Medicine Eindra

HEART FAILURE
DEFINITION

 Heart failure is the state when the heart cannot maintain an adequate cardiac output or can
do so only at the expense of an elevated ventricular filling pressure.

CLASSIFICATION OF HEART FAILURE

According to onset PRECIPITATING / AGGRAVATING FACTORS
 Acute
 A – Arrhythmia ( eg: HF )
 Chronic
 Acute-on-chronic  B – Blood flow ( Ischemia )
 C – Compliance ( Poor compliance )
According to site  D – Demand ( eg: anemia, Hyperthy,
 Right heart failure pregnancy )
 Left heart failure  D – Drugs
 Biventricular failure ( CCF ) ( negative inotropes eg: -blockers
Fluid retaining eg: NSAID, steroids )
According to cardiac cycle  E – Pulmonary embolism
 Systolic failure  F – Fluid overload ( IV infusion )
 Diastolic failure  F – Fever / Infection

According to cardiac output

 Low-output failure
 High-output failure

According to EF
 HF with reduced EF ( <40% )
 HF with preserved EF ( ≥ 50% )

CAUSES OF HEART FAILURE

Reduced myocardial contractility COMMON CAUSES IN MYANMAR
 Myocardial infarct 1. Ischemic heart disease
 Cardiomyopathy 2. Rheumatic heart disease
 Myocarditis 3. Hypertensive heart disease
 Arrhythmia 4. Congenital heart disease
5. Cardiomyopathy
Ventricular inflow obstruction 6. Myocarditis
 MS, TS 7. Anemic HF
8. Beri Beri
Ventricular outflow obstruction
 LHF  AS, systemic hypertension
 RHF  PS, pulmonary hypertension

Reduced ventricular distensibility

 Restrictive CMP
 Cardiac tamponade
 Constrictive pericarditis

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Ventricular volume overload

 LV overload  MR, AR, VSD, PDA
 RV overload  TR, PR
 High-output  anemia, beri beri, hyperthyroid

CLINICAL FEATURES
 Age/sex – Any
 Onset – acute or chronic
 Risk factors – eg: h/o RHD, HT, IHD
 Precipitating factors – eg: poor compliance , Infections

Symptoms
1. Features of left-sided failure
 Due to reduced CO
 Muscle  fatigue, poor effort tolerance, listlessness
 Skin  cold extremities
 Kidneys  oliguria
 Due to pul: congestion
 Dyspnea, orhtopena, PND
 Cough , pink frothy serous sputum

2. Features of right-sided failure

 Due to  pul: perfusion – Dyspnea
 Due to backward congestion
 Liver  abd: discomfort
 LL  odema
 Ascites & pleural effusion ( in severe cases)

3. Features of underlying cause ( eg: chest pain )

Signs
General COMPLICATIONS OF HEART FAILURE
 Thin 1. Renal failure / Uremia
 Dyspnea / orthopnea 2. Impaired liver function
 Pitting odema 3. Electrolytes changes
( Hypo/Hyperkalaemia ,
Systemic Hyponatremia )
1. Pulse 4. Thromboembolism
 Rate – tachycardia ( both pulmonary & systemic )
 Volume – low vol: 5. Arrhythmias
 Character – pulsus alternan

2. JVP  increased
3. Precordial examination
 Features of underlying cause – murmurs

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 Features of HF – S3 / S4 / Triple rhythm / Gallop rhythm / Summation gallop /

bilateral basal crepitation

Abdomen
 Tender hepatomegaly
 Ascites

INVESTIGATIONS
For diagnosis
1. CXR
 Features of pulmonary odema
 Upper lobe veins dilatation
 Perihilar haziness
 Kerley’s B lines
 Bat wing appearance
 Small pleural effusion
 Cardiomegaly may be (+)
 Can detect underlying cause ( eg: mitrilization )

2. ECG
 Can detect underlying cause ( eg: arrhythmia, MI )

3. Echocardiogram
 For diagnosis  EF reduced
 Can detect underlying cause ( eg: valvular disease )

4. B-type Natriuretic peptide ( BNP )

 High BNP  diagnostic
 Can also use as marker of risk

For underlying cause & ppt factors

 For MI  cardiac enzymes
 For infections  Blood for CP
 For hyperthyroidism  Thyroid function tests
 For anemia  Hb%

For complications
 Liver function tests
 Urea & Cr, El

MANAGEMENT
General
 Health education – about the disease & treatment
 Diet – no added slat, weight control, adequate & balanced diet
 Exercise – regular moderate exercise ( 30min/day & 5days/week )
 Lifestyle – give up smoking, moderate alcohol is allowed ( except in alcohol-induced CMP )

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 Vaccination – consider influenza & pneumococcal vaccination

Specific
Medical Tx / Pharmacological Tx
1. Diuretics
 Action
 Reduce preload  improves pulmonary & systemic congestion 
symptomatic relief ( 1st line for symptoms )
 May reduce afterload
 Eg: Frusemide IV or Oral

2. ACEI / ARB
 Action
 Interrupt vicious cycle
 Reduces afterload & preload
 Improve effort tolerance ( ARB – better tolerated )
 Eg: ACEI ( Enalapril / Lisinopril / Ramipril ) , ARB ( Losartan / Valsartan )

3. Beta-blockers
 Action ( Use with action – Start low & Go slow )
 Improves s/s & EF
 Prevent arrhythmia & sudden death ( hospitalization & mortality )
 Bisoprolol, Carvedilol, Metoprolol succinate, Nebivolol

4. Mineralocorticoid R/c anatagonist

 Action
 Inhibit vicious cycle  aldosterone antagonist
 Can also reduce preload
 mortality when added to conventional Rx
 Eg: Spironolactone ( low dose ) or Eplerenone

5. Digoxin
 Action
 Rate control in patients with HF & AF
 Improve symptoms even in those with sinus rhythm

6. Vasodilators
 Action ( valuable in chronic HF )
 Arterial dilators eg: Hydralazine  reduces afterload
 Venodilators eg: Nitrates ( Isosorbide dinitrate )  reduce preload

7. Ivabradine
 Action
 Inhibit 𝐼𝑓 channel in SA node  reduce HR
 Reduce mortality & hospitalization

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8. Neprilysin inhibitors
 Action
 Inhibits neprilysin which is responsible for the breakdown of ANP & BNP
 Additional symptomatic & mortality benefit over ACE inhibition
 Sacubitril is the only drug of this class

Surgical Tx / Role of Surgery

1. Device therapy ( if severe symptomatic HF with medical Rx )
 Implantable cardiac defibrillator ( ICD )
 Cardiac resynchronization therapy ( CRT ) – if asso: BBB(+)
2. Coronary revascularization therapy ( in IHD )
 CABG ( Coronary Artery Bypass Graft )
 PCI ( Percutaneous Coronary Intervention )
3. Valvular Surgery ( in valvular disease )
4. Heart transplantation ( in intractable HF )

NYHA CLASSIFICATION FOR HEART FILURE

Class I No limitation during ordinary activity

Class II Slight limitation during ordinary activity
Class III Marked limitation of normal activities without symptoms at rest
Class IV Unable to undertake physical activity without symptoms, Symptoms may be
present at rest

DRUGS USED IN HEART FAILURE

1. Loop diuretics ( eg: Frusemide )

Action
 Increase Na & water excretion  preload, some degree of arterial & venous
dilatation
Role
 1st line symptomatic Rx
Side effects
 Hypotension, hypokalaemia, hypocalcemia, hyperuricemia, hyperglycemia,
dyslipidemia
Contraindications
 Sulphomaide allergy, severe Hypotension

2. ACEI ( eg: Captropril, Enalapril, Lisinopril )

Action
 Inhibit Angiotensin II synthesis  vasodilatation  afterload
 Inhibit aldosterone formation  inhibit Na & water retention  preload
 Interrupt the vicious cycle  bradykinin breakdown  vasodilation
Role
 Improvement in effort tolerance & mortality , delay the develop: of Ht failure

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Side effects
 Hyperkalaemia, 1st dose hypotension, renal dysfunction, dry cough
Contraindication
 Pregnancy, bilateral renal artery stenosis
3. ARB ( eg: Losartan, Valsartan )
Action & Side-effects & CI
 Similar to ACEI but no effect on bradykinin metabolism ( No dry cough )
Role
 ACEI + ARB – more adverse effect
Beta-blocker
4. Beta-blocker ( eg: Carvedilol, Bisoprolol )  Initiation with std dose can
Action ppt Ht failure
 Inhibit sympathetic stimulation  Given in very small dose
 Inhibit beta-1 R/c on Heart - HR & contraction under careful supervision
 Inhibit vicious cycle  Increase gradually to std Rx
Role ( start low & go slow )
 Prevent arrhythmias & sudden death
 Improve s/s & increase EF
 Reduce frequency of hospitalization & reduce mortality ( additional to ACEI )
Side-effects
 Bronchospasm, bradycardia, rebound phenomenon in abrupt withdrawal
Contraindications
 Asthma, Ht block

