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PANCE review > Cardio 2 > Flashcards

Cardio 2 Flashcards

1
Q

Typical angina of MI

A

crushing chest pain and feeling of impending doom!

midsternal pain which radiates to jaw, neck, shoulder and down left arm

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2
Q

stable vs unstable angina

A

stable - brought on with physical activity and relieved with rest, usually within 30 min

unstable - increasing chest pain at rest or with exercise

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3
Q

Prinzmetal’s angina

A

(aka variant angina)

spontaneous vasospasm of coronary arteries

typically lasts longer than 30 min

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4
Q

Levine’s sign

A

clenched fist held over the heart

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5
Q

ECG findings of ischemia

A

ST depression

Downsloping ST

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6
Q

What lab is done to rule out MI in patient with ischemia?

A

troponins

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7
Q

Quick acting, emergency treatment of ischemia

A

sublingual nitroglycerin

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8
Q

Side effects of vasodilator/nitrate medications

A

hypotension
headaches
N/V

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9
Q

Medications for angina

A 
sublingual nitroglycerin
long-acting nitrates
BBs
CCBs
Aspirin
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10
Q

First line therapy for chronic angina

A

beta blockers

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11
Q

MOA of beta blockers to treat angina

A

lessen heart’s sympathetic response to epi and norepinephrine

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12
Q

MOA of calcium channel blockers to treat angina

A

decrease heart contractility

decrease peripheral vascular resistance

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13
Q

Surgical revascularization procedures for ischemia

A

Balloon angioplasty and stents

CABG = coronary artery bypass grafting

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14
Q

Possible cause of MI in young healthy individual

A

cocaine use

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15
Q

Atypical presentation of MI without chest pain most likely in what patients?

A

women and diabetics

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16
Q

Difference in clinical definition of angina vs MI

A

crushing chest pain in MI lasts longer than 30 min, whereas angina pain resolves within 30 min

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17
Q

Dressler Syndrome

A

post-MI syndrome; 1-2 weeks after MI patient experiences pericarditis, leukocytosis, pericardial effusion, pleural effusion

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18
Q

Changes in serial cardiac enzymes after MI (when do they elevate, peak, and normalize)?

A

Myoglobin: elevates in first 1-3 hrs, peaks at 6-7 hours, and normal by 24 hrs

Cardiac troponins I and K: elevate within 2-12 hrs, peak around 24 hrs, and normal by 2 weeks

CK-MB: elevate within 3-12 hrs, peaks around 24 hrs, and normal by 72 hrs

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19
Q

Progression of ECG findings with MI

A

peaked T waves -> ST segment elevation -> Q waves -> T wave inversion

ST elevation defined as > 0.1mv (one small box)

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20
Q

Using 12 lead how can you determine location of MI?

A 
Inferior – II, III, aVF
Posterior/septal – V1 and V2
Anterior – V3, V4
Anterolateral – V4, V5, V6
Lateral – I, aVL, V5, V6
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21
Q

Treatment of MI

A

“MONA”

Aspirin immediately
Nitroglycerin
Supplemental oxygen
Morphine for pain
Thromobytic
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22
Q

Contraindications of fibrinolytic therapy for STEMI (tPA)

A 
Absolute:
Ischemic stroke or head trauma within 3 months
Intracranial neoplasm
Active bleeding (excludes menses)
Any prior intracranial hemorrhage
Suspected aortic dissection
Relative:
BP > 180/110 or h/o chronic severe HTN
Past ischemic stroke +3 months
Major surgery, prolonged CPR (>10 min), or internal bleeding within 3 wks
Pregnant
Active peptic ulcer
Current use of anti-coags
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23
Q

Thrombolytic therapy (t-PA) for acute MI most effective within _____ hours, but can be used within _____ hours.

A

first 3 hrs

12 hrs

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24
Q

What is given to patient allergic to Aspirin?

A

Clopidogrel (Plavix)

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25
Q

Location of 2 valves between atria and ventricle

A 
mitral = Left
tricuspid = right
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26
Q

Symptoms of mitral valve stenosis and regurgitation

A

exertional dyspnea
orthopnea
paroxysmal nocturnal dyspnea secondary to pulmonary congestion

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27
Q

Way to definitively diagnose valve disorders?

A

Echo with Doppler

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28
Q

Valve disorders have close association with what other pathology?

A

rheumatic fever

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29
Q

Causes of mitral valve regurgitation

A

Mitral valve prolapse most common cause (thin females)
MI
Endocarditis
Ruptured chordae tendineae (d/t MI or endocarditis)

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30
Q

Which murmurs will have rales secondary to pulmonary congestion?

