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Internal Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What does meant by low Pretest probability of CAD?

A

Low (<10%)

Asymptomatic people of all ages
Atypical chest pain in women age <50

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2
Q

What does meant by Intermediate Pretest probability of CAD?

A

Intermediate
(20%-80%)

Atypical angina in men of all ages

Atypical Angina in women age >50

Typical angina in women age 30-50

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3
Q

What does meant by high Pretest probability of CAD?

A

High
(>90%)

Typical angina in men age >40
Typical angina in women age >60

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4
Q

Important point of Aspirin

A

Aspirin is given before heparin in ACA as it reduces the rate of MI, stroke and overall mortality in ACS

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5
Q

How to approach chest Pain In Emergency dept?

A

Take history & do Examination

Check stability—> if unstable then stabilise hemodynamics and find the cause

If stable then do ECG/CXR

If ECG consistent with ACS then give anticoagulants if NSTEMI /// if STEMI then t/m with ER CATH & thrombolysis

If ECG normal—> do CXR—> if diagnostic then t/m the cause Or if non-dx then check underlying other cause of chest pain / check cardiac markers

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6
Q

What medication to hold prior to cardiac stress testing?

A

BB / CCB / Nitrates = hold for 48 hours

Dipyridamole = Hold for 48 hours prior to vasodilator stress test

Caffeine containing food Or Drinks = hold for 12 hours prior to vasodilator stress test

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7
Q

What medication can be continued before doing cardiac stress testing?

A

AIDS

A = ARBs/ACEI
ID = Digoxin / diuretics 
S = statins
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8
Q

How chest wall/ musculoskeletal chest pain presents?

A

Persistent and prolong pain with palpation

Worse with movement Or change in position

Often follows repetitive activity

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9
Q

How pulmonary/pleuritic (pleurisy, pneumonia, pericarditis, PE) chest pain present?

A

Sharp/stabbing pain

Worse with inspiration

Pericarditis:: Worse when lying flat

PE / Pneuomthorax:: Respiratory distress / hypoxia

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10
Q

How GIT/Esophageal chest pain present?

A

Non exertional prolong chest pain lasting>1 hour

Nocturnal pain

Postprandial symptoms

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11
Q

What is the first line agent for stable chronic angina?

A

Beta blocker

But CCB can be combine with BB of angina persist Or as alternate therapy

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12
Q

When to used short acting form and long acting form of nitrates in stable chronic angina?

A

Short acting form is used in the acute setting

Long acting form is an add on therapy for persistent angina

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13
Q

How variant angina different from ACS on the basis of ECG?

A

In variant angina, Transient ST elevation and then return to baseline

Whereas ST depression in unstable angina and longer duration of ST elevation in MI.

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14
Q

Which vessels and what are the ECG findings of Right ventricle MI?

A

RCA

ST elevation in leads V4-V6R

***Right ventricle MI occurs in 50% of inferior MI

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15
Q

Important point of Inferior wall MI

A

Transient bradycardia Or AC block occurs due to enhanced cabal time so give IV fluid unless pulmonary congestion

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16
Q

Important point of RVMI

A

RV MI (Heat failure) leads to decrease preload and resultant hypotension

So avoid all those medications which decreases preload viz nitroglycerin / Diuretics / Opioids)

Also be cautious when using BB and CCB

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17
Q

Which artery and what are the findings of Posterior MI?

A

LCX or RCA

ST depression in leads V1-V3

ST elevation in leads I & aVL (LCX)

ST depression in leads I & aVL (RCA)

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18
Q

Which artery and what are the ECG findings of lateral wall MI?

A

LCX diagonal

ST elevation in leads I, aVL, V5 & V6

ST depression in leads II, III & aVF

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19
Q

Important point

A

Occlusion of LAD can cause 2nd degrees AV block as it perfumed anterior 2/3rd of septum

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20
Q

What is the MC arrhythmia will be seen in setting of acute MI?

A

Ventricular fibrillation

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21
Q

What is the mechanism of arrhythmias within 10 mins of coronary occlusion?

A

Arrhythmia occurring within 10 mins of coronary occlusion—immediate or phase 1a ventricular arrhythmia

MOA:: reentrant arrhythmia

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22
Q

What is the mechanism of arrhythmias within 10-60 mins after acute infarction?

A

Arrhythmia occurring within 10-60 min after acute infarction—delayed or phase 1b arrhythmia—

MOA: abnormal automaticity

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23
Q

How ventricular aneurysm different from MI on ECG?

A

Ventricular aneurysm has persistent ST elevation after recent MI and deep Q waves in same leads

Whereas ST elevation resolve within a few weeks of an MI

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24
Q

What are CXR and Echo findings of ventricular aneurysm?

A

CXR = Prominence Or Bulge among left heart border

ECHO = showing dyskinetic wall motion of a portion of left ventricle

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25
Q

How to t/m dressler syndrome?

A

NSAIDs is mainstay of therapy

Steroids can be used in refractory cases Or when NSAIDs are contraindicated

Avoid to use anticoagulant to prevent development of hemorrhagic pericardial effusion

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26
Q

How to avoid coronary stent thrombosis?

A

Give long term dual anti-platelet therapy with aspirin and platelet P2Y12 receptor blocker

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27
Q

What is the most important intervention to improve long term prognosis of MI esp STEMI?

