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ITE > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Which patients tend to have lower measured levels of BNP, even with heart failure?

A

Obese patients tend to have lower BNP levels.

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2
Q

Which conditions can lead to falsely elevated BNP levels?

A

Advanced age, pulmonary disease, and renal disease can all cause falsely elevated BNP levels.

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3
Q

“Crescendo-Decresendo” mumur =

A

Aortic Stenosis

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4
Q

The following medications should be avoided in a patient with aortic stenosis?

A

Nitroglycerin and vasodilators - don’t reduce their preload, they are preload dependent! Avoid negative inotropes, such as beta blockers and calcium channel blockers.

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5
Q

What maneuvers increase HOCM mumur?

A

-Increase intensity: Valsalva, standing up, giving Nitroglycerin

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6
Q

What maneuvers decrease HOCM mumur?

A

-Decrease intensity: handgrip, leg raise, sitting/laying down, squatting

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7
Q

What underlying pathologic
process distinguishes myocardial
infarction from angina/unstable
angina?

A

Atherosclerotic plaque rupture → exposed endothelium → clot attaches → reduced blood flow; if cell death occurs (usually due to complete vascular obstruction) then positive trop and MI; if no cell death occurs then negative trop and angina/unstable angina

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8
Q

What is the difference between
transmural and non-transmural
infarction?

A

Transmural: usually STEMI, large vessel affected, benefit from
thrombolytics/PCI; Non-Transmural: usually NSTEMI, smaller
subendocardial artery, may benefit from PCI but no thrombolytics

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9
Q

What defines Unstable Angina?

A

Stable Angina + pain at rest, new pain, increasing pain severity,
hemodynamic changes with pain

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10
Q

Acute chest pain at night, EKG
with STEMI, all symptoms and
EKG changes resolve with nitro?

A

Prinzmental’s Angina (coronary spasm, most do not have CAD; treat
with CCBs)

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11
Q

What are early to late EKG
changes with ACS?

A

Hyperacute T’s and Giant R (very early and transient), STE, STD
(ischemia or reciprocal), Q waves (1 square wide, 1/3 height QRS), TWI

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12
Q

Biphasic T-wave in V2/V3

A

Wellen’s Syndrome: biphasic (type A) or deeply inverted, symmetric
(type B) TW in septal leads = early signal of proximal LAD lesion

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13
Q

Chest Pain with STE V1-V4 with
STD II, III, aVL

A

Anterior MI 2/2 LAD occlusion, may affect large territory of LV, septum
and conduction sysytem (high grade blocks, wide complex
bradycardias), commonly have shock, possible ruptures

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14
Q

Chest Pain with STE I, aVL, V5,
V6 with STD V1

A

Lateral MI 2/2 LAD vs LCx occlusion, may affect LV

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15
Q

Chest Pain with STE II, III, aVF
with STD V1-V4

A

Inferior MI 2/2 occlusion of PDA (RCA > LCx), may affect AV node
(usually transient narrow complex bradycardias), may cause papillary
muscle rupture

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16
Q

Chest Pain with STE III > II and
V1 > V2

A

Right Ventricular MI, should get R-sided leads (STE in V4R, V5R), 2/2
proximal RCA lesion, associated with Inferior MI

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17
Q

Chest Pain with STD V1-3

A

Posterior MI, get posterior leads to dx (req only 0.5 mm elevation for
STEMI dx), 2/2 occlusion of Posterior Descending (RCA > L circ)

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18
Q

What meets STEMI criteria for
leads V2-V3 versus all other
leads?

A

V2-V3: ≥2mm in MEN ≥ 40yrs, ≥2.5mm in MEN < 40yrs, or ≥ 1.5mm in
WOMEN; All other leads: STE at the J-point of ≥ 1mm in two contiguous
lead

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19
Q

What distinguishes Type I-Type
V MI?

A

Type I: MI caused by acute atherothrombotic CAD, usually due to
plaque rupture or erosion; Type II: MI 2/2 mismatch of oxygen supply
and demand; Type III: typical MI presentation but death before
biomarkers obtained; Type IV: MI 2/2 PCI; Type V: MI 2/2 CABG

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20
Q

How can you detect MI in
patients with paced rhythm or old
LBBB

A

Sgarbossa Criteria: STE >1mm with concordant (same direction) QRS,
concordant STD >1mm V1-V3, STE >5mm with discordant (opposite
direction) QRS (modified Sgarbossa changes this last rule to discordant
STE >25% preceding S wave)

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21
Q

What is unique about the
management of Inferior MIs?

