Medicine Revision Notes (PDF)

Contents CVS Revision - 1  1 CVS Revision - 2  9 CVS Revision - 3  13 CVS Revision - 4  18 CVS Revision - 5 ...

Contents CVS Revision - 1  1 CVS Revision - 2  9 CVS Revision - 3  13 CVS Revision - 4  18 CVS Revision - 5  22 RS Revision - 1  28 m RS Revision - 2  38 o l.c ai RS Revision - 3  49 gm 2@ Rheumatology Revision - 1  57 t1 ar Rheumatology Revision - 2  66 sm sh Rheumatology Revision - 3  76 yu at Rheumatology Revision - 4  80 pr | Haematology Revision - 1  89 w ro ar Haematology Revision - 2  95 M © Haematology Revision - 3  102 Haematology Revision - 4  110 Endocrinology Revision - 1  118 Endocrinology Revision - 2  127 Endocrinology Revision - 3  134 Endocrinology Revision - 4  145 CNS Revision - 1  157 CNS Revision - 2  161 CNS Revision - 3  165 CNS Revision - 4  170 CNS Revision - 5  176 Nephrology Revision - 1  181 Nephrology Revision - 2  186 GIT Revision  191 Hepatology Revision  198 m o l.c ai gm 2@ t1 ar sm sh yu at pr | w ro ar M ©  CVS Revision - 1 1 CVS REVISION - 1 ----- Active space ----- Aortic Valve Disorders : ↓ ↑ risk of stenosis 3 leaflets/cusps if ↑ ↑ risk of regurgitation N Aortic valve 3 commissures 1 fibrous annulus Aortic Stenosis (AS)  00:04:37 Pathophysiology : Degeneration/calcification Aortic sclerosis Gradient + Aortic stenosis. of aortic valve + Young : Bicuspid valve (BAV). m Inflammation o Elderly : Degeneration & l.c ai (a/w atherosclerosis) calcification. gm 2@ Features : t1 BAV Young patients : Tricuspid valve : > 60 y/o. ar sm - NOTCH 1 defect. sh - Associated with aortopathies (Mandatory CT aortogram). yu at Note Rheumatic etiology : pr Uncommon for AS. | w 15 - 20 y ro Rheumatic fever + Valvulitis RHD (MS + MR > MS + AR > AR + AS. ) ar M (MR > MR + AR) © Hemodynamics : Aortic valve opens at the end of isovolumetric contraction. N gradient b/w LV & aorta is zero (LV = 120 mmHg, Aorta = 120 mmHg). AS : Valve does not open completely Gradient + ∝ Severity of disease. Note : Gradient = Mean transvalvular pressure gradient (MTPG). Severe AS : Given by 40/4/1 rule : MTPG > 40 mmHg (In sclerosis < 20 mmHg). Peak flow velocity > 4 m/s (Across valve). Surface area of valve < 1 cm2 (Normal : 3 - 4). Compensatory mechanism : To maintain cardiac output. Concentric LV hypertrophy ↑ LV mass + ↓ cavity size. Mild/Moderate AS : Severe AS : Very severe AS : Asymptomatic Symptomatic LV failure (Poor prognosis) Medicine Revision v4.0 Marrow 8.0 2024  2 Medicine ----- Active space ----- Clinical Features : Angina Syncope Dyspnea Poor prognosis if untreated after 5 yrs 3 yrs 2 yrs Angina : ↑ LV mass ↑ O2 demand. Tachycardia ↓ perfusion time. ↓ capillary density (w.r.t. wall thickness). Atherosclerosis. Syncope : D/t LV outflow obstruction F ixed cardiac output state even when ↑ demand. Dyspnea : D/t ↑ filling pressure (LVEDP). ↑ LVEDP ↑ LAP ↑ PCWP Fluid escapes into pulmonary interstitium. Exacerbating factors : A - Fib : m o Contribution of atria to cardiac output ↑ (25 40%). l.c ai Thus, A-fib is fatal in AS. gm Systemic HTN : 2@ t1 Masking of severe AS : ar sm ↑ SBP ↑ Aortic pressure ↓ Gradient (Falsely low). sh Thus, strict BP control needed. yu at Diagnosis : pr 1. Transthoracic Echo : To look for 40/4/1 rule. | w 2. Angiogram : Mandatory (To rule out atherosclerosis). ro ar 3. CT aortogram. M © 4. Dobutamine stress echo : To differentiate b/w LV failure d/t AS vs Mild AS with Pre - existing LV failure Low flow low gradient. Examination Findings : Pulse : Slow rising pulse Peak achieved late Severe AS : Pulsus tardus. Very severe AS : Pulsus parvus et tardus. Peak is not achieved BP : D/t LVH Masks AS. JVP : Only elevated in terminal patients (Not relevant). Apex : Laterally displaced Heaving apex (High amplitude sustained apex). Heart sounds : S1 : N (Ejection click Mistaken for loud S1). S2 (A2) Loud : BAV (Young). Soft : Elderly (Calcified valve). Reverse/paradoxical split (P2 A2) : Severe AS. Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 1 3 S3 : N /Less than N filling of a N /More than N filling of a ----- Active space ----- OR non - compliant dilated ventricle. hypercompliant ventricle. Pathological : Physiological. LV failure (Very severe AS). d/t + Non - stenosed mitral valve (No MS). S4 : Specific to AS healthy LA Hypertrophied, non-dilated LV contraction (no MR, AR). Murmur : - Harsh ejection systolic murmur with late systolic accentuation. - Best heard in aortic area & sitting position. - Mixed frequency Low freq : Loud Carotids. High freq : Soft blowing, musical Apex (Gallavardin phenomenon). m Management : o l.c ai 1. Aortic valve replacement (AVR) : gm a. Done in Severe AS. 2@ b. Bioprosthetic valves (No anticoagulation needed). t1 ar c. Asymptomatic severe AS : Follow-up Gradient > 50mmHg OR Symptoms AVR. sm sh Note : AS has a risk of sudden cardiac death. yu 2. Transcatheter Aortic Valve Implantation (TAVI) : If surgery is C/I. at pr Not open surgery; no ICU stay. | w ro Aortic Regurgitation (AR) ar 00:34:33 M © CHRONIC REGURGITATION Etiology : Root issue : vs Valve leaflet issue : Syphilis Rheumatic cause Marfan’s syndrome Quadricuspid valve Ehler Danlos syndrome Takayasu arteritis Takayasu arteritis Ankylosing spondylitis Behcet’s disease IgG4 related disease Specific Cogan’s syndrome Pathophysiology : Hemodynamics : N diastolic gradient between LV (10 mmHg) & aorta (80 mmHg) : 70 mmHg Favours regurgitation. No backleak d/t competent aortic valve. Medicine Revision v4.0 Marrow 8.0 2024  4 Medicine ----- Active space ----- Exacerbating factors : Nocturnal angina : Bradycardia at night More filling Prolonged diastole Angina ↓ Blood to coronary circulation ↑ Regurgitation Systemic HTN :↑ Aortic pressure ↑ Gradient ↑ Regurgitation. Relieving factor : Exercise/NTG/Nitroprusside. Vasodilatation ↓ Aortic pressure ↓ Gradient ↓ Regurgitation. Compensatory mechanism : Eccentric hypertrophy with dilatation. Clinical Features : Mild/moderate AR : Asymptomatic (Since ejection fraction is ↑↑). Occasional palpitation. m o LVEDP & ESV (End systolic volume) is N. l.c ai Severe AR : gm LV failure (Ejection fraction is N to low). 2@ t1 LVEDP ↑↑: Dyspnea. ar sm ESV ↑↑: S3 + ve. sh ↑ SBP & ↓↓↓ DBP (Almost zero) Wide pulse pressure Hill’s sign : yu at Lower limb BP pr exceeds upper limb | w BP by 20 mmHg. ro ar Examination Findings : M © Pulse : Rapid upstroke & downstroke. + 1. Collapsing pulse : High volume Ill - sustained peak. 2. Bisferiens pulse Two peaks in systole. (AR/AR + Mild AS/HCM) Note : Pseudocollapsing pulse N volume+ Rapid upstroke/downstroke (Seen in MR) + well sustained peak. BP : Wide pulse pressure. JVP : Changes only in terminal disease. Apex : Hyperdynamic apex, down & out. Heart Sounds : S1 : Soft S1 (Premature closure). For S1 : Delayed A2 Root issue : Loud S2. Premature : Soft closure. S2 : ↑ Blood in LV + Leaflet issue : Soft S2. Delayed : Loud closure. S3 : Heard in failure. Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 1 5 S4 : Not heard. ----- Active space ----- Murmur : EDM (End diastolic murmur). - High pitched, soft blowing. - Decrescendo. - Austin - Flint murmur : Low pitched d/t displacement of anterior mitral leaflet. Cole Cecil murmur : Radiates to axilla. Management : AVR : Done in symptomatic severe AR. Ejection fraction ≤ 55 %. Asymptomatic patient with 55/50 rule LV end systolic diameter > 50 mm. ACUTE REGURGITATION Presentations : mo Acute pulmonary edema (D/t sudden ↑ LVEDP ↑PCWP) ± Cardiogenic shock. l.c ai Causes : gm Infective endocarditis. 2@ t1 Aortic dissection : Acute AR + chest pain. ar sm Rupture of sinus of Valsalva : Acute AR + Right heart failure symptoms. sh - Immediate Mx : NTG/Nitroprusside. yu at - Definitive Mx : AVR. pr | Mitral Stenosis (MS) 00:52:28 w ro ar Mitral Valve : M 3D structure. © Surface area : 4 - 6 cm2. Parts : - Annulus. - Papillary muscles. - Leaflets with commissures. - Adjacent LV myocardium. - Chordae. Types of MS : 1. Progressive MS : > 1.5 cm2 Asymptomatic 2. Severe MS : < 1.5 cm2 Symptomatic 3. Very severe MS : < 1 cm2 Etiopathogenesis : Main etiology : Rheumatic origin. Main pathology : Commissural fusion Fish mouth abnormality. (15 - 20yrs) MS + MR (M/c). ARF RHD MS + AR. Medicine Revision v4.0 Marrow 8.0 2024  6 Medicine ----- Active space ----- Hemodynamics & compensation : Normal : Ventricular filling is passive > active & occurs across an open valve. In MS : - ↑ LAP at rest for ventricular filling. - On exertion ↓ diastole time ↑↑ LAP for ventricular filling. - Very severe MS : LV failure. Dyspnea