A

PCI

or Fibrinolytic therapy

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28
Q

Name the discharge medication of MI

A
  • Dual anti-platelet therapy
  • BB
  • ACEI or ARB
  • STATINS
  • Aldosterone antagonist if EF <40% with HF symptoms Or DM
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29
Q

Important point

A

ACEi should be started in all pts with MI within 24 hours to prevent remodeling of heart

i.e. dilation of left ventricle with thinning of ventricular wall which takes wks to months

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30
Q

What are the causes of heart failure with preserved left ventricular function?

A
  • Diastolic heart failure (HOCM / Restrictive cardiomyopathy / HTN / Occult CAD)
  • Valvular Heart disease (AR AS / MR MS)
  • Pericardial disease (Constrictive pericarditis / Cardiac tamponade)
  • High Output cardiac conditions ( Thyrotoxicosis / Severe anaemia / Wet beri / Paget’s disease/ AV Fistula)
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31
Q

How to t/m acute decompensated HF with normal Or Elevated BP with adequate end organ damage?

A

Supplemental O2

IV loop diuretics

Consider IV vasodilator Viz nitroglycerin

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32
Q

How to t/m acute decompensated HF with hypotension Or signs of shock?

A

Supplemental O2

IV loop diuretics

IV vasodilator Viz nitroglycerin

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33
Q

What are the laboratory findings suggest poor prognostic factors in systolic HF?

A

Low Serum Sodium

Elevated Pro-BNP level

Renal insufficiency

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34
Q

What are the clinical findings suggest poor prognostic factors in systolic HF?

A

Resting tachycardia with higher NYHA functional class

Elevated JVP with presence of S3 gallop

Low BP and maximal O2 consumption

Moderate to severe MR

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35
Q

What are the ECG and ECHO finding suggests poor prognostic factors in systolic HF?

A

ECG:::
LBBB and QRS>120msec

ECHO:::
Severe LV dysfunction
Concomitant diastolic dysfunction

Reduced Right ventricular function
Pulmonary HTN

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36
Q

What is the initial therapy in hyponatremia in CHF patient?

A

Restrict water intake

ACEi

and loop diuretics

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37
Q

What are the features of Cocaine Induced STEMI?

A

Chest pain due to coronary vasoconstriction

Increase Sympathetic activity Viz pupil dilation /HTN / tachycardia

Blood crusted nose

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38
Q

What are medication not to used in Cocaine Induced STEMI?

A

Beta blockers

Fibrinolytics due to increased risk of intracranial hemorrhage

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39
Q

Where the sound of murmur localized if Aortic regurgitation occurs due to valvular disease?

A

murmur heard along left sternal border (3rd and 4th Intercostal space)

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40
Q

Where the sound of murmur localized if Aortic regurgitation occurs due to aortic root dilation?

A

murmur best heard at right sternal border

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41
Q

Important point

A

If new AV block is present in case of IV drug user alongwith AR murmur, suspect perivalvular abscess extending into adjacent cardiac conduction pathway (conduction defects not common in tricuspid endocarditis)

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42
Q

What are the causes of Dilated Cardiomyopathy?

A

ABCDe

A= alcohol abuse
B= beri beri (wet) / Coxsackie B virus 
C= cocaine / Chagas 
D= Doxorubicin toxicity
E= elsewhere (hemochromatosis / sarcoidosis /peripartum cardiomyopathy
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43
Q

What are the laboratory findings of Dilated Cardiomyopathy?

A

ECHO:::
Dilated heart / systolic regurgitant murmur

CXR:::
Balloon appearance of heart

Miscellaneous:::
Eccentric hypertrophy

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44
Q

How takotsubo cardiomyopathy occurs?

A

Ventricular apical ballooning likely due to increased sympathetic stimulation

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45
Q

What is the histological finding of HOCM?

A

Marked ventricular concentric hypertrophy
(Sarcomere added in parallel)

Myofibrillar disarray and fibrosis

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46
Q

Name the protein get mutated in HOCM?

A

Genes encoding sarcomere protein such as myosin binding protein C and B-myosin heavy chain

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47
Q

Name the condition which cause isolated Right HF

A

Cor pulmonale

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48
Q

What will be detected in physical finding in HOCM?

A

carotid pulse with dual upstroke due to mid-systolic obstruction during cardiac contraction

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49
Q

What are the major causes of sudden cardiac death?

A

CAD
HOCM

Arrhythmia Viz long QT Syndrome
Congenital heart disease

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50
Q

What is Cornell Criteria?

A

It is criteria for HOCM

Tall “R” wave in aVL plus deep “S” wave in V3

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51
Q

What is the difference b/w HOCM and restrictive cardiomyopathy?

A

HOCM:::
Wall is asymmetrical thick

Restrictive cardiomyopathy:::
Wall is symmetrical thick

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52
Q

What is the ECHO findings of amyloidosis?

A

Increased ventricular wall thickness with normal ventricular cavity dimensions (esp in ots without HTN)

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53
Q

What will be ECHO finding of Dilated Cardiomyopathy?

A

echo shows dilated ventricles with diffuse hypokinesia resulting in a low ejection fraction (i.e. systolic dysfunction)

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54
Q

What will be laboratory findings of Cardiac tamponade?

