarteritis nodosa (PAN)
Systemic sclerosis
Chronic pyelonephritis
Polycystic kidneys
Renovascular disease (25%)
Artheromas
Fibromuscular dysplasia (young women)
Endocrine;
Cushings
Conns
Phaeochromocytoma
Acromegaly
Hyperparathyroidism
Others;
Coarctation
Pregnancy
Steroids
MAOI
the pill
Examination
Always examine the CVS and check for retinopathy
Look for signs of renal disease
Radio-femoral delay or weak femoral pulses (coartation)
Renal bruits
Palpable kidneys
Cushings syndrome
Look for end organ damage LVH, retinopathy, proteinuria
Hypertensive retinopathy
I tortuous arteries with thick shiny walls (silver or copper wiring)
II A-V nipping (narrowing where the arteries and veins cross)
III Flame haemorrhages and cotton wool spots
IV Papilloedema
Investigations;
Basic U&Es, creatine, cholesterol. Glucose, ECG, urine analysis
Specific renal ultrasound, renal arteriography, 24hr urinary VMA,
urinary free cortisol, rennin and aldosterone, ECHO

Management
Look for and treat underlying causes
Any adult over 50 would benefit from antihypertensives whatever their
starting BP
Reduce BP slowly, rapid reduction may be fatal
Life style changes
Drugs
If 55 or over and in Black patients 1
st
choice is Ca2+ channel
blocker or thiazide
If <55 1
st
choice in an ACEI
If initial treatment with ACEI isnt working add a thiazide or
Ca2+ channel blocker, if treatment with those arent working
add an ACEI
If treatment with 3 drugs is required try and ACEI, Ca2+
channel blocker and thiazide
If a 4
th
drug is needed consider;
Increasing doses of thiazine
Spironolactone
?-blocker
Selective ?-blocker
?-blockers are not first line for hypertension but consider them
in young people, if intolerant or contraindicated to ACEI or
ARB, if it is a woman of child bearing age or there is increased
sympathetic drive
If a ?-blocker is initiated and a 2
nd
drug is needed add a Calcium
channel blocker and not a thiazide to reduce the risk of diabetes
Malignant Hypertension
Use oral therapy unless there is encephalopathy or CCF
Aim for controlled reduction in BP in days not hours
Avoid sudden drops in BP are cerebral autoregulation is poor so stroke
risk is high
Management;
Best rest there is no ideal hypertensive by atenolol and log
acting Ca2+ channel blockers may be used PO
Encephalopathy aim to reduce the BP to around 100mmHg
diastolic over 4hr
Insert intra-arterial line for pressure monitoring
Furosemide 40-80mg IV then either
IV labetolol or
Sodium nitrprusside infusion
Never use sublingual nifedipine to reduce BP large drop in BP
and high stroke risk

Heart Failure
CO and BP that are inadequate for the bodys requirements
82% die within 6yr of getting diagnosis
Classification
LVF and RVF may occur independently or together as congestive cardiac
failure (CCF)
Low output failure
Pump failure due to;
Heart muscle disease; IHD, cardiomyopathy
Restricted filling; constricitive pericarditis, tamponade,
restricted cardiomyopathy (this may be the mechamism
by which fluid overload causes heart failure as an
expanding right heart can impinge on the LV
Inadequate heart rate; ?-blockers, heart block, post MI
Negative ionotropic drugs; most antiarrhythmic drugs
Excessive preload
Fluid overload
Chronic excessive afterload
Aortic stenosis
Hypertension
High output failure when there are increased needs that the heart fails
to meet
Causes
Pregnancy
Anaemia
Thyrotoxicosis
Pagets disease
AV malformations
Beri beri
Initially associated with features of RHF and later LHF
Symptoms
LHF;
Dyspnoea
Poor exercise tolerance
Fatigue
Orthopnoea, PND
Nocturnal cough, wheeze (cardiac asthma)
Cold peripheries
Weight loss, muscle wasting
RHF
Peripheral oedema
Abdominal distension
Nausea, anorexia
Facial engorgement
Pulsation in the neck and face
Signs
Patient looks ill and exhausted, cool peripheries, peripheral cyanosis
Pulse resting tachycardia, pulsus alternans
Reduced systolic BP, narrow pulse pressure, raised JVP
Praecordium displaced apex (LV dilatation), RV heave (pulmonary
hypertension)
Ausculation S3 gallop, murmurs of the aortic or mitral area
Chest tachypnoea, bibasal end inspiratory crackles, wheeze, pleural
effusions
Abdomen hapatomegaly (pulsatile), ascites
Investigations
If ECG and BNP are normal, heart failure is unlikely
If either is abnormal then ECHO is required
Bloods;
FBC, U&Es, BNP
CXR
Cardiomegaly, prominent uupper lobe veins (upper lobe
diversion), peribronchial cuffing, diffuse interstitial or alveolar
shadowing, perihilar batwing shawdowing, fluid in the fissures,
pleural effusions, Kerley B lines (due to interstitial oedema) and
engorged peripheral lymphatics
ECG may indicate cause;
Ischaemia, MI, ventricular hypertrophy
CXR in LVF;
A Alveolar oedema (bat wings)
B Kerley B lines
C cardiomegaly
D Dilated prominent upper lobe vessels
E Pleural effusion

