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Cardio Flashcards

1
Q

What two signs do you see on EKG for atrial fibrillation?

A
  1. Irregularly irregular rhythm

2. No discrete P waves

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2
Q

What are risk factors for atrial fibrillation?

A

HTN, Cardiovascular disease, heart failure

They all cause atrial dilation

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3
Q

What are consequences of atrial fibrillation?

A
  1. pooling of blood –> formation of clots –> PE or stroke
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4
Q

How do you treat atrial fibrillation?

A

< 48 hours –> synchronized cardioversion (not old afibs because there might be clots that get dislodged)
> 48 hours –> Anti-coagulation with Heparin or Enoxaparin, then Coumadin; Rate control to prevent SVT - Digoxin, Beta blocker, Ca channel blocker; Rhythm control - bring back to sinus rhythm with Sotalol, Amiodarone, Flecainide

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5
Q

How do you identify atrial flutter?

A

Sawtooth appearance

Has p waves, more regular rhythm

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6
Q

What is a 1st degree AV block?

A

Prolonged PR interval (>200 msec); benign condition that is often asymptomatic

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7
Q

What is Mobitz type I block?

A

There is progressive lengthening of PR interval until a beat is dropped (P wave without QRS complex); typically benign (it is a second degree block!)

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8
Q

What organism causes AV block?

A

Borrelia burgdorferi - Lyme disease

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9
Q

What is Mobitz type II block?

A

There is dropped beat with NO warning. Problematic bc can become 3rd degree heart block. Treated with pacemaker.

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10
Q

What is 3rd degree heart block?

A

Atria and ventricles are beating independently of each other; both P waves and QRS waves are present but the P waves bear no relation to QRS complexes. Treated with pacemaker.

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11
Q

What do the QRS complexes look like in 3rd degree heart block?

A

They can be narrow (going through normal conduction) or wide

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12
Q

What is Wolff-Parkinson-White syndrome?

A

Ventricular pre-excitation syndrome
Abnormal fast conduction pathway from atria to ventricle that is not going through the AV node (bundle of Kent instead); This causes early ventrciular depolarization = delta wave and widened QRS complex

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13
Q

Why is it important to identify WPW?

A

It may result in reentry circuit that causes supra ventricular tachycardia

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14
Q

a. How do you treat SVT?

b. How do you treat SVT from WPW?

A

a. Adenosine

b. Procainamide or Amiodarone - tones down tachycardia

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15
Q

Drugs that prolong QT interval

A 
Anti-Arrhythmics (IA, III)
Anti-Biotics (Macrolides, Chloroquine)
Anti-Cychotis (Haloperidol, Risperidone)
Anti-Depressants (TCAs)
Anti-Emetics (Ondansetron)

Anti-HIV protease inhibitors
Methadone

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16
Q

How do you treat Torsades?

A

Mg

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17
Q

What is initial treatment for ventricular tachycardia when there is no pulse?

A

CPR and defibrillation

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18
Q

a. What do baroreceptors in aortic arch respond to?

b. They transmit via which nerve?

A

a. Increases in BP

b. Vagus nerve

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19
Q

What do baroreceptors in carotid sinus respond to?

b. They transmit via which nerve?

A

a. Increase or decrease in BP

b. Glossopharyngeal nerve

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20
Q

Which adrenergic receptors cause vasoconstriction?

A

alpha 1

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21
Q

What is the action of atrial natriuretic peptide?

A

It is released from atrial myocytes in response to increased blood volume and atrial pressure –> it causes vasodilation and reduced Na reabsorption by dilating afferent arteriole and constricting efferent arteriole to increase GFR

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22
Q

What is the action of brain natriuretic peptide?

A

It is released from ventricular myocytes in response to increased stretch/tension –> has similar response of ANP (vasodilation and decreased Na reabsorption) –> it is useful for diagnosing HF

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23
Q

How does Nitroglycerin work to relieve angina?

A

It causes systemic venous vasodilation that decreases preload and reduces the myocardial oxygen demand

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24
Q

How do kidneys regulate BP?

A

Juxtaglomerular apparatus senses low BP and that stimulates production of Renin –> eventually makes Angiotensin II –> vasoconstriction and aldosterone production –> retention of Na and water in kidneys

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25
Q

What substances work on myosin smooth muscle light chain kinase and how does this affect BP?

A

cAMP inhibits myosin light chain kinase to inhibit vasoconstriction –> decreased BP
Calmodulin activates myosin light chain kinase to cause contraction and raise BP

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26
Q

a. What are CXR findings for aortic dissection?

b. What are symptoms?

A

a. Widened mediastinum

b. Tearing chest pain, sudden onset, radiating to back (with unequal BP in arms)

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27
Q

What are the types of aortic dissection?

A

a. Type A (involves ANY portion of aorta - requires surgery) Type B (distal to aortic arch, in descending aorta - treated medically)

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28
Q

What is drug of choice to treat aortic dissection?

A

B blocker - reduce arterial pressure and slope of rise of BP

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29
Q

When should you avoid giving an ACE inhibitor? Why?

A

If the patient has bilateral renal artery stenosis (they decreased GFR –> renal failure)

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30
Q

What drugs can be used for HTN in pregnancy?

A 
Hypertensive Mom's Love Nifedipine
Hydralazine
Methyldopa
Labetalol
Nifedipine
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31
Q

What are adverse effects of Hydralazine? When is it C/I?

A

It can cause compensatory tachycardia, fluid retention, headache, angina, lupus-like syndrome with anti-histone Abs. C/I in patients with CAD/angina.

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32
Q

What is the mechanism of Minoxidil?

A

Opens K channels and hyper polarizes smooth muscle –> resulting in relaxation of vascular smooth muscle

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33
Q

What is a S/E of Minoxidil?

A

Hair growth

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34
Q

Treatment of HTN plus atrial fibrillation

A

Beta blocker or Diltiazem/Verapamil

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35
Q

Which treatments should you avoid in HTN plus bradycardia?

