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Cardiology > Cardiology Part 1 > Flashcards

Cardiology Part 1 Flashcards

1
Q

Hypertension Module

A

x

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2
Q

dx

A

x

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3
Q

what is the measure that raises concern for HTN?

A

BP > 140/90

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4
Q

how many readings do you need to make the dx of HTN?

A

> 140/90 on 3-6 readings over a period of weeks to months.

tyypically >=2 BP readings are necessary

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5
Q

define

A

x

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6
Q

what are the two categories of HTN?

A

primary (essential) or secondary

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7
Q

causes

A

x

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8
Q

what are the causes of secondary HTN?

A

coarctation of aorta, renal or renovascular disease, sleep apnea, pheochromocytoma, cushing syndrome, endocrine disorders

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9
Q

PE

A

x

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10
Q

what are important PE findings to pursue in HTN?

A

fundoscopic exam (HTN retinopathy), pulse palpation (coarctation of aorta), cardiac exam (LVH), abd exam (renal artery bruit)

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11
Q

what type of PE should be done for HTN?

A

full physical exam

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12
Q

workup

A

x

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13
Q

what are important workup labs for HTN module to order?

A

CBC, BMP, UA, lipid profile, and 12 lead EKG, may need microalbumineria screening in diabetics

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14
Q

what imaging should be ordered for HTN?

A

echocardiogram

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15
Q

Management

A

x

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16
Q

first line management for HTN is?

A

lifestyle mods (low salt, regular excercise, no smoking, no alcohol, calorie restriction, low fat diet)

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17
Q

if lifestyle mods fail to alter HTN, what is second line management?

A

pharmacotherapy

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18
Q

what is considered stage I HTN? what is best pharmacotherapy?

A

BP: 140-159/90-99, monotherapy with ACEi/ARB/CCB

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19
Q

what is considered stage II HTN? what is best pharmacotherapy?

A

BP: >=160/>=100, start two drug therapy ACEi/ARB +CCB

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20
Q

Goal of HTN therapy

A

x

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21
Q

what is goal BP for those < 60y.o. and CKD or DM?

A

<140/90

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22
Q

what is goal BP for those >= 60y.o.?

A

<150/90

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23
Q

preferred drugs in select situations

A

x

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24
Q

what is the preferred drug in afib/flutter for BP control?

A

b-blocker, nondihydropyridine CCB

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25
Q

what is the preferred drug in angina pectoris for BP control?

A

b-blocker, CCB

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26
Q

what is the preferred drug in MI for BP control?

A

ACEi/ARB, b-blocker, or aldosterone antagonist

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27
Q

what is the preferred drug in CHF for BP control?

A

ACEi/ARB, b-blocker, diuretic or aldosterone antagonist

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28
Q

what is the preferred drug in DM (no proteinuria) for BP control?

A

diuretic or ACEi

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29
Q

what is the preferred drug in proteinuria for BP control?

A

ACEi or ARB

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30
Q

what is the preferred drug in osteoperosis for BP control?

A

thiazide diuretic

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31
Q

what is the preferred drug in BPH for BP control?

A

alpha blocker (prazosin, terazosin, or doxasozin)

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32
Q

Hypertension

A

x

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33
Q

managment

A

x

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34
Q

what is the most effective non pharm way to decrease BP?

A

10% weight loss (drops SBP by 5-20mm Hg per 10 kg loss)

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35
Q

what is the second most effective non pharm way to decrease BP?

A 
DASH diet (diet high in fruits and veggies and low saturated fat and total fat, high in potassium, calcium and dietary fiber). 
Drops SBP by 8-14mm Hg
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36
Q

what is the third most effective non pharm way to decrease BP?

A

excercise . 30 minutes /day for 5-6 days/week drops SBP by 4-9 mmHg

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37
Q

what is the fourth most effective non pharm way to decrease BP?

A

dietary sodium (<3g/day). Drops SBP by 2-8mmHg

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38
Q

what is the fifth most effective non pharm way to decrease BP?

A

alcohol intake (2drinks/day in men and 1 drink / day in women) drops SBP by 2-4mmHg

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39
Q

trx

A

x

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40
Q

when treating blood pressure in patients what is an effective combination?

A

ACE inhibitor/ARB + CCB (i.e. amlodipine)

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41
Q

Recommendations for treating hypertension

A

x

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42
Q

if Age >=60y.o. , at what BP reading do you initiate treatment of BP?

A

> =150 mm Hg SBP or >90 mm Hg DBP

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43
Q

what is the goal BP if age >= 60 y.o.?

A

< 150/90 mm Hg

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44
Q

if age <60 y.o., CKD , or DM at what BP reading do you initiate treatment of BP?

A

> =140 mm Hg SBP or >90 mm Hg DBP

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45
Q

if age <60 y.o., CKD , or DM what is the goal BP?

A

<140/90 mm Hg

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46
Q

initial anti HTN trx choice in certain populations

A

x

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47
Q

initial treatment for black patients?

A

thiazide diuretics or CCB, alone or in combination (ACEi/ARB, not first line)

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48
Q

initial treatment for other ethnicities ?

A

thiazide diuretics, ACEi, ARB, or CCB, alone or in combination

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49
Q

treatment of all ethnicities with CKD or DM?

A

ACEi or ARB, alone or in combination with other drug classes

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50
Q

Cyanide Accumulation and Toxicity

A

x

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51
Q

risk

A

x

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52
Q

what is the risk of cyanide toxicity?

A

HTN emergency treated with nitroprusside in the setting of chronic renal failure or those receiving a high dose or prolonged infusion (>2ug/kg/min)

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53
Q

pathophys

A

x

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54
Q

what is the pathophys of cyanide accumulation in HTN emergency?

A

nitroprusside infusion to treat high BP. Nitroprusside is metabolized to cyanide, which may accumulate and can be toxic

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55
Q

syx

A

x

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56
Q

what are syx of cyanide toxicity?