5. Spironolactone or Eplerenone
Action
 Inhibit vicious cycle
 Reduce preload
Role
 Reduce mortality when adding to conventional Rx
Side-effects
 Hyperkalaemia, painful gynaecomastia, menstrual inregularity

6. Digoxin
Action
 Inhibit SA node – reduce HR
 Inhibit Na-K pump – increase myocardial contraction
Role
 1st line Rx in patient with AF
 Improve s/s even in those with sinus rhythm
 No effect on overall survival but reduce hospitalization
Side-effects
 Digoxin toxicity ( Nausea, vomiting, diarrhea, VE, VF, VT, bradycardia, altered color
vision) – aggravated by hypokalaemia
Contraindication
 Hypokalaemia , Ht block, ventricular arrhythmia

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7. Vasodilators
 Venodilator ( eg: nitrates )
 Arterial dilator ( eg: hydralazine )

8. Ivabradine
Action
 Inhibit If channel in SA node  reduce HR
Role
 Reduce mortality & hospitalization

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CORONARY HEART DISEASE

CAUSES

 Almost always due to atheroma & its complications particularly thrombosis

 Occasionally – aortitis, polyarteritis, other connective tissue disorder

RISK FACTORS FOR ARTHEROSCLEROSIS

Non-modifiable
 Age
 Sex – male
 Family h/o (+)

Modifiable
 Smoking
 Hypertension
 Dyslipidaemia
 DM
 Central obesity
 Personality
 Hemostatic variables ( platelet activation / hyperfibrinogenemia )
 Lack of exercise & physical activity
 Alcohol ( moderate - risk / Excess alcohol - risk )
 Diet
 Social deprivation

CLINICAL MANIFESTATION & CORE PATHOLOGY

Stable angina Ischemia due to fixed atheromatous stenosis

Unstable angina Ischemia caused by dynamic obstruction of a coronary artery due to
plaque rupture or erosion with superimposed thrombosis
Myocardial infarction Myocardial necrosis caused by acute occlusion of a coronary artery due
to plaque or erosion with superimposed thrombosis
Heart failure Myocardial dysfunction due to infarction or ischemia
Arrhythmia Altered conduction due to ischemia or infarction
Sudden death Ventricular arrhythmia, asystole or massive MI

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STABLE ANGINA
CLINICAL FEATURES
 Age – old age > 40yrs
 Sex – M > F
 Onset – acute or insidious ( off & on )
 Risk factors – eg: smoking, obesity, hypertension, DM, sedentary lifestyle
 Ppt factors
 Common – physical exertion, heavy meals, cold exposure, intense emotions
 Uncommon – lying flat ( decubitus angina ), vivid dreams ( nocturnal angina )

Symptoms
 Chest pain
 Central / retrosternal
 Acute onset
 Constricting in nature
 Radiating to neck, jaw, inner side of left arm
 Aggravated by exertion & other forms of stress
 Relived by rest or nitrates
 Short duration ( eg: < 15min )
 Breathlessness

Signs
 Frequently negative
 Features of risk factors
 Hypercholesterolemia ( eg: xanthoma, xanthelesma )
 Hypertension ( increased BP )
 Obesity
 Features of ppt factors
 Anemia
 Thyrotoxicosis
 Features of Cx
 LVF ( eg: bilateral basal crepts )

INVESTIGATIONS
For diagnosis
1. ECG
 Resting ECG – often normal
 During attack – reversible ST depression with or without T inversion
 Exercise ( Stress ) ECG
 Planar or down sloping ST depression > 1mm ( indicative of ischemia )

2. Myocardial perfusion scan ( with radio-isotopes )

3. Stress echocardiography
4. Coronary angiogram – detail abt extent & nature of disease

For risk factors

 RBS, lipid profile, uric acids
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For ppt factors

 Blood for CP, thyroid function tests, etc …

For complications ( LVF )

 CXR, Echo

MANAGEMENT
General Mx
 Modification of risk factors
 Stop smoking
 Body wt control
 Regular exercise
 Balanced diet
 Avoid ppt factors
 Avoid severe exertion
 Avoid vigorous exercise after heavy meal or in very cold weather
 Advice to take SL nitrate before exertion

Specific Mx
Medical
1. Antiplatelet therapy
 Aspirin or Clopidogrel ( low-dose 75mg )
 Life-long

2. Anti-anginal therapy
i. Nitrates
 For acute attack  GTN SL or aerosol ( spray ) – short acting
 For long term control  Isosorbide mononitrate / dinitrate – long acting
 Need nitrate free interval of 6-8 hr / day

ii. Beta-blockers
 Esp: Cardioselective – atenolol, metoprolol, bisoprolol
 Action – HR , BP & myocardial contractility

iii. Calcium channel blockers

 Rate-limiting CCB – Verapramil, Diltiazam
 Dihydropyridine – Nifedipine, amlodipine
 Action – relax cardiac & arteriolar smooth m/s

iv. Potassium channel activators

 Eg: Nicorandil
 Action – dilates both art: & veins

v. 𝐼𝑓 channel antagonist
 Eg: Ivabradine

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 Action – induce bradycardia by modulating ion channels in SA node

3. Lipid-lowering therapy ( Statins )

 Given in all patients with CAD irrespective of baseline lipid level

Surgical
1. Percutaneous Coronary Intervention ( PCI )
 Method – fine guide wire  position a balloon  dilate the stenosis ± stent
insertion
 Advantage – rapid recovery &  hospital stay
 Disadvantage – high risk of restenosis & repeat revascularization

2. Coronary Artery Bypass Grafting ( CABG )

 Method – use internal mammary artery or reverse seg: of saphenous vein
 Advantage – lower risk of restenosis & repeat revascularization
 Disadvantage – relatively delayed recovery &  hospital stay

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ACUTE CORONARY SYNDROME

MYOCARDIAL INFARCT
TYPES
1. Subendocardial infarct ( NSTEMI ) – Non-Q wave infarct
2. Transmural infarct ( STEMI ) – Q wave infarct

CLINICAL FEATURES
 Age – old age > 40yrs
 Sex – M > F
 Onset – acute, sudden
 Risk factors – eg: smoking, obesity, hypertension, DM, sedentary lifestyle
 Previous h/o angina attack may be ( + )

Symptoms
 Chest pain
 Central / retrosternal
 Acute onset
 Constricting in nature
 Radiating to neck, jaw, inner side of left arm
 Occur on minimal exertion or at rest
 Not relived by rest or nitrates
 longer duration ( usually > 20min )
 Breathlessness
 Syncope or collapse – due to arrhythmia or profound hypotension
 Palpitation
 Anxiety – fear of death
 Nausea & vomiting – due to vagal stimulation

Signs
General
 Very painful expression, pale, anxious, sweating
 Features of risk factors
 Hypercholesterolemia ( eg: xanthoma, xanthelesma )
 Obesity

Pulse
 Rate – tachycardia / bradycardia ( due to autonomic stimulation )
 Rhythm – arrhythmia may be (+)
 Volume – weak
 Cold periphery

JVP
 Raised ( due to impaired myocardial function )

Precordial examination
 Palpation
 Apex beat – diffuse apical impulse
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 Auscultation
 Soft S1, S3
 Bilateral basal crepitation
 Signs of complications – MR ( PSM ) , pericarditis ( pericardial rub )

COMPLICATIONS
Early complications
1. Arrhythmia
 In nearly all patients with AMI
 Common arrhythmia are
 Ventricular/atril fibrillation
 Ventricular/atrial tachycardia
 Ventricular ectopics
 Heart block
 Management
 Pain relief, rest, reassurance & correction of El esp: K+
 Drugs ( eg: Digoxin for AF )
 Defibrillation for VF / 2nd or 3rd Ht block  temporary pacemaker may be
req:
2. Cardiogenic shock & acute circulatory failure
3. Sudden cardiac death
4. Acute pulmonary edema
5. Cerebral anoxia