New York classification of Heart Failure
I heart disease present, but no undue dyspnoea from
ordinary activities
II comfortable at rest, dyspnoea on ordinary activities
III less than ordinary activity causes dyspnoea which is
limiting
IV dyspnoea present at rest, all activity causes
discomfort
Management
Acute heart failure
Medical emergency see below
Chronic heart failure
Treat cause or exacerbating factors
Avoid exacerbating factors NSAIDs (cause fluid retention), verapamil
(negative ionotrope)
Lifestyle diet, stop smoking, limit salt, exercise
Drugs;
Diuretics
Loop diuretuics used to relieve symptoms e.g.
furosemide 40mg/24hr PO (SE ?K+. renal failure)
Monitor U&Es and add spirinolactone if K+
<3.2mmol/L
If refractory oedema consider adding a thiazine e.g.
metolazone 5-20mg/24hr
ACEI
Consider in all patients with LV systolic dysfunction
If cough use angiotensin receptor antagonist e.g.
candesartin
?-Blockers
E.g. carvedilol
Recent RCTs show they reduced mortality
Should be initiated after diuretics and ACEI
Use with caution, start low and go slow
Spironolactone
RALES trial showed it reduced mortality by 30% when
added to conventional therapy
Initiate in patients who remain symptomatic despite
optimal therapy listed above
It improves endothelial function and presents
remodelling
Digoxin
Improves symptoms even in those who are in sinuns
Use if symptoms are controlled by diuretics, ACEI and ?-
blocker or the patient is in AF
Does is 0.125-0.25mg/24hr. monitor U&Es and watch
for K+ rising
Vasodilators
The combination of hydralazine and isosorbide dinitrate
should be used in those intolerant of ACEI or ARB
It also reduces mortality in Black patient with HF
ACE-I
Contraindications/cautions;
Renal failure
Hyperkalaemia, hyponatraemia
Hypovolaemia, hypotension
Aortic stenosis or LV outflow tract obstruction
Pregnancy or lactation
Severe COPD or cor pulmonale
Renal artery stenosis
SE;
Hypotension tell patient to take the first dose before going to
bed
Dry cough
Taste disturbance
Hyperkalaemia
Renal impairment
Urticaria and angioneurotic oedema
If patient has heart failure start ACEI under hospital supervision e.g.
lisinopril 30-40mg/day
If patient has hypertension they can be started s an outpatient e.g.
lisinopril 10mg/day (elderly 2.5mg)
Emergency management of severe pulmonary oedema
Causes;
Cardiovascular usually LVF post MI or ischaemia disease also
mitral stensosi, arrhythmias and malignant hypertension
ARDS
Fluid overload
Neurogenic e.g. head injury
Difficult to distinguish pneumonia, COPD/asthma and
pulmonary oedema therefore start all 3 treatments at once
salbutamol nebuliser, furosemide IV, diamorphine and
amoxicillin
Sit patient upright
100% O2 if no pre-existing lung disease
IV access and monitor ECG treat any arrhythmias
Investigations whilst continuing treatment;
CXR
ECG
U&Es cardiac enzymes, ABG
ECHO
Plasma BNP if diagnosis is in question
Diamorphine 2.5-5mg IV slowly (caution in liver failure and COPD)
Furosemide 40-80mg IV slowly (larger doses required in renal failure)
GTN spray 2 puff sublingual or 2 x 0.3mg tablets sublingual (dont give
is systolic <90mmHg)
Nitrates reduces pre and after load and are coronary artery
dilators
Necessary investigations, history, examination
If systolic >100mmHg start nitrate infusion e.g. isosorbide dinitrate 2-
10mg/hr
If patient is worsening give further dose of furosemide 40-80mg and get
help
If systolic <100mmHg, treat as cardiogenic shock i.e. consider a Swan-
Ganz catheter and inotropic support
If patient fails to improve consider other diagnosis;
Hypertensive heart failure, aortic dissection, PE, pneumonia
Monitor progress via;
BP
Heart rate
Cyanosis
RR
JVP
Urine output
ABG
Once stable and improving;
Weight daily, BP and pulse every 6hr. repeat CXR
Change to oral furosemide or bumetanide
If on large doses of loop diuretic then consider the addition of a
thiazide
ACEI if LVF
Also consider ?-blocker and spironolactone
Is the patient suitable for heart transplant
Consider digoxin and warfarin especially if in AF
Emergency Management of Cardiogenic shock
Caused primarily by the failure of the heart to maintain the circulation
Has a high mortality
Causes;
MI
Arrhythmias
PE
Tension pneumothorax
Cardiac tamponade
Myocarditis myocardial depression (drugs, hypoxia, acidosis,
sepsis)
Valve destruction (endocarditis)
Aortic dissection

Management
If the cause if MI prompt revascularisation
Oxygen
Diamorphine 2.5-5mg
Investigations and close monitoring
Correct arrhythmias, U&E abnormalities or acid-base disturbances
Optimise filling pressure measure pulmonary capillary wedge
pressure (PCWP)
If PCWP is <15mmHg give a plasma expander 100ml every
15mins IV, aim of a PCWP of 15-20mmHg
If PCWP >15mmHg consider ionotropic suppose e.g.
dobutamine 2.5-10?g/kg/min IVI. Aim for a systolic of 80mmHg
Consider renal dose dopamine 2-5?g/kg/min (via central line only)
Consider intra-aortic balloon pump if you expect the underlying
condition to improve or you need time awaiting surgery
Look for and treat any reversible cause; MI or PE consider
thrombolysis. Surgery for acute VSD, mitral or aortic incompetence
Monitor
CVP, BP, ECG, urine output
Swan-Ganz catherter for pulmonary wegde pressure and CO
Arterial line to monitor pressure
Catheterise for accurate urine output
Cardiac tamponade
Causes;
Trauma
Lung/breast cancer
Pericarditis
MI
Bacteria e.g. TB
Rarely raised urea, readitation, myxoedema, dissecting aorta,
SLE
Signs;
Falling BP, rising JVP and muffled heart sounds (Becks traid)
JVP raised on inspiration (Kussmauls sign)
Pulsus paradoxus (pulse fades on inspiration)
CXR
Globular heart
ECG
Electrical alterans
Management
Pericardiocentesis
Whilst awaiting this give O2, monitor ECg, set up IVI. Take
blood for group and save

Rheumatic fever
Still common in developing countries
Peak incidence 5-15 years
Tends to reoccur unless prevented
Pharyngeal infection with Lancefield Group A ?-haemolytic strep
triggers rheumatic fever 2-4 weeks later in the 2% of the susceptible
population
Due to antibody to the carbohydrate cell wall cross reacting with valve
tissue
Diagnosis depends on the Jones criteria
Must have evidence of recent strep infection, 1 major criteria and 2
minor criteria
Evidence of strep infection;
Recent streptococcal infection
History of scarlet fever
Positive throat swab
Increased in anti-streptolysin O
Increase in DNase B titre
Major criteria
Carditis tachycardia, murmurs, pericardial rub, CCF,
cardiomegaly, conduction defects
Arthritis migratory flitting polyarthritis that usually
affects larger joints
Subcutaneous nodules small mobile painless nodules
on extensor surface of joints and spine
Erythema marginatum geographical type rash with red
raised edges and clear centre, occurs mainly on trunk,
thighs and arms
Sydenhams chorea (St Vitus dance) unilateral or
bilateral involuntary semi purposeful movements
Minor criteria
Fever
Raised ESR or CRP
Arthralgia
Prolonged PR interval
Previous rheumatic fever

Management
Best rest until CRP normalises
Benxypenicillin IM stat then penicillin V
Analgesia for arthritis/carditis aspirin, NSAIDs
Immobilse joints in severe arthritis
Haloperidol or diazepam for chorea
Prognosis
60% with carditis develop chronic rheumatic heart disease
Acute attacks generally last 3months
Reoccurrence may be precipitated by another strep infection, pregnancy
or the pill
Cardiac sequelae, valves affected, mitral (70%), aortic (40%), tricuspid
(10%), pulmonary valves (2%)
Incompetent valves develop during attack and stenosis later
Cardiomyopathies
Cardiomyopathy refers to heart disease resulting from a primary
abnormality of the myocardium
Can be divided into;
Dilated
Hypertrophic
Restrictive
Dilated cardiomyopathy
Accounts for 90% of cases
Characterised by progressive cardiac dilation and systolic dysfunction,
usually with concomitant hypertrophy
Only 25% of patients survive >5 years
Pathological mechanisms;
Genetic defects
25-35% have a familial occurrence, most commonly
autosomal dominant inheritance
The genetic abnormalities largely affect the cytoskeleton
Alcohol toxicity
Direct toxicity of alcohol or a metabolite of alcohol on
the myocardium
May also be associated with thiamine deficiency which is
cardiotoxic
Peripartum
Occurs in pregnancy just before or just after birth
Mechanism is unclear but may be due to chronic
hypertension, volume overload, nutritional deficiency,
metabolic derangement or an immune response
Post viral myocarditis
Hypertrophic cardiomyopathy
Heavy, muscular, hypercontractile, poorly compliant heart with poor
diastolic relaxation and reduced cardiac output
Over 50% have an autosomal dominant inheritance
Mutations are in several genes that encode sarcomeric proteins
Increased risk of sudden death
Restrictive cardiomyopathy
Rare with multiple aetiologies
Restrictive ventricular filling leading to reduced cardiac output
Interstitial myocardial fibrosis is usually present
Can be idiopathic or be associated with with distinct disease of the
myocardium, amyloidosis, sarcoidosis, radiation fibrosis, metastatic
tumour
Specific types of restrictive cardiomyopathy are;
Endomyocardial fibrosis
Seen in African children and young adults
Charcterised by ventricular subendocardial fibrosis
Loeffler endocarditis
Similar to subendomyocardial fibrosis but with an eosinophilic
infiltrate and eosinophilia
Endocardial fibroelastosis
Uncommon disorder associated with a fibroelastic thickening of
the endocardium
Hypertrophic CM is a disease caused by mutations in the sarcomere
whilst dilated CM is associated with abnormalities of the cytoskeleton