Moderate MS ↑PCWP First symptom of : Severe MS AS : Angina Pulmonary hypertension ↑Pulmonary artery EDP AR : Palpitation Dyspnea at rest MS : Dyspnea RVH on exertion Hypertensive tricuspid regurgitation m Clinical Features : o l.c Pulmonary hypertension related Ortner’s syndrome : ai gm symptoms. D/t compression of RLN. 2@ Pulmonary edema (In tachycardia). Hoarseness of voice. t1 ar A - fib. Dysphagia : sm sh Hemoptysis : D/t pulmonary D/t compression of esophagus. yu capillary apoplexy. at pr Examination Findings : | w Pulse : Normal. JVP : Elevated (D/t RVH). ro ar BP : Normal. Apex : Tapping apex (Loud, ill-sustained S1). M © Heart Sounds : S1 : Loud S1 ↑ Velocity of valve closure. Downward position of leaflets (D/t inadequate LV filling). Delayed closure. S2 : S3, S4 : Not seen. - Loud, palpable P2 d/t Pulmonary HTN. Murmur : - A2 - P2 widening : Pulmonary HTN with - Low pitched, mid RV failure. diastolic (MDM). Opening snap (OS) : - Presystolic accentuation - Seen in organic MS. (Absent in A - fib). - D/t ↑ LAP. - Severity of MS Long duration of murmur. Short S2 - OS gap. Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 1 7 Management : ----- Active space ----- 1. Pulmonary edema Control heart rate β - blockers Verapamil/Diltiazem 2. Anticoagulation : Oral vitamin K antagonists 3. Surgery : Percutaneous mitral balloon valvotomy /commissurotomy Upon failure : Mitral valve replacement. (1st line for : Calcific MS +/ Mod/Severe MR/LA clot) Dx : Trans esophageal echo Mitral Regurgitation (MR) 01:10:38 Acute MR : D/t posteromedial papillary muscle rupture. Seen in inferior wall MI (RCA involvement). m Chronic MR : o l.c ai gm 1° MR : 2° MR (Innocent bystander mechanism) : 2@ RHD : MS + MR (m/c). MR LV dysfunction Annular dilatation. t1 MVP : Developed countries. begets ar LV remodelling 2° MR. sm SLE/Rheumatoid arthritis. MR sh Pathogenesis : yu at Hemodynamics : Reduction in afterload. pr Worsens with hypertension | LV - LA gradient >>> LV - Aorta gradient. w ( ↑ aortic pressure). ro (LA = 10mmHg; LV = 120mmHg; Aorta = 120mmHg). ar Relieved by Nitrates : M Regurgitation into LA. Vasodialation ( ↓ pressure). © LVEDP N / LV ESV N / Ejection fraction N. Compensation : Eccentric hypertrophy with dilatation of LV. Clinical Features : Mild/Moderate MR : Palpitation/Asymptomatic. Severe MR : LV failure Ejection fraction N / ↓ ↓ + LVEDP/LVESV ↑ ↑. Examinations Findings : Pulse : Pseudocollapsing pulse. Pulse in LV failure : BP : Normal. Pulsus alternans JVP: Normal. Pulsus dicroticus Apex : Hyperdynamic apex; displaced down & out. Heart sounds : S1 : Soft S1 d/t Poor coaptation of leaflet. ↓ ↓ dp/dt of isovolumetric contraction. S2 : Early A2 + Normal P2 Wide split S2. Medicine Revision v4.0 Marrow 8.0 2024  8 Medicine ----- Active space ----- S3 : Heard (Even without failure). S4 : Not heard. Murmurs : Pansystolic murmur. - High pitched. - Soft blowing. - Seen in the apex. - Radiates to axilla. Myxomatous Degeneration : MVP ± MR. MVP Click & murmurs : Non ejection click Dynamic auscultation (Valsalva & standing). m ↓↓LV cavity size ↓↓chordae stretch ↑↑Prolapse o l.c ai gm 2@ Click moves closer to S1 : Long duration murmur. t1 ar All murmurs ↓on dynamic auscultation except : sm sh - HCM : ↑ intensity. yu - MVP : ↑ duration. at pr Management : | w Symptomatic : Surgery (Repair fails Replacement). ro ar Asymptomatic with 60/40 rule : M - Ejection fraction ≤ 60%. © - LV End Systolic diameter ≥ 40mm. Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 2 9 CVS REVISION - 2 ----- Active space ----- Basics of Pulse  00:00:13 Features : Pressure wave. Velocity : 5 m/s. Origin : Aorta. Assesses LV contractile performance. Pulse Wave : 1. Normal wave : P P : Pressure wave T T : Tidal wave (Aortic recoil) m DN DN : Dicrotic notch o l.c DW : Dicrotic wave (Reflected wave) ai gm DW Determined by : Peripheral resistance 2@ t1 S1 S2 ar sm 2. Stiff/non-compliant vessels : Cushioning effect of vessels lost sh T yu ↑ Pulse wave velocity at pr DN P | Augments the T wave (DW arrives early) w ro ar ↑ Central SBP (CSBP) : Best marker for target organ damage M S1 © Abnormalities of Pulse 00:04:43 Relative Bradycardia : Rate of heart rate rise is < 10 beats per 1°F rise in temperature. Causes : - Non - infectious : Lymphoma, drug fever. Rare - Infectious : Typhoid, brucella, Q-fever, dengue, leptospirosis, malaria. Rhythm Abnormalities : Irregularly irregular : A - fib. Regularly irregular : Ventricular premature contractions (VPC). Volume Abnormalities : Low volume (↓ Stroke volume) High Volume (↑ Stroke Volume) 1. Hypokinetic : LV failure 1. Collapsing : AR 2. Pulsus tardus : Severe AS 2. Pseudocollapsing : MR 3. Pulsus parvus et tardus : Very severe AS Medicine Revision v4.0 Marrow 8.0 2024  10 Medicine ----- Active space ----- Contour Abnormalities : 1. Pulsus bisferiens 2. Pulsus dicroticus 3. Pulsus alternans 4. Pulsus bigemini Regular alternating Irregular alternate 1 peak in systole 2 peaks in systole high & low volume high & low volume 1 peak in diastole pulse pulse P>T P 10 mmHg on inspiration. Causes : sm Causes : a. Intermittent positive sh yu i. Cardiac tamponade (m/c). pressure ventilation (IPPV). at pr ii. Constrictive pericarditis (1/3rd cases). b. HCM. | iii. Hyperinflated lung. w ro iv. SVC obstruction. ar M v. Pulmonary embolism. © vi. RCM (Rare). Jugular Venous Pulse 00:14:00 Features : Height of column of blood above the sternal angle at 45°. Semi - recumbent position ≥ 3 cm H2O is elevated. Assess right heart filling IJV used (Directly reflects right atrial pressure). RAP = 5 cm + IJV (Normal = 8 cm H2O). Causes of elevated JVP : Pulseless elevation : SVC obstruction. Pulsatile elevation : 1. Circulatory overload. 4. RV pathology (RVH). 2. Tricuspid valve pathology (TS/TR). 5. Pulmonary valve pathology (PS/PR). 3. Pulmonary artery pathology 6. Right atrial pathology. (Pulm HTN/embolism) Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 2 11 JVP Waveform : ----- Active space ----- Waves Interpretation a Rt Atrial contraction (Presystolic) x x, x’ Atrial relaxation C Upward tricuspid bulge (Coincides with S1) v Atrial filling (Coincides with S2) ‘ y Atrial emptying (70% of ventricular filling) Mitral valve closure Aortic valve closure Abnormalities : Abnormal wave Condition 1. Prominent Tricuspid valve obstruction/RVH/Pulm HTN a wave 2. Giant/Cannon AVNRT/Junctional rhythm/Complete heart block/VT with AV dissociation 3. Absent A-fib/Hyperkalemia mo l.c Prominent/Rapid Cardiac tamponade/RCM/Chronic constrictive pericarditis (CCP) ai x descent gm Absent Tricuspid regurgitation (TR)/RV failure 2@ Diminished Hypovolemia t1 ar v waves ↑ Vena cava pressure : CCP/RV failure sm Prominent 2nd route : ASD/TR (Lancisi sign) sh yu Prominent CCP at y descent pr Slow Tricuspid stenosis (TS) | w Kussmaul’s sign : ro ar Inspiration ↑JVP. M © Causes : CCP/RCM/TS/RV MI. Not seen in cardiac tamponade. Abdominojugular reflex : > 3cm/ > 15s Impending right heart failure. Heart Sounds 00:34:40 Low pitched heart sounds Low pitched murmurs S3 MS S4 TS Tumour plop Austin Flint murmur A. S1 : Cause : Closure of AV valves. Occurrence : Atrial contraction S1 Isovolumetric contraction. Loud S1 : MS. Soft S1 : AR, MR, Good filling of the heart. Medicine Revision v4.0 Marrow 8.0 2024  12 Medicine ----- Active space ----- B. S2 : Split into A2 P2 : D|t hangout interval ∝ Pressure beyond valve. (A2 : 30ms-1; P2 : 80ms-1) ∝ 1 Distensibility of vessel A2 P2 BAV - AS Loud Pulm. HTN (Palpable P2) Root pathology Elderly AS Soft Pulm. stenosis Valve pathology in AR Wide variable split Wide fixed split Paradoxical split Early A2 / Delayed P2. Split does not move with respiration. Loud P2 A2 Cause : MR. Causes : RV failure, ASD. Causes : AR, AS. Note : MS Single loud P2. mo l.c C. S3 : ai gm Pathology : N /Less than normal filling of a non-compliant dilated ventricle. 2@ Seen in : t1 ar - AS/AR with failure. sm - MR with/without failure. sh yu D. S4 : Seen in AS. at pr Added Diastolic Sounds : | w ro O P Time 3 4 ar M Early : © Mid Late Opening snap. Pericardial knock. S3 S4 Tumour plop. Systolic Clicks : 1. Ejection clicks : - Aortic ejection click : BAV. - Pulmonary ejection click (Does not ↑on inspiration). 