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DIT Cards > Cardio Review > Flashcards

Cardio Review Flashcards

1
Q

Which embryologic structure of the heart gives rise to the ascending aorta and pulmonary trunk?

A

truncus arteriosus

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2
Q

Which embryologic structure of the heart gives rise to the coronary sinus?

A

left horn sinus venosus

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3
Q

Which embryologic structure of the heart gives rise to the SVC?

A

R common cardinal vein and right anterior cardinal vein

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4
Q

Which embryologic structure of the heart gives rise to the smooth parts of the left and right ventricles?

A

bulbus cordis

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5
Q

Which embryologic structure of the heart gives rise to the smooth part of the right atrium?

A

right horn sinus venosus

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6
Q

Which embryologic structure of the heart gives rise to the trabeculated parts of the left and right atria?

A

primitive atria

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7
Q

Which embryologic structure of the heart gives rise to the trabeculated parts of the left and right ventricles?

A

primitive ventricles

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8
Q

Which structure divides the truncus arterioles into the aortic and pulmonary trunk? What is the cellular origin of this structure?

A 
spiral septum (aorticopulmonary septum)
neural crest cell origin
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9
Q

Which fetal vessel has the highest oxygenation?

A

umbilical vein

Highest -> Lowest O2
umbilical vein -> ductus venous -> IVC -> R atrium

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10
Q

What causes the ductus arteriosus to close?

A

infant breathing -> increased oxygenation of the aorta -> increased prostaglandins -> closure of ductus arteriosus

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11
Q

What causes the foramen ovale to close?

A

infant breathing -> decreased pulmonary vascular resistance -> increase LA pressure -> pushes septum premium against septum secundum

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12
Q

What are the components of tetralogy of Fallot?

A
  1. pulmonary outflow obstruction (usually pulmonic stenosis)
  2. RVH
  3. VSD
  4. overriding aorta
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13
Q

Explain how the great vessels are attached in transposition of the great vessels.

A

RV -> aorta; LV -> pulmonary vasculature

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14
Q

A 45 year old man presents with a blood pressure of 160/90 mmHg on the right arm and 170/92 mmHg on the left arm. There are no palpable pulses int he feet or ankles. What problem does this patient most likely have?

A

Coarctation of the aorta

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15
Q

What heart defect is associated with chromosome 22q11 deletion?

A

truncus arteriosus, ToF

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16
Q

What heart defect is associated with Down syndrome?

A

ASD, VSD, AV septal defect

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17
Q

What heart defect is associated with congenital rubella?

A

PDA, pulmonary artery stenosis, septal defects

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18
Q

What heart defect is associated with Turner syndrome?

A

bicuspid aortic valve, coarctation of the aorta

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19
Q

Continuous machine-like murmur

A

PDA

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20
Q

Boot-shaped heart

A

ToF, RVH in adult

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21
Q

Rib notching

A

coarctation of aorta

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22
Q

Most common congenital cardiac anomaly

A

VSD

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23
Q

most common congenital cause of early cyanosis

A

ToF

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24
Q

What is the pulse pressure in a patient with a systolic blood pressure of 150 and a mean arterial pressure (MAP) of 90 mmHg?

A 
MAP = 90
MAP = 2/3 diastolic + 1/3 systolic
90 = 2/3x + 1/3 (150)
x=60
Pulse pressure = 150-60 = 90mmHg
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25
Q

What is the basic equation for cardiac output (CO)? What is the Fick principle?

A

CO = SV * HR

Fick principle = CO = rate of O2 consumption/ arterial O2 - venous O2

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26
Q

How can the myocardial oxygen demand be decreased in circumstances where the heart is ischemic?

A

decreased after load (decreased SBP)
decreased contractility
decreased HR
decreased preload

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27
Q

What can make the stroke volume (SV) increase for a given preload?

A

increased contractility (sympathetic stimulation)
inotropic drugs (catecholamines, digoxin)
increased intracellular Ca2+
decreased extracellular Na+
decrease after load (hydralazine, ACEi)

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28
Q

What is the cardiac ejection fraction (EF)?

A

EF = SV/EDV

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29
Q

What are the signs of right sided heart failure?

A

systemic Sx - peripheral edema, increased JVD, hepatosplenomegaly (nutmeg liver)

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30
Q

What are the signs of left-sided heart failure?

A 
lung Sx - pulmonary edema -> rales
orthopnea
dyspnea on exertion
paroxysmal nocturnal dyspnea
dilated cardiomyopathy
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31
Q

How does poor cardiac output result in an increase in aldosterone?