Congenital Heart Disease
Cardiac or great vessel abnormalities present at birth
Mostly due to faulty embryogenesis between weeks 3 to 8
Have an incidence of 1% of live births
Aetiology
Genetic factors identifiable in 10% of cases e,g, Downs syndrome ASD
Environmental factors are congenital rubella infection and teratogens
Clinical features
May be cyanotic
Failure to thrive
Retarded development
Increased risk of chronic or recurrent illness and endocarditis
Two types of abnormality : shunts and obstructions
Shunts
Abnormal communication between heart chambers or between vessels
or between chambers and vessels
Left to right shunts
Induce chronic right sided volume overload and pulmonary
hypertension
Cyanosis occurs late when the pressure within the right side exceeds left
sided pressure to reverse the shunt from right to left
The major left to right shunts are;
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Patent ductus arteriosis (PDA)
ASD
Most common congenital anomaly seen in adults
Primum type 5%. Common in Downs syndrome. Occurs low in the
atrial septum and can be associated with mitral valve defects
Secundum type 90% , occurs at the foramen ovale and is generally
not associated with any other anomalies
Sinus venosum type 5%. Occurs high in the septum near to the SVC
entry
May be asymptomatic until adulthood
VSD
Most common congenital cardiac abnormality
Commonly associated with other anomalies in particular, Tetralogy of
Fallot
90% involve the membranous septum and the rest are muscular of
origin
May spontaneously close
PDA
In the fetus the ductus arteriosus permits blood flow from the aorta to
the pulmonary artery
Closes within a couple of days of birth due to increased oxygen tension
and decreased PGE
Can be closed early with indomethacin
Right to left shunts
Cause cyanosis from the outset
Secondary findings are;
Clubbing
Hypertrophic osteoarthropathy
Polycythaemia
The major right to left shunts are;
Tetralogy of Fallot
Transposition of the great arteries
Tuncus arteriosus
Tetralogy of Fallot
Cardinal findings are;
VSD
Right ventricular hypertrophy
Pulmonary artery stenosis
Aorta overriding the ventricular septum
With complete pulmonary obstruction, survival is through the patent
PDA
Pulmonary stenosis protects the lungs from pressure overload
Right ventricular failure is rare because it can pump excess volume into
the left ventricle and aorta
Transposition of the Great arteries
Aorta arises from the right ventricle and the pulmonary artery from the
left ventricle
Pulmonary and systemic circulations are therefore separate
Particularly common in children of diabetic mothers
Postnatal life depends on there being some mechanism of blood mixing,
PDA, VSD, ASD
Truncus arteriosus
Failure of the aortic and pulmonary artery to separate
Results in a single vessel receiving blood from both left and right
ventricle
Right to left shunting causes early cyanosis
Later the flow reverses resulting in right ventricular hypertrophy and
pulmonary hypertension
Obstructive congenital anomalies
Do not cause cyanosis
Aortic coarctation
Constriction of the aorta
Cardiac hypertrophy can occur due to pressure overload
Clinical manifestations depend on location and severity of the
constriction
Preductal before the ductus arteriosus. Often rapidly fatal
Postductal occurs distal to the ductus arteriosus. Generally
asymptomatic, leads to upper extremity hypertension with lower body
hypotension with arterial insufficiency (claudication, cold sensitivity).
Collateral flow develops around the coarctation via internal mammary
and axillary artery dilation, resulting in intercostals rib notching on CXR
Pulmonary stenosis or atresia
In complete pulmonary atresia the right ventricle is hypoplastic and
there is an ASD with blood entering the lungs via the PDA
Aortic stenosis or atresia
Complete aortic atresia is rare and generally is incompatible with
neonatal survival. The can only surve is a patent PDA allows blood flow
to the aorta and coronary vessels
Resulting underdevelopment of the left ventricle is called hypoplastic
left heart syndrome
Consequences of aortic stenosis are;
Left ventricular hypertrophy
Post-stenotic dilation of the aortic root
Sudden death

Cardiac failure
Definition : impaired cardiac function renders the heart unable to
maintain output sufficient for the metabolic requirements of the body
It is a common result of many forms of heart disease
Regardless of the cause of heart failure the CVS attempts to compensate
for inadequate cardiac output in heart failure by;
Ventricular dilation Frank-Starling Law, increased force of
contraction with myofibril stretch
Blood volume expansion by salt and water retension e.g. via the
renin-angiotensin-aldosterone mech
Tachycardia
In many cases the onset of cardiac failure is preceded by cardiac
hypertrophy, the compensatory response of the myocardium to
increased mechanical work
Most instances of heart failure are the consequence of progressive
deterioration of the contractility of the myocardium systolic
dysfunction e.g with hypertension or ischaemic heart disease
Diastolic dysfunction can occur whereby there is inability of the heart
muscle to relax, expand and fill sufficiently during diastole. This can
occur with massive left ventricular hypertrophy, myocardial fibrosis,
amyloid deposition or constrictive pericarditis
Whatever the cause, heart failure is characterised by diminished cardiac
output of accumulation of blood in the venous system of both
Cardiac hypertrophy
Myocytes cant undergo hyperplasia as they cant synthesise DNA so
arent believed to be able to divide
Increased mechanical load causes an increase in the content of
subcellular components and a consequent increase in cell size. This
results in increased heart size
The weight of the heart depends on the cause of the hypertrophy, hearts
weighing more than 1000g are rare
The pattern of hypertrophy reflects the nature of the stimulus;
Pressure-overload leads to concentric hypertrophy as the
deposition of sarcomeres is parallel to the long axis of the cells,
therefore the cross section of the cell is expanded by the length is not
Volume-overload deposition of new sarcomeres results in
increased cell length and width and is characterised by dilation with
increased ventricular diameter
Hypertrophic states results in increased metabolic demand and
increased wall tension, this was well as increased heart rate and
contractility results in increased oxygen demand
The deleterious alterations associated with hypertrophy are;
Decreased capillary to myocyte ratio
Increased fibrous tissue
Synthesis of abnormal proteins
This can lead to cardiac failure
With the exception of myocyte death, the mechanisms of cardiac
decompensation are not well understood
Left sided heart failure
Most often caused by;
Ischaemic heart disease
Hypertension
Aortic and mitral valve disease
Non-ischaemic myocardial disease
The morphological and clinical effects are due to progressive damming
of blood within the pulmonary circulation and the consequences of
diminished peripheral blood pressure and flow
Morphology
Heart
Hypertrophy and dilation of the LV
There may be fibrosis of the myocardium
Secondary enlargement of the atrium and AF (may result in
blood stasis and thrombus formation)
Lungs
Pulmonary congestion and oedema
Associated with haemosiderin containing macrophages in the
alveoli called siderophages or heart failure cells
Kidneys
Reduced renal perfusion results in;
Salt and water retension
Ischaemic acute tubular necrosis
Impaired waste secretion causing impaired prerenal azotemia
Brain
In advance CHF, cerebral hypoxia may give rise to hypoxic
encephalopathy with symptoms from irritability to coma
Right-sided Heart failure
Usually occurs as a consequence of left sided heart failure
Pure right sided heart failure most often occurs with chronic severe
pulmonary hypertension and is called cor pulmonale overload of the
right ventricle due to increased resistance in the pulmonary circulation
It may also be caused by pulmonary and tricuspid valve disease
Morphology
Liver and portal system
Hepatomegaly with centrolobular congestion and atrophy of
central hepatocytes called a nutmeg appearance
With severe hypoxia, centrilobular necrosis can occur
With high right sided pressure sinusoidal rupture causes central
haemorrhagic necrosis
Subsequent central fibrosis causes cardiac sclerosis
Elevated pressure in the portal vein can lead to congestive
splenomegaly
Chronic oedema of the bowel wall can result in impaired
nutrient absorption and ascites
Kidneys
Congestion of the kidneys is more marked with right sided
failure than left, leading to greater fluid retention, peripheral
oedema and more pronounced azotemia
Brain
Similar to left sided failure
Pleural and pericardial spaces
Accumulation of fluid in the pleural and pericardial space may
occur
Although pulmonary oedema indicates left sided failure, pleural
effusions indicate right sided failure
Subcutaneous tissues
Peripheral, dependant oedema
Sudden cardiac death
Defined as unexpected death from cardiac causes, early after symptom
onset (within one hour) or without symptoms
In older people may be the first sign of IHD
In young people is more likely to be due to other causes;
Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Myocarditis
Dilated or hypertrophic cardiomyopathy
Hereditary or acquired abnormalities in the conduction system
Increased cardiac mass
The ultimate mechanism is generally a lethal arrhythmia