A
  • Skin: Flushing (cherry red color), cyanosis (occurs later)
  • CNS: headache, AMS, seizures, coma
  • Cardiovascular: Arrythmias
  • Respiratory: Tachypnea followed by respiratory depression, pulm edema
  • GI: Abd pain, nausea, vomiting
  • Renal: Met Acidosis (f
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57
Q

trx

A

x

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58
Q

what is the trx of cyanide accumulation?

A

sodium thiosulfate

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59
Q

Nitroprusside

A

x

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60
Q

pathophys

A

x

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61
Q

what is the pathophys of nitroprusside ?

A

potent vasodilator that works on arterial venous circulation

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62
Q

Hypertensive emergency

A

x

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63
Q

ED visit

A

x

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64
Q

what are initial ED orders for HTN emergency prior to physical exam?

A

IV access, oxygen, pulse ox, cardiac monitoring, BP monitor

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65
Q

syx

A

x

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66
Q

what are the symptoms of htn emergency?

A

insidious onset of headaches, nausea, vomiting, which can progress to restlessness, confusion, agitation, seizures, coma.

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67
Q

dx

A

x

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68
Q

how is HTN emergency different than urgency?

A

HTN urgency: SBP >180 and/or DBP>120 with no end organ damage

HTN emergency is DBP > 120 with end organ damage

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69
Q

PE

A

x

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70
Q

what are most important physical exam findings in HTN emergency?

A

fundoscopy, Cardiovascular, and CNS exam.

End organ damage: retinal hemorrhage, papilledema, HTN encephalopathy (n/v, headache, confusion) stroke, malignant nephrosclerosis

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71
Q

work up

A

x

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72
Q

what is the work up for HTN emergency?

A

EKG, CTH, CXR, UA, CBC, BMP, lipid profile (assess for stroke, pulmonary edema, renal impairment, and hemolysis)

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73
Q

what additional orders should be given to a HTN emergency patient?

A

NPO, complete bed rest, monitor urine output

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74
Q

trx

A

x

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75
Q

what is the trx for hypertensive emergency?

A

rapidly lower diastolic pressure to 100-105 mm Hg over 2-6 hours, with a total drop in blod pressure being no more than 25% of the initial value.

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76
Q

what is first line IV BP lowering meds and next steps in addressing HTN crisis?

A

IV nitroprusside to lower BP by 25% while in ICU with arterial line place.

Then transfer to wards to lower BP further with PO meds. D/C art line.

Goal is to lower DBP to 85-90 . over 2-3 months.

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77
Q

what are next steps once BP is under control?

A

discharge home, lipid profile, counseling (medication compliance, smoking cessation, excercise, limit alcohol intake, low salt diet)

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78
Q

if you drop the BP too far what happens?

A

ischemic events (cerebral ischemia, myocardial infarction), AMS, generalized seizures

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79
Q

what are the initial meds used to lower BP?

A

IV nutroprusside, IV hydralazine

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80
Q

what is major side effect of fast acting BP lowering meds?

A

reflex tachycardia

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81
Q

what are alternaive BP lowering meds ?

A

IV labetalol, IV nicardipine

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82
Q

x

A

x

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83
Q

Intracerebral hemorrhage

A

x

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84
Q

syx

A

x

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85
Q

what are the syx of intracerebral hemorrhage?

A

focal neuro deficits, hemiplegia or paresis and hemianopsia.

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86
Q

TCA (tricyclic antidepressant) overdose

A

x

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87
Q

syx

A

x

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88
Q

what are the CNS syx of TCA overdose?

A

-CNS: AMS (drowsiness, delirium, coma); seizures, respiratory depression.

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89
Q

what are the Cardio syx of TCA overdose?

A

NAME?

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90
Q

what are the Anticholenergic syx of TCA overdose?

A

NAME?

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91
Q

complications

A

x

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92
Q

what are the complications of TCA overdose?

A
  • acidemia, which can increase serum potassium due to cellular exchange of hydrogen and potassium.
  • also prolongs QRS interval (>100 ms) and causes arrythmias (eg Vtach, Vfib)
  • can also decrease calcium influx into the myocardium and increase periophera
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93
Q

management

A

x

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94
Q

what is the management of TCA overdose?

A
  • supplemental oxygen, intubation.
  • IV fluids
  • Activated charcoal for patients within 2 hours of ingestion (unless ileus present)
  • IV sodium bicarb for QRS widening or ventricular arryhtmia
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95
Q

how does sodium bicarb owrk?

A

it increases serum pH and extracellular sodium, thereby modifying TCA to their neutral (non-ionized) form, making them less available to bind to the rapid sodium channels.

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96
Q

if patients are refractory to sodium bicarb, what could they respond to?

A

adjuvant magnesium or lidocaine

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97
Q

Salicylate toxicity

A

x

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98
Q

managment

A

x

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99
Q

what do you treat salicylate toxicity with?

A

sodium bicarb , which can alkalanize the urine and enhance salicylate excretion by the kidney

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100
Q

Hyperkalemia

A

x

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101
Q

trx

A

x

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102
Q

what is the treatment of hyperkalemia with EKG changes (peaked T waves, short QT, increased QRS intervals)?

A

sodium bicarb

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103
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A

x

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104
Q

subtypes

A

x

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105
Q

what are the subtypes of PSVT?

A

atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia

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106
Q

pathophys

A

x

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107
Q

what is the pathophys of PSVT?

A

result from secondary conduction pathway that allows abnormal cycling of cardiac conduction and formation of a reentrant circuit

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108
Q

syx

A

x

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109
Q

what are the syx of PSVT?

A
  • intermittent , abrupt onset palpitations accompanied by a sensation of a rapid heartbeat.
  • dyspnea, lightheadedness, chest pain, or rarely syncope, presyncope
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110
Q

PE

A

x

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111
Q

what are physical exam findings of PSVT?

A

HR> 150

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112
Q

dx

A

x

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113
Q

what are EKG findings ?

A
  • narrow complex tachcyardia with regular RR intervals .

- may show retrograde P waves that are typically inverted in the inferior leads (II, III, avF)

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114
Q

trx

A

x

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115
Q

what is the trx for PSVT in HD stable patients?