A

With Inferior MI, always consider RV involvement and get right-sided
EKG leads

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22
Q

What is unique about the
management MI with rightventricular
involvement?

A

They are preload dependent and will become very hypotensive with
nitroglycerin - avoid this, give IVF for hypotension

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23
Q

What are potential early
complications (<24hr) of MI?

A

arrhythmia, shock 2/2 pump failure or valve dysfunction

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24
Q

What are potential late
complications (>24hr) of MI?

A

Thromboembolism, myocardial rupture, valve rupture, CHF, pericarditis

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25
Q

Pleuritic chest pain 4wks after
MI?

A

Dressler’s syndrome: autoimmune pericarditis, typically 2-6wks s/p MI. Tx
it with NSAIDs like any other pericarditis

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26
Q

What artery typically supplies the
SA node and AV node?

A

SA- RCA 60%, LCx 40%; AV- RCA 90%, LCx 10%; concern for
bradycardias if Inferior MI

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27
Q

Cardiac Tamponade after MI

A

Myocardial wall rupture, give IVF and dispo to OR

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28
Q

What EKG finding is classic in
Cardiac Tamponade?

A

Electrical Alternans

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29
Q

Shock + new murmur after recent
MI

A

Papillary muscle rupture, Rx- reduce afterload and dispo to OR; same
treatment if septal wall rupture

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30
Q

What potential treatments for
AMI have been shown to reduce
mortality?

A

Defibrillation for VF/VT (30% mortality reduction), Aspirin (25% mortality reduction)

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31
Q

What is the only contraindication
to aspirin in ACS?

A

True aspirin allergy (anaphylaxis)

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32
Q

What is better for treatment of
STEMI, thrombolytics or PCI?

A

PCI is better. Thrombolytics should only be considered if PCI is not
available at center within 90min or after transfer within 120min

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33
Q

What EKG changes are included
under indications for
thrombolysis?

A

STEMI (STE >2mm for men, >1.5mm for women in V2-3, STE >1mm in
2+ other leads), STD V1-3 (posterior MI), old LBBB + Sgarbossa

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34
Q

What are absolute
contraindications for
thrombolysis?

A

Any previous brain bleed or known mass, ischemic stroke or closed
head injury within 3mo, known bleeding disorder, current active
bleeding, major surgery in the last 2 months, BP > 180/110 *after
treatment, suspected aortic dissection

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35
Q

What are concerning
complications of thrombolysis
and how often do they occur?

A

Intracranial hemorrhage (1/70 to 1/100, >50% mortality), major bleeding
(e.g. GI bleed) in 5%

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36
Q

What EKG changes may occur
with reperfusion?

A

Accelerated idioventricular rhythm, NSVT, PVCs; these should be
transient, are overall benign and do not require additional treatment

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37
Q

What is the appropriate
treatment of ST elevation after
cocaine use?

A

First treat with benzos, aspirin, nitrates, calcium channel blockers or
alpha blockers (e.g. phentolamine) for HTN, thrombolysis only if ST does
not return to baseline after these treatments

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38
Q

What is the appropropriate
treatment for HTN after cocaine
use?

A

Benzos, CCBs or phentolamine; NO Beta Blockers (may theoretically
lead to unopposed alpha stimulation and worsened HTN)

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39
Q

What are key risk factors for
Infective Endocarditis?

A

Diseased valves, artificial valves, IV drug use, dental extractions

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40
Q

What heart valve and what
organism is most common in
Infective Endocarditis?

A

Left sided (mitral most common valve affecred overall) > right sided
(tricuspid > pulmonary); Staph aureus is most common pathogen but
viridans strep if s/p tooth extraction); Tricuspid is most common with IV
drug use (Staph aureus)

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41
Q

Describe the classic physical
exam findings in Infective
Endocarditis?

A

Osler Nodes (painful nodules on fingertips), Janeway Lesions
(nontender hemorrhagic lesions on palms/soles), Roth Spots (retinal
hemorrhages), Splinter hemorrhages (linear on nails), Petechiae, New
Murmur

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42
Q

What is the appropriate
management and treatment of a
patient with suspected Infective
Endocarditis?

A

Blood cultures x 3 (different locations), Echo (transesophageal best),
broad spectrum antibiotics to cover staph/strep/gram negatives (Vanco
+ PCN + Gent)

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43
Q

When should a patient receive
antibiotic prophylaxis for Infective
Endorcarditis prior to a
procedure?

