CVS Revision 1 01 1

CVS REVISION 1 ----- Active space -----

Aortic Valve Disorder 00:02:49

• Lesser the no. of leaflets → chances of stenosis (Unicuspid > Bicuspid).

• More the no. of leaflets → chances of regurgitation (Quadricuspid).

Aortic Stenosis (AS) : 00:04:43

Etiology :
Degeneration / Calcification on Progresses
Aortic Sclerosis Aortic stenosis
top of Tricuspid / Bicuspid valve

Bicuspid aortic valve (M>F) Tricuspid aortic valve (M>F)

Young patient. Elderly patient > 60 yrs.
• Associated with NOTCH 1 defect (endothelial NO -
synthase defect).
• High chance of aortopathy.

Aortic Sclerosis :
• Major cause of Aortic stenosis.
• Gradient < 20 mmHg.
• Associated with Atherosclerosis.
Note :
• Rheumatic etiology is very rare in Aortic stenosis.
• Acute Rheumatic fever : May develop valvulitis. (MR (M/c) > MR+AR).
15 - 20 yrs later
Rheumatic heart disease : (MS + MR (M/c) > MS + AR > AR + AS).

Hemodynamics :
Normally Aortic valve opening produces no sounds
Sometimes Bicuspid aortic valve can produce ejection clicks.
Ventricular systole in aortic stenosis :
Degeneration and Calcification → Incomplete aortic valve opening → Creates a
gradient between LV and Aorta (Gradient > 40 mmHg).
Gradient ∝ Severity of the disease.

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----- Active space -----

40/4/1 rule : Seen in severe aortic stenosis.
• Mean Transvalvular pressure gradient > 40 mm Hg.
• Peak flow velocity across the valve > 4 m/s.
• Aortic valve surface area < 1 cm2.

Compensation :
• Concentric LV Hypertrophy at the expense of cavity size To maintain
• Left Ventricular mass Cardiac output

Symptoms :
• Mild / Moderate AS → Usually asymptomatic.
• Severe AS → Symptomatic.
• Very severe AS → LV Failure.

ASD 5/3/2 rule : Chances of survival if surgery not done,

• Within 5 years from the onset of Angina (1st symptom) → Unlikely to survive.
• Within 3 years from onset of syncope → Unlikely to survive.
• Within 2 years from onset of dyspnea → Unlikely to survive.

Note : Aortic stenosis → Pressure overload condition (Palpitation not

seen as it is seen in volume overload conditions).

Associated conditions :
1. Atrial Fibrillation (AF) : Fatal in patients with Aortic stenosis (Cardiac output is
severely compromised).
2. Systemic Hypertension : Can mask Aortic stenosis.
Uncontrolled Hypertension → Aortic pressure → Falsely low pressure
gradient. Hence, Strict control of blood pressure is needed.

Investigations :
• Trans Thoracic Echocardiogram (IOC) : 40/4/1 rule.
• Angiogram : Detect atherosclerotic changes in Coronaries.
• CT Aortogram in bicuspid valve patients : To r/o Aortopathy.
• Dobutamine Stress ECHO : Differentiate b/w Mild AS and Very severe AS.

Note : In very severe AS, LV fails → Low Flow Low gradient AS.

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Clinical findings : ----- Active space -----

Components Findings
Pulse • Slow rising pulse.
• Severe AS → Pulsus tardus.
• Very severe AS → Pulsus parvus et tardus.
BP • Associated with Left ventricular hypertrophy.
• High BP → Mask aortic stenosis.
JVP • Normal.
• May be elevated in very terminal stages only.
Apex Heaving apex : High amplitude sustained apex.
Heart sound • S1 : Normal.
• S2 : a. Loud S2 : Bicuspid.
b. Soft S2 : Elderly.
c. Reverse/Paradoxical split, P2-A2: Severe AS
• S3 : (+) → Very severe AS (LV Systolic failure).
• S4 : (+) → Seen only in Aortic Stenosis.
Murmurs Mixed frequency murmurs : Harsh Ejection systolic
murmur + Late systolic accentuation → Best heard in
Aortic area and sitting position.
a. Low frequency : Radiated to the carotid.
b. High frequency (soft blowing musical) →
Radiated to the apex (Gallavardin phenomenon).

Note : Production of heart sounds.

• S3 : Normal/less than normal filling of non compliant dilated ventricle OR
of hypercompliant ventricle (Physiological S3).
• S4 : Healthy atria across a non stenosed valve contract vigorously in sinus
rhythm into a hypertrophic non-compliant non-dilated ventricle.

Treatment :
Symptomatic
Aortic Valve
Severe AS Gradient > 50mmHg Replacement (AVR).

Asymptomatic
Observation &
Gradient < 50mmHg
follow-up.
• If bioprosthetic valve is used → No anticoagulation needed .
• Recent update : TAVI → Trans catheter aortic Valve Implantation.

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Aortic Regurgitation (AR) : 00:34:34

Acute aortic regurgitation :

Seen in :
• Aortic Dissection.
• Infective Endocarditis.
• Rupture of sinus of Valsalva.
Presentation :
• Acute Pulmonary edema ± Cardiogenic Shock.
• Acute AR + Chest pain → Suspect Aortic Dissection.
• Acute AR + Right heart failure → Suspect Rupture of Sinus of Valsalva.
Management :
• NTG/ Nitroprusside : Dilate the aorta.
• Aortic Valve replacement : Definitive Management.