A

decreased CO -> decreased BP (detected via JG cells in kidney) -> increased RAAS -> increased aldosterone

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32
Q

What medications are used to treat chronic heart failure?

A 
Symptomatic Relief
- digoxin
- diuretics
- vasodilators
Survival increaseres
- ACE inhibitors
- ARBs
- aldosterone antagonists
- certain beta blockers
- nitrates plus hydralazine
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33
Q

What medications are used to treat acute heart failure?

A

NO LIP
Nitrates
Oxygen

Loop Diuretics
Inotropic drugs
Positioning

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34
Q

What is the MOA of digoxin?

A

blocks Na+/K+-ATPase at myocyte -> increased intracellular Ca2+ -> increased contractility

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35
Q

How does heart failure impact the Starling forces?

A

increased hydrostatic capillary pressure

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36
Q

How does liver failure impact the Starling forces?

A

decreased oncotic capillary pressure

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37
Q

how does oliguric renal failure impact starling forces?

A

increased hydrostatic capillary pressure (increased fluids)

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38
Q

how do infections and toxins impact the starling forces?

A

increased Kf (increased capillary permeability)

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39
Q

how does nephrotic syndrome impact the starling forces?

A

decreased oncotic pressure of the capillaries

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40
Q

how does lymphatic blockage impact starling forces?

A

increased interstitial oncotic pressure (non-pitting edema)

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41
Q

how do burns impact starling forces?

A

increased Kf

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42
Q

How does diuretic administration impact starling forces?

A

decreased hydrostatic pressure of capillaries

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43
Q

How does IV infusion of albumin or clotting factors impact starling forces?

A

increased oncotic pressure of the capillaries

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44
Q

How does venous insufficiency impact starling forces?

A

increased hydrostatic pressure of capillaries (local edema)

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45
Q

How do the vascular resistance and stroke volume change in hypovolemic shock?

A

decreased stroke volume

increased vascular resistance to compensate

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46
Q

How do stroke volume and vascular resistance change in septic shock?

A

decreased vascular resistance

increased stroke volume to compensate

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47
Q

What are some causes of cariogenic shock?

A

CHF, MI, pneumothorax, PE, arrhythmias, cardiac tamponade, cardiac contusion

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48
Q

How is the skin of a patient different in cariogenic shock compared to septic shock?

A

cariogenic shock - cold, clammy, cyanotic, poorly perfused

septic shock - initially warm/flushed

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49
Q

When does isovolumetric contraction take place?

A

systole (after mitral valve closes but before aortic valve opens)

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50
Q

How does an increase in after load affect the stroke volume of the heart assuming contractility remains the same?

A

increased after load = decreased SV (graph gets taller)

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51
Q

What impact does an increase in contractility have on stroke volume assuming preload and after load remain constant?

A

increased contractility = increased SV (graph sifts left)

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52
Q

Which heart sound is associated with dilated CHF? Which heart sound is associated with chronic hypertension?

A 
S3 = dilated CHF
S4 = chronic HTN
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53
Q

What gives rise to the jugular venous a, c, and v waves?

A

JV a = atrial contraction
c = ventricle contraction
v = atrial filling against a closed tricuspid valve

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54
Q

Where does the QRS complex fall in relation to valvular dynamics?

A

QRS correlates to just before closure of the mitral and tricuspid valves

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55
Q

Which murmurs are heard best in the left lateral decubitus position?

A

Left S3 and left S4
mitral stenosis
mitral regurgitation

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56
Q

bounding pulses, head bobbing, diastolic murmur

A

aortic regurgitation

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57
Q

crescendo-decrescendo systolic murmur best heard in the 2nd-3rd right interspace close to the sternum

A

aortic stenosis

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58
Q

early diastolic decrescendo murmur heard best along the left sternal border with BP of 160/55

A

aortic regurgitation

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59
Q

late diastolic decrescendo murmur heard best along the lower left sternal border

A

tricuspid stenosis

60
Q

holosystolic murmur best heard at the apex and often radiates to the left axilla

A

mitral regurgitation

61
Q

late systolic murmur usually preceded by a mid-systolic click

A

mitral valve prolapse

62
Q

crescendo-decrescendo systolic murmur best heard in the 2nd-3rd left interspaces close to the sternum

A

pulmonic stenosis

63
Q

holosystolic murmur best heard along the left lower sternal border

A

tricuspid regurgitation or VSD

64
Q

rumbling, late diastolic murmur with an opening snap, loudest in the 5th interspace in the midclavicular line

A

mitral stenosis

65
Q

What is the mechanism of action of each class of antiarrhythmics?