Late complications
1. Mechanical complications – rupture of necrotic tissue in infarct
 Rupture of papillary m/s  sudden severe MR
 Rupture of interventricular septum  acquired VSD
 Rupture of ventricle  cardiac tamponade
2. Impaired ventricular function
 Ventricular remodeling & ventricular aneurysm
( ACEI can reduce ventricular remodeling & prevent onset of Ht failure )
 Infarct expansion
3. Embolism
 Systemic embolism – due to thrombus on endocardial surface ( eg: Stroke, PVD )
 Pulmonary embolism – due to DVT ( may occur but less common )
4. Pericarditis ( Dressler’s $ - due to autoimmune, few wks to months after MI )
 Persistent fever, pericarditis, pleuritsy
 Rx – self-limiting, may need high dose, NSAID or steroids
5. Post-infarct angina in 50%
 Residual stenosis with viable myocardium still (+)
 Rx as unstable angina with high risk
6. Shoulder-hand $ - pain & stiffness after MI
7. Cardiac psychosis

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INVESTIGATIONS
For diagnosis
1. ECG
 Serial evolution of ECG changes
 Acute ST elevation
 Progressive loss of R & developing Q wave & Resolution of ST elevation
 T version
 Deep Q wave & T inversion
 Persistent Q wave
 Site of infarct
 Changes in lead V1, V2, V3 & V4  anterior infarct
 Changes in lead I, aVL, V5 & V6  lateral infarct
 Changes in lead II, III, aVF  Inferior infarct

2. Cardiac enzymes
Start to rise Peak Fall
Troponin T & I 4-6hr Remain elevated Up to 2wks
CK-MB 4-6hr 12hrs 48-72hrs
AST, LDH After 12hrs 3days 1wks

For complications
 ECG – to detect arrhythmias
 CXR – to detect pul: odema & cardiaomegaly
 Echocardiography – to detect valve regurgitations, septal defects, cardiac tamponade,
thrombus formation, ventricular function ( EF )
 U & Cr, El

For risk factors

 RBS, urinary sugar
 Lipid profile

MANAGEMENT
 It is a medical emergency & urgent Rx is needed !

Immediate Treatment
 Sit the patient upright ( if the patient have APO & dyspnoeic )
 Oxygen ( high flow, high concentration )
 IV access & send blood for Invx
 p.o Aspirin 300mg + Clopidogrel 300-600mg
( Newer & superior alternatives to clopidogrel – Ticagrelor or Prasugrel )
 Beta-blockers ( Metroprolol 50-100mg or 5-15mg IV )
 IV Morphine 5-10mg or Diamorphine slowly + IV antiemetic
 GTN spray 2puffs SL or 0.3mg tablet x 2 SL ( not given if SBP < 90mmHg )
 Monitoring
 Vital signs
 ECG monitoring ( Rx if arrhythmia + )

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 Transfer to a specialist cardiology unit

Acute reperfusion therapy
If PCI available within 120min  Primary PCI ( Tx of choice )
 GP IIb/IIIa R/c followed by Primary / Em PCI

If PCI available within 120min  Thrombolysis / Fibrinolysis ( if no contraindications )

 Thrombolysis
1. Tissue Plasminogen Activator ( tPA ) – Alteplase, Reteplase, Tenecteplase
( Alteplase IV bolus 15mg followed by IV infusion over 90min )
2. Streptokinase
( 1.5 million U in 100ml of N/S IV infusion over 1hr )
 Followed by Anti-coagulant therapy
 s.c Fondaparinux or LMW heparin ( Enoxaparin )

 If thrombolysis fails  refer for Rescuse PCI

 If thrombolysis succeed  refer for early-in hospital coronary angiogram & facilitated PCI

Tx of Emergency Complications ( if present )

 Eg: Tx of APO, cardiogenic shock , Defibrillation for VF

Long-term Mx
Risk stratification by GRACE score
 Depends on
 Degree of residual myocardial ischemia
 Myocardial damage
 Ventricular arrhythmia
 Can predict in-hospital death
 Low risk < 1%
 Medium risk 1-9%
 High risk > 9%

Medical Tx ( for Low risk )

1. Antiplatelet – low dose Aspirin lifelong + ( Clopidogrel / Ticagrelor x 1yr )
 Reduce long-term mortality
2. Beta-blocker – change from IV to oral
 Reduce long-term motality
3. LMW heparin ( Enoxaparin ) s.c x 8 days until discharge
4. ACEI / ARB
 Reduce ventricular remodeling, prevent onset of HF
5. Aldosterone antagonists ( eg: Eplerenone )
 Benefit in AMI with EF <35%
6. For underlying risk factors
 Statins ( In all patients with MI irrespective of baseline lipid level )
 Control of DM & hypertension

Coronary revascularization ( High or Medium risk )

 Coronary angiography + consider GP IIb/IIIa R/c antagonist IV infusion
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 Consider PCI / CABG

Rehabilitation
 Gradually increase activities ( aim to return work at 4-6wks )
 Emotional support & counselling
 Graded exercise

NSTE AC$ (UNSTABLE ANGINA & NSTEMI )

CLINICAL FEATURES
 Age – old age > 40yrs
 Sex – M > F
 Onset – acute, sudden
 Risk factors – eg: smoking, obesity, hypertension, DM, sedentary lifestyle
 Previous h/o angina attack may be ( + )

Symptoms
 Chest pain
 Central / retrosternal
 Acute onset
 Constricting in nature
 Radiating to neck, jaw, inner side of left arm
 Occur on minimal exertion or at rest
 Not relived by rest or nitrates
 longer duration ( usually > 20min )
 Breathlessness
 Syncope or collapse – due to arrhythmia or profound hypotension
 Palpitation
 Anxiety – fear of death
 Nausea & vomiting – due to vagal stimulation

Signs
General
 Very painful expression, pale, anxious, sweating
 Features of risk factors
 Hypercholesterolemia ( eg: xanthoma, xanthelesma )
 Obesity

Pulse
 Rate – tachycardia / bradycardia ( due to autonomic stimulation )
 Rhythm – arrhythmia may be (+)
 Volume – weak
 Cold periphery

JVP
 Raised ( due to impaired myocardial function )

Precordial examination
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 Palpation
 Apex beat – diffuse apical impulse
 Auscultation
 Soft S1, S3
 Bilateral basal crepitation
 Signs of complications – MR ( PSM ) , pericarditis ( pericardial rub )

INVESTIGATIONS
For diagnosis
1. ECG
 Non-specific – ST depression, T inversion ( Typical – deep arrow-headed )
 May be normal

2. Cardiac enzymes – Normal in unstable in angina & increased in NSTEMI

Start to rise Peak Fall
Troponin T & I 4-6hr Remain elevated Up to 2wks
CK-MB 4-6hr 12hrs 48-72hrs
AST, LDH After 12hrs 3days 1wks

For complications
 ECG – to detect arrhythmias
 CXR – to detect pul: odema & cardiaomegaly
 Echocardiography – to detect valve regurgitations, septal defects, cardiac tamponade,
thrombus formation, ventricular function ( EF )
 U & Cr, El

For risk factors

 RBS, urinary sugar
 Lipid profile

MANAGEMENT
 It is a medical emergency & urgent Rx is needed !

Immediate Treatment
 Sit the patient upright ( if the patient have APO & dyspnoeic )
 Oxygen ( high flow, high concentration )
 IV access & send blood for Invx
 p.o Aspirin 300mg + Clopidogrel 300-600mg
( Newer & superior alternatives to clopidogrel – Ticagrelor or Prasugrel )
 Beta-blockers ( Metroprolol 50-100mg or 5-15mg IV )
 IV Morphine 5-10mg or Diamorphine slowly + IV antiemetic
 GTN spray 2puffs SL or 0.3mg tablet x 2 SL ( not given if SBP < 90mmHg )
 Anti-coagulant therapy
 s.c Fondaparinux or LMW heparin ( Enoxaparin )
 Monitoring
 Vital signs
 ECG monitoring ( Rx if arrhythmia + )
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 Transfer to a specialist cardiology unit

Tx of Emergency Complications ( if present )
 Eg: Tx of APO, cardiogenic shock , Defibrillation for VF

Long-term Mx
Risk stratification by GRACE score
 Depends on
 Degree of residual myocardial ischemia
 Myocardial damage
 Ventricular arrhythmia
 Can predict in-hospital death
 Low risk < 1%
 Medium risk 1-9%
 High risk > 9%

Medical Tx ( for Low risk )