Chronic aortic Regurgitation :

Etiology :

Valve Leaflet issues Root issues

• Rheumatic cause. • Syphilis.
• Quadricuspid valve. • Marfan syndrome.
• Takayasu arteritis. • Ehlers Danlos syndrome.
• Ankylosing spondylitis. • Takayasu arteritis.
• IgG4 related disease ( Large vessel
vasculitis).
• Behcet’s disease Variable vessel
• Cogan’s disease vasculitis
Note :
• Takayasu arteritis → Involve both root and the leaflets.
• Cogan’s disease → Interstitial keratitis + Aortitis + Sensorineural hearing
loss.
Hemodynamics :
1. Diastolic pressure gradient :
• Normal ventricular diastole :
Aorta diastolic pressure = 80 mm Hg
High gradient present.
LV diastolic pressure = 10 mm Hg
Competent aortic valve → No back leak despite High pressure gradient.
• Ventricular diastole in AR :
Aortic valve incompetence → Blood flow from Aorta to LV.
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2. Vasodilatation : Pressure in aorta → Pressure gradient → Less Leak. ----- Active space -----
• Exercise → Lead to Vasodilation → Make patient better.
• NTG/ Nitroprusside → Used in Rx of Acute Aortic Regurgitation.
3. Systemic HTN : Pressure in aorta → Pressure gradient → More leak.
4. Nocturnal angina. : Bradycardia at night → filling → Diastole prolonged →
More blood leak (Blood stolen from the Coronaries).
Compensation :
• Eccentric Hypertrophy with dilatation.
• Ejection fraction (EF) : Normal to .
• LV End Diastolic Pressure (LVEDP) : Normal.
• End Systolic Volume (ESV) : Normal.
Presentation :
• Mild/ Moderate AR → Occasional palpitation.
• Severe AR → Dyspnea, S3.
Clinical Findings :
Components Findings
Pulse • Collapsing pulse (High volume pulse).
• Pulsus Bisferiens.
BP Wide Pulse pressure (Hills sign).

JVP • Normal.
• May be elevated in very terminal stages only.
Apex Hyperdynamic (Down and out).

Heart sound • Soft S1 : Premature closure.

• S2 : a. Loud S2 : Root causes.
b. Soft S2 : Leaflet causes.
c. Delayed A2. Sometimes P2-A2 also seen.
• S3 : (+) → LV Systolic failure.
• S4 : Absent.
Murmurs End Diastolic murmur : High pitched, soft blowing murmur.
• Decrescendo murmur : Gradient → Murmur .
• Austin Flint murmur → Displacement of anterior mitral leaflet (Asso-
ciated low pitched murmur).
• Cole cecil murmur → Murmur radiating to the axilla.

Treatment :
• Symptomatic Severe AR : Aortic Valve Replacement.
• Asymptomatic Severe AR : 55/50 Rule.
Ejection fraction < 55 %
LV End Systolic Diameter > 50 mm Aortic Valve replacement

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Mitral Valve Disorder 00:52:19

Mitral Stenosis (MS) :

Etiology :
Rheumatic Heart disease → Commissural fusion (Fish mouth abnormality).
Rx : Percutaneous balloon mitral valvotomy/ commissurotomy.
Acute rheumatic fever 15 - 20 yrs Rheumatic heart disease
(with valvulitis) (MS+MR > MS+AR)

Hemodynamics :
During diastole → Incomplete valve opening → LAP.
• Mild / moderate case (No Symptoms) : LAP not transmitted to the
pulmonary vein.
• Severe cases : PCWP → Pulmonary hypertension → Hypertensive Tri-
cuspid Regurgitation (TR).

Classification of Mitral Stenosis : On basis of Valve Surface area.

• Severe MS ( <1.5 cm2) : Asymptomatic or symptomatic.
• Very severe MS (<1 cm2).
• Progressive MS (>1.5 cm2).

Symptoms :
• Mild MS : Asymptomatic.
• Moderate MS : Dyspnea on exertion (1st symptom).
• Severe MS : Dyspnea at rest + Pulmonary Hypertension (RVH + TR).
• Very severe MS : Left Ventricular Failure.
Other symptoms :
• Hemoptysis.
• Ortner’s Syndrome : compression of the Recurrent Laryngeal nerve.
• Hoarseness of voice.
• Dysphagia.

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Clinical Findings : ----- Active space -----

Components Findings
Pulse Normal.
BP Normal.
JVP Elevated→ Due to RVH.
Apex Tapping apex : Loud S1.
Heart sound • S1 : Loud S1→ Depends on
a. Velocity of closure.
b. Position of leaflets at the end of diastole.
c. Timing (Delayed closure→ Loud sound).
• S2 : Loud palpable P2.
Note : A2-P2 widening→ seen in P. HTN + RV failure.
• Opening snap : seen in Organic MS ( LAP).
Note : Higher LAP → Opening snap occurs earlier.
• S3, S4 : Not heard.
Murmurs Low pitched Mid Diastolic murmur + Pre systolic accentuation.
Note : Presystolic accentuation → Lost in AF.
.
Severity of the Mitral stenosis depends on :
• Long duration of the murmur.
• Short S2-OS gap.

Treatment :
• Control tachycardia→ Beta blockers/ Verapamil/ Diltiazem.
• Anticoagulation→ Oral Vitamin K Antagonist (Risk of Embolization / LA clots).
• Percutaneous Mitral Balloon Valvulotomy/commissurotomy → If it fails,
Mitral Valve Replacement.
• Calcific MS or Associated moderate to severe MR + LA Clot → Mitral valve
Replacement.
Note : Mandatory to do Transesophageal ECHO → To detect LA Clot.