Valvular Heart Disease
Functional regurgitation
When a valve becomes incompetent due to either;
Dilation of the ventricle which causes the papillary muscles to be
pulled out and down
Dilation of the aortic or pulmonary artery, pulling the valve
commissures apart and preventing full closure
Valvular stenosis is almost always due to a primary cuspal
abnormality and is virtually always a chronic process
Valvular regurgitation may result from either intrinsic disease of the
valve cusps or damage or distortion of the supporting structures e.g.
aorta, tendinous cords, papillary muscles and the ventricular free
wall
Major aetiologies of acquired heart valve disease
Mitral stenosis
Post inflammatory scarring rheumatic heart disease
Abnormalities of leaflets and commisures
Post inflammatory scarring
Abnormalities of tensor apparatus
Rupture of papillary muscle
Papillary muscle fibrosis
Rupture of chordae tendineae
Abnormalities of the left ventricle and/or annulus
LV enlargement
Calcification of mitral ring

Aortic stenosis
Post inflammatory scarring rheumatic heart disease
Senile calcific aortic stenosis
Calcification of congenitally deformed valve bicuspid , predisposed
to degenerative change
Aortic regurgitation
Intrinsic valvular disease
Post inflammatory scarring
Aortic disease
Degenerative aortic dilation
Syphilitic aortitis
Ankylosing spondylitis
Marfan syndrome
Congenital Valvular Defects
Pulmonary stenosis
An obstruction in the pulmonary valve that might be mild to severe
It may be an isolated defect or part of a more complex anomaly e.g
Tetralogy of Fallot or transposition of the great arteries
There is often RV hypertrophy
Aortic stenosis
There are three types of aortic stenosis;
Valvular
The cusps may be hypoplastic, dysplastic or abnormal in
number
In severe cases obstruction may lead to;
Underdevelopment of the left atria and
ascending aorta
Subaortic stenosis
Thickened ring or collar of dense fibrous tissue below
the level of the cusps
Supravalvular stenosis
An inherited form of aortic dysplasia in which the
ascending aortic wall is greatly thickened, causing
luminal constriction
May be related to Williams syndrome
Rheumatic Heart Disease
Rheumatic fever is an acute immunologically mediated multisystem
inflammatory disease that occurs a few weeks following an episode of
Group A Streptococcal pharyngitis
The most important consequence of RF are chronic valvular deformities,
characterised by fibrotic valvular disease, most commonly mitral
stenosis which produces permanent dysfunction
Incidence and mortality have decreased due to;
Improved socioeconomic conditions
Improved treatment and diagnosis of streptococcal pharyngitis
Unexplained decrease in the virulence of Group A strep
Morphology
During acute RF, focal inflammatory lesions are found in various tissues
and are most distinctive in the heart where they are called ASCHOFF
BODIES foci of collagen, surrounded by T cells, plasma cells are
macrophages called ANITSCHKOW cells (pathognomonic for RF)
During acute AF, there may be inflammation in any of the three heart
layers e.g. pancarditis. The pericarditis is associated with a serofibrinous
pericardial exudates called a bread and butter pericarditis
Inflammatory valvulitis of the left sided valves, consisting of beady
fibrinous vegetations called verrucae
Chronic rheumatic heart disease is characterised by organisation of the
acute inflammation and fibrosis. This results in;
Fibrinous thickening of the leaflets
Bridging fibrinosis across valve commissures, generating
buttonhole stenosis
Thickened, fused and shortened chordae
Calcification around the fibrous leaflets
Subendocardial collections of Aschoff nodules, usually in the left
atrium, forming thickened MacCallum plaques
In chronic death the mitral valve is generally always affects by the aortic
valve can also be affected and this is often more clinically significant
99% of cases of mitral stenosis are caused by rheumatic heart disease

Pathogenesis
Acute rheumatic fever is believed to be a hypersensitivity reaction
induced by group A strep although exact pathogenesis is uncertain
It is thought that antibodies directed at the M proteins of certain strains
of strep cross react with glycoprotein antigens in the heart, joints and
other tissues
It has been suggested that the streptococcal infection evokes and
autoimmune response against self-antigen
Because only a minority of patients with the infection develop rheumatic
fever, there appear to be genetic susceptibility
The chronic sequelae result from progressive fibrosis due to healing of
the acute inflammatory lesions and the turbulence induced by ongoing
valvular deformities
Clinical features
Major manifestations of disease;
Migratory polyarthritis of the large joints less common in
children
Carditis
Subcutaneous nodules
Erythema marginatum of the skin bathing suit distribution
Sydenham chorea
Diagnosis is established through the Jones criteria;
Evidence of a preceding group A Strep infection and the
presence of 2 major manifestations or one major and two minor
criteria (non specific signs, fever, athralgia, raised
inflammatory markers)
Acute rheumatic fever general occurs 10 days to 6 weeks after a Group A
pharyngitis is 3% of patients
More often occurs aged 5-15
Although cultures are negative by the time the disease starts, antibodies
to streptococcal enzymes may be present
Overall prognosis is good, with only 1% of patients dying
After an initial attack there is increased susceptibility to reactivation of
the disease with subsequent infection. Cardiac damage accumulates
with each reoccurrence
Sequelae of chronic rheumatic heart disease
Cardiac murmurs
Left atrial hypertrophy and enlargement
AF due to atrial dilation
Heart failure with pulmonary congestion
Right ventricular hypertrophy
Arrhythmias
Thromboembolic complications from atrial mural thrombi
Infective endocarditis superimposed on defective valves
Infective Endocarditis
Colonisation of the heart valves or endocardium leading to the
formation of bulky, friable vegetations of thrombotic debris and
organisms and often associated with destruction of the underlying tissue
Most causes are bacterial
Traditionally described as acute or subacute;
Acute is caused by highly virulent organisms e,g, Staph aureus, often
seeding a previously normal valve to produce necrotic ulcerative lesions.
Clinically there is rapidly developing fever and rigors. There may be
embolic complications and splenomegaly. Mortality of 50%
Subacute is generally caused by lower virulence organisms e.g Strep
viridans, seeding a previously injured valve with lesser valve
destruction. Insidious onset with low grade fever, weight loss, flulike
syndrome. Less embolic complications and low mortality rate
Aetiology/Pathogenesis
Patient is predisposed if they are prior valvular abnormalities e.g.
Rheumatic heart disease
Degenerative valvular stenosis
Bicuspid aortic valve
Prosthetic valves
Other predisposing influences are;
Neutropenia
Immunodeficiency
Malignancy
Diabetes
IV drug use
Alcohol
Causative organisms;
Strep viridans in patients with native by previously damaged
valves
Staph aureus more common in IV drug users
Enterococci
HACEK group haemphilus, actinobacilli, cardiobacterium,
eikenella and kingella.
S. epidermidis more common in patients with prosthetic
valves
Other causative agents are gram negative bacilli and fungi
In 10% of cases not organism can be cultured
The portal of entry of infection may be;
Dental or surgical procedure
IV drug use or intravenous cannulaes
Occult source from the gut
Morphology
Friable, bulky, potentially destructive vegetations, containing fibrin,
inflammatory cells and organisms
Aortic and mitral valves are the most common sites of infection
Right sided valves are more commonly affected in IV drug users
The vegetations may erode into the myocardium to produce an abscess
Fungal endocarditis tends to cause bigger vegetations than bacterial
disease
Emboli may break off and go to the brain, kidneys and myocardium
causing septic infarcts
Subacute lesions are generally smaller
Clinical features
Fever is the most consistent sign, also weight loss and flu like syndrome
Complications
Direct injury to valves causing insufficiency with CHF
Direct injury to the myocardium causing abscess and perforation
Emboli to spleen, kidneys, heart and brain, causing infarction or
metastatic infection
Renal injury caused by embolic infarction/infection of antigen-antibody
IC mediated glomerulonephritis causing nephrotic syndrome, renal
failure or both
Clinical signs include;
Splinter haemorrhages
Janeway lesions
Osler nodes
Roth spots
Prevention of IE is done by prophylactic antibiotics in patients with
some form of cardiac anomaly or artificial valve who is about to have a
surgical or dental procedure
Duke criteria for diagnosis
Major criteria
Positive blood cultures
ECHO findings
New valvular regurgitation
Minor criteria
Predisposing heart lesion of IV drug use
Fever
Vascular lesions
Immunological phenomena
Microbiological evidence e.g. a single positive culture