A
  • vagal maneuvers (eg valsalva) can be done

- adenosine administered to slow the AV node and allow for easier idenitifcation of the arrythmia on cardiac monitoring

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116
Q

what is the trx for PSVT in HD unstable patients?

A
  • undergo urgent synchronized cardioversion.

- if needed, cardiac ablation is the definitive treatment of choice

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117
Q

Atrioventricular reentrant tachycardia (AVRT)

A

x

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118
Q

dx

A

x

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119
Q

what are EKG findings of AVRT?

A

can have marked ST segment depression during tachycardia, occurs in young patients in the absence of CAD and does not represent MI

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120
Q

Atrial Fibrillation

A

x

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121
Q

dx

A

x

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122
Q

what are the EKG findings of Afib?

A

irregular rhythm and absent P waves

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123
Q

what is a drug approved for pharmacologic cardioversion of afib?

A

ibutilide (class III antiarrhythmic)

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124
Q

Atrial Flutter

A

x

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125
Q

trx

A

x

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126
Q

what is a good short acting med for trx of Atrial Flutter?

A

esmolol (ultra short acting beta blocker)

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127
Q

what is a drug approved for pharmacologic cardioversion of aflutter?

A

ibutilide (class III antiarrhythmic)

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128
Q

dx

A

x

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129
Q

what are the EKG findings of Aflutter?

A

flutter waves in a sawtooth pattern with a HR> 150 due to 2:1 atrial to ventricular conduction

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130
Q

Multifocal atrial tachycardia

A

x

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131
Q

association

A

x

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132
Q

what is the associated disease with multifocal atrial tachycardia?

A

COPD

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133
Q

dx

A

x

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134
Q

what does EKG show for multifocal atrial tachycardia?

A

irregular, narrow complex tachycardia with variable P wave morphology (p waves higher or lower than others)

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135
Q

Sinus Tachycardia

A

x

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136
Q

dx

A

x

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137
Q

what is the EKG pattern of sinus tachycardia?

A

narrow QRS complexes but normal p waves and often gradual (rather than abrupt) onset.

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138
Q

Wolf Parkinson White Syndrome (WPW Syndrome)

A

x

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139
Q

define

A

x

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140
Q

what is WPW syndrome a type of?

A

a type of tachyarrythmia

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141
Q

syx

A

x

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142
Q

what are the symptoms of WPW Syndrome?

A

syncope, pounding sensation in the chest, nausea, and vomiting

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143
Q

dx

A

x

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144
Q

what are the classic EKG findings of WPW?

A

classic triad = short PR interval + slurred upstroke of the QRS complex + widening of the QRS complex.

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145
Q

what is WPW syndrome?

A

classic triad + symptomatic tachyarrythmia

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146
Q

pathophys

A

x

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147
Q

what is the pathophys of WPW?

A

due to an extranodal accessory conduction pathway that directly connects the atria and ventricles, bypassing the atrioventricular node.THe accessory pathway conducts faster than the AV node and excites the ventricles prematurely, manifesting on EKG as short PR interval with delta wave and widened QRS complex

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148
Q

risk

A

x

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149
Q

what is the risk of WPW syndrome turning into Afib?

A

due to alcohol ingestion, WPW develop afib and conduct down the accessory pathway from the atria to ventricle at such a fast rate that you see syncope

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150
Q

association

A

x

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151
Q

what is the typical rhythm associated with WPW?

A

Atrioventricular reentrant tachycardia (AVRT)

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152
Q

trx

A

x

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153
Q

what is the treatment of WPW that continues to convert to AFib leading to tachyarrythmias causing lightheadedness?

A

catheter ablation (~90% efficacy rate and <5% risk of complications, replacing surgical ablation as the preferred treatment).

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154
Q

Cardiac Risk Stratification for Noncardiac surgical procedures

A

x

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155
Q

dx

A

x

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156
Q

what is dx when determining perioperative cardiovascular risk ?

A

requires consideration of the type of surgery being performed as well as the clinical comorbidities and functional status of the patient

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157
Q

risk

A

x

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158
Q

what are considered low risk (<1%) surgeries of experiencing cardiac death or nonfatal MI?

A

breast, cataract, endoscopic procedure, or ambulatory or superficial procedure

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159
Q

what are considered intermediate risk (1-5%) surgeries of experiencing cardiac death or nonfatal MI?

A

CEA, head and neck, intraperiotoneal and intrathoracic, orthapedic, prostate

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160
Q

what are considered high risk (>5%) surgeries of experiencing cardiac death or nonfatal MI?

A

aortic or other major vascular, peripheral vascular

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161
Q

management

A

x

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162
Q

in patients undergoing low risk surgeries without acutely active cardiac disease (eg decompensated heart failure, unstable angina), what do you do regarding perioperative cardiovascular risk?

A

no further cardiac workup regardless of underlying comorbidities

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163
Q

Moderate- or high-risk patients (ie, with an estimated risk of cardiac death, nonfatal cardiac arrest, or nonfatal MI >1%) may need additional evaluation depending on?

A

functional status

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164
Q

what is considered good functional status?

A

> =4 METs of activity (eg brisk walking, climbing 2 flights of stairs)

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165
Q

if assesing for reduced excercise capacity, what would be appropriate tests?

A

stress testing (excercise EKG, Myocardial perfusion imagin) or repeat echocardiogram

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166
Q

Subacute Stent Thrombosis

A

x

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167
Q

syx

A

x

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168
Q

what are the symptoms of subacute stent thrombosis?

A

substernal chest pressure , mild nausea, all post stenting

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169
Q

dx

A

x

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170
Q

what does EKG show for subacute stent thromobosis?

A

ST elevation in leads II, III, aVF

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171
Q

risk

A

x

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172
Q

risk of subacute stent thrombosis occurs how soon after stent placement?

A

within 30 days

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173
Q

what is the risk of subacute stent thrombosis?