Mitral Regurgitation (MR) : 01:10:35

Acute Mitral Regurgitation :

• Papillary muscle dysfunction /Papillary muscle rupture .
• Inferior Wall MI→ RCA involvement → Posteromedial Papillary muscle
rupture.
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----- Active space -----

Chronic Mitral Regurgitation :
Primary MR Secondary MR
Problem with leaflets. Due to Annular Dilatation
Causes :
• Rheumatic heart disease LV Dysfunction
(MS + MR) : M/c in
Annular Dilatation
developing countries.
MR Begets MR
• Mitral valve prolapse : m.c in 2 Mitral Regurgitation
�
developed countries.
• SLE/ RA LV Remodeling

Hemodynamics :
• Issue in LV Systole.
• When Afterload → Blood Moves from Left ventricle to left atria.

Factors improving and worsening MR :

• Nitrates/ NTG/ Nitroprusside : pressure on the aortic site (Some amount
of blood flow into the aorta).
• S. Hypertension in MR : pressure on the aortic site → More resistance
(Blood moves to the Left atria).

Compensation :
Eccentric Hypertrophy with dilatation of the Left Ventricle.

Mild to Moderate MR Severe/Decompensated MR

Presentation Asymptomatic + On and off LV failure (+) →
palpitation. Predominantly dyspnea.
LV End Diastolic Pressure Normal.
LV End Systolic Volume Normal.
Ejection fraction Normal or Normal to

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Clinical Findings : ----- Active space -----

Components Findings
Pulse • Pseudo collapsing pulse.
• LV failure : Pulsus alternans/ pulsus dicroticus.

BP Normal.
JVP Normal.
Apex Hyperdynamic apex : Displaced down and out.
Heart sound • S1 : Soft S1
a. Poor coaptation of the valve leaflets.
b. dp/dt of isovolumetric contraction not good.
• S2 : Early A2 and Normal P2→ Wide Split S2.
• S3 : Heard even without failure.
• S4 : Not heard.
Murmurs Pan Systolic murmur : High pitched , seen in apex, Soft blowing murmur,
Radiates to the axilla.

Note :
• Myxomatous Degeneration : MVP ± MR.
• MVP : can produce Click + Murmur on Hyperdynamic auscultation.
• LV Size → Chordae stretch → Prolapse (Click will move closer to S1 → Long
duration murmurs).
• Valsalva and Standing :
a. HCM → Intensity of murmur
b. MVP → Duration of murmur

Treatment :
Surgical repair is tried first → If it fails → Replacement.
Indications of surgical repair :
• Symptomatic cases.
• Asymptomatic patient : 60/40 rule.
a. Ejection fraction : ≤ 60%.
b. LV End systolic Diameter : ≥ 40 mm.

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----- Active space ----- CVS REVISION-2

Physiology of Pulse 00:00:11

Wave Coincides with

Percussion wave S1
P wave Peak
Tidal wave Aortic recoil
Dicrotic notch S2
Dicrotic wave Peripheral
(Reflected wave) resistance (PR)

Applied aspect :
Central/Augmented Systolic BP is Best indicator of Target Organ Damage (TOD).
NOTE :
• Pulse apex deficit : Atrial Fibrillation (A-fib).
• Radio femoral delay : Coarctation of aorta.

Abnormalities in Pulse 00:04:30

Rate abnormalities :
Relative Bradycardia : For every 1˚F → in HR by 1o bpm. If in HR is < than
this, then it’s said to be relative bradycardia.
Causes : Infectious : Typhoid, Q-fever, Legionnaires’, Brucellosis.
Non infectious : Lymphoma, Drug fever.
Note : Leptospirosis, Dengue & malaria are very rare causes.

Rhythm abnormalities :
Irregularly irregular : A-fib.
Regularly Irregular : VPC (Ventricular Premature Complex).

Volume abnormalities :
High volume ( Stroke volume) Low volume ( Stroke volume)
Collapsing pulse AR Hypokinetic pulse LV dysunction
Pseudo-collapsing pulse MR Pulsus tardus Severe AS
- Pulsus parvus et tardus Very severe AS

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Contour abnormalities : ----- Active space -----

1. Pulsus bisferiens 2. Pulsus dicroticus

Systolic peak + Prominent dicrotic peak.
Seen in LV systolic failure.

HCM d/t SAM. Severe AR ± Mild AS

3. Pulsus alternans 4. Pulsus bigemini
Regular alternate high & low volume Irregular alternate high & low volume
pulse. pulse.
Seen in LV systolic failure. Seen in VPC.
HCM : Hypertrophic Cardiomyopathy; SAM : Systolic Ant. Motion of mitral valve; VPC : Ventricular Premature Complex

Note : Brockenbrough sign : In HCM → Pulse volume after post VPC pause d/t SAM.
Variations in pulse with respiration :
Reverse Pulsus
Pulsus Normalis Aggregans/ Pulsus paradoxus
paradoxus
SBP falls by > 10 mmHg with inspiration. SBP with inspiration
Seen in : Seen in :
• Cardiac Tamponade (M/c) • IPPV.
• I/3rd cases of CCP. • HCM.
• Hyper inflated lung.
• SVC Obstruction.
• Pulmonary Embolism.
Note : very rare in Restrictive cardiomyopathy.
CCP : Chronic Constrictive Pericarditis; IPPV : Intermittent Positive pressure ventillation

