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MBBS VI - Medicine Final Summary > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

Atrial fibrillation, Heart failure, CAD, Valvular heart disease, Cardiogenic syncope, Hypertension, Myocarditis, IE, Rheumatic fever, Congential heart diseases, Aortic dissection, DVT, PE

1
Q

What is the classification of AF rhythm?

A

AHA guidelines

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2
Q

What are the causes of AF beat?

A
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3
Q

What Ix for AF beat?
What Ix for LA thrombus?

A
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4
Q

What is the triad for treatment principle for AF?

A

Rate control +rhythm control + prevention of thromboembolism

Rate control = blocking the AVN to slow conduction through the AVN

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5
Q

What is the pharmacological rate control of AF?
What is target for symptomatic and asymptomatic rate control

A

Symptomatic: resting HR <80bpm
Asymptomatic + LVEF>40%: HR <100bpm

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6
Q

What is non pharmacological rate control of AF?

A
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7
Q

What is the pharmacological rhythm control for AF?

A
  • None or minimal underlying heart disease = Flecainide/ Propafenone/ Dronedarone/ Sotalol
  • Patients with post-MI/ CAD = Amiodarone/ Dronedarone/ Dofetilide/ Sotalol
  • Patients with heart failure = Amiodarone/ Dofetilide
    o Dronedarone increases mortality in patients with recently decompensated HF and depressed LV function and is contraindicated in patients with NYHA class III or IV HF
  • Patients with hypertension with LVH = Amiodarone
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8
Q

What is non pharmacological rhythm control for AF?

A

Direct current (DC) cardioversion
Indications: haemodynamically unstable patients, refractory to pharmacological cardioversion, rapid control of ventricualr rate during AF is required
Delivery of electrical shock synchronized with QRS complex to avoid inducing VF which can occur by a shock applied during ventricular repolarization of T wave
AF<48 hours of duration: pre and post cardioversion anticoag required only in patients with high risk of thromboembolism
AF >48 hours of duration or unknown duration: precardioversion anticoagulation > 4 weeks. Post cardioversion anticoagulation >4 weeks
Urgent cardioversion: need for restoration of SR takes precedence over need for protection from thromboembolism. Can be anticoagulated acutely with heparin and proceed directly to anticoagulation if no atrial thrombus seen on pre-cardioversion TEE

Catheter ablation
Indicated in patients with symptomatic paroxysmal/ persistent/long standing persistent AF who are refractory or intolerant to >1 class I or III anti arrhythmic drugs when a rhythm control strategy is desired
RFA and cryoballoon ablation. Anticoag required for RFA ablation.
Complications: cardiac tamponade (most common), stroke, TIA or pulmonary veins tenosis

Surgical maze procedure (surgical ablation): indicated in selected patients undergoing cardiac surgery for another indication such as valvular replacement or CABG

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9
Q

What are the indications for anticoags in AF?
What scoring system used

A

 Indications for anticoagulation
* ALL valvular AF (since stroke risk is very high)
* Non-valvular AF with CHA2DS2-VASc score ≥ 2
* Prior stroke or transient ischemic attack

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10
Q

What scoring system for quantification of bleeding risk for anticoagulants use?

A
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11
Q

What are the antithrombotic options for AF?

A
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12
Q

Compare NOACs to warfarin in preventing thromboembolism in AF?

A
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13
Q

What is non pharmacological prevention of AF?
Complication of AF?

A
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14
Q

What is the classification of HF severity?

A

New York Heart association (NYHA)
Quantiy degree of functional limitation impsoed by HF
Classification depends on degree of effort needed to elicit symptoms

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15
Q

What is the staging of heart failure?

A
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16
Q

What are the types of heart failure?

A

Low output heart failure (more common): decreased CO but increased filling pressure
High output heart failure: increased SV and normal or even increased CO, body responds by increasing fluid retention and preload e.g. sepsis/anemia, thyrotoxicosis/AVF or shunting

Left vs right heart failure
Left heart failure (increased left heart filling pressure)
Symptoms: orthopnea, paroxysmal nocturnal dyspnea, dyspnea on exertion, nocturnal cough, palpitation
Signs: tachycardia, presence of S3/S4, cardiomegaly, lung crepitations
RHF
Symptoms: abd distension, ankle swelling
Signs: elevated JVP, hepatojugular reflex, pleural effusion, hepatomegaly, ascites, bilateral ankle pitting edema

HF with reduced ejection fraction <40%: decreased LVEF due to impaired systolyc function, increased LV dilatation
HF with preserved ejection fraction >50%: increased filling pressure but anormal LV filling due to impaired diastolic function. No or niminal LV dilatation

Heart failure according to haemodynamic profile
Presence of congestion = wet vs dry
Adequacy of peripheral perfusion = warm vs cold

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17
Q

What are the causes of heart failure in adults?

A
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18
Q

Causes of heart failure in children and infants?

A
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19
Q

What are the causes of pressure overload and volume overload in causing heart failure (LV and RV)?

A
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20
Q

What is the law that guides heart failure?

A

Frank starling law: SV of heart increases in response to an increase in volume of blood filling the ventricles (preload)
Length-tension relationship in preload phase
When ventricles filled up with larger volume of blood it stretches the ventricular muscle cells and increases sarcomere length
Reduces overlapping of actin and thus increasing cross bridge formation to optimize stroke volume
Overstretching of ventricular wall will lead to actin and myosin being out of reach –> decrease cross bridge formation and decreasing stroke volume

Before optimal point: increased venous return (preload), increased SV and thus CO
After optimal point: increased venous return (preload), decreased SV and thus CO, increasde LV end diastolic pressure, increased LA pressure, increased pulmonary venous pressure

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21
Q

How does the heart compensate for heart failure?
What is decompensation?

A
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22
Q

What is clinical, CXR and ECG findings of pressure overload in heart failure

A

Primary response is ventricular hypertrophy (increased myocardial O2 consumption) but not ventricular dilatation. Imbalance between myocardial O2 demand and coronary flow results in relative myocardial ischemia and myocardial fibrosis. Fibrotic ventricles will eventually dilate (volume overload).
* Clinical
o LV hypertrophy = Strong apical impulse but NO displacement of apex beat
o RV hypertrophy = Left parasternal impulse
* Radiological (CXR)
o LV hypertrophy = NO abnormality seen
o RV hypertrophy = Uptilting of cardiac apex
* Radiological (ECG)
o LV hypertrophy = Left axis deviation/ Deep S wave in V1/ Tall R wave in V6/ T wave inversion in V6 and I (strain pattern)
o RV hypertrophy = Right axis deviation/ Tall R wave in V1/ Deep S wave in V6

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23
Q

What is clinical, CXR and ECG findings of volume overload in heart failure

A

Increased end diastolic volume of ventricles. LV or RV dilates to accomodate the increased amounnt of blood
* Clinical
o LV overload = Strong apical impulse/ Displaced apex beat
o RV overload = Left parasternal impulse
* Radiological (CXR)
o LV overload = Cardiomegaly with apex extending laterally and downwards
o RV overload = Cardiomegaly with apex displaced laterally and tilting upwards
* Radiological (ECG) (similar to hypertrophy)
o LV overload = Left axis deviation/ Deep S wave in V1/ Tall R wave in V6/ T wave inversion in V6 and I (strain pattern)
o RV overload = Incomplete RBBB (rsR’ pattern) (common)/ Right axis deviation/ Tall R wave in V1/ Deep S wave in V6

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24
Q

What are the symptoms of HF in adults?

A
  • Dyspnea (fluid accumulation)
  • Orthopnea: quanity with number of pillows used (redistribution of fluid from splanchnic circulation and LL into central circulation during supine with increase in pulmonary capillary pressure leading to pulmonary congestion
  • Paroxysmal nocturnal dyspnea (PND)
  • Cheyne-Stokes respiration: cyclic breathing in which apnea is followed by gradual increase in RR and TV and then gradual increase in RR and TV until next apneic period. Apenic phase decreases arterial pO2 and increases pCO2 which stimulates the respiratory center resulting in hyperventilation and hypocapnia followed by recurrence of apnea
  • Nocturnal cough
  • Edema (decreased CO –> activation of RAAS, sympathetic nervous system)
  • Fatigue
  • Night sweats
  • Decreased excercise tolerance (decreased CO)
  • Other associateing symptoms: RUQ discomfort (acute hepatic congestion), palpitations, anorexia (poor perfusion of splanchnic circulation)
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25
Q

What are 5 classical symptoms of HF in children

A
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26
Q

What is the diagnostic criteria for congestive heart failure?