A

Diltiazem/Verapamil

B blocker

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36
Q

HTN plus renal insufficiency:

a. Treatment
b. Avoid…

A

a. ACE inhibitor/ARB

b. ACE inhibitor/ARB if there is bilateral renal stenosis (also may increase K) and K sparing diuretics

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37
Q

HTN plus BPH

a. Treatment

A

a. Alpha blocker

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38
Q

HTN plus Hyperthyroidism

a. Treatment

A

Propanolol

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39
Q

HTN plus Hyperparathyroidism

a. Treatment
b. Avoid:

A

a. Loop diuretic

b. Thiazide diuretic (Ca sparing)

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40
Q

HTN plus osteoporosis treatment

A

Thiazide diuretic (Ca sparing)

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41
Q

HTN plus migraines treatment

A

CCB or B blocker

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42
Q

HTN plus essential tremor treatment

A

Propranolol

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43
Q

Treatment of malignant HTN

A

Nitroprusside (increase cGMP –> dilates veins and arteries; short acting given as IV)

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44
Q

What is an adverse effect of Nitroprusside?

A

Cyanide toxicity

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45
Q

Which anti-hypertensives have the following S/E:

a. first dose orthostatic hypotension
b. ototoxic
c. hypertrichosis
d. cyanide toxicity
e. dry mouth, sedation, severe rebound HTN
f. Bradycardia, impotence, asthma exacerbation
g. reflex tachycardia
h. cough
i. avoid in patients with sulfa allergy
j. possible angioedema
k. possible drug induced lupus
l. hypercalcemia, hypokalemia

A

a. Alpha 1 blockers (Zosins)
b. Loop diuretics (esp with aminoglycosides)
c. Minoxidil
d. Nitroprusside
e. Clonidine (alpha 2 agonist)
f. B blocker
g. Nitrates, hydralazine, dihydropyridines
h. ACE inhibitor, ARB
i. Loop and thiazide diuretics
j. ACE inhibitor, ARB
k. Hydralazine
l. Loops and thiazide

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46
Q

a. What do you see on EKG with Prinzmetal angina?
b. What causes Prinzmetal?
c. How do you treat it?

A

a. ST elevation
b. Coronary artery spasm
c. Calcium channel blocker or Nitrates

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47
Q

What are five most deadly causes of chest pain?

A 
Aortic dissection
Unstable angina
MI
Tension pneumothorax
PE
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48
Q

ST segment elevation only during brief episodes of chest pain

A

Prinzmetal’s angina

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49
Q

Patient is able to point to localize the chest pain using one finger

A

Musculoskeletal

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50
Q

Chest wall tenderness on palpation

A

Costochondritis, pulled muscle

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51
Q

Rapid onset chest pain that radiates to the scapula

A

Aortic dissection

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52
Q

Rapid onset sharp pain in a 20 year old and associated with dyspnea

A

Spontaneous Pneumothorax

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53
Q

Chest pain occurs after heavy meals and improved by antacids

A

GERD, Esophageal spasm

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54
Q

Sharp pain lasting hours-days and is somewhere relieved by sitting forward

A

Pericarditis

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55
Q

Pain made worse by deep breathing/motion

A

Musculoskeletal

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56
Q

Chest pain in a dermatomal distribution

A

Shingles

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57
Q

Most common cause of non-cardiac chest pain

A

GERD of musculoskeletal

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58
Q

What is a big side effect of HMG CoA reductase inhibitors?

A

Myopathy

also hepatotoxicity

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59
Q

What is the mechanism of Cholestyramine?

A

Bile acid resin that prevents intestinal reabsorption of bile acids (live must use cholesterol to make more)

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60
Q

What is mechanism of Ezetimibe?

A

Prevents cholesterol absorption at small intestine brush border

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61
Q

a. What is the mechanism of Fibrates?
b. What are their names?
c. Side effects?

A

a. Upregulate LPL –> Increased TG clearance
b. Gemfibrozil, Fenofibrate
c. Myopathy, cholesterol gallstones

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62
Q

What is the mechanism of Niacin?

A

Raises HDL; inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

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63
Q

What are S/E of Niacin?

A

Red, flushed face
Hyperglycemia
Hyperuricemia

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64
Q

a. Best effect on lowering LDL
b. Best effect on raising HDL
c. Best effect on lowering triglycerides

A

a. Statins
b. Niacin
c. Fibrates (Gemfibrozil, Fenofibrate)

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65
Q

How is hypertrophic cardiomyopathy treated?

A

B blocker

Non-dihydropyridine calcium channel blocker (Verapamil)

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66
Q

What is Loffler syndrome?

A

Endomyocardial fibrosis with a prominent eosinophilic infiltrate that causes restrictive cardiomyopathy

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67
Q

What are signs of bacterial endocarditis?

A 
Fever
Roth spots
Osler nodes
Murmur
January lesions
Anemia 
Nail-bed hemorrhage
Emboli
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68
Q

What are the most common causes of bacterial endocarditis? What are features of each?

A 
Staph aureus (30%, acute, large vegetations)
Viridans streptococci (20-30%, subacute, insidious onset, smaller vegetations on abnormal valves, dental procedures)
Enterococci (10%)
Staphylococcus epidermidis (5-10%, IV drug users)
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69
Q

What malignancy is Streptococcus bovis associated with?

A

Colon cancer

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70
Q

What organisms are responsible for culture negative endocarditis?

A 
Haemophilus
Actinobacillus
Cardiobacterium
Eikenella
Kingella
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71
Q

a. What causes Libman-Sacks endocarditis?

b. What is it?

A

a. SLE

b. Sterile vegetations on both sides of the valve

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72
Q

a. What is marantic endocarditis?

b. What is it caused by?

A

a. Non-bacterial

b. Metastatic cancer cells or platelet fibrin aggregates in hypercoagulable states

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73
Q

a. What is a retinal hemorrhage with pale center?

b. When are they seen?

A

a. Roth spots

b. bacterial endocarditis

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74
Q

What is epinephrine reversal? Administration of what drug causes this?

A

Epinephrine is an alpha and beta adrenergic agonist that causes increased BP. BUT when an alpha receptor antagonist like Phentolamine is administered first, it blocks the vasoconstrictive action on arterioles and the administration of epinephrine acts ONLY on the beta receptors to cause vasodilation in skeletal muscle and decrease in BP

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75
Q

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

A

a - atrial contraction
c - ventricular contraction
v - atrial filling against closed tricuspid valve

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76
Q

Which heart murmur is associated with weak pulses?