Jugular venous pulse 00:13:53

Normal JVP waveform :

waveform Corresponds to
a wave RA contraction. Measures active filling of diastole (30% of filling).
x descent Atrial relaxation
Upward bulge of Tricuspid valve into atrium.
c wave
Coincides with S1.
v wave Atrial filling. Coincides with S2
Emptying of Atria.
y descent
Measures passive filling of diastole (70% of filling)

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----- Active space -----

JVP abnormalities :
Abnormality Conditions
Prominent a waves Pulm HTN, Rt. atrial thrombus/mass, TS, RVH.
Cannon a waves Complete AV block, AVNRT junctional rhythm, Vent. tachycardia.
Absent a waves Atrial fibrillation
Absent x descent Severe TR, RV failure.
Prominent/Rapid X
Cardiac tamponade (CT), Chr. constrictive pericarditis (CCP)
descent
Dominant v waves TR, ASD, Vena caval pressure.
Prolonged y descent Tricuspid stenosis (TS)
Prominent y descent CCP, isolated severe TR, RCM
Absent y descent Cardiac tamponade.
Note :
Kussmaul’s Sign :
• Inspiratory rise in JVP.
• Seen in : CCP, Restrictive cardiomyopathy, Right ventricular MI, TS.
• Not seen in cardiac tamponade.
Abd. Jugular reflex (>3cm or >15 s) : Marker of impending Right Heart Failure.

Heart sounds 00:34:36

Mixed murmur Low pitched murmurs Low pitched heart sounds

1. Aortic stenosis : 1. MS 1. S3
Carotids (low pitch) 2. TS 2. S4
Apex of heart (High pitch) 3. Austin flint murmur 3. Tumor plop
Rest all are high pitched sounds.
S1 & S2 :
S1 S2 (A2-P2)
• Occurs just prior to isovolumetric contraction (IVC). • A2 -P2 closure interval is called
• Due to coaptation of mitral & tricuspid valves Hangout Interval (HI).
• Normally A2 occurs prior to P2.
1. Soft S1 1. Loud A2 :
• MR. • Bicuspid aortic valve producing
• Good filling of heart. AS.
• AR. • Root pathologies in AR.
2. Loud S1 2. Soft A2 :
• MS. • Elderly AS.
• Valve pathologies in AR.
3. Loud P2 : Pulmonary HTN.
4. Soft P2 : Pulmonary stenosis.
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Split S2 : ----- Active space -----

Wide variable split Wide fixed split Paradoxical split

Early A2 or Split fails to move P2 first followed by A2.
delayed P2. with respiration. Commonly accompanied by loud P2.
Cause : Causes : Causes :
• MR. • RV failure. • AR.
• ASD. • AS.
S3 :
• S3 in AS/AR is always with heart failure.
• S3 in MR can be heard with or without heart failure.
• Never heard in MS.

S4 : Seen only in AS.

Added diastolic sounds :
Mnemonic : OP Time 3-4.
1. Early diastolic sound :
• Opening snap (High pitch) :
a. Snapping open of mitral valve.
b. S2-OS gap shortens with severity of MS/↑ left atrial pressure.
• Pericardial knock (High pitch).
• Tumor plop (Low pitch).
2. Middiastolic sounds : S3 (Low pitch).
3. Late diastolic sound : S4 (Low pitch).

Added systolic sounds :

1. Ejection clicks :
• Aortic ejection click : Seen in bicuspid aortic valve.
• Pulmonary ejection click.
Note : All right sided heart sounds ↑ with respiration → Carvallo’s sign, except
pulmonary ejection click.
2. Non ejection clicks :
• Seen in mitral valve prolapse.

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----- Active space ----- CVS REVISION 3

Heart Failure 00:00:27

Structural or functional impairment of the ventricle to pump out/fill itself with blood.
Classification :
• HF with reduced EF (HFrEF) (< 40%) : Guideline based management.
• HF with preserved EF (HFpEF) (> 50%) : Comorbidity based management.
• HF with mid range EF (HFmEF) (40-50%).
Staging of HF :
• A : Only risk factors present. Best prognosis.
• B : Risk factors + Structural abnormalities. M/c cause of mortality :
• C : Present or prior symptoms. Sudden cardiac death
• D : Advanced HF (Mortality cause is pump failure).
NYHA grading of symptoms : For angina, palpitation & dyspnea.
Class 1 Symptoms at exertion, no limitation.
Class 2 Mild symptoms at ordinary physical activity, slight limitation.
Class 3 Symptoms at less than ordinary physical activity, marked limitation.
Class 4 Symptoms at rest, severe limitation.

Symptoms :
LV systolic failure LV end diastolic pressure Increase in RVEDP
• Cachexia (TNFα). • ↑ LAP → ↑ PCWP → • Abdomino jugular reflex
• ↓ Urine output (Cardiorenal Dyspnea → Orthopnea → (AJR) → Impending RV
syndrome). PND → Acute pulmonary failure.
• Altered sensorium. edema. • JVP.
• Cold extremities. • O/E : Rales & S4. • Ascites.
• Narrow pulse pressure. • Hepatomegaly.
• O/E : S3 & cardiomegaly. • Edema.