A

mitral stenosis

mitral regurg

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31
Q

opening snap following S2 best heard at apex =

A

mitral valve stenosis

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32
Q

pansystolic blowing murmur with loud S3

A

mitral valve regurg

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33
Q

Hallmark of mitral valve prolapse seen in mitral regurgitation

A

midsystolic click

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34
Q

Most common valvular disease in U.S.

A

mitral regurg

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35
Q

ECG findings of mitral regurg

A

LVH

A-fib

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36
Q

Mitral regurgitation and mitral valve stenosis treatment

A

Treat Afib – cardiovert, warfarin
Pulmonary congestion – diuretics and vasodilators
Surgical – Valve repair for prolapse, Valve replacement

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37
Q

Congenital and acquired causes of aortic stenosis

A

congenital bicuspid or unicuspid valve (middle aged)

acquired degeneration or calcification (over 65)

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38
Q

Symptoms of aortic stenosis

A

exertional dyspnea
syncope
angina - poor profusion of coronary arteries

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39
Q

Characteristics of aortic stenosis murmur

A

harsh crescendo-decrescendo systolic murmur

along right sternal border

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40
Q

Aortic stenosis treatment

A

VALVE REPLACEMENT
prosthetic - long lifespan but require anticoags
pericardial and porcine - shorter lifespan but don’t require anticoags
Ross Procedure - replace with patient’s pulm valve and cadaver to replace pulm valve

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41
Q

Patient with Marfan Syndrome likely has which valvular disorder?

A

Aortic regurgitation

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42
Q

Aortic regurgitation treatment

A

Control BP

Valve replacement if needed

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43
Q

Murmur with chest pain and swelling of feet and ankles?

A

Tricuspid regurg

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44
Q

Causes of pulmonary regurgitation

A 
Pulmonary HTN
Endocarditis
MI
Plaque
Iatrogenic
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45
Q

Valve disorder that causes enlarged right atrium? How does this present on ECG?

A

tricuspid regurg

abnormal p wave

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46
Q

widely split S2 =

A

pulmonary regurg

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47
Q

holosystolic blowing murmur and radiates to right sternum

A

tricuspid regurg

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48
Q

tricuspid regurg treatment

A

Diuretics and salt restriction to decrease fluid volume

Surgical valve repair or replacement

If pulmonary HTN, treat with arterial vasodilators

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49
Q

With mitral valve stenosis it is presumed that the patient has had ________ even if there is no obvious history.

A

rheumatic fever

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50
Q

Pulmonary regurgitation treatment

A

By itself is well tolerated and typically doesn’t require treatment

Valve may be replaced or repaired and underlying causes should be addressed

51
Q

Upon chest auscultation you here an opening snap following S2. You immediately think of what?

A

Mitral valve stenosis

52
Q

Harsh systolic murmur along left sternal border and it may radiate to the neck

A

aortic stenosis

53
Q

Low pitched murmur at the apex

A

mitral stenosis

54
Q

Pansystolic blowing murmur at the apex and radiating to the axilla

A

mitral regurgitation

55
Q

Where is the SA node and what does it do?

A

located in right atrium

pacemaker of the heart

56
Q

Where is the AV node and what does it do?

A

electrically connects atria with ventricles

57
Q

Firing rates of SA node, AV node

A 
SA = 60-100
AV = 40-60
58
Q

Pathway of heart’s electrical conduction system

A

SA node -> AV node -> bundle of His -> L and R bundles -> Purkinje fibers

59
Q

What is rate of sinus bradycardia?

A

under 60 bpm

60
Q

What is rate of sinus tachycardia?

A

> 100 bpm

61
Q

The most common chronic arrhythmia?

A

Atrial fib

62
Q

EKG of A-fib

A

irregularly irregular rhythm

disorganized electrical activity where p waves should be

63
Q

Treatment of atrial fibrillation and atrial flutter

A

Rate control: BBs or CCBs, Digoxin (A-fib)

Anti-thrombotics: Heparin short term, Warfarin long term

Cardioversion: electrical or chemical (AMIODORONE)

Radiofrequency ablation

64
Q

INR goal of A-fib and A-flutter anti-thrombolytic treatment

A

2.0 - 3.0

65
Q

ECG with sawtooth pattern

A

Atrial flutter

66
Q

A vague diagnosis encompassing chronic bradycardia, sinus arrest, and AV node exit block that occurs in elderly patients and is often brought on or exacerbated by drug therapy. Patients may have heart block or A-fib.

A

Sick sinus syndrome

67
Q

Treatment of sick sinus syndrome

A

permanent pacemaker

68
Q

Differences in ECG findings of supraventricular and ventricular arrhythmias?

A

supraventricular - narrow QRS

ventricular - wide QRS

69
Q

Patient comes in with “skipped heart beats.” What is likely arrhythmia?