A

Aortic stenosis

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77
Q

What are the JONES criteria?

A
  • Used to diagnose Rheumatic fever; two major criteria and one minor criteria
  • Joints (migratory polyarthritis)
  • Heart (pancarditis)
  • Nodules (subcutaneous, painless)
  • Erthyema marginatum (creeping ring like rash, comes and goes)
  • Sydenham chorea (chorea of face, hands, upper limbs)
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78
Q

What lab and histology findings are associated with Rheumatic heart disease?

A

Increased anti-streptolysin O titers
Aschoff bodies (granuloma with giant cells)
Anitschkow cells (enlarged macrophages with owl eye appearance)
Mitral valve damage

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79
Q

How does pericarditis present?

A

Sharp pleuritic chest pain, better sitting up and leaning forward
Distant heart sounds
Friction rib on auscultation
Diffuse ST elevation

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80
Q

What are EKG findings for acute pericarditis?

A

Diffuse ST elevation

PR depression

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81
Q

What are long term outcomes of pericarditis?

A

Can spontaneously resolve or cause chronic constrictive pericarditis (Lupus is most common cause)

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82
Q

What sign do you have with chronic constrictive pericarditis?

A

Kussmaul sign = JVD with inspiration

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83
Q

What is the Beck triad of cardiac tamponade?

A

Hypotension
Distended neck veins
Distant heart sounds

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84
Q

What are exam findings for cardiac tamponade?

A 
Hypotension
Distended neck veins
Distant heart sounds
Increased HR
Pulsus paradoxus
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85
Q

a. What is pulses paradoxus?

b. What diseases do you see it in?

A

a. Decrease in amplitude of systolic BP by >10mmHg during inspiration
b. Cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup

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86
Q

Kussmaul’s sign vs. Pulsus paradoxus

a. event
b. mechanism
c. disease

A

a. JVD during inspiration vs. decreased SBP by more than 10 during inspiration
b. decreased capacity of RV vs. decreased capacity of LV
c. constrictive pericarditis > tamponade vs. cardiac tamponade > pericarditis

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87
Q

What is EKG finding of cardiac tamponade?

A

low voltage QRS and electrical alternans (from swinging movement of heart in large effusion)

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88
Q

What is most common cardiac tumor?

A

Metastatic tumor from somewhere else

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89
Q

What is most common primary cardiac tumor in adults?

A

Myxomas - in left atrium

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90
Q

What are complications of left atria myxomas?

A

Multiple syncopal episodes

If they flop into LV you may hear tumor plop on diastole.

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91
Q

What is most common primary cardiac tumor in kids?

A

Rhabdomyoma

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92
Q

What are rhabdomyomas associated with?

A

Tuberous sclerosis

includes Astrocytoma and Angiomyolipomas also

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93
Q

Focal myocardial inflammation with multinucleate giant cells

A

Aschoff bodies

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94
Q

Chest pain and course rubbing heart sounds in patient with Cr of 5.0

A

Uremic pericarditis

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95
Q

Tree-barking of the aorta

A

Tertiary syphilis

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96
Q

Child with fever, joint pain, cutaneous nodules 4 weeks after a throat infection

A

Rheumatic fever

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97
Q

ST elevation in all EKG leads

A

Acute pericarditis

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98
Q

EKG shows electrical alternans

A

Cardiac tamponade

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99
Q

Most common cause of constrictive pericarditis

A

In US - Lupus

In developing countries - TB

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100
Q

Granulomatous nodules in the heart are….

A

Aschoff bodies (seen in rheumatic heart disease)

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101
Q

What is the triad of Granulomatosis with polyangiitis (Wegeners)?

A

Focal necrotizing vasculitis
Granulomas in lung and upper airway
Glomerulonephritis

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102
Q

What are the pathology/lab findings in Microscopic polyangiitis?

A

MPO-ANCA/p-ANCA

No granulomas

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103
Q

What are the pathology/lab findings in Wegeners?

A

c-ANCA/PR3-ANCA

Large nodular densities on CXR

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104
Q

How do you distinguish GPA (Wegeners) and Goodpastures?

A
  1. GPA - affects lungs and upper airway (soft palate, oropharynx, nasal cavity, sinuses); collapse of bridge of nose (saddle nose) and granulomas on lung biopsy, lung disease (dyspnea and hemoptysis) and kidney disease (hematuria)
  2. Goodpastures -
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105
Q

How do you treat GPA?

A

Cyclophosphamide

Corticosteroids

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106
Q

What is classic triad of Henoch Schonlein purpora?

A

Palpable purpura on buttocks/legs
Arthralgias
Abdominal pain (from intestinal hemorrhage)
Renal disease (tetrad)

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107
Q

What vasculitides often follows URI?

A

Henoch Schonlein purpura

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108
Q

What is Churg-Strauss associated with?

A

Asthma
Sinusitis
Skin nodules
Peripheral neuropathy

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109
Q

What is Churg-Strauss?

A

A small vessel vasculitis with granulomatous vasultitis and eosinophilia

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110
Q

What is Polyarteritis nodosa associated with?

A

Hepatitis B seropositivity

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111
Q

What are signs of Polyarteritis nodosa?

A

Fever, weight loss, headache
Abdominal pain, melena
HTN, neurologic dysfunction, cutaneous eruptions, renal damage
does NOT affect lungs

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112
Q

What is presentation of Kawasaki disease?

A 
Conjunctival infection
Rash (polymorphous --> desquamating)
Adenopathy (cervical)
Strawberry tongue (oral mucositis)
Hand-foot changes (edema, erythema)
Fever
CRASH (and burn = fever)
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113
Q

What are potential complications of Kawasaki disease?

A

Coronary artery aneurysms, thrombosis or rupture may cause death

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114
Q

How do you treat Kawasaki disease?

A

Aspirin - important for preventing thrombosis of coronary artery aneurysms

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115
Q

What is Buerger disease?

A

Vasculitis seen in heavy male smokers < 40 years old

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116
Q

What is presentation of Buerger disease?

A

Intermittent claudication –> gangrene, autoamputation of digits, superficial nodular phlebitis
Raynaud phenomenon is often present

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117
Q

a. Who does temporal arteritis affect?

b. Presentation?