A

CXR:::
Enlarged globular cardiac silhouette (water bottle heart shape)

ECG:::
Electrical alternans with sinus tachycardia is highly specific for large pericardial effusion

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55
Q

When to consider S3 sound normal?

A

Children

Young adult

Pregnancy

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56
Q

Important point of S4

A

S4 is heard in acute MI because of ischemia induced myocardial dysfunction

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57
Q

What is the key distinguished feature of benign and pathological murmur?

A

benign Vs pathological murmur is change in instensity with change in position. Position that dec. venous return to heart, dec intensity of innocent murmur.

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58
Q

In which condition Hepatojuglar reflux seen?

A

Common in constrictive pericarditis, right ventricular infarction and restrictive cardiomyopathy

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59
Q

What is Kussmaul’s sign?

A

lack of ↓ or an ↑ in JVP on inspiration

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60
Q

What are the causes of Constrictive pericarditis?

A

Viral pericarditis
Cardiac surgery

Tb
Radiation therapy

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61
Q

Which is the ECHO and CXR finding of Constrictive pericarditis?

A

ECHO:::
Increase pericardial thickness
Abnormal Septal motion
Bi atrial enlargement

CXR:::
Pericardial calcification

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62
Q

What is the JVP finding of Constrictive pericarditis?

A

Prominent X and Y descent

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63
Q

Difference between Pericardial knock and S3

A

Pericardial knock::
Occurs earlier than S3 gallop
Louder and higher pitched than the S3
Heard with the diaphragm over a larger area

S3:::
Best heard with a lightly

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64
Q

How to t/m Constrictive pericarditis?

A

Temporary:::
Diuretics

Definitive:::
Pericardiectomy (also in refractory cases)

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65
Q

Important point of Uremic pericarditis

A

Does not present with classic ECG findings of pericarditis as inflammatory cells do not penetrate the myocardium and lack of involvement of epicardium

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66
Q

What is the effective t/m of Uremic pericarditis?

A

Dialysis is the most effective treatment for UP and can resolve symptoms and decrease the size of any pericardial effusion

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67
Q

How to t/m first degree heart block with normal QRS?

A

No further evaluation needed

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68
Q

What to do if patient has first degree heart block with wide QRS?

A

It should have electrophysiologic testing to determine the site of conduction delay

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69
Q

Difference between first degree heart block with Normal and wide QRS complex?

A

Normal QRS::
due to conduction delay in AV node

Wide QRS::
conduction delay below AV node, mostly bundle branches

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70
Q

What is pacemaker syndrome?

A

uncomfortable sensation of awareness of heart beat due to atrial contraction against close mitral valve during ventricular systole.

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71
Q

At what level there is block in 2nd degree heart block?

A

Type 1::
Usually AV node

Type 2::
Below the level of AV node

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72
Q

How exercise(Or atropine) and vagal maneuvers?

A

Atropine (Or Exercise)::
Improves type 1 block whereas worsen type 2 block

Vagal Maneuvers::
Improves type 2 block whereas worsen type 1 block

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73
Q

What will be the ECG findings type 1 block?

A

Constant P-P interval

Increasing PR interval

Decreasing R-R interval

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74
Q

Difference between first degree and other heart block

A

First degree always have conducted P waves with Qrs , unlike other AV blocks

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75
Q

What are the ECG findings of type 2B block?

A

Normal PR interval

Constant RR interval

Non conducting P waves

Area of drop QRS complex

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76
Q

What are the ECG findings of third degree third block?

A

PP and RR interval constant

Escape rhythm

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77
Q

Important point of third degree heart block

A

Unless an escape rhythm is initiated, ventricle a-systole will occur

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78
Q

Name the drugs contraindicated in third degree heart block

A

Beta blocker and Digoxin

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79
Q

What is the most frequent location of ectopic foci that cause AF?

A

Pulmonary vein

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80
Q

What are the causes of tachycardia mediated cardiomyopathy?

A

AF / atrial flutter

ventricular tachycardia / incessant atrial/junctional tachycardia

and

atrioventricular nodal reentrant tachycardia.

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81
Q

How tachyarrhythmias induced cardiomyopathy occurs?

A

tachyarrhythmias with prolonged periods of rapid ventricular rates can lead to this cardiomyopathy

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82
Q

How to t/m tachyarrhythmias induced cardiomyopathy?

A

AV nodal block agents

Anti arrhythmics agent

Catheter ablation of arrhythmias

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83
Q

Name the pulmonary origin condition associated with A fib

A

Obstructive sleep apnea

Pulmonary embolism

COPD

Acute hypoxia

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84
Q

Name the cardiac origin condition associated with A FIB

A

Hypertensive heart disease
CAD

MR/MS

CHF / HOCM
ASD

Post cardiac surgery

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85
Q

How to control the rate in A fib?

.

A

Rate control is achieved by beta blockers (metoprolol), calcium channel blockers (diltiazem) or digoxin to control ventricular rates.

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86
Q

What are the indications of rhythm control in A fib?