1. Antiplatelet – low dose Aspirin lifelong + ( Clopidogrel / Ticagrelor x 1yr )
 Reduce long-term mortality
2. Beta-blocker – change from IV to oral
 Reduce long-term motality
3. LMW heparin ( Enoxaparin ) s.c x 8 days until discharge
4. ACEI / ARB
 Reduce ventricular remodeling, prevent onset of HF
5. For underlying risk factors
 Statins ( In all patients with MI irrespective of baseline lipid level )
 Control of DM & hypertension

Coronary revascularization ( High or Medium risk )

 Coronary angiography + consider GP IIb/IIIa R/c antagonist IV infusion
 Consider PCI / CABG

Rehabilitation
 Gradually increase activities ( aim to return work at 4-6wks )
 Emotional support & counselling
 Graded exercise

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D.Dx OF CHEST PAIN

COMMON CAUSES OF CHEST PAIN

Central chest pain Peripheral chest pain

Cardiac Pleura
 Myocardial ischemia ( angina, MI )  Pleuritic
 Mitral valve prolapse  Pleural effusion
 Myocarditis  Pneumothorax
 Pericarditis Lungs
Aortic  Pulmonary infarct
 Aortic dissection  Pneumonia
 Aortic aneurysm  TB
Esophageal  Maliganancy
 Esophagitis  Connective tissue d/o
 Esophageal spasm Musculoskeletal
 Mallory-Weiss $  Osteoarthritis
Mediastinal  Rib fracture / injury
 Tracheitis  Costochondritis ( Tietze’s $ )
 Malignancy Neurological
Others  Prolapsed intervertebral disc
 Anxiety  Herpes Zoster
 Massive pul: embolism  Thoracic outlet $
Referred pain ( usually central chest pain )
 Acute pancreatitis
 Peptic ulcer

1. Angina pectoris
Clinical features
 Age & sex – old age, M>F
 Onset – sudden / recurrent
 Risk factors – h/o smoking, DM, hypertension, family h/o
 Symptoms
 Chest pain – central, constricting , radiate to inner side of left arm, jaw &
neck, aggravated by exertion or stress, relived by rest or nitrate, duration <
15min
 Signs
 Usually no physical signs
 Features of risk factors ( eg: obesity, xanthelesma, xanthoma, corneal arcus,
hypertension )

Invx
 ECG – normal between attacks
 Exercise ECG – ST depression & T inversion

2. Myocardial infarction
Clinical features
 Age & sex – old age, M>F

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 Onset – sudden
 Risk factors – h/o smoking, DM, hypertension, family h/o, recurrent attack of angina
 Symptoms
 Chest pain –retrosternal, constriction, radiate to left arm, jaw, neck, more
severe & last longer (>20min), not relived by nitrates & rest
 Breathlessness
 Syncope, palpitation, nausea & vomiting
 Signs
 General – looks very painful, anxious
 Features of acute heart failure – rapid & weak pulse, hypotension, increased
JVP, soft S1, S3 , bilateral basal crepitations

Invx
 ECG – ST elevation, T-inversion, Q wave
 Cardiac enzymes – CK-MB, Troponin T & I

3. Massive pulmonary embolism

Clinical features
 Risk factors – prolonged bed ridden, recent h/o Sx
 Symptoms
 Acute onset of chest pain
 Hemoptysis
 Sudden Syncope or Collapse
 Signs
 General  cyanosis, shock may be (+) – hypotension & tachycardia
 Respi  usually no detectable abnormalities
 JVP  increased
 Lower limb  features of DVT ( eg: Homan’s sign )

Invx
 CXR  Wedge-shaped opacity, oligemic lung field
 ABGA  PaO2 & PaCO2 reduced
 ECG  sinus tachycardia, S1 Q3 T3 pattern, RBBB
 D-dimer, V/Q scan

4. Pericarditis
Clinical features
 Age & sex – any
 Onset – acute or insidious
 Risk factors – rheumatic fever, flu-like prodromal, renal failure
 Symptoms
 Chest pain – central, sharp & stabbing, radiate to shoulder & arm,
aggravated by movement & respiration, relived by sitting & leaning forward
 Low-grade fever is common
 Signs – pericardial rub on auscultation

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Invx
 ECG  wide spread ST elevation with concavity upward, PR depression
 CXR  globular heart ( if asso: with pericardial effusion

5. Dissecting aortic aneurysm

Clinical features
 Age & sex – old age, M:F – 2:1
 Onset – sudden onset
 Risk factors – hypertension , collagen disorders ( eg: Marfan’s $, Ehlers-Danlos )
 Symptoms
 Chest pain – sudden onset, severe sharp & tearing, radiate to the back
 Sudden collapse & shock
 Signs
 General – shock ( hypotension, rapid thread pulse )
 CVS – asymmetry of pulses / absent pulse ( brachial, carotid, femoral ),
asymmetry of BP between arms , EDM due to AR , features of cardiac
tamponade may be (+)

Invx
 CXR  widened mediastinum, distortion of aortic knuckle, lt-sided pl: effustion is
common
 Echocardiogram / CT / MRI

6. Esophageal pain ( GERD / Achlasia / Esophagitis / Esophageal motility disorder )

Clinical features
 Age & sex – any
 Onset – acute or insidious
 Risk factors – risk factors for GERD, alcohol
 Symptoms
 Chest pain – burning or sharp, aggravated by food & drinks, relieved by
nitrate & antacids
 Epigastric pain
 Signs – usually normal

Invx
 ECG, Echo, CXR, Endoscopy
 Esophageal manometry

7. Mitral valve prolapse ( usually due to cong: anomalies or degenerative myoxomatous

changes )
Clinical features
 Age & sex – young ( 14-30 ), F > M
 Risk factors – Marfan’s $, SLE
 Symptoms
 Chest pain – atypical sharp & left-sided chest pain ( similar to angia )
 Palpitation

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 Signs – mid-systolic click  late systolic murmur  lengthen as regurgitation more

severe ( PSM )

Invx
 ECG  T inversion
 Echo  mitral valve bulging toward LA

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CONGENITAL HEART DISEASE

CLASSIFICATION

Acyanotic congenital heart disease

 Ventricular septal defect ( VSD ) – most common congenital heart disease
 Atrial septal defect ( ASD )
 Patent ductus arteriosus ( PDA )

Cyanotic congenital heart disease

 Right to left shunt with pulmonary stenosis
 Tetralogy of Fallot ( TOF ) – most common cyanotic congenital heart disease
 Tricuspid atresia
 Ebstein’s anomaly
 Transposition of Great Vessle ( TGA )
 Total anomalous pulmonary venous connection

VENTRICULAR SEPTAL DEFECT

 likely to close spontaneously
 Membranous VSD

PATHOPHYSIOLOGY
 Defect or hole in ventricular septum  left-to-right shunt
 Blood flows from LV  RV  Pul: A  Lungs  Pul: V  LA  LV
 blood flow & work load in LV  LVH  LV failure

 LVF  pul: congestion  pul: hypertension

 Pul: Hypertension  work load in RV  RVH  RV failure

 LVF + RVF = Biventricular failure ( CCF )

CLINICAL FEATURES
For small VSD ( 0.5-2cm )
 Symptoms – Asymptomatic
 Signs – Loud PSM with thrill ( at left lower sternal edge )

For large VSD ( >2cm )

Symptoms
 Usually present abt 6-10wks of age
 Feeding difficulties
 Features of congestive heart failure – dyspnea, orthopnea, fatigue, effort intolerance
 Repeated chest infection – d/t pul: congestion
 Features of Infective endocarditis – fever, malaise, m/s & joint pain, hematuria
 Poor growth – d/t nutritional deficiency & repeated infections
 Dyspnoea

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Signs
 General examination
 Poor growth, thin, dyspnoeic & orthopneic
 CVS examination
 Pulse – tachycardia ( if CCF + )
 JVP -  ( if CCF + )
 Palpation
o Apex – displaced outward & downward , heaving character ( d/t LVH )
o Pul: area – palpable P2 ( if Pul: hypertension + )
o Lt lower Sternal Edge –systolic thrill
 Auscultation
o LLSE – PSM ( less harsh, more blowing )
o Pul: area – loud P2 ( if Pul: hypertension+)
o MDM at apex ( d/t increased mitral valve flow  relative mitral stenosis )
o ESM at pul: area ( d/t increased pulmonary valve flow  relative pul:
stensosis )

INVESTIGATIONS
1. CXR
 Small VSD – Normal Ht size & normal pul: vascularity
 Large VSD – Gross cardiomegaly (  cardio-thoracic ration ) & plethoric lungs field ( 
pul: vascular markings )