2. Non - ejection click : MVP Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 3 13 CVS REVISION - 3 ----- Active space ----- Heart failure (HF) - Basics 00:00:20 Structural/functional impairment in the ability of the ventricles to pump out blood or fill itself. Types of HF : a. HFrEF : Ejection fraction < 40%. b. HFpEF : Ejection fraction > 50%. c. HFmEF : Mid range ejection fraction (40-50%). Stages of HF : mo l.c A B C D ai gm Only risk factors eg : DM/HTN A + Structural abnormality B + Symptoms (Present/prior) Advanced heart disease 2@ t1 M/C/C of mortality : Sudden cardiac death Pump failure ar sm NYHA Classification : sh yu I II III IV at pr Symptoms on Symptoms on ordinary Symptoms on less than Symptoms at | exertion activity ordinary activity rest w ro NYHA : Only for angina, dyspnea & palpitation (Not syncope). ar M © Heart Failure (HF) - Symptoms 00:06:04 LV systolic failure ↑LVEDP ↑RVEDP Cachexia (TNF-α) ↑LAP ↑PCWP Dyspnea ↑Abdomino jugular ↓ Urine output (Cardio-renal syndrome) reflex Altered sensorium Orthopnea & PND Pulm. edema (Impending failure) Cold extremities O/E : Rales, S4 ↑ JVP (>3cm) O/E : Narrow pulse pressure, S3, Ascites cardiomegaly Edema Hepatomegaly Framingham’s Criteria (Major) : 1. Dyspnea. 5. JVP. 2. Acute pulmonary edema. 6. Abdominojugular reflex. 3. Rales. 7. Cardiomegaly. 4. S3. Medicine Revision v4.0 Marrow 8.0 2024  14 Medicine ----- Active space ----- Dyspnea : Due to ↑LVEDP ↑LAP ↑PCWP. Bendopnea Trepopnea Dyspnea on bending forward Dyspnea while lying on one side Advanced Lt & Rt HF Pleural effusion (more on right side) A/w ↑JVP & ↑PCWP Crepitations : HF : COPD : Fine gravitational crepts Non-gravitational Cold extremities Warm extremities Other Symptoms : Decompensation : 1. Angina : D/t ↑LV mass, LVOT, Factors precipitating acute HF : m Microvascular disease. 1. Non compliance (Diet/drugs). o l.c ai 2. Palpitation : D/t cardiomegaly. 2. Infections (Eg : Infective endocarditis). gm 3. Syncope : D/t LVOT obstruction. 3. Anemia. 2@ 4. Sinus tachycardia : ↑Mortality. 4. Arrhythmia (Eg : A-fib). t1 ar 5. MI. sm sh 6. NSAIDs & β-blockers. yu at Heart Failure (HF) - Management 00:16:18 pr | Investigations : w ro 1. ECG : 2. ECHO : For ejection fraction. ar M - Low voltage in limb leads. 3. Cardiac MRI : Gold standard. © - High voltage in chest leads. - Poor R-wave progression. Treatment Guidelines - HFrEF : Drugs used (Fantastic 4) : Note : 1. SNS blockers : β-blockers HFpEF : Comorbidity Mx. - Metoprolol. HFrEF : Guideline based Mx. - Carvedilol. Vicious cycle of HFrEF : - Bisoprolol (Best : β1 selective). ↓Cardiac Neurohormonal - Started at lowest dose. output compensation - Patient should be dry (No edema). Heart failure 2. RAAS blockers : SNS + ARNI > ACEi > ARBs Cardiac remodelling RAAS + Natriuretic peptide + AT - II inhibitor (Valsartan) + Neprilysin inhibitor (Sacubitril). Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 3 15 3. Mineralocorticoid receptor antagonist (MRA) : ----- Active space ----- - Spironolactone/eplerenone/finrenone. Mortality benefit - S/E : Hyperkalemia, gynecomastia. β-blocker > ARNI > ACEi > ARB > Hydralazine + Nitrate 4. SGLT2 antagonist : Dapagliflozin/Empagliflozin. Hydralazine : Used in renal Add on drugs : failure with HF. Diuretics : Symptomatic relief. Ivabradine : Used if HR > 70 bpm + β-blockers max dose. - Inhibits funny currents. - S/E : Visual field abnormalities. Ventricular Dysfunction 00:29:32 Types : Systolic dysfunction Diastolic dysfunction mo l.c Pumping issue Filling issue ai gm LV defect RV > LV defect F/b diastolic dysfunction May have N systole 2@ t1 ar Constrictive pathology : CCP sm Diastolic dysfunction seen in sh Restrictive pathology (More severe) : RCM yu at Symptoms of Diastolic Dysfunction : pr | 1. ↑RVEDP ↑RAP ↑Pressure in Vena Cava Rt HF. w ro Ascitis precox ↑JVP ar M Edema Hepatomegaly © 2. Systole N ; chamber size N. 3. ECG : Low voltage complexes. 4. Kussmaul’s sign + : CCP, RCM, TS. Acute Pericarditis 00:34:00 Causes : Post viral/uremia. Clinical features : Chest pain. ECG : D/d : MI 1. Global ST elevation (Except V1). 1. Localised ST elevation 2. Concave ST elevation. 2. Convex ST elevation 3. No reciprocal changes. 3. Reciprocal changes + 4. PR depression. 