Framingham criteria :
Major symptoms :
1. Dyspnea/orthopnea/PND. 5. JVP.
2. Acute pulmonary edema. 6. AJR.
3. Rales. 7. Cardiomegaly.
4. S3.
Note : No ascites, edema, hepatomegaly in major Framingham criteria.
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1. Dyspnea : ----- Active space -----

Types of dyspnea :
Bendopnea Trepopnea
• Seen in advanced HF (left & right HF). • Preferred to lie on right side.
• A/w ↑ JVP & PCWP. • Pleural effusion more on right side.
• Along with dyspnea, crepitations (Fine gravitational creps a/w cold
extremities) + S4 can be seen.
2. Angina : D/t ↑ LV mass or LVOT obstruction (not a mandatory symptom of HF).
3. Palpitations : D/t cardiomegaly.
4. Syncope : D/t LVOT obstruction.
Diagnosis :
ECG :
Other symptoms :
• Low voltage in limb leads.
• Sinus tachycardia → ↑ mortality. • High voltage in chest leads.
• JVP (RHF) : ≥ 3 cm elevated from sternal angle. • Poor R wave progression.
• AJR (Impending RHF). Echo : To evaluate ejection fraction.
• Edema, Ascites. Cardiac MRI : Gold standard for EF.
Decompensation :
Factors that precipitate acute HF in a patient with underlying HFrEF/HFpEF :
• Patient related (Non compliant/diet). • Arrhythmias (A. Fib).
• Infection related (Infective endocarditis). • MI.
• Anemia. • NSAIDs & beta blockers.
Mx of HFrEF :
1. Block SNS ( decrease HR & FOC) 2. Block RAAS
• β blockers. • ARNI (Angiotensin II receptor
• Metoprolol/carvedilol/bisoprolol. blocker + Neprilysin inhibitor).
• Bisoprolol (β1 selective) : 1.25 mg - 10 mg. eg. Valsartan + Sacubitril.
• Started at lowest dose. • ARNI > ACE inhibitors > ARBs.
• Patient should not have edema. 4. SGLT 2 antagonist
3. Mineralocorticoid receptor antagonist (MRA)
• Dapagliflozin/empagliflozin.
• Spironolactone/eplerenone/finrenone.
• Produce natriuresis & diuresis
• Side effects : Hyperkalemia,gynecomastia.
without tachycardia.
FOC : Force of contraction.
Mortality benefit : β blockers > ARNI > MRA > Hydralazine + nitrate.
Note : Hydralazine + nitrate is used in renal failure patients with heart failure.

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----- Active space -----

Other drugs :
Diuretics : For symptomatic relief.

Ivabradine :
• Used only if HR > 70 bpm & patient on maximum dosage of β blockers.
• MOA : Inhibits funny currents (Na+).
• S/E : Visual field abnormalities.
No role :
• ACE inhibitor + Neprilysin inhibitor : Omapatrilat.
• Digoxin.

Dysfunction of ventricles 00:29:29

Systolic dysfunction Diastolic dysfunction

Pumping defect Filling defect
Left sided issues Right sided issues (RV > LV)
Always followed by diastolic dysfunction Normal systole possible.

Diastolic dysfunction with normal systole.

Constrictive Restrictive (more severe)

Chronic constrictive pericarditis Restrictive cardiomyopathy

Diastolic dysfunction : ↑ RVEDP → ↑ RAP → Transmitted to SVC, IVC → Right

sided HF (Ascites precox, edema, JVP & hepatomegaly). It has a chronic course.

Acute pericarditis (D/d for MI)

• Clinical features : Elevated ST + chest pain.
• ECG : Global ST elevation (Concave) except lead V1, no reciprocal changes,
PR depression.
• Cause : Post viral (Coxsackie virus), uremia.
Multiple relapses → Rigid, calcific, thickened pericardium with adhesions (Rock
like pericardium) → Chronic constrictive pericarditis.

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Chronic Constrictive Pericarditis (CCP) Restrictive cardiomyopathy ----- Active space -----

Causes : Causes :
• Multiple relapses of acute pericar- • Intercellular accumulation :
ditis. Amyloidosis (Most important cause).
• Post viral > TB. • Intracellular accumulation : Iron
Features : Chronic RHF symptoms. (Hemochromatosis), glycosphingolipids
• Cachexic + malnourished (TB) with (Fabry’s disease) and glycogen
ascites, edema, hepatomegaly. (Pompe’s disease).
• Transmyocardial filling pressure • No accumulation : DM, scleroderma.
= Intracavitary pressure - Intra Features :
pericardial pressure. It is reduced • Stiff hypertrophic, non compliant, non
in CCP. dilated ventricle.
Diastolic dysfunction → Slow, chronic RHF symptoms.
Normal systole. Normal chamber size.
ECG : Low voltage complexes.
Kussmaul sign (↑ in JVP on inspiration) : Fall in intrathoracic pressure is not
transmitted to heart chambers d/t pericardial issue (normally JVP falls with
inspiration).
JVP : JVP :
• Sharp prominent rapid x descent. • Holodiastolic restriction → No y
• Sharp prominent rapid y descent : descent, no square root sign.
Frederichs sign. • Atrial relaxation not adequate → x
Ventricular pressures during diastole descent not prominent.
: Fall → rise → abrupt halt : Square
root sign.
Elevation & equalisation of diastolic Elevation & equalisation of diastolic
pressures after 1/3 of diastole.
rd
pressures not seen.
Pulsus paradoxus seen in 1/3 of rd
Pulsus paradoxus absent.
patients.
Pericardial knock can be heard. S3 can be heard.
Broadbent sign : Indrawing of 11th & No pericardial knock.
12th ribs (systolic retraction of apex).
Ix : MRI (IOC). Ix : Echo.
Rx : Pericardiectomy. Rx : Medical management
(Manage cardiomyopathy/HF).