2. ECG
 Small VSD – Normal
 Large VSD
 LVH – deep S in V1 & tall R in V6
 RVH – Tall R in V1 & deep S in V1
 Pul: hypertension – peak “P” wave ( P- pulmonalae )

3. Echocardiogram
 Can detect defect – size, site
 Can detect cardiac chambers – enlargement, +ce of vegetations
 Can calculate ejection fraction ( to detect heart failure )
 Doppler – pressure gradient across the defect

4. Cardiac catheterization
 Can detect oxygen saturation & pressure -  in RV & pul: artery ( Eisenmenger $ )

OUTCOMES OF VSD
1. Spontaneous closure
 Usually during 1st 2-4 yrs
 Muscular defects are more likely than membranous defects

2. Complications
 Congestive HF
 IE

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 Pulmonary hypertension
 Eisenmenger $ - when blood is shunted from Right-to-Left due to pulmonary
hypertension

TREATMENT
For Small VSD
 Conservative Tx
 Reassurance
 Treatment of Complications if develops
 Long-term follow-up until spontaneous closure occurs

For Large VSD

1. Medical Tx
 Treatment of congestive heart failure if (+)
 Diuretics ( eg: Frusemide )
 Vasodilators ( eg: ACEI )
 Nutritional support for poor growth
 Prevention & treatment of repeated chest infections
 Treatment of IE
 IV broad spectrum antibiotics ( IV Crystalline Pen + Gentamycin )

2. Surgical Tx
 Indications
 (+)ce of uncontrolled congestive HF
 (+)ce of pul: hypertension
 Pul : systemic blood flow > 2:1
 Contraindications
 Severe pul: vascular disease
 Reverse shunt ( Rt-to-Lt )

 Surgical methods
 Closure of defect – by Dacron Patch , by catheter occlusion
 Palliative pulmonary banding with repair

PATENT DUCTUS ARTERIOSUS

 Communication between aorta, distal to origin of left subclavian artery , & the pulmonary
artery , at its bifurcation

RISK FACTORS
 Pre-term infants
 Congenital Rubella $
 Down’s $

PATHOPHYSIOLOGY
 PDA  blood flows from aorta to pul: artery  Left-to-Right Shunt
 Same as VSD

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CLINICAL FEATURES
For Small PDA
 Symptoms – asymptomatic
 Sign – continuous murmur ( loudest at Lt 2nd intercostal space )

For Large PDA

Symptoms
 Usually present abt 6-10wks of age
 Feeding difficulties
 Features of congestive heart failure – dyspnea, orthopnea, fatigue, effort intolerance
 Repeated chest infection – d/t pul: congestion
 Features of Infective endocarditis – fever, malaise, m/s & joint pain, hematuria
 Poor growth – d/t nutritional deficiency & repeated infections
 Dyspnoea
 Palpitation – d/t large stroke volume

Signs
 General examination
 Poor growth, thin, dyspnoeic & orthopneic
 CVS examination
 Pulse – tachycardia ( if CCF + ) , collapsing pulse
 BP – wide pulse pressure ( SBP d/t large stroke vol: , DBP due to diastolic run-off )
 JVP -  ( if CCF + )
 Palpation
o Apex – displaced outward & downward , heaving character ( d/t LVH )
o Pul: area – palpable P2 ( if Pul: hypertension + )
o At Lt 2nd ICS – thrill , with radiation to Lt clavicle or apex
 Auscultation
o At Lt 2nd ICS – continuous machinery murmur , with radiation to Lt clavicle &
back between the scapular
o Pul: area – loud P2 ( if Pul: hypertension+)

INVESTIGATIONS
1. CXR
 Gross cardiomegaly (  cardio-thoracic ratio ) & plethoric lungs field (  pul: vascular
markings )

2. ECG
 LVH – deep S in V1 & tall R in V6
 RVH – Tall R in V1 & deep S in V1
 Pul: hypertension – peak “P” wave ( P- pulmonalae )

3. Echocardiogram
 Suprasternal notch scan – direct visualization of PDA
 Can detect cardiac chambers – enlargement, +ce of vegetations
 Can calculate ejection fraction ( to detect heart failure )
 Doppler

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 retrograde tuburlent flow in pul: artery d/r systole

 aortic retrograde flow in diastole

4. Cardiac catheterization
 Catheter can be passed from pul: artery , through the ductus, into descending aorta
 Can detect oxygen saturation & pressure -  in RV & pul: artery ( Eisenmenger $ )

OUTCOMES OF PDA
1. Spontaneous closure

2. Complications
 Congestive HF
 IE
 Pulmonary hypertension
 Eisenmenger $ - when blood is shunted from Right-to-Left due to pulmonary
hypertension
 Ductus calcification
 Ductus / pul: artery aneyrsm

TREATMENT
1. Medical Tx
 In preterm infants
 Asymptomatic – can wait for spontaneous closure
 Symptomatic – IV indomethacin 0.1mg/kg/day x 3 doses

 Treatment of congestive heart failure if (+)

 Diuretics ( eg: Frusemide )
 Vasodilators ( eg: ACEI )
 Nutritional support for poor growth
 Prevention & treatment of repeated chest infections
 Treatment of IE
 IV broad spectrum antibiotics ( IV Crystalline Pen + Gentamycin )

2. Surgical Tx
 Indications
 As soon as Dx is made
 Preferably before 1yr of age

 Surgical methods
 Ligation & division of ductus ( through left thoracotomy )
 Transcatheter closure ( using umbrella-like devices )

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TETRALOGY OF FALLOT
PATHOPHYSIOLOGY

 Due to anterior deviation of Infandiblar septum ( muscular septum that separates aortic &
pulmonary outflow )
 It consists of
1. Pulmonic stenosis
2. Ventricular septal defect
3. Over-riding of aorta
4. Right ventricular hypertrophy
 Normal venous return to Rt Heart  Due to pulmonic stenosis  deoxygenated blood is
shunted directly to aorta  into systemic circulation  Cyanosis

CLINICAL FEATURES
Symptoms
1. Cyanosis
 Occurs in the 1st year of life ( d/t increasing hypertrophy of Rt ventricle infundibulum
& patient growth )
 Occurs in lips, mouth & nail beds

2. Dyspnoea
 Occurs on exertion ( play for a short time & then, sit down or lie down )
 Relieved by
 Squatting position ( older children )
 Knee-chest position ( infants )

3. Paraoxysmal Hypercyanotic Attacks / Blue spells

 Occurs during 1st 2 years of life
 Occurs after waking up or exerction
 Symptoms – dyspnoeic, cyanosis increases, restless, convulsions , Loss of
consciousness
 Relieved by squatting or knee-chest position

Signs
 General examination
 Poor growth, thin
 Dusky blue skin
 Grey sclerae with engorged blood vessels
 Central cyanosis ( in lips & mouth )
 Peripheral cyanosis ( in nail beds )
 Finger clubbing
 CVS examination
 Pulse, BP & JVP – usually normal
 Palpation
o Bulging of left hemithorax ( d/t RVH )
o Apex – usually Normal
o Left parasternal heaving ( d/t RVH )
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o Systolic thrill along the left sternal border

 Auscultation
o ESM ( Ejection Systolic Murmur ) – at upper sternal border ( left 2nd ICS )
o 2nd heart sound – single or pulmonary component is soft
( in severe pulmonary stenosis  shunting of blood away from RV outflow
through aortic valve )

INVESTIGATIONS

5. CXR
 Heart size – Normal
 Boot-shaped heart ( d/t concavity at pulmonary conus + rounded tilted apex )
 Oligaemic lungs field – d/t pulmonary blood flow

6. ECG
 RVH – Tall R in V1 & deep S in V1
 Right axis deviation

7. Echocardiogram
 Can establish the diagnosis
 Pulmonary stenosis
 Over-riding of aorta
 Right ventricular hypertrophy
 Ventricular septal defect

8. Cardiac catheterization
 Morphological defect
 Systolic pressure in RV almost equal to LV pressure
 Pulmonary artery pressure – markedly reduced
 Oxygen saturation – depend on Rt to left shunt

TREATMENT
Immediate Treatment ( During blue spells )
 One or more of the following in sequence
1. Calming & keeping the infant in knee-chest position
2. Give 100% Oxygen by face mask
3. IV propranolol
 IV 0.1-0.2 mg/kg &
 then prophylactic oral dose 0.5-1 mg/kg/dose 2-3 times/day
 decrease infundibular spasm
 decrease tachycardia
4. sc Morphine ( 0.1mg/kg )
 deceases sympathetic tone & oxygen consumption
 decrease pulmonary vascular resistance
5. IV Sodium bicarbonate
 To reduce respiratory centre stimulating effect of metabolic acidosis
6. Vasopressors ( IV phenylephadrine / methoxamine )
Medical Treatment
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 Nutritional support for poor growth