A

premature cessation of dual antiplatelet therapy with aspirin and platelet P2Y12 receptor blocker (i.e. clopidogrel, prasugrel, ticagrelor)

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174
Q

Acute Decompensated Heart Failure (ADHF)

A

x

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175
Q

syx

A

x

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176
Q

what are the symptoms of acute decompensated heart failure?

A
  • acute dyspnea, orthopnea, paroxysmal nocturnal dyspnea
  • HTN common, hypotension suggests severe disease
  • acute SOB
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177
Q

PE

A

x

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178
Q

what are the physical exam findings of acute decompensated heart failure?

A
  • anxious appearing, diaphoretic
  • JVD, S3 gallop, faint holosystolic murmur over the apex
  • crackles to the midlung level bilaterally, decreased SpO2
  • pitting edema LE
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179
Q

what does the S3 gallop and holosystolic murmur suggest?

A

dilated cardiomyopathy with functional mitral regurg

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180
Q

risk

A

x

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181
Q

what are the risk factors that lead to Acute Decompensated Heart Failure?

A

coronary ischemia, HTN cardiomyopathy, excessive preload(excessive volume resuscitation) or afterload (severe HTN)

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182
Q

pathophys

A

x

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183
Q

what is the pathophys of ADHF?

A

LV systolic and/or diastolic dysfunction (i.e. coronary ischemia, HTN cardiomyopathy), with or without coexisting valvular or coronary heart disease.

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184
Q

a sudden increase in pulmonary capillary wedge pressure (along with atrial and ventricular filling pressures or LV preload) leads to what?

A

accumulation of fluid in pulmonary interstitial and alveolar spaces

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185
Q

treatment

A

x

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186
Q

what is the treatment of normal or elevated BP with adequate end organ perfusion?

A

supplemental O2
IV loop diuretics (eg furosemide)
Consider IV vasodilator (eg nitroglycerin)

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187
Q

what is the treatment for hypotension or signs of shock?

A

supplemental O2
IV loop diuretics (eg furosemide) as appropriate
IV vasodilator (eg norepinephrine)

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188
Q

when improving symptoms of ADHF, what is the most appropriate next steps pathophysiologically?

A

NAME?

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189
Q

when do you need to imporve myocardial contractility with dobutamine and milrinone?

A
  • in severe LV dysfunction and low cardiac output which leads to low cardiac output causing poor peripheral perfusion and end organ dysfunction
  • in patients with inadequate response to diuretic therapy
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190
Q

management

A

x

191
Q

what role does nitroglycerin have in ADHF?

A

venous dilator that leads to decrease in cardiac preload resulting in reduced intracardiac filling pressures and improvement of pulmonary edema

192
Q

what role does milrinone have in ADHF?

A

selective phosphodiesterase 3 inhibitor that causes positive inotropy (as well as reduction in preload and afterload). It can be useful for severe ADHF due to LV systolic dysfunction

193
Q

what med is contrainidcated in acute decompensated heart failure?

A

beta blockers

194
Q

Heart Failure with Preserved Ejection Fraction (HFpEF)

A

x

195
Q

cause

A

x

196
Q

what is the cause of HFpEF?

A

caused by LV diastolic dysfunction

197
Q

pathophys

A

x

198
Q

what is the pathophys of HFpEF?

A

prolonged systemic HTN causes LVH and impaired diastolic filling, eventually leading to decompensated volume overload despite normal LV EF>50%

199
Q

association

A

x

200
Q

what are common associated diseases?

A

obesity, DM, OSA

201
Q

dx

A

x

202
Q

how do you dx CHF?

A

largely based on history and physical exam

203
Q

what do you see on CXR?

A

pleural effusions or pulm edema (kerley b lines=horizontal lines representing interstitial edema)

204
Q

what does echo show?

A

concentric LVH , left atrial enlargement, and LVEF >50%

205
Q

what are BNP levels usually?

A

BNP >100 pg/mL (however obesity lowers BNP levels, making it an unreliable test in these patients)

206
Q

syx

A

x

207
Q

what are the symptoms of HFpEF?

A

dyspnea, orthopnea, PND

208
Q

PE

A

x

209
Q

what are physical exam findings of CHF?

A

elevated JVP, lower extremity edema, S3

210
Q

Obesity Hypoventilation Syndrome (OHS)

A

x

211
Q

syx

A

x

212
Q

what are the syx of OHS?

A

dyspnea

213
Q

PE

A

x

214
Q

what aer the PE of OHS?

A

right sided HF leading to LE edema, hepatomegaly, elevated JVD

215
Q

ST elevation myocardial infarction (STEMI)

A

x

216
Q

syx

A

x

217
Q

what are the symptoms of STEMI?

A

CP like a pick up is right on top of chest, diaphoretic, chest tightness

218
Q

PE

A

x

219
Q

what are the PE findings of STEMI?

A

diffuse mild chest tenderness, low pitched sound at the apex just before S1

220
Q

Dx

A

x

221
Q

what are the classic EKG findings of STEMI?

A

ST elevation of 1.5mm in leads I and aVL with reciprocal changes 1-mm ST depression in II, III, and aVF

222
Q

what are the EKG findings that diagnose STEMI?

A
  • New ST elevation at the J point in >=2 anatomically contiguous leads with the following threshold:
  • ->All leads except V2 and V3: > 1 mm (0.1 mV)
  • ->Leads V2 and V3: > 1.5 mm in women, >2 mm in men age >40, and >2.5 mm in men age <40
  • New left bun
223
Q

what is the J point?

A

point where QRS complex meets the ST segment

224
Q

how tall is each little box on EKG? big box on EKG?

A

little box: 1mm

big box: 5mm

225
Q

trx

A

x

226
Q

what is optimal therapy for STEMI?

A

percutaneous coronary intervention (PCI) within 90 minutes of first medical contact or within 120 mintues for patients who require rapid transfer to a PCI capable facility

227
Q

what are types of fibrinolytic therapy?

A

tenecteplase, alteplase, reteplase

228
Q

when are cardiac enzymes and serial EKGs appropriate?