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----- Active space -----

Cardiac tamponade 00:57:25

Cause : Acute post traumatic event.

Features :
• Acute rise in intrapericardial pressure.
• Presentation : Obstructive shock (Hypotension + shock + disproportionate
dyspnea + tachycardia).
• Beck’s Triad : Hypotension + muffled heart sounds + ↑JVP.
• JVP : Holodiastolic restriction → Absent y descent, no square root sign, no
pericardial knock.
Systolic phase of venous return (Coupled constraint) : X descent is
prominent.
• Holodiastolic elevation & equalisation of diastolic pressures present.
• Transmission of pressure to cardiac chambers can be seen → ↓JVP on
inspiration → No Kussmaul sign.
• Small chambers (as compressed from all sides).
• Pulsus paradoxus (Fall of SBP > 10 mm Hg on inspiration).
ECG : Low voltage complexes (Electrical alternans).
Rx : Emergency pericardiocentesis.

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CVS REVISION 4 ----- Active space -----

Cardiomyopathy :
Myocardial disease in which heart is structurally & functionally abnormal in the
absence of valvular heart disease, congenital heart disease, CAD & HTN.

Classification of cardiomyopathy :
1. Dilated cardiomyopathy (DCM).
2. Hypertrophic cardiomyopathy (HCM).
3. Restrictive cardiomyopathy (RCM).
4. Unclassified.

Dilated cardiomyopathy 00:00:12

Autosomal dominant.
Thin walled dilated LV → Has poor contractility.
Symptoms :
1. Systolic heart failure symptoms :
• Cachectic.
• Cold extremeties.
• Altered sensorium.
• Renal failure symptoms.
• Narrow pulse pressure.
• S3 +ve.
2. Diastolic failure symptoms : Dyspnea.
3. Right sided failure symptoms : JVP, ascites, edema, hepatomegaly.

Causes :
1. 30% genetic : Truncated variant (Tv) Titin mutation (M/c) > myh7 mutation.
2. Peripartum cardiomyopathy :
• Best prognosis.
• D/t anti-angiogenic factors : SFLT 1.
• Risk factors :
a. ↑ Age at pregnancy.
b. HTN with pregnancy.
c. Multiple pregnancy.

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3. Alcohol induced cardiomyopathy :
• Good prognosis (Reversible).
• Patients with ACE polymorphism are at ↑ed risk.
• Precipitated by : Selenium deficiency (Keshan’s disease), thiamine
deficiency & magnesium deficiency.
4. Drug induced cardiomyopathy :
• Worst prognosis.
• Attributed to high dose Anthracycline.
5. Autoimmune : Sarcoidosis & hemochromatosis (DCM > RCM).
6. Endocrine : Pheochromocytoma, thyrotoxicosis & acromegaly.
7. Myocarditis :
• Acute post inflammatory DCM which can occur along with the infection/post
infection period.
• Good prognosis.
• M/c cause : HHV 6 > Chagas disease.

Investigations :
1. ECG findings : Triad
a. Low voltage in limb leads.
b. High voltage in chest leads.
c. Poor ‘R’ wave progression.
2. Echo : Global LV hypokinesia.
3. MRI :
• Gold standard for ejection fraction.
• To look for ischemia vs infract.
4. Angiography.

Restrictive cardiomyopathy 00:14:30

Seen in amyloidosis of heart.

Bad prognosis.

Types of amyloidosis :
1. Primary amyloidosis
2. Secondary amyloidosis : No cardiac involvement.
3. Transthyretin induced
a. Senile systemic amyloidosis (Wild type) → Seen in elderly with carpal
tunnel syndrome.
b. Familial amyloid polyneuropathy (Mutant type) → Severe ANS
symptoms + cardiac symptoms seen.
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Features : ----- Active space -----

• Biatrial enlargement.
• Biventricular hypertrophy.
• Interatrial septal thickening.
• Low voltage complexes.

Investigations :
• IOC : Cardiac MRI (Glittering of myocardium).
• ECG : Pseudo infarct pattern (Infarct pattern on ECG with normal echo).

Unclassified cardiomyopathy 00:17:02

Takotsubo cardiomyopathy :
Aka stress induced cardiomyopathy/neurogenic myocardial stunning/transient
apical ballooning.
M/c : Middle aged females.
Cause : Sympathetic overactivity.
Presents with : ACS like presentation.

Investigations :
• ECG : ST elevation.
• Trop I elevated (Not as much as in ACS).
• NT Pro BNP is high.
• On angiography :
a. Normal coronary arteries.
b. Base is hypercontractile.
c. Bulging apex.
Prognosis :
• Short term complications same as MI.
• No long term complications.

Hypertrophic cardiomyopathy 00:20:12

M/c genetic cardiovascular disease.

Autosomal dominant.
Myosin heavy chain mutation > myosin binding protein C mutation.
Males = females (Females have poorer prognosis).

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Course of HCM :
• 95% -99% → Stable course.
• 1% - 5% → Develop complications like :
1. Progressive heart failure.
2. Arrhythmias (Atrial fibrillation).
3. Sudden cardiac death.
Note : Pompe’s disease mimics HCM.