Hypertensive Heart Disease
Systemic (left sided) Hypertensive Heart Disease
In hypertension hypertrophy of the heart is an adaptive response to
pressure overload that can lead to;
Myocardial dysfunation
Cardiac dilation
Chronic heart failure
Sudden death
The minimal criteria required for a diagnosis for systemic HHD are;
Left ventricular hypertrophy, usually concentric in the absence
of other cardiovascular pathology that might have caused it
A history of pathological evidence of hypertension
Even mild hypertension is sufficiently prolonged induces left ventricular
hypertrophy
Morphology
Left ventricular pressure overload leads to hypertrophy without dilation
The LV wall may be over 2cm thick and the heart may weigh over 500g
In time the thickness of the LV wall imparts a stiffness which impairs
diastolic filling this may then cause atrial thickening
Microscopically the earliest change is an increase in the transverse
diameter of myocytes
At more advanced stages the cellular and nuclear enlargement becomes
more irregular, with variations in cell size amongst adjacent cells and
interstitial fibrosis
Clinical course
May be asymptomatic and only detectable by ECG or ECHO indications
May present with;
AF (due to atrial enlargement)
CHF
Cardiac dilation
Depending on severity, outcomes may be;
Longevity and death from unrelated caused
Development of progressive IHD
Progressive renal failure or cerebrovascular stroke
Progressive heart failure