A

Framingham criteria
 Diagnosis of CHF requires
* Presence of ≥ 2 major criteria (OR)
* Presence of 1 major criteria and 2 minor criteria  Major criteria
* Orthopnea or PND
* Lung crepitations
* Pulmonary edema
* Elevated JVP
* Hepato-jugular reflux
* V enous distension
* Weight loss in response to treatment
 Minor criteria
* Exertional dyspnea
* Nocturnal cough
* Pleural effusion
* Tachycardia
* Hepatomegaly
* Ankle edema

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27
Q

What is the PE for heart failure?

A

Vital signs: BP, RR, HR, pulse (pulsus alternans)
General exam: diminished peripheral pulse, delayed capillary refill, cold, pale or cyanotic extremities
Volume assessment: elevated JVP, peripheral edema: ankle, hepatosplenomegaly
Resp examination: wheezing, basal crepitations (LHF), signs of resp distress: grunting with nasal flaring (infants), insucking of intercostal and subcostal muscles, use of accessory muscles for breathing
CVS exam: presence of S3 (systoloc HF) or S4 (diastolic HF)
S3 = early part of ventricular diastole, when there is rapid ventricular inflow into distended ventricles, the distended and tauted ventricular wall vibrates producing S3
S4 = late part of ventricular diastole, if ventricle is stiff and hardened in ventricular hypertrophy or in patients with MI, the ventricles do not expand properly –> atrium has to contract more strongly than normal to push the blood into ventricles. When atrium strains the blood into stiffed ventricle it will cause S4 (stiffened ventricles vibrate due to strong atrial contraction)

Pulmonary hypertension signs
Single and loud S2: loud P2 (pulmonary component of S2)
Functional PR murmur: early diastolic murmur at left upper sternal border

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28
Q

What is the PE for heart falure in children?

A

General inspection: body weight, height and head circumference (standard growth charts)
Short stature: turner syndrome (associated with coaraction of aorta and bicuspid aortic valve)
Tall stature: Marfan (associated with MVP, aortic root dilatation and AR)
Dysmorphic features: down syndrome, turner syndrome, diGeorge syndrome

General exam
* Cyanosis
* Abnormalities of limbs
Marfan syndrome: arachnodactyly (long slender fingers) + hyperextensible fingers
Down syndrome = clinodactyly + increased space between 4th and 5th finger
* Finger and toe clubbing
* Subcutaneous edema
* Signs of IE: splinter hemorrhage, janeway lesions, osler nodes

CVS
* BP and pulse (rate + rhythm +volume + character): radio-radio delay/pulse volume discrepancy)
* Respiratory distress: tachypnea (increased RR)
* Surgical scars
* Chest wall deformities: pectus excavatum and carinatum (features of Marfans syndrome)
* Visible cardiac pulsation (volume overload or pressure overload)
* Cardiac apex
* Presence of thrills (palpable murmur: at least 4/6)
* Abnormal cardiac impulse: strong apical impulse (LV pressure or volume overload), left parasternal impulse = RV pressure or volume overload
* Heart sounds
S2: pulmonic valve closes
Loud S2: pulmonary hypertension (large left to right heart shunt)
Single S2. Inaudible A2 = critical AS/HLHS, inaudible P2 = PA/critical PS/TGA
Wide fixed splitting of S2: hallmark of ASD
Presence of S3: dilated ventricles (large VSD/PDA/ dilated and hypertrophic cardiomyopathy)
Presence of S4: occurs in decreased ventricular compliance
Heart murmurs

Ejection click in AS or PS
Mid systolic click in MVP
Opening snap in MS

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29
Q

What are biochemical Ix for heart failure?

A

CBC: anemia and infection (leukocytosis) can exacerbate HF
Serum electrolytes: HypoNa (indicator of severe HF)
LFT: hepatic congestion
RFT: increased serum BUN and creatinine level
Urinanalysis
TF
Fasting blood glucose
cTnT/cTnI: for acute decompensated HF or suspected acute coronary syndrome
Plasma BNP level and NT-pro BNP
BNP >400 pg/ml suggestiv eof HF
BNP <100pg/mL is a strong -ve predictor for HF

NT-proBNP (should be similar to BNP): NT-pro BNP is 4x higher than BNP in LV dysfunction

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30
Q

What are the ix for heart failure (apart from biochemical)?

A
  • CXR: heart size (CT ratio >0.5), upper lobe blood diversion (cephalization–> pulmonary venous hypertension)), kerley B lines (periphery of lungs just above costophrenic angle –> edema of interlobular septa), Bat wings appearance (pulmonary edema –> alveolar shadowing from hilum), peribronchial cuffing (edema: interstitial fluid accumulates around bronchi causing thickening of wall –> doughnut like densities in lung parenchyma)
  • ECG
  • Echocardiography
  • Excericse test (risk stratification and determing prognosis) evaluate potential candidates for cardiac transplantation or mechanical circulatory support
  • Cardiac catheterization with angiography (indications –> patients with angina or positive excericse test/CAD is likely to be present)
  • Cardiac MRI: distinguish ischemic heart disease from cardiomyopathy/ identify types of cardiomyopathy
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31
Q

What are the treatment principles of acute heart failure in adults?

A
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32
Q

What is general management of HF?

A

Positioning: prop up the head, sitting up with legs dangling overside of bed. Decrease venous return and thus preload
oxygen supplemenetation: treat hypoxemia only as defined as sO2 <90%
Morphine: reduces anxiety but also induces nausea and respiratory depression
Preload: venodilation which decreases LV filling pressure, afterload = anxiolytic and decrease work of breathing resulting in diminished central sympathetic outflow leading to arterial and venous dilatation

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33
Q

What is medical treatment for acute heart failure?

A

Loop diuretics: indications for volume overload, acute cardiogenic pulmonary edema
MoA: preload (fluid removal by diuresis reduces preload), preload = initial morphine like effect that induces transient venodilation leading to a fall in cardiac filling pressures and decreased pulmonary congestion prior to onset of diuresis mediated by enhanced release of prostaglandins.
Furosmide/bumetanide/torsemide. AE: symptomatic hypotension, hypokalemia, metabolic alkalosis, acute kidney injury
Nitrates: for afterload reduction. Patients with hypertensive emergency, acute MR or AR
Contraindications: hypotension, suspected RV infarcito, HOCM, constrictive pericarditis, intake of PDE5 inhibitors within 24 hours
Nitroglycerin (TNG): venodilation –> arterial vasodilation. Nitroprusside: balanced and venous dilation
Inotropes: indicated for patients with LV systolic dysfunction and low CO. Patients with cardiogenic shock to maintian systemic perfusion and preserve end organ performance until definitive therapy is instituted
Contraindications: not indicated for AHF with HFpEF
Dopamine: D1 receptor. low dose = splanchnic and renal dilatation which improves renal function by increasing renal blood flow and reducing venous pressure. High dose = stimulates alpha-receptors which leads to vasoconstriction
Dobutamine (B1 selective agonist): increase SV and HR and thus CO. Mild decrease in SVR and pulmonary capillary wedge pressure
Milrinone (PDEi): increase myocardial inotropy by inhibiting degradation of cyclic adenosine monophosphate

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34
Q

What are adrenereceptors action and what are the drugs that are agonists of these receptors?

A
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35
Q

What is the pharmacological management of chronic heart failure?

A
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36
Q

When is ACEI/ARB used in chronic heart failure?
What is its moA?

A
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37
Q

What is the indications for using B blockers in chronic heart failure (HFrEF)?
Moa?

A
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38
Q

What is the indications for using diuretics in chronic heart failure (HFrEF)?
Moa?

A
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39
Q

What is the indications for using MRA in chronic heart failure (HFrEF)?
Moa?

A
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40
Q

What is the indications for using ivabradine and hydralazine + nitrates in chronic heart failure (HFrEF?
Moa?

A
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41
Q

What is non pharmacological management of chronic heart failure (HFrEF)?
What is lifestyle modiciation?

A
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42
Q

What is management of chronic heart falure (HFpEF):

A

Treatment for HFpEF has limited and unsatisfactory data

Control of pulmonary congestion and peripheral edema
BP control (prevention of hypretension)
HR control (prevention of tachycardia especially AF)
Management of ischemia (coronary revasuclarization in CAD with ischemia)

Medical
MRA
Diuretics: for LV diastolic dysfunction
SGLT2i
ARNi

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43
Q

What is treatment of chronic heart failure (HFpEF) in children?