A 
Class I (Na+ CB) -> inhibit phase 0 of myocyte
Class II (beta blockers) -> decrease cAMP, decreased Ca2+, phase 4 of pacemaker
Class III (K+ CB) -> inhibit phase 3 of myocyte
Class IV (CCB) -> inhibit phase 0 of pacemaker
66
Q

Which anti arrhythmic has the side effect of cinchonism?

67
Q

What are the potential side effects of amiodarone use?

A 
pulmonary fibrosis
TdP
hyper or hypothyroidism
hepatotoxicity
blue-gray skin discoloration
photodermatitis/photosensitivity
decreased HR
heart block
corneal deposits
neuro problems
constipation
68
Q

What is the mechanism of action of adenomas as an anti arrhythmic?

A

adenosine stops the heart

increases K+ out of cells -> hyper polarizes and decreased Ca2+, decreasing AV node conduction

69
Q

What class of antiarrhythmics does sotalol belong to?

A

Class III (K+)

70
Q

What class of antiarrhythmics does bretylium belong?

A

Class III (K+)

71
Q

What class of antiarrhythmics does quinidine belong?

A

Class IA (Na+)

72
Q

What class of antiarrhythmics does procainamide belong?

A

Class IA (Na+)

73
Q

What class of antiarrhythmics does Lidocaine belong?

A

Class IB (Na+)

74
Q

How does the cause of a narrow QRS complex differ from the cause of a wide QRS complex?

A

Narrow QRS - normal conduction system originating at the top of the heart (sinus beat, ectopic atrial beat, SVT, junctional rhythm)

Wide QRS - PVC (premature ventricular contraction), V tach, BBB

75
Q

What is the ECG axis given the QRS deflections of positive lead I and positive lead II?

A

Normal axis

76
Q

What is the ECG axis given the QRS deflections of positive in lead I, negative in lead III?

77
Q

What is the ECG axis given the QRS deflections of negative in lead I, positive in lead III?

78
Q

What is the ECG axis given the QRS deflections of positive in lead I, negative in aVR?

A

normal axis

79
Q

How does hyperkalemia affect the shape of T waves?

A

causes peaked T waves

80
Q

What are the most common causes of left axis deviation?

A

inferior MI, left anterior fascicular block, left ventricular hypertrophy, left BBB

81
Q

What are the most common causes of right axis deviation?

A

RVH, acute R heart strain (PE), left posterior fascicular block, RBBB

82
Q

What is the treatment for ventricular fibrillation?

A

defibrillation

83
Q

What are the major characteristics of atrial fibrillation?

A

no P waves, increased rate, irregularly irregular

84
Q

What is the hallmark of a third degree AV block?

A

P wave and QRS waves beat separately

85
Q

What drugs are known to prolong the QT interval, increasing the likelihood of TdP in those at risk?

A 
Antiarrhythmics (IA, III)
Antipsychotics (haloperidol)
Antibiotics (macrocodes, chloroquine)
Antidepressants (TCAs)
Anti-HIV protease inhibitors
Methadone
86
Q

What are the two different types of second degree AV block? How do they differ?

A

Type 1 - Wenkebach (gives warning of dropped beat with progressively prolonged PR interval)
Type 2 - no warning before dropped beat

87
Q

Why is warfarin anticoagulation important in patients with chronic atrial fibrillation?

A

prevent clots that patients with a fib are predisposed to

88
Q

What substances act on smooth muscle myosin light-chain kinase? How does this affect BP?

A

Prostaglandins & ephedrine inhibit MLCK -> relaxation
CCB inhibit Ca2+ influx, thus inhibiting MLCK -> relaxation
relaxation = decreased BP (vasodilation)

89
Q

Describe the chain of events in which hypotension causes reflex tachycardia?

A

decreased BP -> decreased PSNS via CN IX and X -> nucleus solitaires -> decrease PSNS and increases SNS -> increase alpha1 stimulation to vasoconstriction -> increase HR via beta1 stimulation

90
Q

What is the blood pressure cutoff for the diagnosis of hypertension?

A

> /= 140/90 on 3 occasions

91
Q

What would you most suspect the cause of HTN to be in a patient with paroxysms of increased sympathetic tone: anxiety, palpitations, diaphoresis

A

pheochromocytoma

92
Q

What would you most suspect the cause of HTN to be in a patient with age of onset between 20 and 50?