Blood supply of the heart
The coronary arteries originate from the aorta immediately distal to the
aortic valve in the sinuses of Valsalva
Consist of epicardial coronary arteries and smaller vessels that penetrate
the myocardium (intramural arteries). These small arteries yield
arterioles and a rich network of capillaries in which there is nearly one
vessel adjacent to each myocyte
The 3 major epicardial coronary arteries are;
LAD branches of which are called the diagonal and septal
perforators
Left circumflex braches of which are the obtuse marginals
Right coronary artery
Most blood flow to the myocardium is during diastole
Perfusion
LAD supplies;
The apex
The anterior wall of the left ventricle
Anterior 2/3 of the intraventricular septum
In a right dominant circulation
The circumflex artery perfuses only the lateral wall of the left
ventricle
The RCA supplies the entire RV free wall and the posterobasal
wall of the left ventricle
Ishaemic Heart Disease
Ischaemia comprises;
Insufficient oxygen
Insufficient nutrients
Inadequate removal of metabolite
The clinical manifestations of IHD can be divided into 4 syndromes;
Myocardial infarction
Angina pectoris
Chronic IHD and heart failure
Acute MI, unstable angina and sudden cardiac death can be referred to
as acute coronary syndrome.
Epidemiology
Leading cause of death for both males and female in the western world
However since the 1960s the overall death rate from IHD has
decreased by 50%. This has occurred by;
Prevention modifiable risk factors such as smoking, high cholesterol
and blood pressure
Diagnostic and therapeutic advances e.g. thrombolysis, coronary
angioplasty, CABG
Additional factors may be, improved sugar control in diabetes, control of
obesity and aspirin prophylaxis
Pathogenesis
Caused by diminished coronary perfusion relative to myocardial
demand due to an interaction between atherosclerotic narrowing of the
coronary arteries, intraluminal thrombosis overlying a disrupted
atherosclerotic plaque, platelet aggregation and vasospasm
In >90% of cases the cause is atherosclerosis of the coronary arteries
reducing perfusion
Narrowing of 75% or greater causes symptomatic ischaemia induced by
exercise
90% stenosis can lead to ischaemia at rest
Slowly developing occlusions may lead to the development collateral
vessels which protect against distant ischaemia and infarction
Role of acute plaque rupture
The acute coronary syndromes are frequently initiated by an
unpredictable conversion of a stable atherosclerotic plaque to an
unstable artherothrombotic lesion, following disruption the
following may happen;
Rupture/fissuring, exposing the highly thrombogenic plaque
contents
Erosion/ulceration, exposing the thrombogenic subendothelial
basement membrane to blood
Haemorrhage into the atheroma, expanding its volume
Statins are thought to help stabilize plaques
Role of inflammation
Inflammation is important in the development of
artherosclerosis as T cells and monocytes enter the arterial wall
as a consequence of the release of chemokines by endothelial
cells and the expression of the adhesion molecules ICAM-1,
ICAM-2, P-selectin and E-selectin by these cells. T cells located
within the wall produce cytokines such as TNF, IFN and IL6
which activate macrophages which become loaded with oxidized
LDL
At later stages the destabilization and weakening of the plaque
may involve the secretion of MMP by macrophages
CRP may serve as a potential marker for atherosclerosis
Role of coronary thrombus
Partial or total thrombosis associated with a disrupted plaque is
critical to the pathogenesis of acute coronary syndromes
It may lead to occlusion of may embolise
Also thrombus is a potent activator of multiple growth related
signals in smooth muscle cells which can contribute to
artherosclerotic lesions
Role of vasoconstriction
Vasoconstriction compromises lumen size and by increasing
local mechanical forces can potentiate plaque disruption
Vasoconstriction may be potentiated by;
Circulating adrenergic agonists
Localized released platelet contents
Impaired secretion of endothelial relaxing factors
relative to contracting factors
Mediators released from perivascular inflammatory cells
Angina pectoris
Symptom complex of IHD, characterized by paroxysmal and usually
recurrent attacks of substernal or precordial chest discomfort caused by
transient myocardial ischaemia that falls short of inducing the cellular
necrosis that defines infarction
There are three patterns of angina pectoris;
Stable
Prinzmental or variant angina
Unstable of crescendo angina
Stable angina
Appears to be caused by the reduction in coronary perfusion to a
critical level by chronic stenosing coronary atherosclerosis
This renders the heart more susceptible to ischaemia whenever
there is increased demand e.g. exercise
Usually relieved by rest and GTN
Prizmental angina
Episodic angina that occurs at rest and is due to coronary artery
spasm
Usually there is ST elevation on the ECG indicating ischaemia
Generally responds to GTN and calcium channel blockers
Unstable angina
Refers to a pattern of pain that occurs with progressively
increasing frequency, with progressively less effort, often occurs
at rest and with prolonged duration
It may be the prodrome of a subsequent MI
Myocardial infarction
Death of cardiac muscle resulting from ischaemia
Leading cause of death in the western world
Most MI are transmural in which the necrosis involves the full thickness
of the ventricular wall in the distribution of a single coronary artery.
This pattern is normally associated with coronary artery
artherosclerosis, acute plaque change and superimposed thrombosis
In a subendocardial infarct, the necrosis is limited to the inner 1/3 of the
ventrical wall and may extend laterally beyond the territory of a single
coronary artery
A subendocardial infarct can occur due to;
A plaque disruption followed by coronary thrombus that becomes lysed
before necrosis extends across the thickness of the wall
Prolonged, severe reduction in systemic blood pressure e.g. in shock. In
which case the are usually circumferential rather than limited to the
distribution of a single coronary artery
Incidence and aetology
More common with increasing age and when predispositions to
atherosclerosis are present;
Hypertension
Smoking
Diabetes
Hypercholesterolaemia
Hyperlipoproteinaemia
Men are more susceptible than women, as women are protected
during their reproductive years
Pathogenesis
Coronary artery occlusion
In typical MI, the following sequence of events can be proposed;
The initial event is a sudden change in the morphology of an
atheromatous plaque
Exposed to subendothelial collagen and necrotic plaque
contents, platelets undergo adhesion, aggregation, activation
and release of potent aggregators including thromboxane A2
and platelet factors 3 and 4
Vasospasm is stimulated by platelet aggregation and the release
of mediators
Other mediators activate the extrinsic pathway of coagulation
adding to the bulk of the thrombus
Frequently within minutes the thrombus evolves to completely occlude
the lumen of the vessel
In around 10% of cases, transmural acute MI is not associated with
atherosclerotic plaque thrombosis. In these situations other
mechanisms may be involved;
Vasospasm sometimes related to cocaine abuse
Emboli from the LA in association with AF, a left sided
thrombosis or vegetative endocarditis or paradoxical emboli
crossing from the right side of the heart through a patent
foramen ovale
Unexplained vasculitis, haemoglobinopathies, amyloidosis
Myocardial response
The principle early consequences of mycocardial ischaemia is the
cessation of aerobic glycolysis, and therefore the initiation of anaerobic
glycolysis within secs leading to inadequate production of high energy
phosphates and the production of potentially noxious breakdown
products such as lactic acid
Myocardial tissue is exceedingly sensitive to ischaemia with a decrease
in contractility after only 60 secs which can precipitate heart failure
Only after 20 -40 mins does irreversible myocyte injury occur
Classic acute MI occurs when the perfusion of the mycocardium is
reduced severely below its needs for an extended interval, usually at
least 2 to 3 hours cusing profound, prolonged ischaemia and resulting in
permanent loss of function of large regions in which cell death has
occurred
Predominant mechanism of cell death is coagulation necrosis
If reperfusion follows briefer periods of flow deprivation, loss of cell
viability can be prevented
Myocardial ischaemia can lead to arrhythmias probably die to electrical
instability
Approximate time onset of key events in ischaemic cardiac
myocytes;
Feature Time
Onset of ATP depletion Seconds
Loss of contractility Less than 2 mins
ATP reduced
To 50% of normal
To 10% of normal

10 mins
40 mins
Irreversibly injury 20-40 mins
Microvascular injury Less than 1 hour
Irreversibly injury occurs first in the sudendocardial zone
The precise location, size and specific morphological features of an acute
MI depends upon;
The location, severity and rate of development of coronary
atherosclerotic obstructions
The size of the vascular bed perfused by the obstructed vessels
The duration of the occlusion
The metabolic/oxygen needs of the myocardium at risk
The extent of collateral vessels
The presence, site and severity of coronary arterial spasm
Other factors such as blood pressure, heart rate and cardiac
rhythm
Morphology
Nearly all transmural infarcts involve a portion of the left ventrical
Isolated RV infarction occurs in only 1-3% of cases
Almost always there is a narrow rim of preserved subendocardial
myocardium sustained by diffusion of oxygen and nutrients from the
lumen
Lesions on the LAD causes infarction of the anterior wall of the LV near
the apex, the anterior portion of the ventricular septum and the apex
itself circumferentially
RCA infarct involves the inferior/posterior wall of the LV, posterior
portion of the ventricular septum and in some cases the
inferior/posterior all of the RV
Left circumflex infarct involves the lateral wall of the left ventricle
The gross appearance of an infarct depends on the survival of the
patient following the MI
Areas of damage undergo a progressive sequence of morphological
changes
Macroscopic
MI less than 12 hours old are not apparent by gross examination
To highlight areas of necrosis after 2-3 hours following infarct,
immerse the tissue in triphenyltetrazolium chloride, which
stains areas with intact dehydrogenase enzymes red with
infracted areas showing up as unstained pale zone
After 12-24hr an infarct can be identified as a red/blue hue
caused by stagnated blood
Progressively the unfarct becomes more sharply defined and
yellowish in colour, within a weak it develops a hyperaemic zone
of highly vascularised granulation tissue
From around 2 weeks scar tissue forms
Histological changes
Typical changes of coagulation necrosis are evident from 4-12
hours with wav fibres being present at the periphery of the
infarct, where viably fibres have tugged on the dead fibres
during systole, stretching an buckling them
In the infarct margin there may be vacuolar degeneration (which
is potentially reversible)
The necrotic tissue elicits acute inflammation (within 2-3 days),
thereafter macrophages remove necrotic myocytes and the
damaged zone is progressively replaced with highly vascular
granulation tissue which progressively becomes less vascularised
and more fibrous (scars forming within 6 weeks)
Infarct healing occurs from the periphery towards the centre
Once a lesion has completely healed it is impossible to
determine its age
Electron microscopy
Within 30mins there is relaxation of the myofibrils, glycogen
loss and mitochondrial swelling
Between to 4 hours there is sarcolemmal disruption and
mitochondrial amorphous densities
Clinical features
Classically diagnosed by typical symptoms, biochemical changes and by
the ECG pattern
10-15% may be an asymptomatic MI more common in the elderly
and diabetics
Troponins are proteins that regulate calcium mediated contraction of
cardiac and skeletal muscle, they have near complete tissue specificity
and high sensitivity. TnI and TnT rise at 2-4hrs after event and stay
high for 7-10 days after acute event
Levels are increased in patients who have had reperfusion due to
washing out of the enzyme from the necrotic tissue
Consequences and complications of MI
Poor prognosis is associated with;
Advanced age
Female gender
Diabetes
Previous MI
Nearly of patients have one or more complication following an MI.
These include;
Contractile dysfunction
MIs produce abnormalities in ventricular function
approximately proportional to their size
May result in hypotension and pulmonary oedema e.g.
cardiogenic shock
Arrhythmias
Conduction disturbance and myocardial irritability
following an MI
Myocardial rupture
Cardiac rupture syndromes result from the mechanical
weakening that occurs in necrotic and inflamed
myocardium;
Rupture of the ventricular wall resulting in cardiac
tamponade
Rupture of the ventricular septum resulting in left-right
shunt
Papillary muscle rupture resulting in acute onset mitral
regurgitation
Pericarditis
A fibrinous or fibrohaemorrhagic pericarditis usually
develops about the second or third following a
transmural infarct and generally resolves over time
Right ventricular infarction
Infarction of the right ventricle often accompanies
ischaemic injury of the adjacent posterior left ventricle
and the ventricular septum
Infarct extension
New necrosis may occur adjacent to the existing infarct
Infarct expansion
Owing to weakening of the necrotic muscle there may be
disproportionate stretching, thinning and dilation of the
infarct region
Mural thrombus
With any infarct the combination of local myocardial
contraction abnormalities and endocardial damage can
result in mural thrombus and potentially
thromboembolism
Ventricular aneurism
Complications of which are mural thrombus,
arrhythmias and heat failure
Papillary muscle dysfunction
Progressive late heart failure chronic IHD
Large transmural infarcts more commonly lead to;
Cardiogenic shock
Arrhythmias
Chronic IHD
Patients with anterior transmural infarct are at increased risk of;
Free wall rupture
Expansion
Mural thombi
Aneurism
Posterior transmural infarcts are associated with;
Conduction defects
Right ventricular involvement
Ventricular septal defects
Prognosis
Total mortality rate within the first year is 30%
Thereafter there is a 3-4% mortality among survivors with each passing
year
Chronic Ischaemic Heart Disease
Describes progressive heart failure as a consequence of ischaemic
myocardial damage
Also called ischaemic cardiomyopathy
In most cases there is a history of prior MI and sometime CABG or other
intervention
Usually constitutes post infaction cardiac decompensation due to
exhaustion of the compensatory hypertrophy of non infracted
myocardium
Patients normally have LV hypertrophy and dilation
Defined as unexpected death from cardiac causes early after symptom
onset (within 1hr) or without symptoms
May be the first clinical manifestation of IHD
Generally causes a lethal arrhythmia
80-90% caused by atherosclerosis
With decreasing age, other non atherosclerotic causes of sudden cardiac
death are more likely, such as;
Congenital structural or coronary artery abnormalities
Aortic valve stenosis
Myocarditis
Dilated or hypertrophic cardiomyopathy
Increased cardiac mass seen in atheletes