A

Correct unerlying precipitating factors: infection, electrolyte disturbance and cardiac arrhythmias
Mechanical circulatory support for potentially reversible pump failure due to myocardial dysfunction: IABP, ventricular assist device

Medical treatment
* Diuretics: furosemide + spironolactone
Furosemide is potent and effective for preload reduction, spironolactone added to maintain normoK by reducing K+ in urine
MoA = preload reduction which reduces the volume load on heart and the congestion of systemic and pulmonary circulations
Furosemide = hypoNa/hypoK, metabolic alkalosis, hyperuricemia
Spironolactone = hyperK/metabolic acidosis/endocrine abnormalities

Inotrope: digoxin (enhance myocardial contractility by increasing intracellular Ca2+ as well as neurohumoral effect through decreasing central sympathetic outflow to the heart

Vasodilators (ACEI/nitrates)
ACEI (captopril, enalapril0
Nitrates (IV nitroprusside/nitroglycerine)

Inodilators: amrinon/milrinone
inhibits PDEIII which prevents inactivation of cAMP, increased cAMP elevates Ca2+ and augments contractility. Increased cAMP inactivates protein kinase in vascular smooth muscle leading to vasodilation and afterload reduction

B blockers: improve cardiac contractility, increase excercise tolerance.
Myocardial shielding from toxic effects of catecholamines, afterload reduction due to vasodilation

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44
Q

Differentiate cardiogenic and non cardiogenic pulmomary edema

A

Cardiogenic pulmonary edema: increased transudation of protein poor fluid into pulmonary interstitium and alveolar space leading to decreased diffusing capacity, hypoxemia and dyspnea
High pulmonary capillary pressure is responsible for abnormal fluid movement. Rise in pulmonary capillary pressure results from an increase in pulmonary venous and LA pressure

Non cardiogenic pulmonary edema: presence of radiographic evidence of alveolar fluid accumulation in the absence of elevated pulmonary capillary wedge pressure (PAWP <18mmHg)
Most common mechanism for rise in transcapillary filtration is an increase in capillary permeability

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45
Q

What is the etiology of cardiogenic pulmonary edema and precipitating factor of acute edema?

A
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46
Q

What is the etiology of non cardiogenic pulmonary edema?

A
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47
Q

What are Ix for pulmonary edema?

A
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48
Q

What is treatment protocol for acute pulmonary edema?

A
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49
Q

Compare stable vs unstable angina

A
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50
Q

What are the causes of CAD (coronary artery disease)?

A
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51
Q

What is non invasive and invasive testing for CAD (coronary artery disease)?

A

Excercise tolerance test (with ECG/imaging): use Bruce protocol. High risk test results (requiring coronary angiography)
Pharmacological stress test (with imaging only). Coronary vasodilator = adenosine (relative coronary steal phenomenon), inotrope = dobutamine (more physiological but longer test duration)

SPECT (rMPI= radionuclide myocardial perfusion imaging) enables evaluation of cardiac perfusion and function at rest and at stress
Echocardiography
Cardiac MRI (viability assessment for patients with significant coronary artery narrowing): helps to determine if PCI or CABG will lead to improvement in cardiac function
MDCT (multidetector row CT scan) for coronary artery calcium (CAC) score. Sensitive but not specific to coronary artery disease.
CTA/MRA (detects coronary artery steosis and estimates %stenosis before applying invasive coronary angiography)

Invasive assessment: invasive coronary angiography (gold standard)
Indications in stable CAD or asymptomatic patients: high risk patients after non invasive testing

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52
Q

What is the guideline directed medical therapy (GDMT) in coronary artery disease? (ABCDE mnemonics)

A
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53
Q

What are the 2 methods for coronary revascularization in stable CAD (SIHD)?

A
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54
Q

When is CABG indicated over PCI for stable CAD (SIHD)?

A

3 vessel disease of significant stenosis >70%
2 vessel disease involving proximal LAD of significant stenosis >70%

Unprotected left main disease with significant stenosis >50% –> CABG prefferred/ PCI alternative
Survivors of sudden cardiac death with presumed ischemia-mediated VT –> CABG/PCI both are preferred

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55
Q

What are poor prognostic factors for coronary artery disease?

A
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56
Q

Compare usage rate, durability, thrombogenic risk, anticoag use in mechanical vs bioprosthetic valve

A
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57
Q

What are indications for mechanical heart valves

A
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58
Q

What are the indications for bioprosthetic heart valves?

A
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59
Q

What is antithrombotic prophylaxis for mechanical heart valves?
Target INR for mechanical aortic valve/mitral valve

A
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60
Q

What is antithrombotic prophylaxis for bioprosthetic heart valves?

A
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61
Q

What is the periprocedural bridging of anticoagulation in patients with mechanical heart valves?

A
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62
Q

What is the correction of ovar-anticoagulation?

A
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63
Q

What are the complications of valve replacement?

A
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64
Q

What are the causes of mitral stenosis?

A
  • Rheumatic heart disease (>95%): fish mouth opening and shortening of chordae tendineae due to repetitive valve scarring. Leaflet thickening and calcification due to stress of chronic turbulent flow through a deformed valve
  • Mitral annular calcification
  • Congenital heart disease
  • Rheumatological diseases (SLE, RA)
  • Miscalleneous: infective endocarditis, carcinoid syndrome
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65
Q

What are SS of mitral stenosis?

A
  • Exertional dyspnea (most common): pulmonary venous hypertension –> reduced compliance of lungs and decrease in vital capacity
  • Decreased excercise tolerance
  • Hemoptysis: increased pulmonary pressure and vascular congestion can lead to haemoptysis. Sudden hemorrhage due to rupture of thin walled and dilated bronchial veins when there is sudden increase in LA pressure
  • Hoarseness: Ortners syndrome which refers to compression of recurrent laryngeal nerve by the LA enlargement
  • Malar flush: pulmonary hypertension
  • Fatigue: reduction of CO
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66
Q

What PE findings of mitral stenosis?

A

Inspection: malar flush, JVP (elevated in RHF, loss of a wave if AF is present, prominent a wave (elevtaed RA pressure in pulmonary hypertension), prominent v wave (functional TR in pulmonary hypertension). Pulse: small volume due to low CO, AF due to LA enlargement

Palpation
Non displaced taping apex beat.
Left parasternal heave: RV hypertrophy, pulmonary hypertension

Auscultation
* Loud S1
* Loud S2 due to pulmonary hypertension
* Opening snap
* Mid diastolic murmur: low pitched rumbling murmur heard maximally over apex. Louder in left lateral decubitus during expiration.

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67
Q

What Ix for mitrals tenosis and findings?

A

CXR
* Left atrial enlargement: straightening of left heart border, riht doubel density, displaced left mainstem bronchus
* Enlargement of main pulmonary artery due to pulmonary hypertension
* Pulmonary vascular congestion or cephalization of pulmonary blood flow to upper lobes

ECG
* P mitrale: broad and bifid P wave
* AF
* RVH

Echocardiography: structural changes of mitral valve leaflets such as thickened and calcified mitral valve
Echocardiographic parameters of MS
* Mean transvalvular gradient
* Diastolic pressure half time
* Mitral valve area
* Pulmonary artery systolic pressure

Cardiac catheterization: indicated if echocardiography is non diagnostic or conflicts with clinical findings

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68
Q

What is medical and surgical management of mitral stenosis?

A
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69
Q

What are the complications of mitral stenosis?

A
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70
Q

What is the classification of MR
What is the staging of MR?

A

Acute MR: pathological regurgitation of blood due to acute events such as acute MI, infective endocarditis and trauma
Chronic mitral regurgitation (MR): primary (degenerative) or secondary (functional)
Primary degenerative MR due to structural abnormalities in >1 of the following mitral valve apparatus components: valve leaflets, papillary muscles, chordae tendinae
Secondary functional MR characterized by structurally normal mitral valve with regurgitation cauased by ventricular remodelling due to ischemic or non ischemic cardiomyopathy (valve leaflet tethering with associated annular dilation)

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71
Q

Causes of acute, chronic MR, chronic functional MR?

A
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72
Q

What is the consequence of acute and chronic MR?

A
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73
Q

What are SS of acute MR
What is PE?

A

SS
* Cardiogenic shock: hypotension
* Heart failure (pulmonary edema): orthopnea, PND, dyspnea on exertion, reduced excercise tolerance

Palpation
* Pulse: AF
* Pansystolic thrill
* Left parasternal heave due to enlarged LA
* Apex beat: displaced and diffuse apex beat due to LV dilatation, thrusting apex beat due to volume overload

Auscultation
* Soft or absent MI
* Widely split S2: early A2 due to decreaed LV afterload, late P2 due to pulmonary hypertension
* Presence of S3
* Pan systolic murmur: high pitch blowing holosystolic murmur maximal over apex, radiates to axilla. Louder with handgrip and softer with Valsalvas maneuver

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74
Q

What Ix for mitral regurgitation and results?