A

essential HTN

93
Q

What would you suspect the cause of HTN to be in a patient with abdominal bruit?

A

renal artery stenosis

94
Q

what would you most suspect the cause of HTN to be in a patient with blood pressure in arms > legs?

A

coarctation of the aorta

95
Q

what would you most suspect the cause of HTN to be in a patient with a family history of HTN?

A

essential HTN

96
Q

What would you most suspect the cause of HTN to be in a patient with tachycardia, heat intolerance, diarrhea?

A

hyperthyroidism

97
Q

what would you most suspect the cause of HTN to be in a patient with hyperkalemia?

A

renal insufficiency

98
Q

what would you most suspect the cause of HTN to be in a patient with hypokalemia?

A

hyperaldosteronism (Conn syndrome)/renal artery stenosis

99
Q

What would you most suspect the cause of HTN to be in a patient with central obesity, moon-shaped face, hirsutism?

A

Cushing syndrome

100
Q

What would you most suspect the cause of HTN to be in a young individual with acute onset tachycardia?

A

illicit drugs - cocaine, amphetamine

101
Q

What would you most suspect the cause of HTN to be in a patient with proteinuria?

A

kidney disease

102
Q

What chest X-ray finding is a possible sign for aortic dissection?

A

widening of mediastinum

also think of: ruptured esophagus, lymphoma

103
Q

Which category of BP medications is preferred in the treatment of aortic dissection?

A

beta blockers

104
Q

What antihypertensive causes hypertrichosis?

A

(hair growth) Minoxidil

105
Q

What antihypertensive causes cyanide toxicity?

A

Nitroprusside

106
Q

What antihypertensive causes reflex tachycardia?

A

vasodilators (hydralazine, nitrates, dihydropyridines)

107
Q

What antihypertensive causes cough?

A

ACE inhibitors

108
Q

What antihypertensive causes possible development of a drug-induced lupus

A

hydralazine

109
Q

What antihypertensive causes possible angioedema?

A

ACE inhibitors and ARBs

110
Q

Which antihypertensives are particularly beneficial to heart failure patients?

A 
ACE inhibitors/ARBs
beta blockers (not in acute decompensated HF)
aldosterone antagonist
111
Q

Which antihypertensives are safe to use in pregnancy?

A 
Hypertensive Moms Love Nifedipine
Hydralazine
Methyldopa
Labetalol
Nifedipine (and other dihydropyridines)
112
Q

Which serum lab markers are commonly used to diagnose an MI?

A

troponin, CK-MB, CK

Troponin I is the most sensitive and specific

113
Q

Which coronary artery is most commonly occluded in an MI?

114
Q

What is the most common lethal complication after an MI?

A

v-fib (1-3 days after)

115
Q

What is the most common complication from an MI days 1-3 after?

A

arrhythmia

116
Q

What is the most common complication from an MI days 3-14 after?

A

ventricular wall rupture -> cardiac tamponade
papillary muscle rupture
ventricular aneurysm

117
Q

Chest pain, pericardial friction rub, and persistent fever occurring several weeks after an MI

A

Dressler syndrome

pericarditis post MI

118
Q

What wall is perfused by the LAD artery? What ECG leads would show an MI?

A

Anterior wall; V1-V4, V5

119
Q

What wall is perfused by the left circumflex artery? What ECG leads would show an MI?

A

Lateral wall; aVL, V5, V6

120
Q

What wall is perfused by the right coronary artery? What ECG leads would show an MI?

A

Inferior wall; II, III, aVF

AND posterior wall: R precordial ECG: V4

121
Q

What would cause cardiac tamponade following an MI?

A

ventricular wall rupture

122
Q

What would cause severe mitral regurgitation following an MI?

A

papillary muscle rupture

123
Q

What would cause a new VSD following an MI?

A

intraventricular septum rupture

124
Q

What would cause a stroke following an MI?

A

mural thrombus formation

125
Q

How would you manage a patient presenting with an acute MI?