Atherosclerosis
Characterised by intimal lesions called atheromas or fibrofatty plaques
These protrude into and obstruct the vessel lumen and weaken the
underlying media
The American Heart Association classification divides atherosclerosis
into 6 types;
Type I initial lesion of isolated macrophage foam cells
Type II fatty streak, mainly intracellular lipid accumulation
Type III type II changes plus small extracellular lipid deposits
Type IVatheroma lesion, type II change plus core of extracellular
lipid
Type V fibroatheroma
Type VI complicated lesion with surface defect
Fatty streaks are the earliest lesions, composed of lipid filled foam cells
They are not raised and dont disrupt blood flow
They begin as small (<1mm) multiple yellow flat spots and coalesce to
form larger lesions
They appear from before the age of 1 and are present in all children by
the age of 10
Fatty streaks are related to the known risk factors for atherosclerosis,
support the hypothesis that they are the precursors of atherosclerotic
plaques
However they often occur in vascular areas where atheroma is
uncommon and in individuals in populations which are unlikely to get
atheromas therefore although they may be the precursors of
atherosclerotic plaques, not all fatty streaks will become so
Atherosclerotic plaques generally affect elastic arteries (e.g. aorta,
carotid and iliac arteries) and large and medium sized muscular arteries
(e.g. coronary and popliteal arteries)
Symptomatic disease can involve the vessels of the heart, brain, kidneys
and lower extremities
Major consequences of artherosclerosis;
MI
Cerebral infarction
Aortic aneurisms
Peripheral vascular disease
Mesenteric occlusion
In smaller vessels, atheroma can occlude vessels causing ischaemic
injury
Plaques can undergo disruption and precipitate thrombi which can
further obstruct blood flow
In large arteries they can encroach on the media, weakening the vessel
wall causing aneurisms which may rupture
Atheromas may be friable and shed emboli into the distant circulation
Morphology
The key processes are intimal thickening and lipid accumulation
An atheroma consists of a raised focal lesion derived from the intima
with a soft yellow core of lipid covered by a firm, white fibrous cap
They vary and size and sometimes coalesce to form larger masses
They usually involve only partial circumference of the vessel
They are focal and patchy at first and then become more numerous and
diffuse as disease progresses
Abdominal aorta is more commonly involved that the thoracic and
lesions tend to be prominent around the ostia of major branches
After the abdominal aorta the most commonly affected vessels in order
are, coronary arteries, popliteal arteries, internal carotid arteries and the
vessels of the circle of Willis
Atherosclerotic plaques generally have 3 principle components;
Cells smooth muscle cells, macrophages and other
leukocytes
ECM collagen, elastic fibers and proteoglycans
Lipid extracellular and intracellular
The fibrous cap is composed of SMC and relatively dense ECM
Beneath and at the shoulder is a cellular area consisting of
macrophages, SMC and T cells
Deep to the fibrous cap is a necrotic core containing a disorganized mass
of lipid, cholesterol, dead cell debris, foam cells and fibrin
Foam cells are large lipid laden cells that derive predominantly from
macrophages but SMCs can also take up lipid to become foam cells
Finally, particularly around the periphery of the lesion, there is
neovascularisation
Plaques continue to change and remodel and can often calcify
The advanced lesion of atherosclerosis is a risk of the following
pathological events which have clinical significance;
Focal rupture, ulceration or erosion of the luminal
surface resulting in exposure of highly thrombogenic
substances which induce thrombus formation or can be
released into the bloodstream as microemboli
Haemorrhage into a plaque especially in the coronary
arteries, may be due to rupture of the fibrous cap or of
the thin walled vessels which vascularise the plaque. The
resulting haematoma may expand or rupture the plaque
Superimposed thrombus usually occurs on disrupted
lesions and may occlude the lumen. Thrombi may heal
and become incorporated thereby enlarging the plaque
Aneurismal dilation due to weakening of the vessel
media
Epidemiology and risk factors
The risk factors that predispose to artherosclerosis have been identified
by a number of prospective studies, most notably the Framingham study
and the Multiple Risk Factor Intervention Trial. These risk factors
include;
Age between 40 and 60 the incidence of MI rises 5 fold
Sex M>F, until after the menopause, probably due to a decrease in
oestrogen.
Genetics most likely familial predisposition in polygenic. They may
relate to other risk factors such as hypertension and diabetes or to
derangements in lipid metabolism resulting in excessively high blood
lipid levels
The four major risk factors potentially controllable are;
Hyperlipidaemia hypercholesterolaemia, particularly
associated with a high LDL and low HDL
Hypertension both systolic and diastolic levels are
important in increasing risk
Cigarette smoking
Diabetes mellitus
Other factors
Hyperhomocystinaemia
Caused by low folate and Vit B intake
In patients with homocystinurua, an inborn error of
metabolism resulting in high levels of homocysteine and
urinary homocysteine
Markers of haemostatic function e.g. elevated plasminogen
activator inhibitor-1 and inflammation e.g. CRP
Lipoprotein Lp(a) is an altered form of LDL that has been linked
to coronary and cerebrovascular disease
There is a protective role for a moderate intake of alcohol
Multiple risk factors have a multiplicative effect
Pathogenesis
Response to injury hypothesis considers artherosclerosis to be a
chronic inflammatory response of the arterial wall initiated by injury to
the endothelium. The lesion is sustained by interactions between
modified lipoproteins, macrophages, T cells and the normal constituents
of the vessel wall
Central to this hypothesis are the following;
Chronic endothelial injury, resulting in endothelial dysfunction causing
increased permeability, leukocyte adhesion and thrombotic potential
Accumulation of lipoproteins, mainly LDL within the vessel wall
Modification of the lipoproteins by oxidation
Adhesion of blood monocytes to the endothelium, followed by their
migration into the intima and their transformation into macrophages
and foam cells
Adhesion of platelets
Release of factors from activated platelets, macrophages or vascular
cells that cause migration of SMC from the media into the intima
Proliferation of SMC in the intima and elaboration of the extracellular
matrix leading to accumulation of collagen and proteoglycans
Enhanced accumulation of lipids both intracellularly and extracellularly
Causes of endothelial dysfunction;
Haemodynamic disturbances turbulent flow
Cigarette smoke
Homocysteine
Infectious agents
Inflammatory cytokines e.g. TNF
Role of inflammation
Upregulation of endothelial adhesion molecules VCAM which binds
monocytes and T cells
After adhering to the endothelial cell, monocytes migrate between the
cells stimulated by chemokines and transform into macrophages that
engulf oxidized LDL
Macrophages contribute to the growth of the lesion by;
Producing IL-1 and TNF which increases adhesion of leukocytes
Produce chemokines e.g. MCP-!
Produce reactive oxygen specifies which cause oxidation of the LDL in
the lesion
Produce growth factors which stimulate SMC proliferation
CD4 and CD8 T cells are recruited by chemoattractants and produce
IFN and TNF which stimulates macrophages, SMC and endothelial
cells
Role of lipids
The mechanisms by which hyperlipidaemia contributes to atherogenesis
include;
Impairement of EC function through increased production of oxygen
free radicals that deactivate NO, the major endothelial relaxing factor
With chronic hyperlipidaemia, lipoproteins accumulate within the
intima at sites of increased endothelial permeability
Oxidized lipid generated by free radicals generated in macrophages or
EC is ingested by macrophages via the scavenger receptor distinct from
the LDL receptor thus forming foam cells
It increases monocyte accumulation in lesions
Stimulates release of growth factors and cytokines
Cytotoxic to EC and SMC
Role of smooth muscle cells
SMC migrate from the media to the intima, where they proliferate and
deposit ECM components, converting a fatty streak into a fibrofatty
atheroma, thus contributing to the progressive growth of the
atherosclerotic lesion
Growth factors that have been implicated in the proliferation of SMC;
PDGF
FGF
TGF-
SMC may also take up oxidized lipids to form foam cells
Other factors in atherogenesis
Oligoclonalitiy of lesions plaques may be equivalent to benign
neoplastic lesions
Infection Chlamydia pneumonia
Hypertension
Hypertension is a risk factor for coronary artery disease and
cerebrovascular accidents
It is raised pressure in a vascular bed
It can lead to;
Cardiac hypertrophy
Heart failure
Aortic dissection
Renal failure
Hypertension is defined as a sustained systolic pressure of >140 mm Hg
and a sustained diastolic pressure of >90 mm Hg. By these criteria 25%
of persons in the general population are hypertensive
Prevalence increases with age and is higher in African Americans
Systolic blood pressure is more important that diastolic pressure as a
determinant of cardiovascular except in young individuals
Factors controlling blood pressure
Blood pressure = cardiac output x peripheral resistance
Cardiac output depends up;
Cardiac factors e.g heart rate and contractility
Blood volume e.g. sodium, mineralocorticoids
Peripheral resistance
Humoral factors
Constrictors;
Angiotensin II
Catecholamines
Thromboxane
Leukotrienes
Endothelin
Dilators
Prostaglandins
NO
Local factors
Autoregulation
Ionic (pH, hypoxia)
Neural factors
Constrictors - adrenergic
Dilators -adrenergic
Causes
95% of cases are idiopathic and termed essential hypertension
Causes of secondary hypertension;
Renal
Acute glomerular nephritis
Chronic renal disease
Renal artery stenosis
Renal vasculitis
Endocrine
Adrenocortical hyperfunction Cushing syndrome,
primary aldosteronism, congenital adrenal hyperplasia
Exogenous hormones glucocorticoids, oestrogen,
sympathomimetics
Pheochromocytoma
Acromegaly
Hypothyroidism
Hyperthyroidism
Cardiovascular
Coartation of the aorta
Vasculitis
Increased intravascular volume
Increase cardiac output
Neurological
Increased ICP
Sleep apnoea
Stress
Pathogenesis
The major factors that determine blood pressure are age, gender, body
mass index and diet, particularly sodium intake
The kidney plays an important role in blood pressure;
Via the renin-angiotensin syndrome. Angiotensin II raises BP by
increasing peripheral resistance and by increasing blood volume
(increasing distal tubular reabsorption of sodium)
Produces vascular relaxing substances such as NO and
prostaglandins
When BP is reduced the GFR falls leading to increased sodium
reabsorption and expanding blood vol
Natriuretic factors, including those secreted by the atrial and
ventricular myocardium act on the distal tubules to cause
sodium excretion and diuresis
When renal artery excretory function is impaired, the increased
arterial pressure is a compensatory mechanism that helps
restore fluid and electrolyte balance