A

CXR:
* LA enlargement (straightening of left heart border
* right double density
* displaced left mainstem bronchus)
* cardiomegaly (left ventricular dilatation)
* pulmonary congestion (enlargement of main pulmonary artery due to pulmonary hypertension)
* pulmonary vascular congestion or cephalization of pulmonary blood flow to upper lobes

ECG
* P mitrale: broad and bifid P wave (LA enlargement)
* AF
* LVH

Echocardiography: LV size and function, LA size and pulmonary arter pressure
TEE or cardiac MRI indicated when transthoracic echocardiography not sufficiently informative

Cardiac catheterization: indicated in primary degenerative MR if there is discrepancy between symptoms and severity of MR

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75
Q

What is the medical and surgical treatment of acute mitral regurgitation?

A
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76
Q

What is the medical and surgical treatment of chronic mitral regurgitation?
Indications for surgical treatment

A
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77
Q

What is the medical and surgical treatment of chronic secondary (functional) mitral regurgitation?

A
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78
Q

What is the most common cause of LV outflow obstruction in children and adults?

A

Aortic stenosis?

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79
Q

how to classify the severity of aortic stenosis?

A
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80
Q

What are primary causes of aortic stenosis?

A
  • Rheumatic heart disease
  • Congenital abnormal aortic valve
  • Degenerative calcification
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81
Q

Natural history of aortic stenosis
Signs and symptoms

A

Symptoms rarely occur until stenosis is severe: transvalvular velocity >4m/s, mean gradient >40mmHg, valve area <1cm

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82
Q

What is PE for aortic stenosis?

A

Palpation
* Carotid and peripheral pulse: small volume and slow rising
* Apex beat: heaving apex due to pressure overload in LVH
* Systolic thrill at aortic area

Auscultation
* Presence of S4
* Soft, single or reversed spliting S2
* Ejection systolic murmur
Early peaking murmur is mild to moderate AS, late peaking murmur is severe AS. Maximal over aortic area at right upper sternal border (RUSB), radiates to both sides of carotid artery

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83
Q

What are the 5 common signs of severe AS?

A
  • Slow rising carotid pulse
  • Reduced intensity of S2
  • Single or reversed splitting of S2
  • Presence of S4
  • Late peaking intensity of the murmur
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84
Q

What Ix for aortic stenosis and findings?

A

CXR:
* Cardiomegaly
* Pulmonary edema
* Calcification of aortic valve leaflets and aortic root
* Rounding of the LV apex indicated LVH
* Dilation of ascending aorta: post stenotic dilatation, tissue abnormalities associated with bicuspid aortic valve

ECG
* Primary findings in AS is the presence of LVH
* Assess for LA enlargement (LAE), LBBB and AF

Echocardiogram
* Valvular anatomy and structure, maximal aortic jet velocity, mean transvalvular pressure gradient, aortic valve area, left ventricular ejection (LVEF), left ventricular ize

Cardiac catheterization: indicated in patients with suspected AS but discrepency between clinical evaluation and echocardiography

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85
Q

What is surgical treatment for aortic stenosis?

A
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86
Q

What are the complications of aortic stenosis?

A
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87
Q

What are the different types of aortic regurgitation?

A

Acute aortic regurgitation
* Rapid cardiac decompensation and death can occur if left untreated: inability of LV to quickly fdilate and adapt to rapid increase in LV end diastolic pressure caused by regurgitant blood. This leads to cardiogenic shock.
* Acute pathologic regurgitation of blood from aorta to LV during disatole due to >1: malcoaptation of aortic leaflets due to abnormality of aortic leaflets (infective endocarditis or dilated left ventricle). Abnormality of aortic annulus/aortic root supporting strictures (e.g. aortic dissection)

Chronic aortic regurgitation

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88
Q

What are the causes of acute and chronic AR?

A
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89
Q

What is the physiology of wide pulse pressure in aortic regurgitation?

A
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90
Q

What are the SS of acute vs chronic AR?

A
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91
Q

What is the PE and findings of aortic regurgitation?

A

General exam: BP (wide pulse pressure due to increased SV)
Palpation
Pulse: prominent carotid pulsation (Corrigans sign), collapsing pulse, pulsus bisferiens. Displaced and thrusting apex beat. Diastolic thrill on left lower sternal border

Auscultation
* Soft S1 due to early closure of mitral valve
* Soft A2
* Loud P2 due to pulmonary hypertension
* Presence of S3
* Early diastolic murmur
* Austin flint murmur (mid to late diastolic rumble heard at apex which mimics MS): AR jet interfering with mitral inflow

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92
Q

What Ix for aortic regurgitation and how to assess the severity

A
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93
Q

What is treatment for acute and chronic AR?

A
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94
Q

What is cause of primary and functional tricuspid regurgitation?

A
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95
Q

What SS for TR?
What is the PE for tricuspid regurgitation?

A

SS related to RHF: dilated neckveins (elevated JVP), painful hepatosplenomegaly (pulsatile liver), pleural effusion, ascites, sacral edema, bilateral ankle pitting edema

PE
General exam: pulsatile liver, pleural effusion, ascites, sacral edema, bilateral ankle pitting edema
Inspection: elevated JVP (giant v wave due to systolic regurgitation into RA), jugular vein is very pulsatile, jugular venous distension more prominent with inspiration (Kussmauls sign)

Palpation: pulse (AF), left parasternal heave (RV heave)
Auscultation: presence of S3, pansystolic murmur (maximal over left lower sternal border (LLSB), louder on inspiration, softer on expiration

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96
Q

What Ix and findings for tricuspid regurgitation?

A

CXR: pleural effusion, upward displacement of diaphragm due to ascites
ECG: right axis deviation, P pulmonale, RVH, RBBB
Echocardiography: tricuspid valve motion, dilation of RA and RV, RV function

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97
Q

What is medical and surgical treatment for TR?

A
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98
Q

Define syncope
Define presyncope

A

Syncope = sudden transient loss of consiousness specifically caused by global cerebral hypoperfusion must often due to abrupt disease in systemic BP and
* Spontaneously self limited condition with recovery
* Inadequate cerebral blood flow is tupically of brief duration of 8-10s, loss of postural tone and subsequent gravitationally neutral position generally restores cerebral blood flow

Presyncope = prodrome of light headedness without TLOC

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99
Q

What is ddx of non syncopal cause of TLOC (not true syncope)?

A

 Neurological causes
* Seizure/ Epilepsy
* Traumatic brain injury
 Endocrine disturbances
* Hypoglycemia
* Hypoxia
* Hypocapnia
 Psychiatric causes
* Panic disorders
* Hysteria
 Intoxication
 Anaphylaxis

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100
Q

What are the causes of syncope (cardiac, orthostatic, neurocardiogenic, neurological)?

A
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101
Q

What is the pathophysiology of syncope?

A
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102
Q

What are the SS of syncope?
What witness signs?

A
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103
Q

What is the history taking for syncope?

A

HPI
Number, frequency and duration of episodes. Multiple episodes occuring over a short period of time suggests serious underlying disorder such as intermittent high grade heart block or paroxysmal VT
Onset of syncope: extended symptoms with classic prodrome associated with vasovagal form of reflex syncope.
Duration of syncoep: TLOC is compatible with syncope. Prolonged loss of consiousness may indicate a seizure or conversion reaction
Prodromal symptoms: light headedness/ feeling of warm or cold/ pallor/palpitation/ sweating/nausea
Position before incident (supine, sitting, standing): reflex syncope commonly occurs when patient is upright and almost never supine. Syncope resulting from orthostatic hypotension occurs when change from supine to erect posture but severeal minutes may pass between arising and the collapse
Activity before the incident (trigger factors)
* Situational syncope: coughing, sneezing, defacation, swallowing, urination, post prandial
* Vasovagal syncope: emotional stress, fear or intense pain
* Carotid sinus hypersensitivity: immediately after abrupt neck movements/head turning/shaving
* Cardiac syncope: during excercise
* Orthostatic hypotension: standing up, prolonged stanging

Medical history
DM: orthostatic hypotension secondary to autonomic neuropathy or apparent syncope due to hypoglycemia
Hypertension: orthostatic hypotension secondary to antihypertensives
Structural heart disease: CAD, VHD, congenital heart disease, cardiomyopathy
Neurological disease: seizure disorder/epilepsy, migraine headaches, parkinsons disease, stroke
Intoxication: alcoholism, illicit drug use

Surgical history: previous cardiac surgery

Drug history
* Diuretics
* Nitrates (hydralazine/nitroglycerin)
* Alpha blockers (terazosin)
* B blockers (propranolol)
* CCB
* PDE inhibiotrs (sildenafil)
* Antidepressants (SSRIs/ TCAs/MAOI)
* Antipsychotics
* Antiarrhythmics (Class 3): torsade de pointes

Family history
* Sudden death at a young age <40: brugada syndrome, congenital or acquired long QT syndrome (LQTS)
* Familial cardiomyopathy: HOCM, arrhythmogenic right ventricular cardiomyopathy
* Seizure disorders
* Migraine headaches

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104
Q

What is done for PE of syncope?