Features of hypertrophy :
• LV thickness ≥15 mm with no cause & no dilatation .
• Asymmetric hypertrophy : Only septum + anterior wall hypertrophies.
• Inappropriate hypertrophy : Absence of any factor causing ↑ in afterload.
• Concentric LVH → ↓ Cavity size → ↑ LVEDP.
Left ventricular outflow tract (LVOT) obstruction :
• First 1/3rd : Fixed obstruction.
• Second 1/3rd : No obstruction.
• In last 1/3rd : Dynamic obstruction.

Pathophysiology :
1. Diastolic dysfunction with normal systolic function :
Concentric LVH → ↓Cavity size → ↑ LVEDP → ↑LAP → ↑PcWP → Dyspnea
(M/c symptom). A-fib
2. Systolic motion of anterior mitral leaflet (SAM) :
• Asymmetrical septal hypertrophy → LVOT obstruction → ↑ Velocity of
blood across the obstruction → Low pressure zones across the outflow
tract → Anterior mitral leaflet sucked into septum (Occurs in mid to late
systole).
• SAM will lead to 2˚ MR.
3. Angina (2nd m/c symptom) with normal coronaries : D/t microvascular
dysfunction.

Factors influencing obstruction :

• ↑ Preload →↓Gradient ↓ LVOT obstruction
• ↑ Afterload →↓Gradient
• ↑ Force of contraction →↑ Gradient → ↑ LVOT obstruction.

Clinical features :
• Most patients are asymptomatic.
• Atrial fibrillation.
• Angina, syncope, & dyspnea (Features of LVOT obstruction).
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Findings : ----- Active space -----

• Pulse : Pulses bisferiens ( In HCM p wave > t wave).
• JVP : Normal
• Apex : Double /triple apex (d/t SAM).
• S1 : Normal
• S2 : Normal/reverse split.
• S3 : May be heard.
• S4 : May be heard.
• Murmurs :
a. Lower left sternal border : Ejection systolic murmur (D/t SAM).
b. Apex : Pan systolic murmur (D/t 2˚ MR).
• Biopsy : Myofibre disarray.

Dynamic auscultation :
All the murmurs in cardiology ↓se with valsalva or standing except :
1. MVP : ↑Duration of murmur.
2. HCM : ↑ Intensity of murmur.

To differentiate b/w MVP & HCM

Post VPC pulse volume

Increased Decreased (Brocken brough sign)

MVP HCM

Rx :
• DOC : β blockers (Propranolol).
• 2nd DOC : Verapamil > diltiazem.
• If no adequate response : Add Disopyramide (Class 1a).
Side effects of disopyramide :
a. QT prolongation.
b. Anticholinergic side effects.
c. Reduce ejection fraction by 5% - 10%.
• If medical Mx fails → Surgery : Septal myomectomy.
• If family h/o sudden cardiac death or spontaneous sustained VT → Im-
plantable cardioverter-defibrillator (ICD).

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Myocardial Infarction (MI) 00:00:20

Coronary circulation :

Dominance of coronary circulation :

Based on origin of posterior descending
artery (which supplies Inferior wall) :
• Right dominant (80%) : If arises
from right coronary artery (RCA).
• Left dominant (20%) : If arises
from left circumflex artery (LCX).

Origin of Acute marginal artery (AMA)

demarcates RCA into Proximal & Distal
segments.
Acute marginal art. supplies RV free
wall. Occlusion of AMA → RVMI.

Inferior wall MI (IWMI), Right ventricular MI (RVMI), Posterior wall MI (PWMI) :

Inferior Wall MI Can occur d/t Occlusion of Proximal RCA, Distal RCA or LCx.
Involvement of Post. Descending artery : IWMI ± PWMI.

In a right dominant person :

• Proximal RCA occlusion : RvMI + IWMI ± PWMI.
• Distal RCA occlusion : IWMI ± PWMI.
Posterior wall can be supplied by obtuse marginal artery (branch of LCx), hence
can be spared in RCA occlusion.

In a left dominant person :

• LCX occlusion : Definitely IWMI + PWMI.
• Proximal RCA occlusion : Only RvMI.
• Distal RCA occlusion : No MI.

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IWMI & RVMI Features : ----- Active space -----

• SA nodal branch → Bradycardia.
• Clear lungs, ↑ JVP, hypotension in RVMI.
• Posteromedial papillary muscle rupture → 20 MR.
• ST elevation : II, III, aVF (Inferior wall).

Identifying site of occlusion in IWMI :

ST ↑ ST ↓
RCA Lead III > II aVL > aVR
LCX Lead II > III aVR > aVL

RVMI : V1 shows ST ↑ (or) flat/depressed ST which is discordant with V2, V3, V4.
Findings :
1. ST elevation in leads II, III, aVF. IWMI
2. Reciprocal changes in V2,V3,V4.
3. ST ↑ in III > II
RVMI with
& ST ↓ in aVL > aVR proximal RCA
4. ST in V1 discordant to V2, V3.
Diagnosis : IWMI + RVMI with proximal RCA occlusion.

Anterior wall MI (AWMI) : 00:09:30

Left coronary artery (LCA) branches into : Left anterior descending (LAD) & LCX.

Blood supply Area Corresponding leads

LAD (D1) or LCX High lateral wall I, aVL
LAD (S1) Septum V1 >> V2
LAD (D2) Anterior wall V2, V3, V4
LAD (D3) or LCX Lateral wall V5, V6

Findings :
1. ST elevation in V2, V3, V4.
2. Reciprocal changes in leads II, III, aVF.
3. ST ↑ in V1 → Above S1.
4. ST ↑ in I & aVL → Above D1.
Diagnosis : Extensive antero high lateral MI.