A

Hemodynamic unstable patient with rapid A fib
Not responding to rate controlling drugs

recurrent symptomatic episodes (eg, palpitations, lightheadedness, dyspnea, angina) or

heart failure symptoms in setting of underlying left ventricular systolic dysfunction

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87
Q

Important point of A FIB

A

Attempting cardioversion for an unknown duration or >48 hours without adequate anticoagulation inc. risk of systemic thromboembolism

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88
Q

How to valvular Afib or mechanical/prosthetic valve?

89
Q

What will be t/m if CHADVASc score is more than 2?

A

Oral anticoagulants

90
Q

What will be t/m if CHADVASc score is 1?

A

Aspirin Or Oral anticoagulants

91
Q

What will be t/m if CHADVASc score is zero?

92
Q

What is lone AF?

A

presence of paroxysmal, persistent or permanent atrial fibrillation with no evidence of cardiopulmonary or structural heart disease.

Required no treatment

93
Q

How Atrial premature beats occur?

A

depolarization of the atria originating in a focus outside SA node
Check the ECG

94
Q

Difference between HTN urgency and HTN emergency?

A

HTN urgency:::
BP more than >180/120 with no Sx or acute end organ damage

HTN E/R:::
Severe HTN with acute, life threatening end organ damage

95
Q

Important point of atrial premature beats?

A

P wave has a d/f shape from one originating from SA node

96
Q

What is malignant HTN?

A

Severe HTN with retinal hemorrhages, exudates or papilledema

there can also be malignant nephrosclerosis but non-dx and not always present

97
Q

What is HTN Encephalopathy?

A

Severe HTN with cerebral edema, non-neurological signs and symptoms

98
Q

Important point of t/m in HTN Emergency

A

BP should be lowered 10-20% in 1st hour and 5-15% in next 23 hours - Excessive drop in BP results cerebral ischemia with altered mental status and/or generalized seizures

99
Q

Name the initial HTN medication for black ethnicities

A

Thiazide Or CCB

but not ACEI and ARBs

100
Q

Name the initial HTN medication for non black ethnicities

A

ACEI / ARBs

Thiazide / CCB

101
Q

How to isolated systolic HTN?

A

monotherapy with low dose thiazide diuretic, ACEi or a long acting calcium channel blocker

102
Q

What is the most effective method to control HTN?

A

Life style modification

Obese ppl:: Reducing weight
Non obese:: DASH diet

103
Q

Name the anti HTN contraindicated in pregnancy

A

ACEi
ARBs

Aldosterone antagonist
Direct renin inhibitors

Furosemide
Nitropursside

104
Q

What are first and 2nd line anti HTN medication in pregnancy?

A

First line:::
Methyldopa > Labetolol > hydralazine > CCB (nifedipine)

2nd Line:::
Thiazides
Clonidine

105
Q

How cyanide toxicity occurs?

A

If it is given in high amount or prolong.

SxS ::: alter mental status / lactate acidosis / fits and coma

106
Q

How to counter the Edema due to CCB?

A

By giving ACEi Or ARBs

107
Q

How to t/m BB toxicity?

A

Secure airway

Give isotonic fluids bolus and IV atropine for low BP and bradycardia

If refractory Or severe hypotension then give IV glucagon

108
Q

Important point of HTN

A

All pts with resistant HTN, severe or malignant HTN, sudden BP rise in a pt with previously controlled BP, age of onset <30 years without family h/o HTN should be screened for 2* causes of HTN

109
Q

How to d/f bruit of AAA and Renal artery stenosis?

A

AAA:::
Bruit only heard in systolic

Renal Artery Stenosis:::
Bruit heard in systolic and diastolic

110
Q

Triad of Renal artery stenosis

A

Severe HTN with atherosclerosis and abdominal bruit

Increase serum creatinine after starting ACEi Or ARBs

asymmetric kidney size or a small atrophic U/L kidney

111
Q

How to d/f difference in BP of upper limb causes?

A

Difference in BP in arms more in left than right—-> subclavian atherosclerosis

Difference in BP in arms more in right than left—-> coarctation proximal to left Subclavian artery origin

112
Q

Name the condition which has both abdominal and carotid bruits

A

Fibromuscular dysplasia

113
Q

Triad of Renal Artery stenosis

A

Young Female with Secondary HTN

Flank pain

Neurological features viz TIA / stroke / Recurrent Headache / Pulsatile tinnitus

114
Q

Name the imaging used for diagnosing Fibromuscular dysplasia

A

Preferred Imaging:::
Duplex US
CTA
MRA

Others::: catheter based arteriography

115
Q

How to t/m fibromuscular dysplasia?

A

Anti HTN:::
ACEi / ARBs first line

2nd Line:::
PTA

Do surgery if PTA unsuccessful

116
Q

At what area murmur of coarctation of aorta is heard?

A

Systolic ejection murmur at left interscapular area

117
Q

What are the Chest X Ray findings of co arctation of aorta?

A

3 sign from aortic indentation

Notching of 3rd to 8th ribs from enlarged intercostal arteries

118
Q

How to t/m aortic co arctation?

A

Balloon angioplasty with or without stent

119
Q

Important point of digoxin toxicity

A

Atrial tachycardia with AV block is arrythmia specific for digitalis toxicity

  • Multifocal atrial tachy is rarely associated with digitalis toxicity. It is more commonly a consequence of pulmonary
    dis.
120
Q

Name the medication which can cause digoxin toxicity

A

Amiodarone
verapamil
quinidine
and propafenone increases the serum levels of digoxin and can lead to toxicity

121
Q

What skin changes occur due to digoxin toxicity?