A
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105
Q

What is the treatment for syncope?

A
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106
Q

What are the leading causes of sudden cardiac death in young athletes?

A

 Hypertrophic obstructive cardiomyopathy (HOCM)
 Arrhythmogenic right ventricular dysplasia (ARVD)
 Congenital anomalies of coronary arteries
 Atherosclerotic coronary heart disease (probably homozygous familial hyperlipidemia)

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107
Q

What is the cut off for hypertenson?

A
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108
Q

What is white coat hypertension?
Ambulatory and BP monitoring of hypertension

A
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109
Q

What is the clinical presentation of malignant hypertension?

A
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110
Q

What is emergency hypertension and management?

A
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111
Q

What is the cause of primary (essential) hypertension?

A
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112
Q

What are the causes of secondary hypertension?

A
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113
Q

What are the SS of hypertension
What target organ damage

A
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114
Q

How to make a dx of hypertension?

A
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115
Q

What history taking for hypertension
What PE done?

A
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116
Q

What biochemical tests for hypertension?

A
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117
Q

What non basic Ix for hypertension to rule out secondary causes?

A
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118
Q

What is BP goal depending on age
What non pharmacological treatment?

A
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119
Q

What are the adrenoreceptors and their function?

A
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120
Q

What are ACEI and ARB options for hypertension?
What is their mechanism and adverse effects?

A
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121
Q

What are BB and CCB options for hypertension?
What is their mechanism and adverse effects?

A
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122
Q

What are diuretics (loop, thiazide diuretics, K+ sparing) options for hypertension?
What is their mechanism and adverse effects?

A
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123
Q

What is the treatment combination for hypertension?

A
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124
Q

What are the contraindications to specific drugs used to treat hypertension?

A
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125
Q

How to treat hypertensive crisis?

A
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126
Q

What is the treatment of hypertension in pregnancy?

A
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127
Q

What are the complications of hypertension?

A
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128
Q
A
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129
Q

What are the histological findings of renal disease induced by hypertension?

A

 Nephrosclerosis
* Macroscopic
o Kidneys are shrunken and scarred
* Microscopic
o Obsolescence of glomeruli
o Interstitial fibrosis
o Arterial intimal fibroplasia
o Hyalinization in small arteries

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130
Q

What is the treatment of malignant hypertension?

A
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131
Q

When should you refer to a specialist with hypertensive patient?

A

 Young hypertensive patients (< 40 years old)
 Patients with secondary hypertension
 Patient with severe hypertension that is difficult to control

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132
Q

What are the different methods of investigation for hyperlipidemia?

A
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133
Q

What are major risk factors that modify LDL cholesterol goal?

A
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134
Q

What are the types of hyperlipidemia?

A
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135
Q

What are types of primary hyperlipidemia?

A
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136
Q

What are the causes of secondary hyperlipidemia?

A
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137
Q

What are the genetics of familial hypercholesterolemia
Clinical manifestation
dx
treatment?

A
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138
Q

What are the mechanism of statins, clinical use, AE and eg
Same for fibrates

A
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139
Q

What are the mechanism of resin, clinical use, AE and example
Same for niacin and cholesterol absorption inhibitors

A
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140
Q

Summary of action of lipid lowering agents in hyperlipidemia?

A
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141
Q

What combination therapy given for hyperlipidemia?

A

 Highly synergistic combinations
* Statins + Resins
* Stains + Cholesterol absorption inhibitors

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142
Q

Familial hypercholesterolemia
What other treatment apart from medical treatment would you give?

A

Plasmapharesis

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143
Q

What differential diagnosis do you have?

A

 Endocrine disease
* Hypothyroidism
o ↓ LDL cell surface receptor and activity and hence decreased catabolism of LDL-C
o TH has permissive effect on stimulating LDL receptor activity
 Liver disease
* Cholestatic disease
 Renal disease
* Nephrotic syndrome
o Hypoalbuminemia triggers increased synthesis of lipoproteins in liver
o Abnormal transport of circulating lipid particles
o Impairment of peripheral breakdown of lipoproteins
o Leads to hyperlipidemia and lipiduria

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144
Q
A

 Gastroenteritis
 Pancreatitis
 Appendicitis
 Cholecystitis
 Diabetic ketoacidosis (DKA)

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145
Q

Explain why serum amylase is normal.
What can contribute to hypertriglyceridemia?

A

 Elevation in serum amylase to 3x ULN may NOT be seen in
* 20% of patients with alcoholic pancreatitis due to inability of parenchyma to produce amylase
* 50% of patients with hypertriglyceridemia-associated pancreatitis since TG interfere with amylase assay

 Renal disorders
* Nephrotic syndrome
* Renal failure
 Endocrine disorders
* DM
* Hypothyroidism
* Hypercortisolism
* Estrogen excess
* Glycogen storage disease
 Others
* Alcoholism

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146
Q

Compare stable and unstable angina by causes, chest pain and relieving factors?

A
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147
Q

What are the causes of coronary artery disease?

A
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148
Q

What is the clinical manifestation of stable angina?

A
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149
Q

What PE and results of coronary artery disease?

A
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150
Q

What non invasive invasive and invasive assessment of CAD?

A

Stress testing
indications: d of stable ischemic heart disease, risk stratification after acute coronary syndrome, evaluate excercise tolerance, localization of ischemia

Excercise tolerance test (with ECG and imaging)
Pharmacological stress test (with imaging only)

Imaging
SPECT
Echocardiography
Cardiac MRI: viability assessment for patients with significant coronary artery narrowing: assess for viable myocardium in the territory affected which helps to determine if PCI or CABG will lead to an improvement in cardiac function
MDCT (multidetector row CT) for coronary artery calcium score: recommended in asymptomatic patients with framingham intermediate risk for screening of CAD. Estimates the plaque burden but not % of coronary stenosis.
CAC sc

Coronary CT/MR angiography: anatomical assessment of coronary arteries and myocardium. Detects coronary artery stenosis and estimate % stenosis before applying invasive coronary angiography.
Indicated in patients with intermedate pre test probability of CAD who are unable to perform or have equivocal result from excercise test, stress echocardiography or nuclear stress test

Invasive coronary angiography (gold standard) indications
* High risk patients after non invasive testing
* Non invasive testing is contraindicated or inconclusive
* Survivors of sudden cardiac arrest of life threatening arrhythmia
* Unacceptable ischemia on guideline directed medical therapy and candidacy for revascularization

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151
Q

What is done for excercise tolerance test (high risk test results that require coronary angiography) and pharmacological stress test (drugs used)?

A
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152
Q

What is medical treatment principle of coronary artery disease?

A
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153
Q

What is the coronary revascularization treatment in stable CAD?
What are the best conduits used?

A
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154
Q

What are the indications for coronary revascularization in stable CAD?

A
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155
Q

What are poor prognostic factors for CAD (coronary artery disease)?

A
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156
Q

Compare stable angina –> unstable angina –> acute MI in pain and triggers

A
157
Q

What is the classification of acute coronary syndrome?

A
158
Q

What is the classification for types of MI?

A
159
Q

What is the precipitating factors of MI?

A
160
Q

What is the clinical timeline for MI?

A
161
Q

What are the different arteries of the heart from RCA, supplies what part of heart, areas of infarct corresponding to RCA occlusion?

A
162
Q

What are the different arteries of the heart from LCA, supplies what part of heart, areas of infarct corresponding to LCA occlusion?

A
163
Q

What are SS of MI
What are incompatible description of chest pain that are not characteristic of MI?

A
164
Q

What is the ddx for MI?

A
165
Q

What is the diagnostic criteria for MI?

A
166
Q

What are the roles of biochemical markers of ACS?

A
167
Q

What is ddx of elevated cTn?

A
  • Coronary artery spasm
  • Myocarditis/ Pericarditis
  • Pulmonary embolism
  • Chronic kidney disease (CKD)
  • Subarachnoid hemorrhage (SAH)
168
Q

What is the timing of release of various biomarkers after acute ischemic MI?

A
169
Q

In ECG what leads to look for ECG changes according to artery occluded?

A
170
Q

What ECG changes will occur in MI?

A
171
Q

What antiplatelet therapy used in MI?

A
172
Q

What anticoag therapy for acute MI?
AE

A
173
Q

What is the antiischemic therapy in acute MI?

A
174
Q

Apart from antiplatelets, anticoags and antiischemic agents what other medication given for acute MI?

A
175
Q

What are the indications and contraindications/relative contraindications for coronary revascularization (fibrinolytic therapy) in AMI

A
176
Q

What are the indications for coronary revascularization (percutaneous intervention (PCI)) in AMI

A
177
Q

What are the complications of PCI for MI?