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Acute coronary syndrome Mx algorithm :
Golden hour : 6 hours.
First medical contact
Diagnosis (preferably <10 mins)

24 hour PCI capable center Centre not capable for PCI

PCI within 60 mins

Shift for PCI, if PCI Can’t shift within 120 mins
possible in < 120 mins
Thrombolysis (Tenecteplase
0.5 mg/kg as bolus)

Shift to PCI capable center

Repeat ECG within 60-90 minutes

Resolution No resolution
Plan PCI within 2 to 24 hours Rescue PCI
Note : Pharmacoinvasive approach : PCI within 2 - 24 hours following successful
thrombolysis.
Medical management after initial stabilisation :
• Aspirin 300 mg.
• Clopidogrel 300 mg.
• For a patient planned with PCI : Ticagrelor/Prasugrel & Clopidogrel 600 mg.
• Statin 20-40 mg.
• Anticoagulation 30 mg s/c (Before PCI).
• ACE inhibitors & β blockers started within 24 hours.
• Life long aspirin & statin.
• 2nd antiplatelet for 1 year.

Arrhythmias 00:19:32

Narrow QRS tachycardia Slight wide QRS tachycardia Wide QRS tachycardia
QRS < 0.12 s QRS 0.12-0.16 s QRS > 0.16 s
Origin : Above bundle of His. Origin : Above bundle of His. Origin : Ventricles.
• Atria : Atrial tachycardia (focal/ But, conducted with a • Ventricular tachycardia.
multifocal). bundle branch block
• AV node : Junctional tachycardia.
• AVNRT, AVRT, AF, atrial flutter.
Note : Paroxysmal atrial tachycardia with AV block (d/t Digoxin).

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Narrow QRS tachycardia : ----- Active space -----

Regular RR interval Irregular RR interval

AVNRT : • Atrial fibrillation.
• No P waves. • Multifocal atrial tachycardia.
• P wave just outside QRS, with short RP & long
PR interval (only in 1/3rd patients).
AVRT :
• P wave just outside QRS, with short RP (> 80 to
100 ms) & long PR interval.
Focal atrial tachycardia :
• Long RP, short PR interval with morphologically
abnormal P waves.

M/c narrow QRS tachycardia : Sinus tachycardia.

Findings :
1. Narrow QRS tachycardia
(Rate > 150/min).
2. P wave just before QRS
complex → Long RP & short
PR.
Diagnosis : Atrial tachycardia.
Findings :
1. Narrow QRS tachycardia.
2. P wave just after T wave.
Diagnosis : Atrial tachycardia.

Management :
1. AVNRT :
• Adenosine.
• In COPD → Verapamil → no response → Metoprolol. Defibrillation done in :
• Pulseless VT.
• Synchronised DC cardioversion.
• Ventricular fibrillation.
2. Atrial tachycardia : Verapamil, β blockers. • Polymorphic VT.

Multifocal atrial tachycardia :

• 3 different morphologically abnormal P waves can be identified.
• Can be precipitated by Theophylline

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----- Active space ----- Atrial fibrillation (AF) : 00:35:27

Findings :
1. Irregular RR interval.
2. Fibrillatory waves.
3. No identifiable P waves.
Diagnosis : AF.
Valvular AF : AF seen in MS (or)
prosthetic mitral valve.
Types :
1. Paroxysmal : Lasts for < 7 days. Reverts back spontaneously (or) with drugs.
2. Persistent : Lasts for > 7 days.
3. Permanent : LA dilatation > 4 cm. Rhythm can’t be reverted back to normal.
Complications : Thromboembolism.
Management :
Hemodynamically unstable : DC cardioversion (100 J → 100 J).
Hemodynamically stable
Transthoracic echo
Normal
Duration of AF
LA > 4 cm
Indicates : > 48 hours < 48 hours
Structural heart disease (or) unknown
Rhythm control :
Rate control : CCBs. Transesophageal echo (or) • Ibutilide.
cardiac CT to visualise clot • Amiodarone (Structural
If clot + heart disease)
3 weeks anticoagulation f/b
Rhythm control f/b 4 weeks
anticoagulation
Wide QRS tachycardia :
Ventricular tachycardia :
• Sustained VT , rate > 100/min.
• ≥ 3 VPCs.
• Capture beat, fusion beat maybe present.
Management Monomorphic VT
.

Unstable Stable

Synchronised DC cardioversion • Procainamide.

(100 J → 100 J → 100 J → 60J) • Amiodarone in structural heart disease.
• Lignocaine : Post MI.

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Polymorphic VT + prolonged QT : Torsades de pointes. ----- Active space -----

Precipitating factors
• Class Ia, Ic, III anti arrhythmic
drugs.
• Terbinafine.
• Macrolides.
• Hypokalemia, hypocalcemia,
hypomagnesemia.
• Hypothermia.

Torsades de pointes
Mx (All patients unstable) :
Defibrillation (200 J) + 2g I/v MgSO4.

Hyperkalemia : 00:45:20

Causes :
• Renal failure (M/c).
• Hypoaldosteronism.
• Pseudo hypoaldosteronism : RTA type IV.
• Spironolactone.
ECG findings Serum K+
(mEq/L)
Tall T waves 6-7
ST segment ↓, 7-8
PR segment ↑
Wide QRS 8-9
P wave absent >9
Mx of hyperkalemia : Calcium gluconate.

Hypokalemia : 00:47:22

Findings :
1. Sagging of ST segment.
2. Prominent U waves.

Mx : I/v KCl.

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