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Cardiology Flashcards

1
Q

What are the Class III antiarrythmics?

A

-“tilide” drugs (dofetilide, ibutilide)
Sotalol
Amiodarone

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2
Q

What are some of the MANY side effects of amiodarone?

A 
Pulmonary fibrosis
Hypo OR hyper thyroidism
Hypersensitivity hepatitis
Risky in heart failure patients
Grey corneal deposits
Grey-blue skin discoloration in sun
CYP450 inhibitor
LOW incidence of torsades (sotalol and the ilide drugs have a higher risk)
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3
Q

What is the action of class III antiarrhythmics?

A

Block K+ channels that depolarize the myocardium thereby causing prolonged depolarization (prolonged action potential) and prolonged refractory period

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4
Q

How is Digoxin cleared/metabolized? What are signs of toxicity?

A

Renally

Toxicities: yellow tinting, anorexia, n/v, abdominal pain

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5
Q

Although digoxin can cause _____kalemia, toxicity is actually exacerbated by _____kalemia because it increases Digoxin binding to the Na/K ATPase pump.

A

Digoxin can cause hyperkalemia (blocked pump prevents sodium coming out and thus exchange for K in).

However hypokalemia increases Digoxin binding so it can make toxicity (yellow tinted vision and GI disturbances) worse.

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6
Q

What are the most common causes of nonbacterial thrombotic endocarditis (NBTE)?

A
  1. Advanced malignancy
  2. Chronic inflammatory diseases (SLE, antiphospholipid syndrome, DIC)

NBTE is characterized by sterile platelet-rich thrombi on the valves

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7
Q

Although Digoxin is primarily used to increase contractility, it may also be used for rate control. What is the mechanism by which Digoxin slows ventricular rate during atrial fibrillation?

A

Increasing parasympathetic tone via the Vagus nerve -> ultimately inhibits AV nodal conduction

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8
Q

What is the mechanism of action of dobutamine? What is the signaling cascade?

A

Beta 1 agonist:

Gs signaling -> increased cAMP -> calcium channel activation -> increased Ca2+ = increased contractility and heart rate (and thus cardiac output overall)

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9
Q

What cardiac defects result from doxorubicin (or other anthracyclines like daunorubicin)?

What can be co-administered to prevent these effects?

A

Dilated cardiomyopathy due to formation of iron-containing complexes that produce DNA-damaging free radicals.

Dexrazoxane is a chelating agent that can block the free radicals.

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10
Q

Which organ is most likely to suffer from infarction/thromboembolism in emboli generated in Afib?

A

Kidneys due to higher perfusion rate

Infarction will appear as a wedge-shaped lesion on CT

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11
Q

What is the classic triad of physical exam findings seen in cardiac tamponade?

A
  1. Muffled heart sounds
  2. JVD
  3. Hypotension (+ pulsus paradoxus!)
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12
Q

How does Digoxin increase myocardial contractility?

A

Competes for the Na/K ATPase, reducing its activity. This prevents Na efflux (and K influx).

Na builds up but then escapes through another Na/Ca2+ exchanger. This floods the cell with calcium, causing increased contractility.

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13
Q

(+) Inotropy will increase cardiac output INDEPENDENT of ______.

A

EDV (cardiomyocyte stretching)

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14
Q

Total peripheral resistance is MOSTLY determined by what vessels?

A

Arterioles

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15
Q

In what situations will you often see a decrease in TPR?

A

i.e. arteriolar dilation

Exercise
Arterio-venus shunts

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16
Q

An S4 heart sound is a sign of ______ dysfunction.

A

Diastolic

It occurs due to a sudden rise in end-diastolic ventricular pressure caused by atrial contraction against a stiff ventricle.

Occurs in any condition that reduces ventricular compliance (e.g. hypertensive heart disease, aortic stenosis, hypertrophic cardiomyopathy).

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17
Q

What causes the S3 heart sound?

A

Rapid passive filling of ventricles in diastole.
Sudden cessation of filling as ventricle reaches elastic limit.

Occurs in systolic heart failure, mitral regurg, and high-output states

Think of lots of blood sloshing around slamming against the wall

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18
Q

What is the major determining factor of severity of a case of Tetralogy of Fallot?

A

Degree of RVOT obstruction

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19
Q

What compensatory mechanisms are initiated by the kidneys in response to decreased renal perfusion (e.g. as in CHF)?

A
  1. RAAS activation: sodium retention, aldosterone production, vasoconstriction
  2. Sympathetic output: epinephrine and norepinephrine increase HR and contractility and increase in peripheral arterial resistance increasing afterload.
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20
Q

Class IB antiarrhythmics are useful for treating _____-induced ventricular arrhythmias.