A

Blue gray skin discolouration

122
Q

What are the examination findings of cor pulmonale?

A

Peripheral Edema with pulsatile liver from congestion

Right sided heave with TR murmur

Loud S2

Increase JVP with Prominent “a” wave

123
Q

What is the gold standard test for Cor pulmonale?

A

Right HEART CATH:::

elevated pulmonary artery systolic pressure (<25 mmHg).

Right ventricular dysfunction

Pulmonary HTN

No left heart disease

124
Q

What are ECG findings of cor pulmonale?

A

Right BBB

Right axis deviation

Right ventricular hypertrophy

Right atrial enlargement

125
Q

What is the normal right atrial pressure?

A

Mean of 4 mmHg

126
Q

What is the normal PCWP?

A

Mean of 9 mmHg

127
Q

What is the normal cardiac index?

A

2.8–4.2 L/min/m2

128
Q

What changes occur in hyperdynamic phase of Septic shock?

A

Hyperdynamic phase

dec in SVR

dec. BP,
inc. HR

and CO (warm shock)

129
Q

What changes occur in hypodynamic phase of Septic shock?

A

inc. SVR,

dec. in CO grave deterioration (cold shock)

130
Q

Triad of Exerational heat stroke

A

Body temperature >104 ‘F

Alter metal status

Multi organ failure

131
Q

What are the risk factors for Exerational heat stroke?

A

Physical activity in hot and humid weather
Dehydration and obesity

Lack of physical fitness with poor acclimatization

Medication viz anticholinergic / anti histamine / tricyclic / phenothiazine

132
Q

How non Exerational heat stroke occur ?

A

More freqeuntly affect elderly pt with significant underlying comorbidities that limit their ability to escape or cope with excessive heat

133
Q

How to t/m non Exerational heat stroke?

A

evaporative cooling (eg spraying lukewarm water while fans blod air on pt) is more imp than ice immersion which is associated with inc mortality in this case

134
Q

What amount of lipid lowering agents given in patient whose age is ≤75 with atherosclerotic diseases?

A

High intensity statin

135
Q

What amount of lipid lowering agents given in patient whose age is ≥75 with atherosclerotic diseases?

A

Moderate intensity statin

136
Q

What amount statin given patient whose LDL is ≥190?

A

High intensity statin

137
Q

What amount of lipid lowering agents given in patient whose age is 40-75 with diabetes?

A

If 10 years ASCVD risk <7.5%::
Moderate intensity statin

If 10 years ASCVD risk >7.5%::
High intensity statin

138
Q

How to t/m the patient whose TAG level is 150-500mg/dl?

A

Lifestyle modification

If CVS risk then give statin

139
Q

How to t/m the patient whose TAG level is ≥1000mg/dl?

A

Initially to prevent pancreatitis by giving fibrates and fish oil / abstinence from alcohol

Once TAG reach ≤500mg/dl then do lifestyle modification and add statin if CVS risk

140
Q

What are the risk factors for cholesterol crystal embolism?

A

Invasive procedures like cardiac cath Or Vascular procedure

Comorbidities like HTN / DM / High cholesterol)

141
Q

What are important or different features of Cholesterol crystal embolism?

A

Blue toe syndrome:
cyanotic toes with intact pulses.

Livedo reticularis:
blanches with pressure application

Hollenhost spots:
bright, yellow, refractile plaques in retinal artery

142
Q

What are laboratory findings of cholesterol crystal embolism?

A

Increase eosinophils in cbc as well in urine D/R

High creatinine with low complement levels

Renal Or skin Biopsy::
Biconvex, needle shaped clefts within occluded vessels
Perivascular inflammation with eosinophils

143
Q

How acute lower limb ischemia?

A

pain
pallor

poikilothermia (cool extremity)
paresthesia

pulselessness
and paralysis

144
Q

How to t/m acute limb ischemia?

A

Give heparin before proceeding for surgery as this drug will stop propagating the thrombus

145
Q

What are the indications for carotid endarterectomy in female?

A

Do it in female whether asymptomatic or symptomatic with stenosis 70-99%

146
Q

What are the indications for carotid endarterectomy in Male ?

A

Asymptomatic with stenosis 60-69%

Symptomatic::
50-69% stenosis
70-99% stenosis

147
Q

What does it mean to be symptomatic if patient has carotid stenosis?

A

Symptomatic means:

occurence within past 6 months of sudden onset focal neurological symptoms corresponding to a carotid artery lesion

148
Q

Triad of Vagovagal syncope

A

There is always trigger

Prodrome Sx before unconscious viz pallor, nausea, dizziness and diaphoresis

Short duration of syncope which improve with supine position

149
Q

What is orthostatic Hypotension?

A

Drop in systolic BP >20mmHg and diastolic >10mmHg on standing from sitting position within 2-5min of standing from supine position

150
Q

What are main causes of orthostatic Hypotension?

A

decreased baroreceptor sensitivity

Hypovolemia

151
Q

What is PULSUS PARVUS ET TARDUS?

A

Arterial pulse with decreased amplitude and delayed peak.