Mechanisms of essential hypertension
Genetic factors
Single gene disorders are rare and cause severe forms of hypertension
Gene defects involved in aldosterone metabolism e.g. aldosterone
synthase, 11-hydroxylase and 17-hydroxylase. These lead to an
increase in aldosterone secretion, increased salt and water reabsorption
and therefore plasma volume
Mutations in proteins that affect sodium reabsorption e.g. Liddle
syndrome, caused by a mutation in ENaC leading to increased
reabsorption of sodium induced by aldosterone
There are different hypothesis put forward to explain essential
hypertension
Reduced renal sodium excretion in the presence of normal arterial blood
pressure, leading to increased fluid volume, increased cardiac output
and peripheral vasoconstriction, thus elevating blood pressure. At this
higher setting enough additional sodium could be excreted by the
kidneys to equal intake and prevent fluid retention. Thus an altered
state of sodium excretion could be achieved but with the expense of a
stable increase in blood pressure
An alternative hypothesis is one of vasoconstrictive influences as the
primary cause of hypertension. Chronic or repeated vasoconstrictive
influences may cause structural thickening of the vessels
Environmental factors;
Can modify the expression of the genetic determinants of increased
pressure
Stress
Obesity
Smoking
Physical inactivity
Heavy consumption of salt (also augments the disease in
secondary hypertension)
Vascular pathology in hypetension
Accelerates atherogenesis
Causes degenerative changes in the walls of large and medium arteries
that potentiate aortic dissection and cerebrovascular haemorrhage
It is also associated with 2 forms of small vessel disease;
Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis

Diseases of Heart Muscle

Загружено:

Сведения о документе

Авторское право

Доступные форматы

Поделиться этим документом

Поделиться или встроить документ

Параметры публикации

Этот документ был вам полезен?

Это неприемлемый материал?

Авторское право:

Доступные форматы

Diseases of Heart Muscle

Загружено:

Авторское право:

Доступные форматы

Diseases of heart muscle

Вам также может понравиться