 Treatment of IE
 IV broad spectrum antibiotics ( IV Crystalline Pen + Gentamycin )

Surgical Treatment
 Palliative ( Systemic to pulmonary artery shunt )
1. Blalock-Taussig shunt – between subclavian artery & pulmonary artery ( most
commonly used )
2. Waterson shunt – between ascending aorta & Rt pulmonary artery
3. Pott’s shunt – between descending aorta & Lt pulmonary artery

 Curative
 Open heart surgery & repair
 Relieve Rt ventricular outflow obstruction & closure of VSD

Prevention & Treatment of Complications

 Prevention & prompt treatment of dehydration
 Adequate hydration
 Maintenance of Hct around 60%
 In extreme polycythemia & symptomatic patients
 Venesection & volume replacement with albumin or saline
 For brain abscess – BS Antibiotics & operation to drain the abscess

COMPLICATIONS
1. Hypercyanotic attacks
2. Infective endocarditis
3. Delayed growth & development
4. Polycythemia ( d/t persistently low arterial oxygen saturation )
5. Cerebral thrombosis & embolization ( d/t polycythemia ppt by dehydration )
 Common in <2yrs of age
6. Brain abscess
 Common in >2yrs of age
7. Iron Deficiency anemia

ATRIAL SEPTAL DEFECT

PATHOPHYSIOLOGY
 Most are ostium secundum defects, involving fossa ovalis which in utero was the foramen
ovale
 May be due to Ostium primum defects which result from a defect in the atrioventricular
septum & are associated with a cleft mitral valve ( Split anterior leaflet )

 Defect in atrial septum  left to Rt shunt ( according to Pressure gradient )

 Blood flows from LA  RA  RV  Pul: A  LA  RA
 blood flow & work load in Rt heart  RVH  RVF

 Later  blood flow to pul: circulation  pul: hypertension develops ( Eisenmenger’s $ )

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 When Eisenmenger’s $  pul: resistance  Rt to left shunt ( according to Pressure

gradient )

CLINICAL FEATURES
Symptoms
 Usually asymptomatic for many years ( up to 5th decade )
 Feeding difficulties
 Features of congestive heart failure – dyspnea, orthopnea, fatigue, effort intolerance
 Repeated chest infection – d/t pul: congestion
 Features of Infective endocarditis – fever, malaise, m/s & joint pain, hematuria
 Poor growth – d/t nutritional deficiency & repeated infections
 Dyspnoea
 Palpitation ( arrhythmia esp: aF )

Signs
 General examination
 Poor growth, thin, dyspnoeic & orthopneic
 CVS examination
 Pulse – tachycardia ( if CCF + )
 JVP -  ( if CCF + )
 Palpation
o Pul: area – palpable P2 ( if Pul: hypertension + )
o Left parasternal heaving ( + )
 Auscultation
o S2 wide fixed splitting S2
( Wide – because of delayed RV ejection )
( Fixed – because septal defect equalizes left & Rt atrial pressures
throughout repi: cycle )
o Systolic flow murmur ( ESM ) over the pul: area
o Diastolic flow murmur ( MDM ) over tricuspid valve in childen with a large
shunt
COMPLICATIONS
 Heart failure
 Chest failure
 Arrhythmias
 Paradoxical embolism ( rare )
 Pulmonary hypertension & reversal of left of right shunt ( Eisenmenger $ )
 Pulmonary & tricuspid regurgitation

INVESTIGATIONS
1. CXR
 Small aortic knuckle
 Pulmonary plethora
 Progressive

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2. ECG
 RBBB with LAD & prolonged PR interval ( primum defect ) or RAD ( secundum defect)

3. Echocardiogram
 Can detect defect – size, site
 Can detect cardiac chambers – enlargement, +ce of vegetations
 Can calculate ejection fraction ( to detect heart failure )
 Doppler – pressure gradient across the defect

4. Cardiac catheterization
 Can detect oxygen saturation & pressure -  in RV
TREATMENT
1. Medical Tx
 Treatment of congestive heart failure if (+)
 Diuretics ( eg: Frusemide )
 Vasodilators ( eg: ACEI )
 Nutritional support for poor growth
 Prevention & treatment of repeated chest infections
 Treatment of IE
 IV broad spectrum antibiotics ( IV Crystalline Pen + Gentamycin )

2. Surgical Tx
 Indications
 Symptomatic
 Pul: to systemic blood flow ratio – 1.5:1

 Contraindications
 Severe pul: vascular disease
 Reverse shunt ( Rt-to-Lt )

 Surgical methods
 Closure of defect – by Dacron Patch , by catheter occlusion

COARCTATION OF THE AORTA

PATHOPHYSIOLOGY
 Narrowing of aorta ( most commonly in the region where the ductus arteriosus joins the
aorta ,i.e, at the isthmus just below the origin of the left subclavian artery
 Mostly congenital ( M:F – 2:1 )
 Frequent Associated abnormalities
 Bicuspid aortic valve
 Berry aneurysms of cerebral circulation
 Turner’s $
 Acquired coarctation of the aorta is rare but may follow trauma or occur as a Cx of a
progressive arteritis ( eg: Takayasu’s disease )

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CLINICAL FEATURES
Symptoms
 Headache ( due to pressure proximal to the coarctation )
 Weakness or cramps in the legs ( due to circulation in the lower part of the body )

Signs
 Pulse – radio-femoral delay, weak femoral pulse
 BP - in the upper limbs but normal or low in the lower limbs
 Auscultation
 scapular bruit, systolic murmur ( best heard over the left scapula )
 If bicuspid aortic valve (+)  may be an ejection click & systolic murmur in aortic
area

COMPLICATIONS
 Heart failure
 Infective endocarditis
 Hypertension & its complications
 In untreated cases, death may occur from left ventricular failure
 Dissection of aorta or cerebral H’ge

INVESTIGATIONS
1. CXR
 Often normal in childhood
 Older age  changes in the contour of aorta ( indentation of descending aorta, 3
sign ), Notching of the under surfaces of the ribs from collaterals
2. MRI – Ideal for demonstrating the lesion
3. ECG – features of LVH may be (+)

MANAGEMENT
 Surgical correction
 Advisable in all but the mildest cases
 If done early in childhood, persistent hypertension can be avoided
 Recurrence of stenosis may occur as the child grows & can be managed by balloon
dilatation, which can also be used as the primary Tx in some cases

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HYPERTENSION
CLASSIFICATION & DEFINITION

Category Systolic BP ( mmHg ) Diastolic BP ( mmHg )

BP
 Optimal  <120  <80
 Normal  <130  85
 High normal  130-139  85-89
Hypertension
 Grade 1 ( mild )  140-159  90-99
 Grade 2 ( moderate )  160-179  100-109
 Grade 3 ( severe )  ≥180  ≥110
Isolated systolic hypertension
 Grade 1  140-159  <90
 Grade 1  ≥160  <90

CAUSES OF HYPERTENSION ( ERECT )

Primary/Essential hypertension ( >95% )

 Multifactorial
 Genetic ( 40-60% )
 Environmental ( high salt intake, heavy alcohol consumption, obesity, lack of exercise, IUGR )
 Metabolic $ / Syndrome X / Reaven’s $ / Insulin Resistance $
 Hyperinsulinemia
 Type 2 DM
 Hypertension
 Low HDL cholesterol, elevated TGs
 Central ( visceral ) obesity
 Microalbuminuria
 Increased fibrinogen
 Increased plasminogen activator inhibitor -1
 Elevated plasma uric acid
 Increased CRP
 Associated disorders – PCOS, NAFLD

Secondary Hypertension ( 5% ) – esp: < 40yrs ( young hypertension )

1. Renal causes ( Renal hypertension )
 Renal vascular disease – RAS
 Parenchymal renal disease – particularly GN
 Polycystic kidney disease
 Chronic renal failure

2. Endocrine causes
 Pituitary – acromegaly
 Thyroid – thryrotoxicosis, primary hypothyroiditsm
 Parathyroid – Hyperparathyroidism
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 Adrenal cortex – Conn’s $, Cushing’s $, Glucocorticoid-suppressible

hyperaldosteronism
 Adrenal medulla – pheochromocytoma
 Congenital adrenal hyperplasia
 11- hydroxysteroid dehydrogenase deficiency
 Liddle’s $ ( imporper stimulation of Na+ channel )