Common in severe aortic stenosis

152
Q

What is PULSUS BISFERIENS (OR BIPHASIC PULSE)?

A

Two strong systolic peaks or aortc pulse from left ventricular ejection separated by a midsystolic dip.

Can be palpated in pts with significant aortic regurgitation with or without stenosis, HOCM, and occasionally large PDA

153
Q

What are the immunologic phenomena seen in infective endocarditis?

A

Osler nodes:: Painful, nodules violaceous seen on the finger and toes

Roth spots:: edematous and haemorrhagic lesion of the retina

154
Q

How to t/m Infective endocarditis?

A

Empirically with vancomycin after taking blood culture

T/m::
Penicillin susceptible strains should be treated with IV aqueous penicillin G (every 4-6 hours or 24 hours continuous infusion) or IV ceftriaxone (once daily) for 4 weeks.

155
Q

What is the MCC of death in infective endocarditis?

A

Valvular insufficiency

156
Q

What is the preferred prophylactic medication for Rheumatic fever?

A

IM Benzathine penicillin G for every 4 weeks

157
Q

Important point of aortic dissection

A

50% cases in ppl <40 years are due to Marfan syndrome but HTN is most common risk factor seen in 75% patients

158
Q

Name imaging test to dx aortic dissection

A

TEE>TTE

CT and MRI are alternatives if emergency TEE is not available

159
Q

How HOLT-ORAM SYNDROME (HEART HAND SYNDROME) presents?

A

Both upper limb defects (e.g. deformities of radius and carpal bone)

and atrial septal defect

160
Q

What are the causes of A-systole/PEA?
5Hs

And

5Ts

A

5Hs::
Hypovolemia
Hypoxia

Hydrogen ion (acidosis)
Hypo/hyper kalemia

Hypothermia

5Ts::
Tension pneumothorax
Tamponade cardiac

Toxins
Thrombosis

Trauma

161
Q

What is synchronised cardio version and when to use it?

A

Synchronized cardioversion delivers energy synchronized to QRS complex—

used in symptomatic or sustained monomorphic VT(unresponsive to antiarrhythmics) AND hemodynamically unstable atrial fibrillation with rapid ventricular response.

162
Q

What is un-Synchronized cardio version and when to use it?

A

Defibrillation delivers energy randomly during cardiac cycle without synchronization to QRS complex.

Needed for pulseless ventricular tachycardia and ventricular fibrillation

163
Q

How to avoid cardiac complication when doing Central venous catheter?

A

To avoid myocardial perforation, catheter tip should be located proximal to either cardiac silhouette or the angle between the trachea and the right mainstem bronchus.

Ideally catheter tip should lie in superior vena cava. Tip placement in smaller vessels can cause perforation

164
Q

WHO classification of Pulmonary HTN

A

Group 1::
Due to unknown PAH

Group 2::
Due to left heart disease

Group 3
Due to chronic lung disease

Group 4::
Due to thromboembolic occlusion of the pulmonary vasculature

Group 5::
Due to haematological /metabolic / systemic disorder

165
Q

What are the chest X-ray findings of thoracic Aorta aneurysm?

A

CXR in TAA:

widened mediastinal silhoutte

↑ aortic knob

and tracheal deviation

166
Q

How to d/f thoracic aortic aneurysms from tortuous aorta?

A

CXR cannot distinguish TAA from tortuous aorta

confirm with CT with contrast

167
Q

What are the causes of thoracic aortic aneurysms?

A

Ascending aorta aneurysms:::

cystic medial degeneration (cox of aging) or connective tissue disease ( eg Marfan and Ehler Danlos)

Descending aorta aneurysms:::

due to atherosclerosis; risk factor: HTN, hypercholestrolemia and smoking

168
Q

What is basic difference b/w thoracic and abdominal aorta aneurysms?

A

unlike thoracic aortic aneurysm, it does not form false lumen and an intimal flap and is composed of all 3 layers

169
Q

Important point of AAA

A

AAA >3cm

Imaging modality of choice:
abdominal ultrasound

Screen the men who smoke with age of 65-75years

risk of AAA formation and expansion is lower in diabetics than non-diabetics

170
Q

What are the risk of AAA which increases the chances of rupture?

A

large aneurysm diameter (>/=5.5cm)

aortic expansion rate >0.5cm/6mo and >1cm/year

female gender, current ongoing smoking and HTN
(HTN has weak association with AAA formation and expansion and rupture)

171
Q

What are the indications for surgical repair Or Endovascular repair of AAA?

A

size >5.5cm,

rapid rate of expansion >0.5cm/6months and >1cm/year

and presence of symptoms (abdominal, back or flank pain; limb ischemia) regardless of size

172
Q

Triad of Leriche syndrome

A

Erectile dysfunction

Buttock and hip pain

Absent femoral pulse on examination

173
Q

What to do if ankle brachial index test comes positive?

A

Arterial duplex US

174
Q

How to t/m peripheral arterial disease?

A

Start with::
Anti platelets agents with lipid lowering agents and exercise

If not settle out with above therapy do::
Cilostazol
Percutaneous or surgical revascularization

175
Q

How to approach DVT?