A

patients with suspected but undiagnosed ACS

229
Q

Acute Inferior wall STEMI

A

x

230
Q

pathophys

A

x

231
Q

what is the pathophys of sinus brady in acute inferior wall STEMI ?

A

due to ischemia of the SA node and right ventricular wall triggering an increase in vagal tone

232
Q

dx

A

x

233
Q

what is the diagnosis of acute inferolateral wall STEMI?

A

ST elevation in leads II, III, aVF

234
Q

complications

A

x

235
Q

what is a common complication of acute inferior wall STEMI?

A

bradyarrhythmias, typically transient

236
Q

acute inferior wall STEMI can lead to severe bradycardia leading to inadequate LV cardiac output causing what?

A

pulmonary edema (evidenced by bibasilar crackles) and cardiogenic shock

237
Q

trx

A

x

238
Q

how do you treat acute inferolateral wall STEMI?

A

IV atropine

239
Q

Acute Anterior wall MI

A

x

240
Q

trx

A

x

241
Q

do these patients respond to atropine in setting of bradycardia?

A

no they don’t becasue the bradyarrhyhtmias of anterior wall MI are commonly due to damage to the conduction system below the AV node (AV block in this setting is unlikely to respond to atropine)

242
Q

once cardiac pacing is initiated for bradycardia, what is the next step in the setting of ST elevation in either lateral or inferior leads?

A

PCI

243
Q

Persistent bradycardia secondary to anterior or inferior wall acute MI?

A

x

244
Q

trx

A

x

245
Q

what is the trx of choice?

A

cardiac pacing if syx (hypotenision, dizziness, heart failure, syncope) and not responsive to atropine

246
Q

Post MI Sexual Activity

A

x

247
Q

issue

A

x

248
Q

what is the issue after an MI in engaging in sexual activity?

A

sexual activity associated with increased in HR and BP, and a small but measurable absolute increase in teh risk of MI

249
Q

metabolic equivalents

A

x

250
Q

what is the metabolic equivalents for sexual activity?

A

3-4 METs

251
Q

what is the metabolic equivalents for rest?

A

1 METs

252
Q

what is the metabolic equivalents for walking?

A

2 METs

253
Q

what is the metabolic equivalents for housework?

A

2-4 METs

254
Q

what is the metabolic equivalents for moderate walking, sexual intercourse?

A

3-4 METs

255
Q

what is the metabolic equivalents for climbing stairs, golf, ballroom dancing?

A

4-5 METs

256
Q

what is the metabolic equivalents for weight lifting?

A

5-7 METs

257
Q

what is the metabolic equivalents for aerobic sports (cycling, tennis, basketball)?

A

8-10 METs

258
Q

what is the metabolic equivalents for running?

A

8-12 + METs

259
Q

CVD status and sexual activity

A

x

260
Q

CVD status in regards to sexual activity can be divided into three categories. what are they?

A

Low risk
High Risk
Indeterminant/Intermediate Risk

261
Q

What are low risk patients?

A

light intensity excercise without syx and should be able to initiate or resume sexual activity (ex include-those with few CVD risk factors, controlled hypertension, asymptomatic left ventricular dysfunction, or successful revascularization of clinically significant lesions (>50%-60%))

262
Q

what are high risk patients?

A

referred for a detailed assessment prior to advising on activity. Examples include (refractory angina, NYHA class IV heart failure, significant arrythmias, severe valvular disease)

263
Q

what are indeterminate/intermediate risk patients?

A

stress testing recommended to reclassify them as low or high risk and to help guide decisions

264
Q

managment

A

x

265
Q

what do you tell low risk patients about resuming sexual activity post MI?

A

safely resume intercourse soon after the MI, within 3-4 weeks and possibly as early as 1 week

266
Q

Acute Pericarditis

A

x

267
Q

dx

A

x

268
Q

what are the EKG findigns of acute pericardiits?

A

diffuse ST elevation with PR depression

269
Q

what does echo show for acute pericarditis?

A

pericardial effusion

270
Q

PE

A

x

271
Q

what does PE findings show Acute Pericarditis?

A

pleuritic CP (decreases with sitting), pericardial friction rub (highly specific)-scratchy sound heard during ventricular systole along the left sternal border

272
Q

causes

A

x

273
Q

what are the causes of acute pericarditis?

A

viral or idiopathic, autoimmune disease (eg SLE), uremia (acute or chronic renal failure), post MI (early: peri-infarction pericardiits; late: dressler syndrome)

274
Q

trx

A

x

275
Q

what is the treatment for acute pericarditis?

A

NSAIDs and colchicine for viral or idiopathic, variable for other etiologies

276
Q

Acute Pericarditis Module

A

x

277
Q

syx

A

x

278
Q

what are syx of Acute Pericarditis?

A

sharp, retrosternal chest pain worsened with inspiration and relieved by leaning forward, fever

279
Q

what are common preceding syx of viral Acute Pericarditis ?

A

preceding flu like illness , febrile over the days prior to admission

280
Q

DDx

A

x

281
Q

what is on the differential for Acute Pericarditis?

A

Acute MI, Pulm Embolism, PNA, GERD, MSK pain

282
Q

initial orders

A

x

283
Q

what are important initial orders for Acute Pericarditis?

A

IV access, Oxygen therapy, pulse ox, cardiac monitoring, EKG

284
Q

Dx

A

x

285
Q

what does EKG for Acute Pericarditis classically show?

A

diffuse ST segment elevation

286
Q

PE

A

x

287
Q

what do you appreciate on Physical exam for Acute Pericarditis?

A

pericardial friction rub

288
Q

causes

A

x

289
Q

what are causes of Acute Pericarditis?

A

viral agents, neoplasm, uremia, autoimmune disease, TB, bacteria, acute MI, and trauma

290
Q

workup

A

x

291
Q

what are important initial dx orders for Acute Pericarditis?

A

CBC (infxn, inflammation), BMP (to evaluate uremia), CXR, echo (to rule out cardiac tamponade), blood culture (in febrile patients), ESR.