A

a. Elderly females

b. Unilateral headache, jaw claudication; may lead to irreversible blindness from ophthalmic artery occlusion

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118
Q

What are clinical findings of temporal arteritis?

A

Elevated ESR

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119
Q

What is pulseless disease?

A

Takayasu arteritis

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120
Q

What is Takayasu arteritis?

A

Causes granulomatous inflammation of arteries of aortic arch –> poor pulses in extremities

121
Q

Who does Takayasu affect?

A

Young Asian women

122
Q

Vasculitides associated with this history:

a. 2 year old Asian female
b. 20 year old Asian female
c. Associated with asthma
d. Young male smoker
e. Associated with polymyalgia rheumatica
f. Associated with IgA nephropathy
g. Associated with hepatitis B

A

a. Kawasaki disease
b. Takayasu arteritis
c. Churg-Strauss (Eosinophilic granulomatosis with polyangiitis)
d. Buerger disease
e. Temporal arteritis
f. Henoch Schonlein purpura
g. Polyarteritis nodosa

123
Q

Vasculitides with the following presentation:

a. Elderly woman with jaw claudication and vision loss
b. Strawberry tongue
c. Desquamation of the hands/feet
d. Poor pulses in the arms
e. Palpable purpura on the legs
f. Vasculitis of the kidney and GI tract, spares the lungs
g. Vasculitis of the kidney, upper airway and lungs

A

a. Giant cell arteritis
b. Kawasaki disease
c. Kawasaki disease
d. Takayasu (pulseless disease)
e. Henoch Schonlein Purpura
f. Polyarteritis Nodosa
g. GPA (Wegeners)

124
Q

What is the treatment for Raynaud phenomenon?

A

Dihydropyridine Calcium channel blockers because they vasodilate Aspirin - prevents clotting

125
Q

What is Raynaud’s disease?

A

Primary

Arterial vasospasm causes decreased blood flow

126
Q

Which disease are frequently found in those with Raynaud phenomenon?

A

Lupus
CREST scleroderma
Buerger disease
Mixed CT disease

127
Q

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

A

Cherry hemangioma

128
Q

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

A

Strawberry hemangioma

129
Q

Lesion caused by lymphoangiogenic growth factors in an HIV patient

A

Kaposi sarcoma

130
Q

Polypoid red lesion found in pregnancy or after trauma

A

Pyogenic granuloma

131
Q

Benign, painful, red-blue tumor under fingernails

A

Glomus tumor

132
Q

Cavernous lymphangioma associated with Turner syndrome

A

Cystic hygroma

133
Q

Skin papule in AIDS patient caused by Bartonella

A

Bacillary angiomatosis

134
Q

What divides the right and left atria?

A

Septum primum and septum secundum

135
Q

How is the blood shunted from the right atrium to the left atrium in an embryo?

A

Through the foramen oval (of septum secundum) and ostium secundum (of septum primum)

136
Q

What grows to separate the atria and ventricle?

A

Superior endocardial cushion and inferior endocardial cushion

137
Q

What genetic abnormality is commonly associated with endocardial cushion defects?

A

Trisomy 21

138
Q

What are the abnormalities associated with conotruncal abnormalities? (when the truncus arteriosus rotates to form aorticopulmonary septum/spiral septum)

A

Transposition of great vessels
Tetralogy of Fallot
Persistent truncus arteriosus

139
Q

What are the abnormalities associated with conotruncal abnormalities? (when the truncus arteriosus rotates to form aorticopulmonary septum/spiral septum)

A

Transposition of great vessels
Tetralogy of Fallot
Persistent truncus arteriosus

140
Q

How does the ductus arteriosus close at birth?

A

At birth, there is an increase in O2 from respiration and a decrease in prostaglandins from placental separation –> DA closes

141
Q

How does the ductus arteriosus close at birth?

A

At birth, there is an increase in O2 from respiration and a decrease in prostaglandins from placental separation –> DA closes

142
Q

What fetal structures do each adult part come from:

a. ascending aorta and pulmonary trunk
b. coronary sinus
c. superior vena cava
d. smooth parts of the L and R ventricles
e. smooth part of right atrium
f. trabeculated left and right atria
g. trabeculated parts of left and right ventricles

A

a. Truncus arteriosus
b. Left horn of sinus venosus
c. R common cardinal vein, R anterior cardinal vein
d. Bulbus cordis
e. right horn of sinus venosus
f. primitive atria
g. primitive ventricle

143
Q

Which fetal vessel has the highest oxygenation?

A

Umbilical vein > ductus venosus > inferior vena cava > right atrium

144
Q

Which cell types are rich in smooth ER?

A

Hepatocytes

Steroid hormone-producing cells of the cortex

145
Q

What are overdose antidotes for Heparin and Warfarin?

A

Heparin - Protamine sulfate

Warfarin - Fresh frozen plasma and vitamin K

146
Q

What is Eisenmenger syndrome?

A

An uncorrected left to right shunt causes increased pulmonary blood flow and remodeling of the vasculature that causes pulmonary arterial HTN –> RVH compensates and eventually the right pressure becomes so much greater that shunt becomes right to left –> causes clubbing, cyanosis and polycythemia

147
Q

What is Coarctation of the aorta?

A

Aortic narrowing near insertion of doctor arteriosus; HTN in upper extremities and weak, delayed pulse in lower extremities. With age you see rib notching from the collateral arteries eroding.

148
Q

What are the four defects in Tetralogy of Fallot?

A

Pulmonary infundibular stenosis (most important determinant for prognosis) –> forces R to L flow across VSD, RVH
Right ventricular hypertrophy (boot shaped heart on CXR)
Overriding aorta
VSD

149
Q

Why does squatting improve cyanosis in Tetralogy of Fallot?

A

It increases systemic vascular resistance (SVR) –> decreased R to L shunt –> improves cyanosis

150
Q

What is most common cardiac congenital anomaly?

151
Q

How are aorta and pulmonary trunk attached in transpositions of great vessels?

A

Pulmonary trunk comes off left ventricle and aorta comes off right ventricle

152
Q

Boot shaped heart

A

Tetralogy of Fallot, RVH in adult

153
Q

Rib notching

A

Coarctation of aorta

154
Q

Most common congenital cause of early cyanosis

A

Tetralogy of Fallot

155
Q

Which type of collagen is found in

a. slippery tissue
b. bloody tissue

A

a. Type II

b. Type III

156
Q

What enzymes are used in metabolism of NE?