A
178
Q

What are the signs of reperfusion post AMI treatment?

A
179
Q

What is summary of medical treatment for UA/NSTEMI?

A
180
Q

What is the antithrombotic therapy in UA/STEMI?

A
181
Q

What is antiischemic therapy and other therapy in UA/STEMI in AMI

A
182
Q

What are the risk stratification scores for coronary revascularization in AMI?

A
183
Q

What are the factors associated with approrpriate selection of early invasive strategy or ischemia guided strategy in patients with NSTE-ACS?

A
184
Q

What is the treatment for STEMI?

A
185
Q

What is the general management of STEMI?

A
186
Q

What is the antithrombotic therapy in STEMI?

A
187
Q

What is the antiischemic therapy, fibrinolytics and PCI/CABG therapy for STEMI?

A
188
Q

What is long term post MI management?

A
189
Q

What are the structural, conduction and circulatory complications of AMI?

A
190
Q

What are other complications apart from structural, conductin and circulatory complications for AMI?

A
191
Q

What are infectious and non infectious causes of myocarditis?

A
192
Q

What is the SS for myocarditis?

A
193
Q

What are the basic Ix done for suspected myocarditis?

A
194
Q

What imaging ix done for myocarditis?

A
195
Q

What is the treatment principle for myocarditis?

A
196
Q

What is the pericardium made up of?

A
  • Fibrous pericardium = Outer sac
  • Parietal pericardium = Serous layer lining fibrous pericardium
  • Visceral pericardium (Epicardium) = Serous layer lining heart and proximal great vessels
  • Pericardial cavity = Contains 15 – 50 mL of ultrafiltrate between visceral and parietal pericardium
197
Q

What are the causes of pericarditis?

A
198
Q

What are the SS of pericarditis?

A
199
Q

What Ix done for pericardiocentesis and why?

A
  • CBC with DC: leukocytosis or lymphocytosis sugests bacterial infection or haematological malignancy
  • Serum inflammatory markers: ESR and CRP
  • cTn and CK-MB: indicates inflammatory damage of subepicardial myocardium close to the pericardium (myopericarditis) or myocarditis with pericardial involvement
  • Serum autoimmune markers: ANA
  • Tuberculine skin test/IFNgamma release assay (QuantiFERON TB)
  • Routine viral serology is not recommended except HIV serology since the yield is low and management is not altered
  • Pericardiocentesis and pericardial biopsy: indicated in patients with pericardial effusion. Fluid samples should be sent for gram stain, bacterial culture, AFB smear, culture and PCR as well as cytology.
    Pericardial biopsy indicated in patients with recurrent pericardial effusion and cardiac tamponade after prior pericardiocentesis or patients with illness lasting >2 weeks despite treatment without definitive dx

Imaging
* CXR: evaluate cardiac silhouette (uncommon but cardiac silhouette is enlarged if at least 200ml of pericardial fluid)
* Echocardiogram: normal in patients with pericarditis. Look for evidence of pericardial effusion and cardaic tamponade which is a gold stsandard for detecting and quantifying effusion. Absence of pericardial effusion does not exclude pericarditis

200
Q

What is treatment of pericarditis?

A

 Pericardiocentesis
* Indicated in patients with cardiac tamponade or large pericardial effusion not responsive
to medical treatment
 Pericardiectomy
* Surgical removal of all or part of pericardium is virtually never required for treatment of acute pericarditis
* May only be considered in patients with frequent and highly symptomatic recurrences of pericarditis resistant to medical treatment

201
Q

What is the RF for infective endocarditis?

A
202
Q

What is the micbio of infective endocarditis?

A
203
Q

What is the pathogenesis of infective endocarditis?

A
204
Q

What is the SS of infective endocarditis
symptoms of complications

A
205
Q

What is the diagnostic criteria for infective endocarditis?

A

Modified Dukes criteria

Pathological criteria
Pathological lesiosn: demonstration of active endocarditis on histology of a vegetation or intracardiac abscess
Microorganism: demonstrated by culture or histology of a vegetation or intracardiac abscesses

Clinical criteria
2 major clinical criteria or
1 major + 3 minor clinical criteria or
5 minor criteria

Possible dx of IE
1 major and 1 minor clinical criteria or
3 minor criteria

Rejected IE: firm alternative dx is made, clinical criteria for possible or definitive IE are not met. Resolution of clinical manifestation occurs after <4 days of antibiotic therapy. No pathological evidence fo IE found at surgery or autospy after <4 days of antibiotic therapy

206
Q

What is the history taking for infective endocarditis?

A
207
Q
A
208
Q

What is done for the general examination for infective endocarditis?

Obvious auscultation necessary for murmurs to indicate involvement of which valve

A
209
Q

What blood tests done for infective endocarditis?

A
210
Q

What is the imaging ix done for infective endocarditis?

A
211
Q

What is the medical treatment for infective endocarditis
What indications for surgical intervention?

A
212
Q

What are high risk patients that may need antibiotic prophylaxis to prevent infective endocarditis
And in under what circumstances?

A
213
Q

What are the complications of infective endocarditis?

A
214
Q

Q1: What investigations will you perform to establish the diagnosis?Q2: How do you treat his infective endocarditis?
Q3: What is the relationship of the febrile episode in childhood to this admission?
Q4: What is the cause of hematuria in infective endocarditis?

A

1.
 Persistent bacteremia as revealed by 3 positive blood cultures will establish the diagnosis
 CBC
* WBC and ESR increases in infection
 Echocardiography (Trans-esophageal)
* Establish status of cardiac disease
* Visualization of vegetation

  1.  Medications
    * IV penicillin at high-dose (3 Mega units) every 4 hours for 4 weeks
    * IV gentamicin 60 mg every 8 hours for 2 weeks
     Modify antibiotics according to culture and sensitivity results
     Monitor patient temperature, changing murmur and cardiac symptoms, urine, ESR, renal function

3.
 Febrile illness in childhood could represent an episode of rheumatic fever

4.
 Emboli
 Glomerulonephritis
 History of urinary catheterization

215
Q

What are the general features of group A streptococcus pharyngitis and acute rheumatic fever complications?

A
216
Q

What is the pathogenesis of acute rheumatic fever?

A
217
Q

What is the diagnostic criteria for acute rheumatic fever?

A
218
Q

What Ix done for acute rheumatic fever?

A
219
Q

What is the treatment principle and medical treatment for acute rheumatic fever?

A
220
Q

What is the primary and secondary prevention of acute rheumatic fever?

A
221
Q

What is the classification of tachycardia according to origin of depolarization?

A
222
Q

What is the classification of tachycardia according to QRS complex?

A
223
Q

What are the different ECG changes in different types of tachycardia?

A
224
Q

What is the diagnostic algorithm for narrow QRS tachycardia?

A
225
Q

What is the Brugada algorithm for wide complex tachycardia?

A
226
Q

What is LBBB vs RBBB pattern (V1 and V6)?

A
227
Q

What is the immediate management of tachycardia?

A

unstable patient: immediate synchronized DC cardioversion
Stable patient: differentiate (1), (2) and (3)

228
Q

What are the different classes of antiarrhythmics?
What are there indicated usages?

A
229
Q

What is the management of stable regular narrow complex tachycardia?

A
230
Q

What is the management of stable wide complex tachycardia?

A
231
Q

What is the vagal manouvre and ATP used in initial management of stable regular narrow coplex tachycardia?

A
232
Q

What is the management of AF and atrial flutter
Control of underlying cause
Control of ventricular rate
Termination of arrhythmia
Prevention of recurrence
Anticoag to prevetn stroke

A
233
Q

What is the management of the differen types of regular narrow complex tachycardia?

A
234
Q

What is the management of the different types of irregular narrow complex tachycardia?

A
235
Q

What is the management of the different types of wide complex tachycardia?

A
236
Q

What is hte classification of bradycardia?

A
237
Q

Compare description, ECG findings and casues for 1st, 2nd and 3rd degree heart block?

A
238
Q

Compare RBBB and LBBB in ECG presentation and cause?

A
239
Q

Compare left anterior fascicular block (left anterior hemiblock), bifascicular block, sick sinus syndrome in description and ECG presentation?

A
240
Q

What is management of bradycardia
Management of stable and unstable patients

A
241
Q

What is mx of VFib or pulseless ventricular tachycardia?

A
242
Q

What is the 6Hs and 6Ts of pulseless electrical activity?

A
243
Q

What is management of pulsless electrical activity?

A
244
Q

What are causes of asystole
What is management?

A
245
Q

A patient presented with irregularly irregular pulse. What are the 6 main differential diagnosis?