292
Q

where do you admit patient after ordering those labs for Acute Pericarditis?

A

into the wards

293
Q

what are other important labs to order in Acute Pericarditis in whcih the underlying cause is not readily apparent (URI, uremia, post MI, cardiac surgery)?

A

ANA, HIV, TB skin testing

294
Q

management

A

x

295
Q

when is pericardiocentesis indicated in Acute Pericarditis?

A

if echo shows cardiac tamponade

296
Q

what are the criteria for hospitilization of Acute Pericarditis ?

A

fever >100.4, cardiac tamponade, failure to respond to NSAIDs within one week, immunosuppressed, anticoagulated, acute trauma, elevated cardiac trops

297
Q

what is initial best management for Acute Pericarditis?

A

NSAIDs and colchicine for idiopathic or viral pericarditis,

298
Q

how long do you continue NSAIDs and colchicine in Acute Pericarditis?

A

NSAID should be continued while the patient is symptomatic . (generally <2 weeks)

colchicine should continued for 3 months

299
Q

in which patient population of Acute Pericarditis should you avoid NSAIDs (other than aspirin)?

A

post-MI pericarditis

300
Q

in which patient population of Acute Pericarditis do you use steroids as second line ?

A

idiopathic or viral pericariditis that is resisitant to NSAIDs and colchicine

301
Q

in which patient population of Acute Pericarditis do you give steroids as first line trx?

A

in autoimmune disease Acute Pericarditis

302
Q

if you have uremia induced Acute Pericarditis, what do you manage with ?

A

dialysis

303
Q

Peri-infraction Pericarditis (PIP)

A

x

304
Q

timing

A

x

305
Q

when does pericardiits typically occur post MI?

A

<4 days following MI

306
Q

risk

A

x

307
Q

what increases the risk of developing PIP?

A

delayed coronary reperfusion following STEMI (eg >3 hours from symptom onset)

308
Q

syx

A

x

309
Q

what are the symptoms of PIP?

A

pleuritic CP that worsens with deep inspiration and improves with sitting up. Pain is usually located retrosternally and often radiates posteriorly to the bilateral trapezius ridges (lower porition of the scapulae). +/- low grade fever

310
Q

PE

A

x

311
Q

what does cardiac ausculation show?

A

triphasic pericardial friction rub(heard in atrial systole, ventricular systole, and early ventricular diastole

312
Q

trx

A

x

313
Q

what is the trx for those with significant discomfort?

A

high dose aspirin (650mg 3x/day)=analgesia and anti-inflammatory effects

314
Q

for patients with persistent symptoms despite high dose aspirin, what is the trx?

A

colchicine or narcotic analgesics (eg oxycodone)

315
Q

why is aspirin a better choice over other NSAIDs?

A

Other anti-inflammatory agents (eg, other nonsteroidal anti-inflammatory drugs, glucocorticoids) should be avoided as they may impair myocardial healing and increase the risk of ventricular septal or free wall rupture.

316
Q

complications

A

x

317
Q

what are the complications of PIP?

A

right ventricular failure (acute), papillary muscle rupture (acute or within 3-5 days), interventricular septum rupture (acute or w/n 3-5 d), free wall rupture (within 5d-2wks), left ventricular aneurysm (up to several months),

318
Q

Right Bundle Branch Block (RBBB)

A

x

319
Q

dx

A

x

320
Q

what are the EKG findings of RBBB?

A

R prime wave (second R wave) in V1 accompanied by a widened S wave in V6

321
Q

association

A

x

322
Q

what are the associated RBBB inducing diseases?

A

pHTN or acute PE

323
Q

Right Heart Strain

A

x

324
Q

dx

A

x

325
Q

what are EKG findings of right heart strain?

A

T wave inversion in Leads II,III, aVF

326
Q

Ventral Septal Defect (VSD)

A

x

327
Q

PE

A

x

328
Q

what are the physical exam findings of VSD?

A

a harsh, 4/6 holosystolic murmur is heard at the 4th left intercostal space close to the sternal border accompanied by a thrill

329
Q

the murmur is ___ in a small restrictive VSD, but the murmur is ___ in a large nonrestrictive VSD?

A

small VSD has a loud murmur

large VSD has a soft murmur (due to equalization of right and left ventircular pressures)

330
Q

epid

A

x

331
Q

what is the epidemiology of VSD?

A

most common congenital heart defect at birth

332
Q

trx

A

x

333
Q

what is the trx for VSD?

A

spontaneous closure in 40-60% of patients during early childhood

334
Q

syx

A

x

335
Q

what are syx of VSD?

A

asyx

336
Q

dx

A

x

337
Q

what does the echo show for VSD?

A

right ventricle dilation along with enlargement of the left ventricle, left atrium, and pulmonary arteries due to volume overload in pulm circulation

338
Q

Atrial Septal Defect (ASD)

A

x

339
Q

PE

A

x

340
Q

what is murmur heard on exam for ASD with large left to right shunt and normal pulm artery pressure?

A

wide and fixed splitting of the second heart sound

341
Q

what is the auscultation sounds of ASD?

A

mid-systolic ejection murmur resulting form increased flow across the pulmonic valve, and a mild diastolic rumble from increased flow across the tricuspid valve

342
Q

what does the murmur of ASD sound like if there is a left to right shunt?

A

mid- systolic murmur at the left upper sternal border with right atrial and ventricular dilation

343
Q

pathophys

A

x

344
Q

what is the pathophys of ASD?

A

left to right shunt with increased flow through the pulmonic valve.

345
Q

syx

A

x

346
Q

what are the syx of ASD?

A

most patients asyx. those with significant shunt flow have decreased excercise tolerance (dyspnea and fatigue), other complicatoins like pulm HTN, right CHF, stroke due to paradoxical embolization, atrial arrythmias (afib or aflutter)

347
Q

dx

A

x

348
Q

what does Echo show?

A

normal LV size and function and right atrial and ventricular dilation

349
Q

what does EKG show?