A

Ischemia-induced

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21
Q

Class IC antiarrhythmics have the strongest binding to sodium channels and thus are slowest to dissociate causing cumulative effects, thus they are especially useful in treating what type of arrhythmia?

A

Tachyarrhythmia

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22
Q

Aortic regurgitation murmur is best heard in which position?

A

Sitting up and leaning forward with breath held at end-expiration

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23
Q

Midsystolic click followed by a Mid- to late systolic murmur = ?

A

Mitral valve prolapse with mitral regurgitation

The click results from the sudden tensing of the chordae tendineae as they are pulled taut by the ballooning valve leaflets

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24
Q

What are the only two murmurs that DECREASE with increased preload/venous return?

A

Mitral valve prolapse

Hypertrophic cardiomyopathy systolic murmur at cardiac apex

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25
Q

Which class of anti-arrhythmics work by blocking voltage-dependent sodium channels (i.e. depolarization) of the cardiac AP?

A

Class I

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26
Q

What do endothelial cells secrete to prevent platelet aggregation and adhesion to the vascular endothelium?

A

Prostacyclin

Damaged endothelial cells lose the ability to synthesize prostacyclin, predisposing them to the development of thrombi and hemostasis.

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27
Q

What are the 2 main effects of milrinone (a PDE3 enzyme inhibitor)?

A
  1. Positive inotropy

2. Vasodilation (arterial AND venous)

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28
Q

Nesiritide and is a synthetic form of what endogenous peptide?

A

BNP

thus causes naturesis and arteriolar and venous dilation

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29
Q

Due to the very high myocardial oxygen extraction (up to 75%), what vessel in the body has the absolute lowest oxygen saturation?

A

The coronary sinus (drains the venous blood of the heart itself)

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30
Q

What are the actions of nitroprusside?

A

Short-acting arteriolar and venous dilation

As such, it decreases both preload and afterload, allowing adequate CO to be delivered at lower LVEDPs.

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31
Q

What pathologies can cause wide splitting (i.e. P2 heart sound, delayed pulmonary valve closing)?

A

Right bundle branch block

Pulmonic valve stenosis

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32
Q

What pathologies can cause fixed splitting (i.e. P2 heart sound, delayed pulmonary valve closing that doesn’t change with inspiration/expiration)?

A

ASD

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33
Q

What pathologies can cause paradoxical splitting (i.e. P2 heart sound pulmonic valve closing before A2 aortic valve)?

What will bring them back closer together?

A

Increase in left ventricular volume
Left bundle branch block)
Aortic valve stenosis

Inspiration will bring them back together (though P2 will still occur before A2, you just won’t be able to hear it).

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34
Q

Hand grip increases ___load. It therefore increases the intensities of which murmurs?

A

Afterload

MR
AR
VSD

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35
Q

Rapid squatting increases ______ and _____. Ultimately what murmurs are decreased

A

Preload AND afterload

AS
MR
VSD

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36
Q

Valsalva decreases ____load.

A

Preload by increasing thoracic pressure

Decreases most murmurs but NOT MVP or HCM

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37
Q

New onset mitral valve regurgitation may be due to an infarct in _______ because it supplies the _____ valve leaflet.

A

RCA

Posterior valve leaflet

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38
Q

In what part of systole does mitral and tricuspid regurg present?

A

All of it! (they are holosystolic)

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39
Q

Patients with what type of diseases are predisposed to mitral valve prolapse?

A

Connective tissue diseases

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40
Q

VSD and tricuspid regurgitation are both holosystolic murmurs heard best at the LSB…so how can you tell them apart?

A

Tricuspid regurg will radiate to the right shoulder

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41
Q

Opening snap + diastolic rumble = ?

A

Mitral regurgitation

42
Q

What is an important side effect of vinblastine other than the stocking glove neuropathy?

A

Myelosuppression

43
Q

What ion is responsible for the upstroke in cardiac PACEMAKER cells?

A

ICa2+

44
Q

What ions are responsible for Ifunny in cardiac pacemaker cells?

A

Na and K+

45
Q

How is atrial flutter discernible from atrial fibrillation?

A

Atrial flutter produces a 4:1 sawtooth pattern with intact p waves and regular spacing of R-R intervals

46
Q

Mobitz Type I/Wenkebach 2nd degree heart block results in what?

A

Gradual increase in PR intervals until you get

Dropped QRS complexes

47
Q

Mobitz Type II 2nd degree heart block results in what?

A

Randomly dropped QRS complexes, PR interval is fixed

Should be treated with a pacemaker

48
Q

Lyme disease is associated with ____ degree heart block.