157
Q

What are clinical applications of Atropine?

A 
Decreased airway secretions
Pupillary dilation and cycloplegia
Decreased stomach acid
Decreased gut motility
Decreased urgency 
Treats Bradycardia
158
Q

What structures do these embryologic structures give rise to?

a. Truncus arteriosus
b. Bulbus cordis
c. Primitive atrium
d. Primitive ventricle
e. Primitive pulmonary vein
f. Left horn of sinus venosus
g. Right horn of sinus venosus
h. Right common cardinal vein and right anterior cardinal vein

A

a. great vessels –> aorta and pulmonary trunk
b. smooth parts of left and right ventricles (outflow tract)
c. Trabeculated part of atria
d. Trabeculated part of ventricles
e. Smooth part of left atrium
f. coronary sinus
g. smooth part of right atrium
h. superior vena cava

159
Q

When does the heart start beating in the embryo?

160
Q

What is the purpose of cardiac looping?

A

The primary heart tube loops to establish left-right polarity beginning in the fourth week of gestation

161
Q

Defect in left-right dynein

A

Dextrocardia

162
Q

Steps of septation of chambers

A
  1. Septum primum grows towards endocardial cushions, narrowing foramen primum
  2. Foramen secundum forms in septum primum and foramen primum disappears
  3. Septum secundum develops as foramen secundum maintains R to L shunt
  4. Septum secundum expands and covers most of the foramen secundum (residual foramen is the foramen ovale)
  5. Remaining portion of septum primum forms valve of foramen ovale
  6. Septum scandium and septum primum fuse to form the atrial septum
  7. Foramen ovale usually closes soon after birth because of increased LA pressure
163
Q

Where do VSDs more commonly occur?

A

In the membranous septum

164
Q

Heart morphogenesis of ventricles

A
  1. Muscular ventricular septum forms; opening is called inter ventricular foramen
  2. Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous inter ventricular septum. closing inter ventricular foramen
  3. Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of inter-ventricular septum
165
Q

Outflow tract formation

A

Truncus arteriosus rotates; neural crest and endocardial cell migrations –> truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum –> ascending aorta and pulmonary trunk

166
Q

Valve development

A

Aortic/pulmonary: derived from endocardial cushions of outflow tract
Mitral/tricuspid: derived from fused endocardial cushions of AV canal

167
Q

Fetal erythropoiesis occurs where?

A

Yolk sac: 3-8 weeks
Liver: 6 week - birth
Spleen: 10-28 weeks
Bone marrow: 18 weeks to adult

168
Q

Embryonic hemoglobin

A

Hemoglobin gower: two zeta and two epsilon chains

169
Q

Fetal hemoglobin

A

HbF: alpha2 gamma 2

170
Q

How does fetal Hgb affinity for oxygen differ from adult Hgb?

A

Fetal Hgb has higher affinity for oxygen due to less avid binding of 2,3 BPG - this allows fetal Hgb to extract O2 from maternal Hgb across the placenta

171
Q

Describe fetal circulation

A
  1. Blood enters fetus through umbilical vein and goes through ductus venosus into the IVC (bypasses hepatic circulation)
  2. Highly oxygenated blood from IVC enters right atrium: most of it goes through foramen ovale into the left heart and is pumped out to the rest of the body
  3. Blood from SVC (deoxygenated) –> goes from right atrium to right ventricle –> main pulmonary artery –> PDA –> descending aorta
172
Q

How is the shunt from right atrium –> PDA –> Aorta possible in fetal circulation?

A

There is HIGH fetal pulmonary artery resistance

173
Q

What happens to fetal circulation at birth?

A

When the infant takes it’s first breath, the pulmonary vasculature resistance decreases and left atrial pressure increases compared to right atrial pressure. The foramen ovale closes. The increase in O2 and decrease in prostaglandins close the ductus arteriosus

174
Q

What can you use to close PDA?

A

Indomethacin - inhibits prostaglandins E1 and E2 that keep the PDA open

175
Q

Fetal-postnatal derivatives

a. AllaNtois –> urachus
b. Ductus arteriosus
c. Ductus venosus
d. Foramen ovale
e. Notochord
f. UmbiLical arteries
g. Umbilical vein

A

a. MediaN umbilical ligament
b. ligamentum arteriosum
c. ligamentum venosum
d. Fossa ovalis
e. Nucleus pulposus
f. MediaL umbilical ligaments
g. Ligamentum teres hepatis (in falciform ligament)

176
Q

Which artery supplies the SA and AV nodes?

A

RCA; infarct may cause nodal dysfunction (bradycardia or heart block)

177
Q

What does right dominant circulation mean?

A

The Posterior descending artery arises from the RCA (85% of people)

178
Q

What does left dominant circulation mean?

A

PDA arises from the LCX (8% of people)

179
Q

Where does coronary artery occlusion most commonly occur?

A

In the LAD - “widow maker”

180
Q

What part of the heart makes up the posterior part of the heart?

A

Left atrium

181
Q

Cause of dysphagia or hoarseness

A

Left atrium enlargement –> dysphagia (compression of esophagus) or hoarseness (due to compression of left recurrent laryngeal nerve)

182
Q

3 properties of heart circulation

A
  1. Heart is perfused during diastole
  2. Myocardial oxygen requirement is very high; resting myocardium extracts 75-80% of oxygen from blood - exceeds ALL other tissues
  3. Coronary flow is regulated by local metabolic factors including hypoxia and adenosine accumulation
183
Q

What is the pulse pressure? It is proportional to what?

A

Systolic pressure - diastolic pressure

Proportional to SV, inversely proportional to arterial compliance

184
Q

How is CO maintained during exercise?

A

Early exercise - increased HR and increased SV

Late exercise - Increased HR (SV plateaus)

185
Q

What conditions increase pulse pressure?

A 
Hyperthyroidism
Aortic regurgitation
Aortic stiffening
Obstructive sleep apnea
Exercise
186
Q

What conditions decrease pulse pressure?

A

Aortic stenosis
Cardiogenic shock
Cardiac tamponade
Advanced heart failure

187
Q

What does LCX artery supply?