A

 Atrial fibrillation
 Atrial flutter with variable AV block
 Atrial tachycardia with variable AV block
 Multi-focal atrial tachycardia (MAT)
* Atrial rate > 100 bpm
* Absence of one dominant pacemaker
* P waves of at least 3 morphologies
 Multi-focal atrial rhythm (MAR)
* Atrial rate ≤ 100 bpm
* Absence of one dominant pacemaker
* P waves of at least 3 morphologies
 Very frequent ectopic beats

246
Q

What is the cause of Brugada syndrome?

A

Genetic mutations
* Autosomal dominance (AD) inheritance
* 12 genetic mutations identified most commonly in
o SCN5A gene encoding for cardiac Na+ channels 2+
o CACN1Ac gene encoding for α-subunit of cardiac Ca
channel

247
Q

What are provative factors of Brugada syndrome
What are SS?

A
248
Q

What are different ECG patterns for Brugada syndrome?

A
249
Q

What is the diagnostic criteria for Brugada syndrome?

A
250
Q

What is treatment for Brugada syndrome?

A
251
Q

What is long QT syndrome?
What are associated conditions

A
252
Q

What is the etiology of LQTS?

A
253
Q

What is the diagnostic criterai for LQTS?

A
254
Q

What Ix done for LQTS?

A
255
Q

What is treatment of congenital LQTS?
Acquired LQTS?

A
256
Q

What are the complications of lQTS?

A
257
Q

What are the types of hypertrophic cardiomyopathy?

A
258
Q

What is the general features of hypertrophic cardiomyopathy?

A
259
Q

What are the morphological variants of hypertrophic cardiomyopathy?

A

 Can be classified by portion of LV with hypertrophy
* Asymmetric hypertrophy without obstruction
* Asymmetric hypertrophy with obstruction
* Symmetric hypertrophy
* Septal hypertrophy
* Apical hypertrophy

260
Q

What are the genetic causes of hypetrophic cardiomyopathy?

A
261
Q

What is the ddx of hypertrophic cardiomyopathy?

A
262
Q

What is the pathophysio of hypertrophic cardiomyopathy?

A
263
Q

What is the histological findings of hypertrophic cardiomyopathy?

A
264
Q

What are the SS of hypertrophic cardiomyopathy?

A
265
Q

What is the PE of hypertrophic cardiomyopathy?

A
266
Q

What Ix should be done for hypertrophic cardiomyopathy?

A
  • ECG
  • Ambulatory ECG monitoring (Holter)
  • Echocardiogram
  • Excercise treadmill test (performed before initiation of therapy)
  • Cardiac MRI: indicated in patients with inconclusive echocardio findings
  • CT coronary angiography: detection of coexisting CAD
  • Cardiac catheterization: identification of coexisting CAD
    Others: genetic testing to identify genotypes for family screening
267
Q

What is the diagnostic for HCM?

A
  • 1 Major criteria in echocardiogram
  • 2 Minor criteria in echocardiogram
  • 1 Minor criteria in echocardiogram + 2 Minor ECG criteria
268
Q

What ECG in hypertrophic cardiomyopathy?

A
269
Q

What is major and minor criteria for echocardiogram of hypertrophic cardiomyopathy?

A
270
Q

What is the use of excercise treadmill testing for hypertrophic cardiomyopathy?
What are important clinical findings?

A
271
Q

What are medical, surgical and non pharmacological treatment of HCM?
What complications of HCM?

A
272
Q
A
273
Q

How do you determine severity of aortic stenosis clinically?

A

 History of syncope, angina and heart failure
 Physical examination shows systolic thrill, slow rising and small volume pulse, soft aortic component of S2
 Displaced apex beat
* Late event and associated with heart failure

274
Q

What are the causes of exercise-induced syncope in this HOCM patient who excercises?

A

 Dynamic outflow obstruction
 Exercise-induced atrial or ventricular arrhythmia
 Reflex vasodilation

275
Q

How do you investigate this patient?
What results would expect?

A
276
Q

How would treat this patient?

A
277
Q

What is dilated cardiomyopathy?

A

 MOST common type of cardiomyopathy
 Cardiomyopathy associated with ventricular dilatation and decreased contractility (LV systolic dysfunction) ± decreased wall thickness in the ABSENCE of myocardial disease caused by ischemic or infarct, valvular heart disease or hypertension

278
Q

What are the causes of dilated cardiomyopathy?

A
279
Q

What is PE and blood tests for for dilated cardiomyopathy?

A
280
Q

What non basic Ix done for dilated cardiomyopathy?

A
281
Q
A

 Cardiac catheterization
* Document pressure in chambers, cardiac function and presence of coronary artery disease
 Endomyocardial biopsy
 Thallium scan
* Elicit myocardial ischemia
 Thyroid function test
 Serum ferritin level (Cardiac hemochromatosis)
 Antibody titres (Acute myocarditis)
 Skeletal muscle biopsy (Primary muscle disease)
 HIV test
 Drug screen (Illicit drugs such as cocaine)

282
Q

What are the causes of heart failure?

A

 Hypertension
 Ischemic heart disease
 Valvular heart disease
 Cardiomyopathy
 Previous MI
 High output failure
* Thyrotoxicosis * Anemia

283
Q

How do you treat heart failure in this patient?

A
284
Q

What is the prognosis of dilated cardiomyopathy?

A
285
Q

Can virus cause dilated cardiomyopathy?

A

 Viruses, parasites, protozoan and fungi can all cause myocarditis
* Coxsackie B virus
* Hepatitis C virus
* HIV
 Pathogenesis
* Viral infection leads to infiltration of NK cells, macrophages and T lymphocytes in myocardium
* Leads to apoptosis, necrosis and fibrosis

286
Q

Is dilated cardiomyopathy hereditary?

A

 At least 1/4 of cases have a family history
 Screening the relatives may reveal LV enlargement that may progress into cardiomyopathy
 A number of genes are implicated
* Dystrophin gene

287
Q

What are the general features of restrictive cardiomyopathy?

A
288
Q

What are the secondary causes of restrictive cardiomyopathy?

A
289
Q

What is the pathophysio of restrictive cardiomyopathy?

A
290
Q

What is the SS of restrictive cardiomyopathy?

A
291
Q

What is the PE and Ix done for restrictive cardiomyopathy?

A
292
Q

What is treatment for restrictive cardiomyopathy?

A
293
Q

What are the general features of atrial septal defect?

A
294
Q

What is the embrology of formation of atrial septum?

A
295
Q

What is the classification of ASD?

A
296
Q

What is the perinatal physiology of atrial septum. Before birth and after birth?

A
297
Q

What is the physiology of ASD?
What are consequences?

A
298
Q

What is the pathophysio of pulmonary hypertension in ASD?

A
299
Q

What is PE findings in ASD: general exam and cardiovascular exam

A
300
Q

What are cardio exam PE findings in ASD?

A
301
Q

What are the Ix done for ASD and results?

A
302
Q

What is management of patients with ASD?

A
303
Q

What are the general features of ventricular septal defect?
What is occurence rate?

A
304
Q

What is the classification of congenital heart diseases (acyanotic and cyanotic)?

A
305
Q

What are the different types of VSD?

A
306
Q

What is the pathophysio before and after birth for VSD?

A
307
Q

What is the physiology of VSD?

A
308
Q

What is the natural history fo VSD?

A
309
Q

What is the pathophysio of pulmonary hypertension in VSD?

A
310
Q

What is PE findings for general and cardiovascular exam?

A
311
Q

What are the cardiovascular PE findings of VSD?

A
312
Q

What are the non blood tests and findi for VSD?

A
313
Q

What is the treatment of VSD?
What indications for surgery?

A
314
Q

What are the complications of VSD?

A
315
Q

What is atrioventricular septal defect?

A

 Comprises cardiac lesions that have deficient AV septation and AV valves (mitral valve and
tricuspid valve) and a common atrioventricular (AV) junction
 Also known as AV canal defect or endocardial cushion defect
 Caused by a disruption of the normal development of endocardial cushions

316
Q

What is the classification of atrioventricular septal defect?

A
317
Q

What are the associated conditions with ASVD?

A
318
Q

What is the haemodynamic consequence of AVSD?
What complications

A
319
Q

What PE and findings for ASVD?

A
320
Q

What are the signs of heart failure in AVSD for infanat?

A
  • Affected infants present with tachypnea, poor feeding, sweating, failure to thrive and pallor at around 1 – 2 months of age as pulmonary vascular resistance (PVR) falls
  • Chest infection are common manifestation due to microatelectasis caused by increased pulmonary blood flow and interstitial pulmonary edema
321
Q

What are Ix done for ASVD and the findings?

A
322
Q

What is treatment of AVSD?

A
323
Q

What is the general features of patent ductus arteriosus?

A
324
Q

What is the embyrology of patent ductus arteriosus?