4. No PR depression Medicine Revision v4.0 Marrow 8.0 2024  16 Medicine ----- Active space ----- CCP vs RCM 00:39:10 Chronic Constrictive Pericarditis Restrictive Cardiomyopathy Multiple relapses : Acute pericarditis Stiff, hypertrophic, non-compliant, non-dilated Pathology Rock like pericardium : ventricle Rigid, calcific, thickened, fibrous pericardium with adhesions Diastolic dysfunction 1. Intercellular accumulation : Amyloidosis (M/c) 2. Intracellular accumulation : m a. Hemochromatosis (Iron) o l.c Causes Post viral > TB b. Fabry’s disease ai gm 2@ (Glycosphingolipids) c. Pompe’s disease (Glycogen) t1 ar 3. No accumulation : sm DM/Scleroderma sh yu Rapid x-descent at X-descent is not prominent pr Rapid y-descent : Friedreich’s | No y-descent w JVP sign ro No square root sign ar Square root sign + M ↑On inspiration : Kussmaul’s sign © Elevation & After 1/3rd of diastole Equalisation Absent (Pericardial knock + ) of pressures Cachexic & malnourished patient S3 + Pulsus paradoxus (1/3rd of No pulses paradoxus patients) Other No pericardial knock Pericardial knock + features ↓Transmyocardial filling Broadbent sign : Systolic pressure retraction of apex (11th/12th rib indrawing) ECG : low voltage complexes Ix MRI (IOC) ECHO Rx Pericardiectomy Medical management Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 3 17 Cardiac Tamponade 00:57:03 ----- Active space ----- Cause : Post-traumatic Acute rise in intrapericardial pressure. Features : Holodiastolic elevation & equalisation of pressures No filling. Small chambers. Diastolic dysfunction. Clinical Features : Hypotension Obstructive shock : Hypotension. Shock. Beck’s m Disproportionate dyspnea. triad o l.c Tachycardia. Muffled ↑JVP ai gm heart sound 2@ On Examination : t1 JVP : ar sm - Prominent x-descent (Coupled constraint : Heart acts as one chamber). sh - No y-descent. yu at - No square root sign. pr No pericardial knock. | w ro No Kussmaul’s sign. ar Pulsus paradoxus (Inspiration M SBP decreases > 10 mmHg). © Management : Investigations : 1. ECG : Electrical alternans (low voltage complexes). 2. ECHO. Treatment : Emergency pericardiocentesis. Medicine Revision v4.0 Marrow 8.0 2024  18 ----- Active space ----- CVS REVISION - 4 Dilated Cardiomyopathy (DCM) 00:02:40 Pathology : Large, dilated, thin walled LV Poor contractile Poor relaxation. Clinical features : 1. Systolic failure : ↓ cardiac output. Cachectic (TNFα). O/E : Narrow pulse pressure. Cold extremities. S3 +. m Altered sensorium. Cardiomegaly. o l.c Renal failure (CRS). ai gm 2. Diastolic failure : Dyspnea (↑LVEDP ↑PCWP). 2@ 3. Right heart failure : ↑JVP, ascites, edema, hepatomegaly. t1 ar sm Etiology : sh 1. Genetic : Autosomal dominant Truncated variant titin mutation (M/C). yu at Myh7 (Myosin heavy chain 7) mutation. pr 2. Peripartum cardiomyopathy : | w Best prognosis. ro ar D/t antiangiogenic factors : SFLT 1. M © R/F : - ↑Age. - HTN. - Multiple pregnancies. 3. Alcohol induced : 4. Drug induced : Anthracyclines Good prognosis. (Worst prognosis). A/w ACE polymorphisms. 5. Autoimmune : Precipitated by deficiency of : Sarcoidosis. a. Selenium : Keshan’s disease. Hemochromatosis. b. Thiamine. c. Mg2+. 7. Acute post inflammatory DCM : 6. Endocrine : Myocarditis in the infection/post infection period. Pheochromocytoma. New onset HF : ↑↑Trop I. Thyrotoxicosis. Hypotension. M/C/C : HHV6 > Chagas. Acromegaly. Chest pain. Mx : Supportive. Tachycardia. Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 4 19 Investigations : ----- Active space ----- 1. ECG : Triad Low voltage in limb leads. High voltage in chest leads. Poor R-wave progression. 2. Echo : Global LV hypokinesia. 3. Cardiac MRI : Ischemia vs infarct; ejection fraction (Gold std). 4. Angiography. Restrictive Cardiomyopathy 00:14:30 Seen in amyloidosis of the heart. 1. Primary. 2. Secondary : No cardiac involvement. m 3. Transthyretin induced : o l.c a. Senile systemic (Wild type) : Elderly patient with carpal tunnel syndrome. ai gm b. Familial amyloid polyneuropathy (Mutant) : Severe ANS symptoms + 2@ Cardiac involvement. t1 ar Features : sm 1. Biatrial enlargement. sh yu 2. Biventricular hypertrophy. Cardiac MRI : IOC. at pr 3. Interatrial septal thickening. Glittering/sparkling myocardium Bad prognosis | 4. Low voltage complexes. w ro ECG : Pseudo infarct pattern. ar M © Takotsubo Cardiomyopathy 00:17:10 AKA s tress induced cardiomyopathy/neurogenic myocardial stunning/ transient apical ballooning. Cause : Sympathetic overactivity M/C in middle aged females. Features : ACS like presentation ST elevation. ↑Trop I (Not as high as ACS). ↑↑NT Pro BNP. Angiography Normal coronary arteries. Hypercontractile base. Bulging apex. Prognosis : Short term : Like MI. Long term : Good. Medicine Revision v4.0 Marrow 8.0 2024  20 Medicine ----- Active space ----- Hypertrophic Cardiomyopathy 00:20:12 M/C genetic CVS disease. AD. Mutation : Myosin heavy chain > Myosin binding protein C. Males = Females Poorer prognosis (More progressive disease). 