3. Coarctation of aorta
4. Toxins
 Alcohol
 Drugs
 OC pills ( estrogen ) , anabolic steroid
 Corticosteroids
 NSAIDs, carbenoxolone
 Sympathomimetic drugs

5. Others
 Pre-eclampsia
 Obesity
 Increased ICP

TARGET ORGAN DAMAGE / COMPLICATIONS

CNS
 TIA
 Stroke – infarct ( thrombosis ) or Hemorrhage ( ruptured Charcot Buchard Aneurysm )
 Hypertensive encephalopathy ( hypertensive emergency ) – rare

Retina ( Hypertensive Retinopathy )

 Grade I – arteriolar thickening tortuosity & reflectiveness ( silver wiring )
 Grade II – Grade I + constriction of veins at arterial crossing ( AV nipping )
 Grade III – Grade II + evidence of retinal ischemia ( flame-shaped H’ge & cotton wool
exudates )
 Grade IV – Grade III + Papillodema

CVS
 Heart – LVH / LVF, Angina, MI , AF
 Vessel – artherosclerosis, peripheral vascular disease, dissecting aortic aneurysm, carotid
artery aneurysm ( atherosclerotic )

Renal ( Hypertensive nephropathy )

 Proteinuria
 Progressive renal failure / CKD
 Malignant nephrosclerosis ( Acute RF )

Hypertensive crisis ( Severe elevation of BP – SBP > 200 , DBP >120 )

 Hypertensive urgency – high BP without acute TOD
 Hypertensive emergency – high BP complicated by acute target organ dysfunction

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( eg: Retinopathy grade 3 or 4 / renal dysfunction / hypertensive encephalopathy )

INVESTIGATIONS
Invx done on all patients
 Urinalysis / Urine RE – for blood protein & glucose
 Blood U&Cr, El
 Blood glucose
 Lipid profile
 12-lead ECG ( LVH, IHD, AF , etc ….. )

Invx done on selected patients ( esp: young hypertension )

 CXR
 Cardiomegaly
 Features of pul: odema
 Dock’s sign / rib notching ( in COA )
 Echocardiogram – LVH & associated valvular pathology
 Renal USG – Renal size , PCK , ect ……..
 Abdominal USG – for adrenal tumor , etc …….
 Radio-isotope scans for localization of adrenal tumors ( eg: MIBG scan for
pheochromocytoma / iodocholerstrol scna for cortisol tumors )
 Renal arteriogram – for renal artery stenosis
 Aortogram – for COA
 Ambulatory BP recording – for borderline / white-coat hypertension
 Urinary catecholamines / VMA level – increased in pheochromocytoma
 Plasma renin & aldosterone – for primary hyperaldosteronism
 Urinary cortisol / dexamethasone suppression test – for Cushing’s $

MANAGEMENT
Immediate Treatment ( if any hypertensive Em + )
 Bed rest
 In most patients  can avoid parenteral Rx & treated with oral drugs
May also require parenteral Rx ( require special care preferably in ICU )
 Eg: IV Labetalol
 IV GTN
 IM hydralazine
 IV sodium nitroprusside
 Symptomatic Rx for encephalopathy, APO , etc …….

General Mx
 Stop smoking / moderation of alcohol intake
 Avoid high salt & fatty diet
 Regular Physical exercise
 Avoid stressful life-style

Medical Treatment
Anti-hypertensive drugs
1. ACEI ( eg: Captopril, Enalapril, Ramipril ) Or ARB ( eg: Losartan )

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2. Beta-blockers ( eg: Atenlol, Bisoprolol )

3. Calcium channel blockers (
 Dihydropyridines – Nifedipine, Amlodipine
 Rate limiting CCB – Verapamil, Diltiazam
4. Diuretics
 Thiazides ( eg: Bendrofluzanide, Indapamide )
 Frusemides
5. Others
 Vasodilators – Alpha-blockers ( eg: Prazosin, hydralazine, Minoxidil )
 Centrally acting drugs ( eg: Methyldopa )

 Targets of BP control
Clinical BP Ambulatory BP
< 80yrs < 140/90 < 135/85
≥ 80yrs < 150/90 < 140/85

 Choices of Drugs ( NICE guidelines )

Adjuvant drugs Rx
 Anti-platelet – Aspirin ( low dose )
 Lipid-lowering agents – Statin

Treatment of underlying cause

 Treat or control secondary causes in refractory hypertension

Treatment of complications
 Eg: Tx of heart failure, renal failure

Regular follow-up & monitoring

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SURGICALLY CORRECTABLE CAUSES OF HYPERTENSION

 Hyperthyroidism
 Hyperparathyroidism
 Coarctation of aorta
 Renal artery stenosis
 Unilateral renal parenchymal disease
 Conn’s $
 Cushing’s $
 Pheochromocytoma

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CARDIOMYOPATHY
TYPES OF CARDIOMYOPATHY

1. Hypertrophic cardiomyopathy
 Asymmetric septal hypertrophy ( ASH ) with systolic anterior motion of the mitral
valve ( SAM ) causing mitral reflux & dynamic LV outflow tract obstruction
 Concentric hypertrophy
 Apical hypertrophy

2. Dilated cardiomyopathy
3. Arrhythmogenic right ventricular dysplasia
4. Obliterative cardiomyopathy
5. Restrictive cardiomyopathy

DILATED CARDIOMYOPATHY
AETIOLOGY
 A dilated flabby heart of unknown cause
 M > F ( 2:1 )
 Associations –alcohol, hypertension, haemochrmatosis, viral infection, autoimmune,
thyrotoxicosis, peri- or postpartum, congenital ( X-liked ) eg: Becker & Duchenne

CLINICAL FEATURES
Symptoms
 Fatigue, dyspnea, sporadic chest pain, heart failure
Signs
 Pulse – tachycardia, hypotension
 JVP – raised
 Palpation – displaced & diffuse apex
 Auscultation – S3, Gallop, Mitral or Tricuspid regurgitation – PSM
 Signs of HF – pleural effusion, odema, jaundice, hepatomegaly, ascites

COMPLICATIONS
 Heart failure, arrhythmia ( eg: AF, VT, thromboembolism & sudden death )

INVESTIGATIONS
 CXR – cardiomegaly, pulmonary odema
 ECG – tachycardia, non-specific T wave changes, poor R wave progression
 Echo – globally dilated hypokinetic heart with low EF, also look for MR, TR, LV mural
thrombus

MANAGEMENT
Medical
 Control heart failure – bed rest, diuretics, digoxin, ACEI, anticoagulation ( to reduce risk of
sudden arrhythmic death )
Surgical
 Consider cardiac transplantation
 Consider for implantation of a cardiac defibrillator and/or cardiac resynchronization therapy

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HYPERTROPHIC CARDIOMYOPATHY
AETIOLOGY
 Most common form of cardiomyopathy
 Genetic disorder – autosomal dominant
( Beta-myosin heavy chain mutations, Troponin mutations, Myosin-binding protein C
mutations )
 Septal hypertrophy may cause dynamic left ventricular outflow tract obstruction ( HOCM )

CLINICAL FEATURES ( similar to those of aortic stenosis )

Symptoms
 Effort-related symptoms ( angina, Dyspnea, Syncope )
 Palpitation, Sudden death

Signs
 Jerky pulse
 Double apical impulse ( palpable 4th heart sound due to LA hypertrophy )
 Mid-systolic murmur / ESM at the base/ PSM ( due to MR ) at the apex
( Signs of left ventricular outflow tract obstruction which may be augmented by standing up
( reduced venous return ), inotropes & vasodilators ( eg: sublingual nitrate )

COMPLICATIONS
 Arrhythmia ( AF, WPW $, ventricular ectopics, VT ) &
 Sudden death – typically during or just after vigorous physical activity
( Hypertrophic CMP is the most common cause of sudden death in young athletes )

INVESTIGATION
 ECG – LVH, variety of bizarre abnormalities ( eg: pseudo-infarct pattern, deep T-inversion ),
arrhythmia
 Echo – usually diagnostic, but diagnosis may be difficult when another cause of LVH is
present, asymmetrical septal hypertrophy, small LV cavity with hypercontractile posterior
wall
 Cardiac catheterization – to assess severity of gradient , CAD or MR
 Genetic testing – may facilitate diagnosis in the future

MANAGEMENT
Medical Tx ( No pharmacological Tx is definitely known to improve prognosis )
 Beta-blocker & rate limiting CCB ( eg: Verapramil ) – to relieve angina & sometime prevent
syncope
 Amiodarone – to treat arrhythmia
 Digoxin & vasodilator – may increase outflow tract obstruction & should be avoided