A

Afib with RVR

350
Q

Mitral Valve Prolapse (MVP)

A

x

351
Q

PE

A

x

352
Q

what is the murmur heard on exam for MVP?

A

single or multiple non ejection clicks (due to snapping of the mitral chordae as the valve cusps extend into the atrium during systole) and/or mid to late systolic murmur of mitral regurg that is best heard at or just medial to the cardiac apex.

353
Q

what maneuvers cause the systolic murmur of MVP start earlier (and is longer and softer) from decreased venous return ?

A

standing, valsalva, inhalation of amyl nitrate

354
Q

what maneuvers cause the systolic murmur of MVP to be delayed in onset (late in systole) or may not be reached at all (dissapearance of the click)?

A

squatting, leg elevation, and handgrip

355
Q

pathohpys

A

x

356
Q

what is the most important factor in affecting the onset of the click (early vs late) in MVP?

A

LVEDV (LV end diastolic volume).

  • The LVEDV is relatively high with increased venous return (squatting, supine leg raise), causing a later click in systole of the MVP murmur.
  • The LVEDV is relatively low with decreased venous return (eg standing, valsalva), causing an earlier click in systole of the MVP murmur
357
Q

x

A

x

358
Q

Tetralogy of Fallot (TOF)

A

x

359
Q

epid

A

x

360
Q

what is the frequency of Tetralogy of Fallot ?

A

most common cyanotic congenital heart defect

361
Q

dx

A

x

362
Q

what are the components of TOF?

A

right ventricular outflow tract (RVOT), overriding aorta, right ventricular hypertrophy, and VSD

363
Q

pathophys

A

x

364
Q

what is the pathophys of TOF?

A

as RVOT obstruction increases , it leads to decreased pulm blood flow, resulting in cyanosis early in life.

365
Q

Tricuspid Regurgitation

A

x

366
Q

PE

A

x

367
Q

what is the physical exam sound of tricuspid regurg?

A

holosytolic murmur at the lower sternum that increases with inspiration

368
Q

Tricuspid Valve Stenosis

A

x

369
Q

dx

A

x

370
Q

what is the heart murmur associated with tricuspid valve stenosis?

A

mid-diastolic rumble best heard along the left sternal border

371
Q

Anomalous Coronary Artery/Anomalous Aortic Origin of a Coronary Artery (AAOCA)

A

x

372
Q

syx

A

x

373
Q

what are common syx

A

exertional angina, lightheadedness, or syncope. Sudden cardiac death in young athletes

374
Q

epid

A

x

375
Q

what population is most commonly affected?

A

young athletes (<35y.o. )

376
Q

pathophys

A

x

377
Q

what is the pathophys of AAOCA?

A

-Two types of AAOCA commonly associated with Sudden Cardiac Death are the left main coronary artery originating from the right aortic sinus (with right coronary artery also originating from the same side) and the right coronary artery originating from the

378
Q

dx

A

x

379
Q

what does the EKG of AAOCA normally show?

A

resting EKG is typically unremarkable

380
Q

Brugada Syndrome

A

x

381
Q

dx

A

x

382
Q

what are the EKG findings of Brugada Syndrome?

A
  • right bundle branch block

- ST elevation in leads V1-V3

383
Q

Long QT syndrome

A

x

384
Q

dx

A

x

385
Q

what are the EKG findings of Long QT syndrome?

A

Men: QTc>450 ms
Women: QTc>470 ms

386
Q

syx

A

x

387
Q

what is an uncommon presentation of long QT syndrome?

A

sudden cardiac death

388
Q

Hypertrophic Obstructive Cardiomyopathy (HOCM)

A

x

389
Q

epid

A

x

390
Q

what population is most commonly affected?

A

young athletes

391
Q

what is the most common cause of sudden SCD in young athletes?

A

HOCM

392
Q

genetics

A

x

393
Q

what is the genetic mutaiton?

A

myosin gene

394
Q

dx

A

x

395
Q

what do you see on EKG?

A

LV hypertrophy ( Add the R wave in aVL and the S wave in V3. If the sum is greater than 28 millimeters in males or greater than 20 mm in females, LVH is present. Or look at increased voltage in precordial leads (V1-V5)

396
Q

what do you see on Echo?

A

small left ventricular cavity, LV hypertrophy (often asymmetric and involving the septum), and increased LV outflow tract gradient pressure that increases with valsalva.

397
Q

what else do you see on echo for HOCM?

A

echo shows left atrial enlargement , intraventricular septal thickness increased, and posterior left ventricular wall thickness increased. There is a systolic anterior moition of the mitral valve.

398
Q

PE

A

x

399
Q

what do you hear on PE for HOCM?

A

harsh crescendo-decresendo systolic murmur heard best at the apex and lower left sternal border.

murmur increases in intensity with valsalva and also when rising from sitting or squatting position

400
Q

what maneuvers increase murmur intensity?

A

decrease preload: which decrease LV Blood volume: valsalva, abrupt stending , nitroglycerin administration

401
Q

what maneuvers decrease murmur intensity?

A

increase afterload: sustained hand grip
squatting: increase afterload and preload
passive leg raise: increase preload

All increase LV blood volume, which decrease murmur intensity

402
Q

Syx

A

x

403
Q

what are the symptoms of HOCM?

A

asyx or severe fatigue, exertional dyspnea, CP, palpitations, presyncope, or syncope

404
Q

Trx

A

x

405
Q

what is the treatment of HOCM?

A

negative inotropic agents (beta blockers, verapamil or disopyramide)

usually start with beta blockers and then add verapamil or disopyramide

406
Q

what is the treatment in those with refractory HOCM?

A

-Alcohol septal ablation (injecting ethanol into the first or second septal perforator artery to cuase a localized MI in the basal septum leading to localized scarring and remodeling over time and leads to a reduction in LVOT gradient with improvment in s

407
Q

what are indications for ICD (implantable cardioverter -defibrillator)?