A

3rd

49
Q

An increase in BNP is used to diagnose ______.

A

Heart failure

50
Q

Oxygen is only sense by chemoreceptors in the ______ nervous system.

A

Peripheral

51
Q

What will a tetralogy of fallot heart look like on CXR?

A

A boot

52
Q

Do VSDs usually close on their own?

A

Yes

53
Q

Endothelin is a vaso______

A

constrictor

54
Q

What is the most common congenital heart defect in Down syndrome and what are the sequelae?

A

Endocardial cushion defects ->

i.e. causes AV defect, ASD, VSD

55
Q

What is the most common congenital heart defect associated with babies born to moms with DM? What about a spinal defect?

A

Transposition

Caudal regression syndrome (problems forming the lumbar, sacrum, coccyx regions)

56
Q

What congenital heart defects are associated with Marfans?

A

Mitral Valve Prolapse

Aortic aneurysms and aortic dissection

57
Q

What congenital heart defects are associated with Turner Syndrome?

A

Bicuspid aortic valve and coarctation

58
Q

What congenital heart defects are associated with Williams Syndrome?

A

Supravalvular aortic stenosis

59
Q

22q11 defect patients have problems with their ______ cells, leading to what common heart defects?

A

Neural crest cells
Aorticopulmonary defects
Persistent truncus arteriosus
TOF

60
Q

If you see symptoms of superior vena cava syndrome but it is UNILATERAL rather than bilateral, you’ve likely occlude what vein?

A

Brachiocephalic

61
Q

S3 heart sounds may be normal in which patients?

A

Young individuals and pregnant women

62
Q

What are the 2 major local effectors of coronary vasodilation (i.e. myocardial oxygen supply) involved in autoregulation?

A

Adenosine and NO

63
Q

Which class of calcium channel blocker has effects the SA node and can cause bradycardia?

A

Non-dihydropyridine (i.e. verapamil, diltiazem)

64
Q

Which antiarrhythmic class is efficacious in ischemia-induced ventricular arrhythmias?

A

Class IB (lidocaine, mexilitine, phenytoin)

They are the weakest sodium channel blockers and thus dissociate the fastest. Ischemic myocardium has higher than normal (less negative)

65
Q

How does adenosine work as an antiarrhythmic? What are the side effects?

A

Adenosine blocks conduction through the AV node and can thus be used to treat PSVTs.

Side effects = rapid-onset and short-lived flushing, chest burning (due to bronchospasm), hypotension, and high-grade AV block

66
Q

What are the side effects of niacin?

A

Cutaneous flushing, warmth, and itching mostly mediated by the release of prostaglandins.

Pre-treatment with aspirin can reduce niacin side effects.

67
Q

What is acute decompensated heart failure?

A

Reduced cardiac output from excessive ventricular filling pressures triggers a compensatory neurohumoral stimulation:

  1. Sympathetic nervous system activation
  2. RAAS activation
  3. Antidiuretic hormone secretion

All of which can cause vasoconstriction, edema, and deleterious cardiac remodeling which exacerbate problems with cardiac output.

68
Q

What is Ortner syndrome?

A

A rare cardiovocal syndrome and refers to recurrent laryngeal nerve palsy from cardiovascular disease.

Most common cause is a dilated left atrium due to mitral stenosis, but other causes, including pulmonary hypertension, thoracic aortic aneurysms, an enlarged pulmonary artery and aberrant subclavian artery syndrome have been reported compressing the nerve.

69
Q

DM (elevated blood glucose) leads to what type of arteriolosclerosis?

A

Non-enzymatic glycation leads to hyaline deposition -> hyalinosis ateriolosclerosis

70
Q

HTN leads to what type of arteriolosclerosis?

A

Fibrinous/”onion skinning” arteriolosclerosis

71
Q

Monckeberg sclerosis aka ?

A

Medial calcific sclerosis

Often occur in popliteal. Does NOT decrease size of the lumen because it only thickens the medial layer

72
Q

What type of aortic aneurysm is seen in tertiary syphilis?

A

Thoracic AA due to spirochetes embedding themselves in the vasa vasorum causing cystic medial inflammation/fibrosus

73
Q

What distinguishes type A vs type B aortic aneurysms? Which is more stable (and thus can be treated medically)?

A

Type B begins after the aortic arch

B = more stable
can be treated with a Beta Blocker

Remember: B = beyond (aortic a.), Beta Blocker

74
Q

What vessels are at risk of compression from Type A and B aortic aneurysms?

A

Left subclavian vessels -> leads to uneven pressure readings between L and R arms

75
Q

Chronic/stable angina is _______, while prinzmetal/vasospastic is ___________.