A

Lateral and posterior walls of left ventricle

Anterolateral papillary muscle

188
Q

What does LAD artery supply?

A

Anterior 2/3 of IV septum
Anterolateral papillary muscle
Anterior surface of left ventricle

189
Q

What does PDA supply?

A

Posterior 1/3 of IV septum
Posterior walls of ventricles
Posteromedial papillary muscle

190
Q

What forms diaphragmatic surface of heart?

A

Inferior wall of left ventricle

191
Q

What artery supplies right ventricle?

A

Right marginal artery

192
Q

What three things affect Stroke Volume?

A

Contractility, Afterload, Preload

Increased with increased contractility, increased preload and decreased afterload

193
Q

What things increase contractility?

A

Catecholamines (increased activity of Ca pump in SR)
Increased intracellular Calcium
Decreased extracellular Na (Na/Ca exchanger)
Digitalis (blocks Na/K pump –> increased intracellular Na)

194
Q

What things decreased contractility?

A 
Beta 1 blockade (decreased cAMP)
HF with systolic dysfunction
Acidosis
Hypoxia/hypercapnia
Non-dihydropyridine Ca Channel blockers (Verapamil, Diltiazem)
195
Q

What increases myocardial oxygen demand? (four things)

A

Increased contractility
Increased afterload
Increased HR
Increased diameter of ventricle (because it increases wall tension)

196
Q

What approximates preload? What determines this?

A

Ventricular EDV; depends on venous tone and circulating blood volume

197
Q

What approximates afterload? What determines this?

A

MAP

Increased afterload -> increased pressure –> increased wall tension

198
Q

What drugs decrease preload?

A

Venodilators (nitroglycerin)

199
Q

What things decrease afterload?

A

Vasodilators (Hydralazine)

ACE inhibitors and ARBs

200
Q

Normal ejection fraction

A

> 55%; this is an index of ventricular contractility

EF is decreased in systolic HF, normal in diastolic HF

201
Q

Force of contraction is proportional to what?

A

End diastolic length of cardiac muscle fiber (preload)

202
Q

Velocity of blood flow from highest to lowest

A

Aorta, large vessels –> vena cava –> large veins –> small arteries –> arterioles –> small veins –> venules –> capillaries

203
Q

What vessel accounts for most of TPR?

A

Arterioles

204
Q

Which vessels provide most of blood storage capacity?

205
Q

How does organ removal affect TPR and CO?

A

Increases TPR and decreases CO

206
Q

What is biggest determinant of viscosity of blood?

How does it increase and decrease?

A

Viscosity depends mostly on Hematocrit
Decreased in anemia
Increased in hyperproteinemic states (like multiple myeloma) and polycythemia

207
Q

Which part of the cardiac cycle has the highest O2 consumption?

A

Isovolumetric contraction (between mitral valve closing and aortic valve opening)

208
Q

Cause of normal splitting of heart sounds

A

On inspiration there is drop in intrathoracic pressure that increases venous return –> increased RV filling –> increased RV stroke volume –> increased RV ejection time –> delayed closure of pulmonic valve

209
Q

Cause of wide splitting of heart sounds

A

Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block) –> delay in RV emptying causes delayed pulmonic sound and exaggeration of normal splitting

210
Q

Cause of fixed splitting of heart sounds

A

Seen in ASD –> there is left to right shunt that causes increased RA and RV volume –> increased flow through pulmonic valve so that regardless of breath the pulmonic closure is greatly delayed

211
Q

Cause of paradoxical splitting

A

Seen in conditions that delay aortic valve closure (aortic stenosis, left bundle branch block); normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound (on inspiration, P2 closes later and moves closer to A2 paradoxically eliminating the split)

212
Q

How does hand grip affect the following?

a. Mitral regurgitation
b. Aortic regurgitation
c. VSD murmur
d. Hypertrophic cardiomyopathy murmur
e. Mitral Valve prolapse

A

(Increasing Afterload)

a. Increased intensity
b. Increased intensity
c. Increased intensity
d. Decreased intensity
e. Later onset of click/murmur

213
Q

How does Valsalva affect the following?

a. Most murmurs in general
b. Hypertrophic cardiomyopathy murmur
c. MVP

A

(Decreasing preload)

a. Decreased intensity
b. Increased intensity
c. Earlier onset of click

214
Q

How does rapid squatting affect the following?

a. Hypertrophic cardiomyopathy murmur
b. AS murmur
c. MVP

A

(Increased venous return, increased preload)

a. Decreased intensity
b. Increased intensity
c. Later onset of click

215
Q

Crescendo decrescendo systolic ejection murmur loudest at heart base

A

Aortic stenosis

216
Q

Holosystolic high pitched blowing murmur

A

Mitral/tricuspid regurgitation

217
Q

Mitral regurgitation is often due to…

A

Ischemic heart disease post MI

218
Q

Tricuspid regurgitation is most often caused by:

A

RV dilation

219
Q

Causes of Mitral or Tricuspid regurgitation

A

Rheumatic fever, Infective endocarditis

220
Q

Late systolic crescendo murmur with mid systolic click

A

Mitral valve prolapse

221
Q

MVP predisposes to:

A

Infective endocarditis

222
Q

Causes of MVP

A

Myxomatous degeneration (Marfans, Ehler Danlo)
Rheumatic fever
Chordae rupture

223
Q

Holosystolic harsh sounding murmur loudest at tricuspid area

A

Ventricular Septal Defect

224
Q

High pitched blowing early diastolic decrescendo murmur

A

Aortic regurgitation

225
Q

Causes of aortic regurgitation

A

Aortic root dilation, Bicuspid aortic valve, endocarditis, rheumatic fever

226
Q

Murmur that follows opening snap; delayed rumbling late diastolic murmur

A

Mitral stenosis

227
Q

Chronic mitral stenosis can cause:

A

LA dilation

228
Q

Myocardial action potential

a. Phase 0
b. Phase 1
c. Phase 2
d. Phase 3
e. Phase 4

A

a. Phase 0 = rapid upstroke and depolarization from Na influx
b. Phase 1 = Repolarization; inactivation of Na channels; voltage gated K channels open
c. Phase 2 = Calcium influx through voltage gated Ca channels balances K efflux; Ca triggers Ca release from SR and myocyte contraction
d. Phase 3 = Rapid depolarization by massive K efflux from opening of slower K channels and closure of voltage gated Ca channels
e. Phase 4 = resting potential; high K permeability through K channels

229
Q

How long is the effective refractory period normally?