A

MONA - supp O2 if pulse ox <90%, nitroglycerin, aspirin
Beta blocker - metoprolol or atenolol
Statin - atorvastatin
Antiplatelet therapy - clopidogrel or ticagrelor
Anticoagulant therapy: unfractionated heparin if undergoing PCI; enoxaparin for those not undergoing PCI
Potassium and Mg2+ to keep above 4 and 2, respectively
STEMI - Cath lab or fibrinolysis
NSTEMI - NO fibrinolysis; Cath lab

126
Q

Giant Cell Arteritis

A

AKA - temporal arteritis
elderly females
unilateral headache, jaw claudication
may lead to irreversible blindness due to ophthalmic artery occlusion
associated with polymyalgia rheumatica (pain and stiffness in head, shoulders, hips)
muscle wasting of temple
enlarged temporal artery tender to palpation
increased ESR (screening tool)
definitive diagnosis = temporal artery biopsy
Tx = high dose corticosteroids
(affects large arteries)

127
Q

Takayasu arteritis

A

mostly teens-20s
Asian females
“pulseless disease” - weak upper extremity pulses
granulomatous thickening and narrowing of the aortic arch and proximal great vessels
increased ESR
(affects large arteries)

128
Q

Polyarteritis nodosa (PAN)

A 
middle-aged men
associated with HepB and HepC
typically involves renal and visceral vessels BUT SPARES THE LUNGS
p-ANCA NEG
Tx = corticosteroids, cyclophosphamide
(affects medium vessels)
129
Q

Kawasaki disease (mucocutaneous lymph node syndrome)

A 
asian children <4 yo
conjunctival injection, rash, adenopathy, strawberry tongue, hand-foot changes (desquamation), fever (CRASH and burn)
may develop coronary artery aneurysms
Tx = IV immunoglobulin and aspirin
(affects medium vessels)
130
Q

Buerger disease (thromboangiitis obliterans)

A 
heavy smokers, males <40 yo
intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis
Raynaud phenomenon often present
Tx = smoking cessation
(affects medium vessels)
131
Q

Granulomatosis with polyangiitis (Wegener)

A

upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
Triad: 1. focal necrotizing vasculitis
2. necrotizing granulomas in the lung and upper airway
3. necrotizing glomerulonephritis
saddle nose
PR3-ANCA/c-ANCA positive
Tx = cyclophosphamide and corticosteroids
(affects small vessels)

132
Q

Microscopic polyangiitis

A

necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purport
No granulomas
MPO-ANCA/p-ANCA positive
Tx = cyclophosphamide and corticosteroids\
(affects small vessels)

133
Q

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

A

asthma, sinusitis, skin nodules or purport, peripheral neuropathy (wrist/foot drop)
Granulomatous, necrotizing vasculitis with eosinophils
MPO-ANCA/p-ANCA positive, increased IgE levels
(affects small vessels)

134
Q

Henoch-Schonlein purpura

A

most common childhood systemic vasculitis
often follows URI
Triad: 1. skin: palpable purpura on buttocks/legs
2. arthralgias
3. GI: abdominal pain
Also: renal disease: IgA nephropathy
vasculitis secondary to IgA immune complex deposition
self-limiting
(affects small vessels)

135
Q

Hereditary hemorrhagic telangiectasia

A

autosomal dominant
findings: telangiectasias (esp in mouth?), recurrent epistaxis, skin discolorations, arteriovenous malformations (AVMs), GI bleeding (can cause iron deficiency anemia), hematuria.
AKA Osler-Weber-Rendu syndrome

136
Q

Most common vasculitis

A

Giant Cell Arteritis

137
Q

Which disorders are commonly discovered in patients with Raynaud phenomenon?

A

SLE, CREST scleroderma, Thromboangiitis obliterans (Buerger Dz), Mixed connect tissue disease

138
Q

Benign, raised, red lesion about the size of a mole in older patients

A

cherry hemangioma

139
Q

raised, red area present at birth, increases in size initially then regresses over months to years

A

strawberry hemangioma

140
Q

lesion caused by lymphoangiogenic growth factors in an HIV patient

A

Kaposi sarcoma (HHV-8)

141
Q

Polypoid red lesion round in pregnancy or after trauma

A

pyogenic granuloma

142
Q

benign, painful, red-blue tumor under fingernails

A

glomus tumor

143
Q

cavernous lymphangioma associated with turner syndrome

A

cystic hygroma

144
Q

skin papule in AIDS patient caused by Bartonella spp.

A

Bacillary angiomatosus

145
Q

What organisms cause infective endocarditis?

A

S. viridians, S. epidermidis, S. aureus (most common), enterococci, S. Bovis
HACEK: H. influenza, Actinobacillus, cardiobacterium, eikenlla, kingella
Rare: Coxiella, borrelia, brucella

146
Q

What is pulsus paradoxus and what causes it?

A

drop in systolic BP >10mmHg with inspiration

occurs with hyperinflation of the lungs (asthma, COPD, croup) and cardiac tamponade

DIT Cards (16 decks)

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