95-99% Stable course 1-5% Complications : 1. Progressive HF. 2. Arrhythmias (A-Fib). 3. Risk of sudden cardiac death. D/D : Pompe’s disease. m o Hypertrophy : l.c ai Concentric, inappropriate, asymmetrical hypertrophy. gm 2@ LV thickness ≥ 15mm No cause. Left side : t1 ar No dilatation. Septum + Anterior wall >> Posterior wall. sm ↓cavity size sh yu ↑LVEDP at Obstruction in HCM pr Clinical Features : 1/3 : Fixed obstruction. rd | w 1/3rd : No obstruction. ro 1. Dyspnea (M/C) : D/t diastolic dysfunction. 1/3rd : Dynamic obstruction ar 2. Angina with normal coronaries (2nd M/C) : M (Depends on cavity size). © D/t microvascular dysfunction. 3. Systolic Anterior Motion (SAM) : SAM pathophysiology D/t asymmetrical septal hypertrophy. Septal hypertrophy Leads to 2˚ MR. LVOT obstruction 4. A-fib : D/t ↑LAP. 5. LVOT obstruction Angina ↑velocity of blood across obstruction Syncope Anterior mitral leaflet sucked into septum Dyspnea (Mid-late systole) Note : Most patients are asymptomatic. ↑obstruction Examination Findings : Pulse : Pulsus bisferiens (P>T). S1 : Normal. BP : Normal. S2 : Normal/reverse split. JVP : Normal. S3 : ± Apex : Double apex/triple apex. S4 : ± Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 4 21 Murmurs : ----- Active space ----- Lower left sternal border Ejection systolic murmur (D/t SAM). Apex Pansystolic murmur (D/t 2˚ MR). Biopsy : Myofibre disarray. Dynamic auscultation : Factors affecting LVOT obstruction Intensity of murmur ∝ LVOT obstruction. ↑Preload ↑Force of contraction Valsalva, standing ↑Afterload (Amyl nitrate, isoproterenol) (↓Preload and afterload) ↑cavity size ↓cavity size - ↑Intensity of murmur in HCM. - ↑Duration of murmur in MVP. ↓obstruction ↑obstruction Brockenbrough sign : ↓Post-VPC pulse volume in HCM (D/t SAM). mo Note : MVP and HCM are exceptions. Valsalva/standing ↓ all other murmurs. l.c ai gm Treatment : 2@ β-blocker (DOC) : 2mg/kg propranolol t1 If C/I ar sm sh Verapamil/diltiazem Max dose : 480 mg yu (Not combined with β-blocker) Fails QT prolongation. at Add Disopyramide S/E pr Fails Anticholinergic S/E. | ↓ejection fraction (5-10%). w ro ar If Medical Mx fails M © Sx : Septal myomectomy Indications for ICD (Implantable cardioverter defibrillator) : Family h/o sudden cardiac death. H/o spontaneous sustained VT. Medicine Revision v4.0 Marrow 8.0 2024  22 ----- Active space ----- CVS REVISION - 5 Inferior Wall MI (IWMI)  00:00:35 Dominance of Coronary Circulation : aVL(-30˚) Depends on supply of PIVA/PDA Lead I RCA LCx Lead II1 Lead II Right dominant (80%) Left dominant (20%) aVF (120˚) (90˚) (60˚) m Arteries Supplying Inferior Wall : o l.c ai Inferior wall leads gm RCA OR LCx 2@ Note : t1 1. RVMI : V3r, V4r, V5r ar Proximal OR Distal sm 2. PWMI : V7, V8, V9 sh yu Landmark : Acute marginal A. (Only branch supplying RV free wall) at pr RCA Branches : | w 1. SA nodal branch ro Anterior branches Block IWMI + RV-MI ± PWMI ar 2. Atrial branch M © 3. Acute marginal artery 4. AV nodal branch Posterior branch Block IWMI (No RVMI) ± PWMI. LCx block : IWMI + PWMI. Features of RCA block : 3. ↑JVP 1. Bradycardia : D/t SA nodal branch block, vagal stimulation. 2. Posteromedial papillary muscle rupture 2° MR. RVMI (Single blood supply RCA) Clear lungs Hypotension Rx : Hydration Occluded artery : ST ↑ ST↓ RCA Lead III > II aVL > aVR LCx Lead II > III aVR > aVL IWMI : ST ↑in lead II, III, aVF + RVMI (Proximal RCA) : V1 ST ↑/Discordance with V2,V3,V4 Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 5 23 Anterior Wall MI (AWMI) 00:09:37 ----- Active space ----- LCA LAD. LCx. Blood supply Area ECG leads (In order) LAD (D1) or LCx High lateral wall I, aVL LAD (S1) Septum V1 >> V2 LAD (D2) Anterior wall V2, V3, V4 LAD (D4) or LCx Lateral wall V5, V6 Note : D Diagonal ; S Septal mo l.c ai gm 2@ t1 ar sm sh yu at pr Extensive antero high lateral MI (Above D1, S1, D2, D3) : | ST ↑in V2, V3, V4. w ro Reciprocal changes in II, III, aVF. ar M V1 ST↑. © ST↑ in I & aVL. ACS Management 00:14:02 Acute Coronary Syndrome : 1 out of 5 : Myocardial injury 1. Clinical evidence of ischemia 2. ECG evidence of ischemia ↑Cardiac troponin (> 99th percentile) + 3. Pathological Q-waves & 4. Echo changes Rise & fall of troponin 5. Angio changes Medicine Revision v4.0 Marrow 8.0 2024  24 Medicine ----- Active space ----- ACS Protocol : First medical contact (Diagnosis in 10 min) Golden hours : 6 hours. 