230
Q

What initiates depolarization in cardiac nodal cells?

A

They spontaneously depolarize during diastole resulting in automaticity due to If channels (funny current responsible for slow mixed Na/K inward current)

231
Q

Pacemaker action potential

a. Phase 0
b. Phase 3
c. Phase 4

A

a. Phase 0 = upstroke; from opening of voltage gated Ca channels; fast voltage gated Na channels are permanently inactivated because of less negative resting voltage of these cells) –> results in slow conduction velocity that is used by AV node to prolong transmission from atria to ventricles
b. Phase 3 = repolarization; inactivation of Ca channels and activation of K channels -> K efflux
c. Phase 4 = slow spontaneous diastolic depolarization as Na conductance increases

232
Q

What part of pacemaker action potential determines HR?

What factors affect this?

A

Slope of phase 4 in the SA node
Decreased by Ach/Adenosine
Increased by Catecholamines

233
Q

How does sympathetic stimulation cause increase HR through pacemaker cells?

A

They increase the chance that I(f) channels are open

234
Q

a. Normal PR interval

b. Normal QRS complex

235
Q

What causes U wave?

A

Hypokalemia, Bradycardia

236
Q

Speed of conduction; fastest to slowest

A

Purkinje fibers > atria > ventricles > AV node

237
Q

Conduction pathway of heart

A

SA node –> atria –> AV node –> common bundle –> bundle branches –> fascicles –> Purkinje fibers –> ventricles

238
Q

Blood supply to AV node

Location of AV node

A

RCA supplies AV Node

Located in posteroinferior part of interatrial septum

239
Q

Shifting sinusoidal waveforms

A

Torsades de pointes

240
Q

What can Torsades de pointes progress to?

A

Ventricular fibrillation

241
Q

Treatment for Torsades de pointes

A

Magnesium sulfate

242
Q

Romano Ward syndrome

A

Autosomal dominant
Congenital long QT syndrome –> increased risk of sudden cardiac death from torsades de points
Pure cardiac phenotype

243
Q

Jervell and Lange-Nielsen syndrome

A

Autosomal recessive; congenital long QT syndrome that increases risk of sudden cardiac death from torsades de points
ALSO sensorineural deafness

244
Q

Brugada syndrome

A

Autosomal dominant - most common in Asian males
Pseudo-right bundle branch block and ST elevations in V1-V3
Increased risk of Ventricular tachyacchythmias and SCD
Prevent SCD with ICD

245
Q

WPW

A

Ventricular pre-excitation syndrome
Abnormal fast accessory pathway from atria to ventricle bypasses the rate slowing AV node –> ventricles depolarize too early and you see delta wave in QRS complex

246
Q

Complication of WPW

A

Reentry circuit that causes supra ventricular tachycardia

247
Q

Cause of 3rd degree heart block

A

Lyme disease

248
Q

What is Nesiritide?

A

Brain natriuretic peptide used in treatment of HF

249
Q

Hypertension, Bradycardia, Respiratory depression

A

Cushing reaction

250
Q

What is the Cushing reaction?

A

Increased intracranial pressure constricts arterioles –> cerebral ischemia –> increased pCO2 and decreased pH –> central reflex sympathetic increase in perfusion pressure (HTN) –> increased stretch –> peripheral reflex baroreceptor induced bradycardia

251
Q

PCWP is a good approximation of which pressure?

A

Left atrial pressure

252
Q

In mitral stenosis how does LA pressure compare to LV diastolic pressure?

A

LA pressure > LV diastolic pressure; this means PCWP > LV pressure

253
Q

Autoregulation controlled by:

a. Heart
b. Brain
c. Kidneys
d. Lungs
e. Skeletal muscle
f. Skin

A

a. Local metabolites like adenosine, NO, CO2 and decreased O2 are vasodilatory
b. Local metabolites like CO2 are vasodilatory
c. Myogenic and tubuloglomerular feedback
d. Hypoxia causes vasoconstriction
e. Local metabolites during exercise (lactate, adenosine, K+, H+, CO2) and at rest (sympathetic tone)
f. Sympathetic stimulation most important mechanism: temp control

254
Q

Cause of transposition of great vessels

A

Failure of aorticopulmonary septum to spiral

255
Q

Most common cause of ASD

A

Osteum secundum defect

256
Q

Congenital cardiac defect associations:

a. Alcohol exposure in utero
b. Congenital rubella
c. Down syndrome
d. Infant of diabetic mother
e. Marfan syndrome
f. Prenatal lithium exposure
g. Turner syndrome
h. Williams syndrome
i. 22q11 syndrome

A

a. VSD, PDA, ASD, tetralogy
b. PDA, pulmonary artery stenosis, septal defect
c. AV septal defect
d. Transposition of great vessels
e. MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
f. Ebstein anomaly
g. Bicuspid aortic valve, coarctation of aorta
h. Supravalvular aortic stenosis
i. Truncus arteriosus, tetralogy

257
Q

What is Monckeberg arteriosclerosis?

A

Medial calcific sclerosis
Calcification of elastic lamina of arteries –> vascular stiffening without obstruction; Intima NOT involved
Pipestem appearance on X-ray

258
Q

Which vessels does Arteriolosclerosis affect? What are the types?

A

Small arteries and arterioles

1) Hyaline - thickening of vessels walls in essential HTN or diabetes
2) Hyperplastic - onion skinning in severe HTN with proliferation of SMCs

259
Q

How do you treat Prinzmetal angina?

A

Calcium channel blockers, nitrates and smoking cessation

260
Q

How do you differentiate Unstable angina and NSTEMI?