A

prevention of SCD in patients with hx of cardiac hx or sustained VT. HCM patients have high risk of malignant arrythmias (fam hx of SCD, recurrent or exertional syncope, nonsustained VT, hypotension w excercise, extreme LVH)

408
Q

Constrictive Pericarditis

A

x

409
Q

cause

A

x

410
Q

what is the cause of constrictive pericarditis?

A
  • idiopathic or viral pericarditis
  • cardiac surgery or radiation therapy
  • TB pericarditis (in endemic areas)
411
Q

syx

A

x

412
Q

what are the symptoms?

A

fatigue, DOE, peripheral edema

413
Q

PE

A

x

414
Q

what are the physical exam findings of constrictive pericarditis?

A

increased JVD, pericardial knock (mid diastolic sound) may be heard, pulsus paradoxus, kussmaul’s sign (increa or lack of decrease in JVP on inspiration), hepatic congestion with hepatomegaly

415
Q

what does cardiac auscultation show?

A

mid diastolic murmur

416
Q

dx

A

x

417
Q

what are EKG findings for constrictive pericarditis?

A

nonspecific or show atrial fibrillation or low voltage QRS complex

418
Q

what are CXR findings for constrictive pericarditis?

A

calcified cardiac borders

419
Q

what does jugular venous pulse tracings show?

A

prominent x and y descents

420
Q

what does echo show for constrictive pericarditis?

A

pericardial thickening and calcification , atrial enlargement, and abnormal septal motion

421
Q

what is considered elevated JVD?

A

> 8cm H20

422
Q

risk

A

x

423
Q

what is a common risk for constrictive pericarditis?

A

post op from CABG

424
Q

pathophys

A

x

425
Q

what is the pathophys of constrictive pericarditis post CABG surgery?

A

post pericardial effusions commonly form and eventually continued inflammation over months may lead to development of thickened, fibrous pericardium and constrictive pericarditis

426
Q

trx

A

x

427
Q

what are the treatment options for constrictive pericarditis?

A
  • supportive care (anti-inflammatory agents)

- pericardiectomy for refractory causes

428
Q

Amiodarone Toxicity

A

x

429
Q

side effects

A

x

430
Q

what are side effects of amiodarone?

A

thyroid dysfunction, hepatotoxicity, cardiac bradyarryhtmias, chronic interstitial pneumonitis, neuorlogic symptoms (eg ataxia, peripheral neuropathy), blue-gray skin discoloration, and visual disturbances.

431
Q

timeline

A

x

432
Q

what is the timeline for amiodarone toxicity?

A

prolonged treatment

433
Q

syx

A

x

434
Q

what are syx of amiodarone toxicity?

A

photosensitivity, skin discoloration, bone marrow suppression, thyroid dysfunction, abnormal liver function tests, and pulmonary toxicity

435
Q

Pulmonary Toxicity from Amiodarone

A

x

436
Q

forms

A

x

437
Q

what are forms of Pulmonary Toxicity from Amiodarone?

A

chronic interstitial pneumonitis, organizing pneumonia, acute respiratory distress syndrome, and rarely with a solitary pulmonary mass

438
Q

which is the most common form of Pulmonary Toxicity from Amiodarone?

A

Chronic interstitial pneumonitis,

439
Q

Chronic interstitial pneumonitis

A

x

440
Q

features

A

x

441
Q

what are features of Chronic interstitial pneumonitis?

A

nonproductive cough, fever, pleuritic chest pain, weight loss, dyspnea on exertion and a focal or diffuse interstitial opacity on the chest radiograph

442
Q

risk

A

x

443
Q

what is the risk dose of amiodarone to lead to pulm toxicity?

A

higher maintenance doses (more than 400 mg/day)

444
Q

management

A

x

445
Q

what is the mainstay of management of Pulmonary Toxicity from Amiodarone?

A

`Discontinuation of amiodarone is the mainstay of treatment for amiodarone-induced pulmonary toxicity

Corticosteroids can be used in patients with severe or life-threatening pulmonary disease

446
Q

prognosis

A

x

447
Q

what is the prognosis of Pulmonary Toxicity from Amiodarone?

A

good , majority of patients either stabilize or improve after the complete withdrawal of the drug

448
Q

Cardiac Amyloidosis

A

x

449
Q

dx

A

x

450
Q

what would EKG show?

A

low voltage on EKG

451
Q

what woudl Echo show?

A

increased ventricular wall thickness with normal LV cavity dimensions

452
Q

syx

A

x

453
Q

what do syx of cardiac amyloidosis show?

A

unexplained CHF

454
Q

Superior Vena Cava Syndrome

A

x

455
Q

pathophys

A

x

456
Q

what is the pathophys of SVC Syndrome?

A

obstruction of blood flow (typically due to external compression from a tumor)

457
Q

syx

A

x

458
Q

what are the SVC syndrome syx?

A

facial swelling, JVD, distended chest wall veins

459
Q

Blunt Cardiac Injury

A

x

460
Q

risk

A

x

461
Q

what is the major risk of blunt cardiac injury?

A

Motor Vehicle Collision

462
Q

syx

A

x

463
Q

what are the syx of Blunt Cardiac Injury?

A

acute heart failure, cardiac arrythmias, myocardial ruputure, superficial injuries across chest

464
Q

complications

A

x

465
Q

what are the complications of blunt cardiac injury?

A

pericardial effusion, tamponade, and cardiogenic shock

466
Q

what are the rapidly fatal injuiries in blunt cardiac injury?

A

pneumothorax, aortic dissection, hemoperitoneum, pericardial effusion leading to tamponade

467
Q

dx

A

x

468
Q

what is the best initial dx test to rapidly identify rapidly fatal injuires in blunt cardiac injury?

A

FAST (bedside U/S)

469
Q

what happens to cardiac biomarkers in blunt thoracic trauma?

A

elevated troponins (non specific)

470
Q

what are the best proceeding dx test to after FAST to identify rapidly fatal injuires in blunt cardiac injury?

A

CXR, CT scan of chest

471
Q

PE

A

x

472
Q

what are the physical exam findings of blunt cardiac injury?

A

bruises over the anterior chest

473
Q

x

A

x

Cardiology (7 decks)

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