A

PVC

70
Q

Bigeminy, trigeminy, unifocal, and multifocal PVCs

A

Bigeminy – PVC every other beat
Trigeminy – PVC every third beat (2 normal beats followed by a PVC)

Unifocal – all PVCs originate at same place within the ventricles and therefore all PVC QRS complexes look the same
Multifocal PVC – PVCs originate at different places and therefore QRS complexes appear different

71
Q

ECG findings of premature ventricular contractions

A

beat without a p wave that has wide QRS and a compensatory pause before the next beat

72
Q

PVC treatment

A

No treatment if asx

Beta blockers if sx

73
Q

A run of 3 or more PVCs is considered _______.

A

V-tach

74
Q

ECG of V-tach

A

Rate of 160-240

Several wide QRS waves with no p waves

75
Q

Treatment of V-tach

A

Cardioversion:
Defibrillation for pulseless V-tach
Synchronized if pulse present

Medications:
BBs for sustained V-tach to reduce incidence of sudden death
Lidocaine for stable sustained V-tach

76
Q

What is Torsades de Pointes?

A

deadly form of V tach where QRS complexes appear twist around isoelectric line

77
Q

How is Torsades de Pointes treated?

A

Bolus of Magnesium

Cardioversion prn

78
Q

Treatment of Ventricular Fibrillation

A

Immediate intervention to prevent sudden death

Defibrillation and lidocaine

79
Q

Pathophysiology and ECG findings of 1st degree AV block

A

All SA node signals get through AV node to ventricles but are a little delayed

PR interval greater than 0.20 seconds (1 box)

80
Q

Pathophysiology of 2nd degree AV block

A

Only some signals from SA node get to ventricles

81
Q

What are the two types of 2nd degree AV blocks and what do they appear like on ECG?

A

Mobitz Type 1: longer and longer PR intervals until one impulse (QRS complex) is dropped

Mobitz Type 2: intermittent dropped ventricle impulses without lengthened PR intervals

82
Q

What does 2:1 AV block mean?

A

two p waves for every QRS complex

83
Q

How are 2nd degree AV blocks treated?

A

Type 1 may be benign
Type 2 requires pacemaker

  • may use ACLS guidelines if symptomatic (Atropine or transcutaneous pacing)
84
Q

Pathophysiology of 3rd degrees AV block? Tx?

A

No impulses reach ventricles = complete heart block

Requires pacemaker

85
Q

Pathophysiology and ECG findings of Bundle Branch Block?

A

damaged bundle of His; AV node must propagate through muscle itself which is slower

ECG shows wide QRS wave as ventricles depolarize

86
Q

Predisposing factors to endocarditis

A

Most commonly bacterial infection with damaged or prosthetic heart valves - strep viridian’s, staph aureus, enterococci

Post op valve replacement (infection w/i 2 mon) - staph aureus, fungi, G-

Dental work, IV drug use, central line, surgeries/procedures

87
Q

PE findings of endocarditis

A 
New or changed murmur
Splinter hemorrhages
Janeway lesions
Osler nodes
Roth spots
Petechia
88
Q

Difference between Janeway lesion and Osler nodes?

A

both found on palms and soles but Osler nodes are painful and Janeway lesions aren’t

“Jane is nice”

89
Q

Duke Criteria for endocarditis

A

2 major, 1 major + 3 minor, 5 minor

Major Criteria
2 positive blood cultures that grow organism that typically causes endocarditis
Positive echo findings - New regurge, Abscess, Oscillating mass

Minor Criteria
Predisposing factor (eg. prosthetic heart valve, post op)
Fever
Embolic events - Janeway lesions, Petechia, Splinter hemorrhages
Immunologic events - Glomerulonephritis, Osler nodes
Positive blood culture not satisfying major criteria

90
Q

Endocarditis treatment

A

Prophylactic antibiotic use for patients with predisposing cardiac issues undergoing higher risk surgical procedures

4-6 weeks of IV antibiotics

Surgical: Valve replacement or Debridement of abscess or infected material

91
Q

Causes of pericarditis

A

Viral infection is the most common cause – echovirus, coxsackie, flu, HIV
Bacterial is more rare and typically follows respiratory infection
Post MI – Dressler Syndrome
Post cardiac surgery
Radiation
Autoimmune
Kidney failure

92
Q

Patient came in because of dyspnea, diaphoresis, and looks extremely ill. There is a pericardial friction rub heard in on lung exam and WBC’s are elevated. Likely dx?

A

Pericarditis

93
Q

ECG findings of pericarditis

A

ST-T wave changes

It begins with ST elevation. There is a return to baseline, and then a T wave inversion

94
Q

Treatment of pericarditis

A

Treat underlying issue

High doses of NSAIDS to reduce inflammation (eg. Colchicine)

Corticosteroids if NSAIDS not effective

Diuretics

Pericardiocentesis
Pericardiotomy

95
Q

___________ is when the pressure from a pericardial effusion constricts the heart to a point where it begins to affect cardiac output.