A

No cardiac biomarker elevation in unstable angina

Both may have ST depression or T wave inversion

261
Q

Causes of sudden cardiac death

A

Lethal arrhythmia after MI
Cardiomyopathy (hypertrophic or dilated)
Hereditary ion channelopathies (Brugada, long QT)

262
Q

0-4 hours after MI

a. Gross
b. Microscope
c. Complications

A

a. None
b. None
c. Arrhythmia, HF, cardiogenic shock

263
Q

4-24 hours after MI

a. Gross
b. Microscope
c. Complications

A

a. Dark mottling; pale with tetrazolium stain
b. Early coagulative necrosis; release of necrotic cell contents into blood; edema; hemorrhage; wavy fibers; neutrophils appear; Reperfusion injury may cause contraction bands (due to free radical damage)
c. Arrhythmia, HF, cardiogenic shock

264
Q

1-3 days after MI

a. Gross
b. Microscope
c. Complications

A

a. Hyperemia
b. Extensive coagulative necrosis; tissue surrounding infarct shows acute inflammation and neutrophils
c. Post-infarction fibrinous pericarditis

265
Q

3-14 days after MI

a. Gross
b. Microscope
c. Complications

A

a. Hyperemic border; central yellow brown softening; maximally yellow and soft by 10 days
b. Macrophages, then granulation tissue at margins
c. Free wall rupture –> tamponade; papillary muscle rupture –> mitral regurgitation; interventricular septal rupture due to macrophage mediated structural degradation; LV pseudoaneurysm (risk of rupture)

266
Q

2 weeks to several months
a. Gross
b. Microscope
C. Complications

A

a. Recanalized artery, gray-white
b. Contracted scar complete (Type III collagen replaced by Type I collagen)
c. Dressler syndrome, HF, arrhytmias, true ventricular aneurysm (risk of mural thrombus)

267
Q

When does cardiac troponin rise? How long is it increased?

A

Rises after 4 hours; is increased for 7-10 days

268
Q

When does CK-MB rise? How long is it increased? What is it useful for?

A

Rises are 6-12 hours; levels return to normal after 48 hours so it is useful for diagnosing re-infarction following acute MI

269
Q

EKG localization of STEMI

a. LAD - anteroseptal
b. distal LAD - anteroapical
c. Anterolateral (LAD or LCX)
d. Lateral (LCX)
e. Inferior (RCA)

A

a. V1-V2
b. V3-V4
c. V5-V6
d. aVL, I
e. aVF, II, III

270
Q

Causes of dilated cardiomyopathy (ABCCCD)

A 
Alcohol
wet Beriberi
Coxsackie B virus
Chronic cocaine use
Chugs disease
Doxorubicin/Daunorubicin
Hemochromatosis
Sarcoidosis
Peripartum cardiomyopathy
271
Q

Eccentric hypertrophy - sarcomeres added in series

A

Dilated cardiomyopathy

272
Q

Findings in dilated cardiomyopathy

A

HF, S3, systolic regurgitant murmur, dilated heart on echo, balloon appearance of heart on CXR

273
Q

Systolic or diastolic dysfunction?

a. Dilated cardiomyopathy
b. Hypertrophic cardiomyopathy
c. Restrictive cardiomyopathy

A

a. Systolic
b. Diastolic
c. Diastolic

274
Q

Myofibrillar disarray and fibrosis

A

Hypertrophic cardiomyopathy

275
Q

Causes of restrictive cardiomyopathy

A

Sarcoidosis
Amyloidosis
Postradiation fibrosis
Endocardial fibroelastosis (young children)
Loffler syndrome (eosinophilic infiltrate)
Hemochromatosis

276
Q

Cause of hemosiderin laden macrophages in lungs

A

Pulmonary edema from increased pulmonary venous pressure –> increased pulmonary venous distension and transudation of fluid

277
Q

Causes of nonbacterial endocarditis

A

Malignancy
Hypercoagulable state
Lupus

278
Q

Tricuspid valve endocarditis bugs

A

Associated with IV drug use

S. aureus, Pseudomonas, Candida

279
Q

Aschoff bodies

A

granuloma with giant cells; associated with Rheumatic fever

280
Q

Enlarged macrophages with ovoid, wavy rod-like nucleus

A

Anitschkow cells seen in Rheumatic fever`

281
Q

Causes of acute pericarditis

A

Idiopathic (most common - probably viral)
Confirmed infection (Coxsackievirus)
Neoplasia
Autoimmune (SLE, rheumatoid arthritis)
Uremia
Cardiovascular (STEMI or Dressler syndrome)
Radiation therapy

282
Q

Equilibration of diastolic pressures in all 4 chambers

A

Cardiac tamponade

283
Q

Beck triad: hypotension, distended neck veins, distant heart sounds

A

Cardiac tamponade

284
Q

Kussmaul sign

A

Chronic constrictive pericarditis (JVD with inspiration)

285
Q

Rhabdomyoma association

A

Tuberous sclerosis (hamartomas, seizures, astrocytomas, cortical and retinal hamartomas, intellectual disability)

286
Q

Vascular tumor associated with radiation therapy and chronic post mastectomy lymphedema

A

Angiosarcoma

287
Q

Cancer association with vinyl chloride and arsenic exposure

A

Hepatic angiosarcoma

288
Q

Blood vessel malignancy in elderly

A

Angiosarcoma - in sun exposed areas

289
Q

Benign capillary skin papule found in AIDS patients

Cause?

A

Bacillary angiomatosis

Bartonella henselae infection

290
Q

How do you differentiate Kaposi sarcoma and Bacillary angiomatosis?

A

Both in AIDS patients but Bacillary angiomatosis has neutrophilic infiltrate; Kaposi has lymphocytic infiltrate

291
Q

Benign capillary hemangioma of the elderly

A

Cherry hemangioma; does not regress

292
Q

Cavernous lymphangioma of the neck

What is it associated with?

A

Cystic hygroma

Associated with Turner syndrome

293
Q

Benign, painful, red-blue tumor under fingernails

A

Glomus tumor

294
Q

Polypoid capillary hemangioma that ulcerates and bleeds

Associations?

A

Pyogenic granuloma

Trauma and pregnancy

295
Q

Benign capillary hemangioma of infancy; grows rapidly and regresses spontaneously by 5-8 years old

A

Strawberry hemangioma

296
Q

Histology of Temporal arteritis

A

Granulomatous inflammation

297
Q

Vasculitis that spares the lungs

A

Polyarteritis nodosa

298
Q

Palpable purpura on buttocks/legs, arthralgia, abdominal pain

A

Henoch-Schonlein purpura

-Associated with IgA nephropathy (Berger disease)

Step 1 AB (29 decks)

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