Surgical Tx
 Relieve outflow tract obstruction by
 Partial surgical resection ( myocetomy ) OR
 Iatrogenic infarction of basal septum ( Septal ablation ) using a catheter-delivered
alcohol solution
 Implantable cardiac defibrillator ( ICD ) – considered if risk factors for sudden death

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INFECTIVE ENDOCARDITIS
DEFINITION

 Microbial infection of a heart valve ( native or prosthetic ) , lining of a cardiac chamber or

blood vessel or a congenital anomaly ( eg: Septal defect )

CAUSAL ORGANISMS
Subacute IE
 Streptococci
 Viridans group ( URT commensal ) – Strep mitis, Strep mutans, Strep sanguis
 Enterococci ( bowel & urinary commensal ) – E. faecalis, E. faecium
 Strep bovis & Strep milleri
 Gram (-)ve – HACEK group ( Hemophilus, Actinobacillus, Cardiobacterium, Eikenella,
Kingella)
 Brucella, Coxiella

Acute IE
 Staph aureus ( skin infection, Abscess, IV site, IVDU )
 Strep pneumonia, Strep pyogenes
 Coagulase (-)ve Staph – Staph lugdenesis
 Fungi in immunocompromised pts – Candia, Aspergillus

Acute IE Subacute IE
1. Highly virulent organism Low virulent organism
2. Absence of underlying heart disease & Presence of underlying heart disease &
endothelial damage endothelial damage or prosthetic
3. Sudden onset Insidious onset
4. Severe febrile illness Persistent fever
Cardiac or renal failure rapidly Clinical stigmata (+)
Clinical stigmata of chronic IE (-)

CLINICAL FEATURES
 Age > 60yr ( in 50% )
 Sex – M > F
 Risk factors – underlying Ht disease ( but 32% has no pre-existing cardiac abnormalities )
 Ppt factors – any sepsis ( esp: tooth & throat infection )

Symptoms
Due to vegetation
 Changed or new murmur ( typically seagull murmr )
 Heart failure
 Conduction defect

Due to bacteremia
 Fever ( persistent ), rigors, malaise, night sweats, wt loss
 Anemia, Jaundice

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Due to immune complex deposition

 Subconjunctival hemorrhage, Roth’s spot ( fundoscopy )
 Petechial / purpura
 Splinter H’ge, Clubbing, Osler’s nodes, Janeway lesion
 Splenomegaly
 Hematuria ( microscopic )

Due to Septic embolization

 Brain infarct / abscess
 Splenic infarct / abscess
 Renal infarct / abscess
 Bone infarct / abscess

INVESTIGATIONS
For diagnosis
1. Blood culture
 6 specimens at different sites before antibiotics
 Both aerobic & anaerobic culture

2. Echo – to detect vegetation / valve damage & abscess / underlying heart disease
 TTE – detect vegetation > 2mm
 TOE – detect vegetation ≥1mm

3. Blood for CP / ESR / CRP

For complications
 CXR – features of heart failure
 ECG – conduction defect
 Urine RE – microscopic hematuria

DIAGNOSIS ( Duke’s Criteria )

Major Criteria 1. Positive blood culture
 Typical organism from 2 cultures
 Persistently (+)ve blood cultures taken >12hr apart
 3 or more (+)ve cultures taken over > 1hr
2. Endocardium involvement
 Positive Echo findings of vegetations
 New valvular regurigitation
Minor Criteria 1. Predisposing valvular or cardiac abnormality
2. IVDU
3. Pyrexia ≥ 38C
4. Embolic phenomenon
5. Vasculitic phenomenon
6. Suggestive blood cultures : organisms grown but not achieving major
criteria
7. Suggestive echo findings

 Definite IE  2 major OR ( 1 major + 3minor ) OR 5 minors

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 Possible IE  ( 1 major + 1 minor ) OR 3 minor

MANAGEMENT
General Mx
 Bed rest
 Nursing care
 Monitoring

Specific Mx
Tx of IE ( Antibiotic therapy )
 Choice of Antibiotics
Before C&S result
 For subacute  IV Benzyl penicillin + Gentamycin
 For acute  IV Flucloxacillin + Gentamycin
 In pen allergy / MRSA / prosthetic valve  IV Vancomycin + IV Gentamycin + oral
oral Rifampicin
After C&S result
 Change according to C&S result Role of Surgery in IE
 Route – parenteral ( IV )
1. Heart failure due to valve
 Duration – 4-6 wks
damage
2. Failure antibiotic therapy
Tx of Complications
( persistent or uncontrolled
 Treatment of heart failure
infection )
 Treatment of conduction defects etc …..
3. Large vegetations on left-sided
valves with evidence or high risk
Tx of underlying cause
of systemic embolic
 Treatment of underlying heart disease etc …
4. Abscess formation

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PERICARDIAL DISEASE
ACUTE PERICARDITIS
DEFINITION
 Inflammation of the pericardium which may be primary or secondary to systemic disease

CAUSES
Common
 Acute myocardial infarction
 Viral ( eg: Coxsackie B, but often not identified )

Less common
 Uremia
 Trauma ( eg: blunt chest injury )
 Malignant disease
 Connective tissue disease ( eg: SLE )

Rare
 Bacterial infection
 Rheumatic fever
 TB

CLINICAL FEATURES
Symptoms
1. Chest pain
 Retrosternal chest pain
 Sharp pain
 Radiate to shoulders & back
 Aggravated by deep breathing, movement & change of position, exercise &
swallowing
2. Low grade fever ( common )

Signs
 Auscultation – pericardial friction rub (high-pitched superficial scratching or crunching noise)

INVESTIGATIONS
For diagnosis
 ECG – ST elevation with concavity upward ( which may be widespread )
 CXR – cardiomegaly ( large globular heart ) indicates pericardial effusion
 Echo – if pericardial effusion is suspected

For underlying cause

 Blood for CP, ESR, U&E, cardiac enzymes, viral serology, etc ….

TREATMENT
For pericarditis
 NSAIDs for pain relief

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 Corticosteroid may suppress symptoms but there is no evidence that they can accelerate
cure

For underlying cause

 Viral pericarditis  recover within a few days or weeks
 Purulent pericarditis  Rx with Antibiotics or pericardiocentesis & surgical drainage ( if
necessary )

CONSTRICTIVE PERICARDITIS
DEFINITION
 The heart is encased in a rigid pericardium

CAUSES
 TB pericarditis ( common )
 Hemopericardium, Viral pericarditis, Rheumatoid arthritis & purulent pericarditis

CLINICAL FEATURES
Symptoms
 Fatigue dyspnea

Signs
 Pulse – low-vol: pulse, pulsus paradoxus ( in some cases )
 JVP – increased with prominent x & y descent, Kussmaul’s sign ( paradoxical  JVP during
inspiration )
 Palpation – soft, diffuse apex beat
 Auscultation – quiet heart sounds, loud & early S3 or diastolic pericardial knock
 Hepatomegaly , ascites, peripheral odema

INVESTIGATIONS
1. CXR – small heart ± pericardial calcification
2. Echo – often help to establish Dx
3. CT & MRI

MANAGEMENT
 Surgical resection of diseased pericardium ( carries a high morbidity )

CARDIAC TEMPONADE
DEFINTION
 Accumulation of pericardial fluid raises intra-pericardial pressure  poor ventricular filling &
fall in cardiac output

CAUSES
 Any pericarditis ( above )
 Aortic dissection, hemodialysis, Wafarin , Trans-septal puncture at cardiac catheterization ,
post-cardiac biopsy

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CLINICAL FEAUTRES
Symptoms
 Symptoms of acute heart failure Beck’s Triad

1. Falling BP
Signs 2. Rising JVP
 Pulse – rapid, low-vol: pulse, Pulsus paradoxus 3. Small & quiet heart
 BP – hypotension
 JVP – raised, Kussmaul’s sign
 Auscultation – muffled S1 & S2

INVESTIGATIONS
 CXR – large globular heart ( if > 250cc )
 ECG – low voltage QRS ± electrical alternans
 Echo – diagnostic

MANAGEMENT
 Seek expert help
 Pericardiocentesis – needs urgent drainage
 A wide bore needle is inserted under LA to the left of the xiphisternum, between the
angle of the xiphisternum & rib cage
 The needle is advanced towards the tip of the scapula into pericardial space
 Sent fluid for culture, ZN stain & other Invx