A

Through WELLS criteria if high chance of DVT then do compression U/S—> if positive—>give anticoagulant
If negative—> repeat the test after a week

——

If low chance of DVT—>check D dimer—>if increase—>follow the above pattern

If decreases—>unlikely DVT

176
Q

Which anticoagulant to give for DVT?

A

Proved DVT:

begin anticoagulation with Heparin followed by warfarin, rivaroxaban or apixaban

177
Q

Important findings of CXR in PE

A

,Westermark’s sign
(peripheral hyperlucency due to oligemia)

Hampton’s hump
(peripheral wedge of lung opacity due to pulmonary infarction)

and

Fleishner’s sign
(enlarged pulmonary artery)

178
Q

How to t/m Torsades de pointes?

A

IV MgSO4 doesn’t matter if magnesium is normal

If cause of torsades de pointe is quinidine then use Sodium bicarbonate

179
Q

How to managed Wide complex tachycardia if there is no AV dissociation or fusion/capture beats?

A

Consider it SVT with aberrancy
If vitally stable—>vagal maneuver, rate/rythm control

If vitally unstable—> Direct cardioversion

180
Q

How to managed Wide complex tachycardia if there is AV dissociation or fusion/capture beats?

A

DX of VT

If vitally stable—> amidarone

If vitally unstable—> DC cardioversion

181
Q

Important point of Acute MR

A

Short time so no compensatory changes made result left atrial and ventricular size remain normal with normal or increase EF

182
Q

Important point of Chronic MR

A

Enough time so compensatory changes made result left atrial and ventricular size increases with normal or increase EF initial but wall stress would eventually leads to decrease in EF

183
Q

Important point of Preload / After load and CO

A

1) Sepsis:: Both Preload Afterload decrease and CO initially increase and then Decrease
2) Adrenergic agonist like epi activate both alpha and Beta result increase Afterload, Preload and CO
3) Increase Afterload and Preload with Decrease CO seen in Decompensated HF

184
Q

What are the cardio origin syncope causes?

A

LV outflow obstruction
VT

Conduction impairment like sick sinus syndrome or AV block

185
Q

What are the orthostatic origin syncope causes?

A

1) vasodilator Medication like alpha blocker/ anti HTN
Inotropic / chronotropic blocker like BB

2) hypovolemia
3) Autonomic dysfunction more seen in DM/ parkinson

186
Q

What are the Reflex syncope causes?

A

Vasovagal

Situational

Carotid hypersensitivity

187
Q

Why sedation and Intubation avoided in HYPOVOLEMIC SHOCK?

A

Intubation or Positive pressure ventilation increases Intra thoracic pressure result Decrease venous return

Sedation dilated the vein result pooling of blood

188
Q

How much alcohol intake would cause hypertension?

A

More than 2 drinks per day
Or
More than 5 drinks in single sitting

189
Q

How to Approach STEMI?

B-SOMAN

A

LIFE saving treatment is PCI or tPA
But initially
BB, Statin, O2, Morphine, aspirin plus , Nitrates

190
Q

Name the medicine avoided/given in STEMI in specific situation

A

1) Give BB but avoid if low BB and pulse, sxs of HF or heart block
2) Lasix if pul-edema but avoid if patient has low BP Or dehydrated
3) Unstable sinus bradycardia—-> IV atropine
4) Avoid Nitrates if low BP, R-heart infarction or severe aortic stenosis

191
Q

Triad of Vasospastic angina

A

Chest pain occur at Rest or sleep (not on exertion)

Seen in young age with positive hx of cocaine and smoking

Transient ST elevation with no blockage of coronary artery on angiography

192
Q

How to manage Vasospastic angina?

A

CCB as preventive

Nitroglycerin as abortive

193
Q

Important point of Vasospastic angina and raynaud phenomenon;; Claudication and angina

A

Both have same pathophysiology that is hyperactivity of muscle of arteries

Both Claudication and angina have same pathophysiology somehow

194
Q

What are the surgical indications of Infective Endocarditis?

A

If patient developed sxs like HF
Bacteremia even on ABx

Large vegetation or persistent septic emboli
Fungus Or MDR pathogen result d/f to eradicate organism

Extension of infection viz abscess, fistula or heart block

195
Q

Name the medicine given for Chronic stable angina

A

1) First line—> BB
Cardiac selective CCB alternative to BB if BB CI

2) Add non cardiac selective CCB (with BB) which dilates coronary and systematic artery result reduced Afterload
3) Nitrates if still persistent or Ranolazine if refractory angina which decrease calcium influx in myocardiocytes

196
Q

What is the typical finding of Pericarditis?

A

Pericarial frictional rub which is triphasic that is heard in atrial systole, ventricular systole and early ventricular diastole

197
Q

What are the PRIMARY PREVENTION indications for statin therapy in prevention of ASCVD?

A

1) Age more or at least 40 with DM regardless of LDL level

Or
2) LDL more than 190mg/dl

Or
3) Estimated 10 year risk of ASCVD >7.5%-10%

198
Q

What are the SECONDARY PREVENTION indications for statin therapy in prevention of ASCVD?

A

Already established ASCVD like
Acute coronary syndrome

Stable angina

Stoke TIA PAD

Arterial Revascularization like CABG

199
Q

What are the CNS and CVS complications of aortic dissection?