A

Cardiac tamponade

96
Q

Pathognomonic ECG finding of cardiac tamponade?

A

Electrical alternans = QRS amplitudes fluctuate beat to beat

97
Q

CXR of cardiac tamponade

A

water bottle heart

98
Q

How is cause of pericarditis definitively dx’d?

A

Pericardiocentesis for culture and cytology

99
Q

Treatment of cardiac tamponade

A

Small, stable effusions may be watched carefully

Treat underlying cause

Pericardiocentesis may be required

Pericardiectomy

100
Q

How is endocarditis cause confirmed?

A

blood cultures

101
Q

What is jaw claudication? What is it a hallmark sign of?

A

pain in jaw muscle or ear while chewing

Giant Cell Arteritis (aka temporal arteritis)

102
Q

What is an aneurysm? Where is it most common?

A

abnormal widening or ballooning of an artery due to weakness in the vessel wall

abdominal aorta

103
Q

Likely causes of aneurysm

A

Secondary to atherosclerosis - CAD, smoking, HTN, hyperlipidemia, etc.

104
Q

What congenital conditions are risk factors for aneurysms?

A

Marfan’s Syndrome

Ehler’s Danlos type IV

105
Q

Best diagnostic study for abdominal aneurysms?

A

Abdominal U/S

106
Q

Blood work of temporal arteritis or Giant Cell arteritis

A

LFT with elevated Alk phos
Elevated C-reactive protein
Elevated Sed rate

107
Q

Treatment of temporal arteritis or Giant Cell arteritis

A

High dose prednisone 40-60 mg po daily for 1-2 months followed by tapering over the period of 1-2 years

Aspirin 81 mg may help reduce risk of stroke and blindness etc.

108
Q

Gold standard for diagnosis for temporal arteritis

A

Biopsy of temporal artery

109
Q

List the six P’s of arterial occlusion.

A 
pain
pallor
pulselessness
paresthesias
poikilothermia (cold)
paralysis
110
Q

I came in to see my physician assistant because of…

Claudication – pain with exertion
Ischemia in lower extremities - numbness, tingling, +/- ulcers
Erectile dysfunction

A

PVD

111
Q

Diagnostic imaging of PVD

A

Doppler U/S flow studies
Ankle brachial index
Arteriography
CT/MRI angiography

112
Q

What is a normal ankle brachial index? What does lower value indicate?

A

Normal ABI is 1.0-1.4

Peripheral arterial disease (PAD) is less than 0.9

113
Q

Treatment of peripheral vascular disease

A

Lifestyle modifications to reduce atherosclerosis
Aspirin 81mg daily
Surgical intervention - Endovascular stenting and angioplasty, Bypass grafting

114
Q

___________ is venous inflammation as a result of a blood clot. This tends to be superficial following trauma.

A

Thrombophlebitis

115
Q

Causes and risk factors of DVT

A 
Trauma
Major surgery
Prolonged bed rest or immobilization
Smoking on oral contraception
Cancer
Pregnancy
Genetic clotting issues/ FHX
116
Q

Homan’s sign

A

pain and tenderness in the calf with a straight knee and dorsiflexion of foot

117
Q

Gold standard for DVT and varicose vein diagnosis

A

U/S doppler

118
Q

How to prevent DVTs?

A 
Leg exercises
Compression stockings
Sequential compression devices
Freq ambulation
Anticoag therapy: Warfarin, Lovenox, Heparin
119
Q

DVT treatment

A

Anticoags: Heparin, Warfarin
Filter for inferior vena cava
Thrombolysis
Thromboectomy

120
Q

Risk factors of varicose veins

A 
Pregnancy
Genetic predisposing factors
Valvular incompetence
Increased abdominal pressure
Long periods of standing
121
Q

Treatment of varicose veins

A

Behavioral changes - avoid long periods of standing, elevate legs when possible
Graduated elastic stockings
Vein stripping
Sclerotherapy

122
Q

I came in to see my physician assistant because of…

Progressive edema beginning at the ankles and moving up
Skin changes –
Hyperpigmentation
Shiny
Atrophic
Dermatitis
Painful ulcerations
A

Chronic Venous Insufficiency

123
Q

Treatment of Chronic Venous Insufficiency

A

Behavioral changes - avoid long periods of standing, elevate legs when possible
Graduated elastic stockings
Heat
Ambulatory exercise

124
Q

When can fibrinolytic therapy be done for chest pain?

A

ST elevation MI (STEMI) on ECG

Onset of angina

PANCE review (18 decks)

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