A

Subendocardial

Transmural

76
Q

Chronic/stable angina will cause ST _______, while prinzmetal/vasospastic will cause ST ___________. Unstable angina will cause ST _____.

A

Stable: Depression

Prinzmetal: Elevation

Unstable: Depression (and also possibly T wave inversion)

77
Q

What is Brugada Syndrome?

A

AD disorder most common in Asian males.

ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3. Increased risk of Vtach and SCD.

78
Q

What type of heart defect is seen in Friedrich’s Ataxia?

A

Hypertrophic cardiomyopathy

79
Q

In which type of shock will patients be cold and clammy due to increased peripheral resistance (SVR and CVP elevated)?

A

Cardiogenic shock

80
Q

In which type of shock will patients be warm and dry due to decreased peripheral resistance (SVR and CVP DROP, vessels wide open)?

A

Distributive shock: Septic shock /anaphylaxis/CNS failure

HR will increase to compensate

81
Q

The first sign of shock will always be:

A

Tachycardia

82
Q

What are the major drugs that cause drug-induced Lupus?

A

Procainimide
Hydralazine

look up the rest

83
Q

Nitroprusside can actually cause cyanide poisoning. How is it treated?

A

Thiosulfate

84
Q

Nitrates primarily cause ____dilation.

A

Venodilation

85
Q

Which antiarrhythmic class is best post MI?

A

Class IB (lidocaine)

86
Q

Which antiarrhythmic class is contraindicated post MI?

A

Class IC (fleicanide, propafenone)

Generally bad in any heart with structural defect or previous ischemia

87
Q

Mg2+ can be used to treat ______ toxicity.

A

Digoxin

88
Q

Ivabradine inhibits _________ which prolongs phase _____ of the pacemaker cells.

A

funny current
Phase 4 by decreasing the slope of depolarization

Does not hurt contractility!

89
Q

Acetazolamide inhibits _______ (enzyme) resulting in reduced _______ reabsorption in the PCT.

What are the metabolic consequences of this inhibition?

A

Carbonic anhydrase
Sodium bicarb reabsorption inhibited

Causes a normal anion gap metabolic acidosis/hyperchloremia

Note that the efficacy of acetazolamide decreases because the body will start to absorb more Na distally to compensate

90
Q

Loop diuretics and thiazides can cause contraction ____osis.

A

Alkalosis

Hypovolemia caused by the diuretics can cause an upregulation of RAAS which pulls in Na in exchange for H+

91
Q

Unlike other diuretics, K-sparing diuretics (triamterenes, spironolactone, eplerenone) cause metabolic _____osis/

A

Acidosis

92
Q

How do calcium channel blockers/class 4 antiarrhythmics (diltiazem, verapamil) work as rate control?

A

Slow the funny current/slow depolarization phase/phase 4 in the pacemaker cells. Most dramatic effect is slowing the rate at the AV node.

93
Q

Migratory thrombophlebitis, known as Trousseau syndrome, should raise suspicious for ______.

A

Cancer

esp visceral adenocarcinomas of the pancreas, colon, and lung due to hypercoaguable state.

94
Q

Cyanosis that affects the lower extremities more than the upper extremities is indicative of what congenital heart defect?

A

PDA

95
Q

What drug is given to treat beta blocker overdose?

A

Glucagon

96
Q

What is the cellular signaling/MOA of glucagon in beta blocker overdose.

A

Increases HR and contractility independent of adrenergic receptors via:

Increased G-protein-coupled receptors on cardiac myocytes -> increased adenylate cyclase -> increased cAMP -> increased calcium release from internal stores and SA nodal firing

97
Q

Beta blockers slow the AV nodal conduction, prolonging the ___ interval.

A

They do not have any specific effects on QRS or QT interval durations.

98
Q

What is Osler-Weber-Rendu syndrome?

A

AKA hereditary hemorrhagic telangiectasia

AD condition marked by congenital telangiectasias to the skin and mucous membranes. May involve mucosa of lips, oronasopharynx, resp tract, GI tract, or urinary tract. They may cause epistaxis, GI bleeding, and hematuria.

Rarely can occur in the brain.

99
Q

What is another name for Neurofibromatosis Type I?

A

Von Recklinghausen’s disease

This is marked by cafe au lait spots, lisch nodules, optic nerve gliomas, and of course neurofibromas

100
Q

How do small VSDs present?

A

Loud blowing holosystolic murmurs mid/lower LSB and NO SYMPTOMS!

The murmur is usually not detectable at birth, but rather 4-10 days later as pulmonary vascular resistance continues to decline, permitting L to R shunting.

101
Q

Cardiomyocytes stop contracting within __________(time) of ischemia.

A

60 seconds

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