A

CNS
Stoke due to carotid artery

Horner syndrome due to carotid sympathetic plexus

Lower extremity paraplegia (spinal arteries)

CVS::
Acute AR due to aortic root / valve

MI due to coronary artery Ostia

Pericardial effusion or tamponade (pericardium)

200
Q

What are the complications of pulmo, Abdominal and Renal complications of Aortic Dissection?

A

Pulmo::
Hemothorax due to pleural cavity

GIT:
Abdominal pain (mesenteric arteries)

Renal:
Renal injury due to renal arteries

201
Q

What Factors leads to S.aureus and S.epidermis induced Infective Endocarditis?

A

Prosthetic device

Intravascular catheter

Implanted devices (Pacemaker / defibrillator)

202
Q

What Factors leads to Viridian streptococci induced Infective Endocarditis?

A

Gingival manipulation

Respiratory tract incision or biopsy

203
Q

What Factors leads to Enterococci induced Infective Endocarditis?

A

Nosocomial UTI

204
Q

What Factors leads to fungi induced Infective Endocarditis?

A

Prolonged Abx therapy

Intravascular catheter

Immuno incompetent

205
Q

Name the parameters of CHA2 DS2 VASc for non Valvular A.fib

Patient is assigned in one of the “age” group

A

C CHF
H HTN
A2 >75
D DM

S2 stroke Or TIA
V vascular disease like prior MI

A 65-74
Sc sex category like female

206
Q

Name the anti diabetic meds given for CVS patient

A

Metformin
GLP-1 Agnoist like Liraglutide
SGLT2 Inhibitor like Empagliflozin

207
Q

How Post cardiac surgery syndrome occur and what are the causes of it?

A

Form of acute pericarditis due to “”immune mediated inflammation (deposition of Immune complex)”” in the pericardium occur to exposure of antigen

Causes are PCI , Cardiax surgery or trauma and MI (dressler syndrome)

208
Q

How to treat post cardiac surgery syndrome?

If not manage properly—> leads to constrictive pericarditis

A

Tx
NASID and colchicine
Steroid if refractory cases

209
Q

If JVP pulse shows (1)Prominent V wave and absent X descent what condition is it?

1a) if shows Prominent A wave and flattened Y wave descent what condition is it?

And if (2)shows flattened Y wave what condition is it?

A

1) Tricuspid Regurgitation
Absent X wave descent due to elevated R-atrial pressure throughout ventricular systole

1a) Tricuspid stenosis

2) Pericardial effusion
External right ventricular compression with restricted diastolic filling

210
Q

What is Cannon A waves?

A

Prominent A waves cause by surge in JVP due to R-atrium contraction against a closed tricuspid valve

Seen in AV dissociation (v-tach Or complete AV block)

211
Q

Name the d/f types of Stress Test

A

1) If able to reach HR—> exercise ECG test
2) if Patient has LBBB, pacemaker placed Or unable to reach HR—-> pharma stress test with adenosine or dipyridamole
3) If patient has reactive airway disease Or unable to reach HR—> dobutamine Stress echo

212
Q

What are different types of stress test contraindications?

tHR (Targeted HR)

A

1) Don’t do Exercise ECG test if patient has LBBB, Pacemaker placed or Unable to reach tHR
2) Don’t do pharma stress test of patient has reactive airway diseases or patient taking theophylline/dipyridamole
3) Don’t do Dobutamine stress Echo—> if patient has tacchyarrhythmia

213
Q

Name the Antiarrhymatic increase the PR, QRS and QT interval

Start with QT then QRS and then PR

A

1) Amidarone increases the duration of all three
2) Class 1a, Class 3 and Sotalol increases QT interval
3) Class 1c also increases QRS besides amidarone
4) Class 2, 4 , Sotalol and amidarone increase PR interval

214
Q

Name the Antiarrhymatic increase the PR, QRS and QT interval

Start with QT then QRS and then PR

A

1) Amidarone increases the duration of all three
2) Class 1a, Class 3 and Sotalol increases QT interval
3) Class 1c also increases QRS besides amidarone
4) Class 2, 4 , Sotalol and amidarone increase PR interval

215
Q

What are the causes of Multifocal Atrial tachycardia and how to manage it?

A

Surge of Catecholamines like in sepsis

Imbalance lytes like low potassium
Exacerbation of Pulmonary disease like COPD

Rx
t/m underlying cause
If condition persist even after t/m underlying cause then give AV nodal blocking agent

216
Q

What are the causes of Stress induced (Takotsubo cardiomyopathy) and how to manage it?

A

Post menopausal female
Recent physical or emotional stress

Rx is supportive care as it will resolve on its own

217
Q

What are d/f test to dx Stress induced (Takotsubo cardiomyopathy)?

A

ECG—>shows Ischemic changes in chest leads

Cath—> no blockage in coronary arteries

ECHO shows hypokinesis in apical LV whereas hyperkinesis in Basilar

218
Q

How BB toxicity present physically and on ECG?

A

AMS with breathing d/f ( bronchospasm)
Low BP, HR and Glucose
Fits

EKG show Increase PR interval and bradycardia

219
Q

How to manage BB toxicity?

A

First secure airway Along with IV fluid infusion
Not response—->.IV atropine
Not response——–> IV glucagon.

Internal Medicine (14 decks)

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