A

 Ductus arteriosus (DA) derives from embryonic left 6th aortic arch
* Aortic end arises distal to left subclavian artery
* Pulmonary end insets at the junction of main and left pulmonary arteries

325
Q

What is the pathophysio of patent ductus arteriosus before and after birth?

A
326
Q

What is the physiology of PDA?

A
327
Q

What is pathiophysio of pulmonary hypertension in patent ductus arteriosus?

A
328
Q

What is general exam for PDA?

A
329
Q

What is cardiovascular PE findings for PDA?

A
330
Q

What is Ix and findings for PDA?

A
331
Q

What is the treatment for PDA?

A
332
Q

What are the complicatiaons of PDA?

A
333
Q

What is the general features of coarctation of aorta?

A
334
Q

What associated syndrom with PDA?

A
  • Turner’s syndrome (loss of an X chromosome) (5 – 15% in females)
    o Neonates may have congenital lymphedema of hands and feet, webbed neck and a low hairline
    o Women may have broad, shield-shaped chest with widely spaced nipple
335
Q

What is the pathogenesis of coarctation of aorta?

A
336
Q

What is the before and after birth perinatal physiology of coarctation of aorta?

A
337
Q

What is the general exam for coarctation of aorta?

A
338
Q

What is the cardiovascular exam and results of coarctation of aorta?

A
339
Q

What Ix for coarctation of aorta and results?

A
340
Q

What is the treatment of coarctation of aorta?

A
341
Q

What is general features of tetralogy of fallot?

A
342
Q

What are the associated cardiac features with tetralogy of Fallot?

A
  • Right aortic arch (20 – 25%)
  • LAD arising from RCA (9%)
    o Critical to identify prior to complete repair since the course of the artery may run directly across the RV outflow tract and inadvertent transection will leads to catastrophic consequences
  • Aorticopulmonary collateral vessels
  • Patent ductus arteriosus (PDA)
  • Aortic regurgitation
343
Q

What are the syndromal conditions assocaited with TOF?

A
344
Q

What is the physiology of TOF?

A
345
Q

What is the SS of TOF?
What is the PE findings?

A
346
Q

What Ix done and results for tetralogy of fallot?

A
347
Q

What is treatment of tetralogy of Fallot?

A
348
Q

What are the general features of transposition of great vesels
What associated conditions

A
349
Q

What is the physiology of D-transposition of great vessels?

A
350
Q

What is the physiology of L-transposition of great vessels?

A
351
Q

What is the in utero circulation of D-TGA?

A
  • O2-rich blood from umbilical vein is largely directed from RA across fossa ovalis into LA and into LV where it is pumped into pulmonary artery and across ductus arteriosus (DA)
    into systemic circulation
  • Vascular resistance provided by placenta is lower than pulmonary capillary bed which allows for right-to-left blood flow through DA and into descending aorta
352
Q

What is the clinical course, PE and results of transposition of great vessels?

A
353
Q

Whst are the Ix done for transposition of great vesels?

A
354
Q

What is treatment of transposition of great vessels?

A
355
Q

What are the different kinds of cyanosis?

A
356
Q

How to categorize cyanotic heart disease (decreased pulmonary blood flow, increased pulmonary blood flow, severe heart failure)

A
357
Q

How to manage ductal dependent congenital heart diseases?

A
358
Q

What are the different types of duct dependent circulation?

A
359
Q

What is the physiology before and after birth in ductus arteriosus?

A
360
Q

What are the cardiac causes of cyanosis?

A
361
Q

What are the cyanotic cogenital heart disease causes of decreased pulmonary blood flow?

A
362
Q

What are the cyanotic cogenital heart disease causes of increased pulmonary blood flow?

A
363
Q

Describe the congenital cyanotic heart disease causes that increased pulmonary blood flow and their physiology and management?
Transposition of great vessels, truncus arteriosus, total anomalous pulmonary venous return (TAPVC)

A
364
Q

What are the cyanotic cogenital heart disease that cause heart failure
Their general features and physiology?

A
365
Q

What are the ddx of cyanosis in newborn?

A
366
Q

What is general feature of aortic dissection?

A

 Aortic dissection is defined as separation of layers of aortic wall by intimal injury
* Allows blood to travel between intima and media resulting in creation of two flow channels known as the true lumen and false lumen
 Ascending aorta dissections are 2x more common than descending aorta
* Right lateral wall of ascending aorta is the most common site of aortic dissection

367
Q

What is the anatomical classification of aortic dissection?

A
368
Q

What are the acute aortic syndromes?

A
369
Q

What is the RF of aortic dissection?

A

 HT (most important)
 Collagen disorders
* Marfan syndrome
* Ehlers-Danlos syndrome
 Aortic aneurysm
 Bicuspid aortic valve
 Family history of aortic dissection

370
Q

What is the physiology of aortic dissection?

A

 Tear in aortic intima layer and blood passes into aortic media
 Creates a false lumen as it separates intima from surrounding media and adventitia
 False lumen dilation and true lumen collapse immediately following dissection
* False lumen dilation depends on BP, size of entry tear, depth of dissection plane within media and percentage of aortic circumference involved
* True lumen collapses due to pressure differential between true and false lumen and can be exacerbated by intrinsic recoil of muscular elements within dissection flap
 Leads to an increase in aortic cross-sectional area

371
Q

What is SS and PE for aortic dissection?

A
372
Q

What is the ddx of aortic dissection?

A

 Pneumothorax
 Pulmonary embolism
 Pericarditis
 Acute pancreatitis
 Acute myocardial infarction (AMI)

373
Q

What are the Ix done for aortic dissection?

A

Blood tests: cTnT, cTnI, CK-MB
CXR: irregualr or way aortic outline, swidening of aortic silhouette, widening of mediasitnum (erect PA=6cm and supine AP=8cm)
ECG: differentiate aortic dssection from AMI
Echo: aortic regurgitation, pericardial effusion of dissection flap

374
Q

What is treatment of aortic dissection?

A
375
Q

What is complication of aortic dissection?

A
376
Q

How is DVT of lower extremity subdivided into 2 categories?

A
  • Proximal vein thrombosis
    o Thrombi involves popliteal, femoral or iliac veins
    o Clinically more significant as it more commonly associates with PE
  • Distal (Calf) vein thrombosis
    o Thrombi involves deep calf veins
377
Q

What is the risk factors for thrombosis?

A
378
Q

What is the non thrombotic etiology of PE?

A
  • Tumor embolism
  • Air embolism
  • Fat embolism
    o Following pelvic or long bone fracture
379
Q

What is virchows triad?

A

 Stasis + Endothelial injury + Hypercoagulability
* Stasis = Prolonged bed rest/ Air travel > 6 hours/ Congestive heart failure (CHF)/ Cerebrovascular accident within 3 months
* Endothelial injury = Surgery/ Trauma/ Prior DVT/ Central catheter placement
* Hypercoagulability = See risk factors above

380
Q

What is SS of DVT/PE?

A
381
Q

What is the ddx of DVT?

A
  • Muscle strain/ tear/ twisting/ injury to leg
  • Cellulitis
  • Superficial thrombophlebitis
  • Lymphangitis
  • Lymphedema
  • Venous valvular insufficiency
  • Ruptured Baker’s cyst
382
Q

What is the diagnostic criteria for PE?

A

Wells score

383
Q

What PE and Ix done for PE?

A

PE
Vital signs: sinus tachycardia, hypotension, fever
Resp exam: tachypnea, cyanosis, pleural frictions rub, crepitations
CVS exam: elevated JVP, right sided S3, graham steell (PR) murmur

384
Q

What non blood tests done for PE?

A

ECG: sinus tachycardia, S1 (right axis deviation or deep S wave in lead I), Q3 (Q wave in lead III), T3: inverted T wave in leadIII. Evidence of right heart strain: R axis deviation, T inversion in V1-4, incomplete or complete RBBB
CXR: Hamptoms hump (hump shaped opacity or density in the periphery of lung with its base abutting the pleura), westermark sign (avascularity distsal to the PE: distal hypoperfusion in a segmental distribution within the lung), pleural effuson, atelactasis (collapse of segment which is infarcted due to embolism)
Venous duplex USG: duplex =B mode USG +doppler technique. Lower extremity compression USG to look for evidence of DVT
CT pulmonary angiogram:confirmatory test that is diagnostic
Ventilationperfusion scan: hihg sensitivity but low specificyt
Echocardiogram (transthoracic/transsophageal): identify saddle, right or left main PE. Mcconnels sign: hypokinesis of RV free wall

385
Q

What is treatment approach to PE and DVT?

A
386
Q

What are alternatives to heparin/add on for treatment of PE?

A
387
Q

What is surgical treatment of PE?

A
388
Q

What is 1st line management of PE?

A

MBBS VI - Medicine Final Summary (20 decks)

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