24hr PCI capable catheter No PCI capability PCI within 60 min PCI possible within 120 mins if shifted Medical Mx after Stabilising Pt : 1. Aspirin 300 mg. No Yes 2. Clopidogrel 300 mg (600 mg for PCI) Thrombolysis (If PCI planned : Ticagrelor/Prasugrel). Tenecteplase : 0.5 mg/kg bolus Shift 3. Statin 20-40 mg. 4. Anticoagulant 30 mg s/c (Before PCI). Repeat ECG (Within 60-90 mins) 5. ACEi & β-blockers (Within 24 hours). 6. Lifelong aspirin & statins. Resolution No resolution m 7. Antiplatelet for 1 year. o l.c PCI within 2-24 hours Rescue PCI ai gm Arrythmia 2@ 00:19:43 t1 ar Mechanisms of Arrhythmias : sm 1. Abnormal enhanced automaticity : Focal/MAT; Junctional tachy; Ischemic VT; sh yu Digoxin toxicity. at pr 2. Triggered activity : Long QT syndromes; Catecholamine induced tachy. | w 3. Re-entry : AVNRT; A. Fib; Brugada Sx; AVRT & A. Flutter; Scar VT. ro ar TYPES OF TACHYARRHYTHMIAS M © Narrow QRS Slightly wide QRS Wide QRS QRS interval < 0.12 seconds 0.12 - 0.16 seconds > 0.16 seconds Above Bundle of His bifurcation + Bundle Origin Above Bundle of His bifurcation Ventricles branch block Atrial tachycardia Polymorphic VT; Examples Junctional tachycardia - Monomorphic VT; AVNRT, AVRT, A-fib, atrial flutter Torsades de pointes Narrow QRS Tachycardia : Regular R-R interval Irregular R-R interval 1. AVNRT : - No P-waves OR - P wave after QRS complex with short RP & long PR interval. 1. Atrial fibrillation 2. AVRT : P wave after QRS complex with short RP (>80-100 ms) 2. Multifocal atrial tachycardia (MAT) : & long PR interval 3 distinct P-wave morphology seen 3. Focal atrial tachycardia : - Long RP, short PR interval (P before QRS). - Abnormal P-wave. Medicine Revision v4.0 Marrow 8.0 2024  CVS Revision - 5 25 ----- Active space ----- Atrial tachycardia Management : 1. AVNRT : m - Adenosine. o l.c - COPD : Verapamil Fails Metoprolol. ai gm - Synchronized DC cardioversion. 2@ 2. Atrial Tacycardia t1 Rate lowering agents ar 3. MAT (A/w COPD Rx with theophyline) (Verapamil, β-blockers ) sm sh yu Note : Indications for unsynchronized cardioversion Pulseless VT; V. Fib.; at Polymorphic VT. pr | w Atrial Fibrillation : ro ar Features : Types : M Reverts spontaneously © 1. Irregular R-R interval. 1. Paroxysmal : 7 days. OR With drugs 3. No identifiable P-wave. 3. Permanent : LA dilatation >4 cm Cannot be reverted back to normal. Complications : Thromboembolism. Risk factors : 1. Age. 2. HTN. 3. Associations : - Structural heart/lung disease. - OSAS. - Thyroid patients. - Psoriasis. 4. Mitral stenosis, prosthetic valve : Valvular A-fib. Medicine Revision v4.0 Marrow 8.0 2024  26 Medicine ----- Active space ----- Management : Hemodynamically stable Hemodynamically unstable Transthoracic Echo DC cardioversion (100J x 2) LA dilated > 4cm LA N (Structural heart disease) > 48 hrs (Or) < 48 hrs Rate control : CCB unknown duration Rhythm control : TEE/Cardiac CT Ibutilide Amiodarone m Clot + o l.c (Structural heart disease) ai gm Anticoagulation X 3wks Rhythm control Anticoagulation X 4wks 2@ (Drugs > DC cardioversion) t1 ar sm Wide QRS Tachycardia : sh 1. Monomorphic Ventricular Tachycardia : yu at Sustained VT + rate >100/min. pr | ≥3 VPC. w ro Capture beat/fusion beat ±. ar M Management : © Monomorphic VT Unstable Stable : 1. Procainamide. Synchronised DC cardioversion 2. Amiodarone (Structural heart disease). (360J) 3. Lignocaine : Post MI. 2. Torsades de Pointes/Polymorphic VT : - Polymorphic VT + QT prolongation. - Precipitating factors : a. Antiarrhythmics : Class Ia, Ic, Class III. b. Terbinafine, macrolides. c. Hypokalemia, hypocalcemia, hypomagnesemia. d. Hypothermia. - Mx : Defibrillation (200J) + 2g MgSO4 I.V. Polymorphic VT Med