A

High-risk procedures: dental or invasive respiratory; GI/GU
procedures don’t need abx. High risk pts: Aritficial or damanged valves,
ANY congnetial heart dz hx; Rx: Amoxicillin (dental procedures)

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44
Q

What left sided murmurs are
systolic?

A

Aortic stenosis and mitral regurg

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45
Q

What left sided murmurs are
diastolic?

A

Aortic insufficiency and mitral stenosis

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46
Q

Syncope + systolic murmur
radiating to neck

A

Aortic Stenosis, syncope is poor prognostic sign, requires surgical
consult; causes L heart strain. Patients generally present with angina,
then syncope and then heart failure.

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47
Q

Chest pain with new diastolic
murmur

A

Aortic dissection causing aortic insufficiency, may have “water-hammer”
pulse

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48
Q

Pregnant women with sudden
cardiovascular collapse during
labor

A

Mitral Stenosis, high output during labor causes LA enlargement, AFib and arrhythmia

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49
Q

Treatment for decompensating
patient with diastolic murmur,
opening snap

A

Cardiovert, suspect mitral stenosis and AFib

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50
Q

MI followed by hypotension and
new murmur

A

Mitral Regurgitation 2/2 ruptured cordae tendineae/papillary muscle; Tx
decrease afterload and cardiac surgery

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51
Q

What are the most likely causes
and signs/symptoms of Right
and Left sided Heart Failure?

A

Right: MC 2/2 L-sided failure, lung disease, PE, symptoms include JVD,
peripheral edema, hepatic congestion; Left: 2/2 ischemia, valves, HTN,
symptoms include SOB, orthopnea, PND, potential R-sided failure

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52
Q

What distinguishes systolic vs
diastolic heart failure?

A

Systolic: failed forward flow; Diastolic: failed filling

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53
Q

What is the general approach for
treatment of decompensated
heart failure?

A

Decrease LVEDV to improve SV and CO (Starling curve); Reduce
preload with nitroglycerin and diuretics (Lasix; caution if diastolic failure),
BiPAP; consider afterload reduction (nitroglycerin); give inotropes for
shock

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54
Q

What are classic causes of high
output cardiac failure?

A

Hyperthyroidism, Beriberi, AV fistula, Paget’s dz, severe anemia,
pregnancy

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55
Q

What are classic CXR findings
with heart failure?

A

Big heart, fluffy infiltrates, Kerly B lines, blunted CVA (effusion)

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56
Q

What does BiPAP help patients
with heart failure?

A

Decreases work of breathing, decreases preload (positive pressure
increases intrathoracic pressure and decreases venous return)

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57
Q

What is the most common cause
of acute Right Heart Failure (Cor
Pulmonale)?

A

Pulmonary Embolism; Left heart failure is most common chronic cause

58
Q

Dx and Tx of Dilated
Cardiomyopathy

A

H/o HTN or ischemia, big heart on CXR, low EF on echo; Tx underlying
cause/CHF/dysrhythmias, anticoagulate if mural thrombus, transplant if
severe

59
Q

Dx and Tx of Restrictive
Cardiomyopathy

A

2/2 fibrosis, radiation, TB causing stiffness; normal heart on CXR, poor
filling on echo; Tx underlying cause/CHF/dysrhythmias

60
Q

Dx and Tx of Hypertrophic
Cardiomyopathy

A

Classically with septal hypertrophy, severe symptoms/syncope with exercise, EKG with LVH (tall QRS, needle-like Q waves);
Tx avoid exertion, beta blockers (slow rate and ↑ ventricular filling), AICD for ventricular arrhythmias, surgical ablation

61
Q

Describe the typical mumur of
Hypertrophic Obstructive
Cardiomyopathy (HOCM)

A

Harsh, systolic crescendo-decrescendo murmur; ↑ with Valsalva,
standing up (↓ LV blood volume); ↓ squatting, trendelenberg (↑ LV
blood volume)

62
Q

What is the typical time frame for
developing peripartum
cardiomyopathy?

A

Last trimester to 5 months postpartum

63
Q

What are the classic clinical clues
for diagnosis of Pericarditis?

A

Triad: fever + dyspnea + chest pain (pleuritic chest pain radiating to
neck, worse with laying flat), recent viral syndrome; exam- intermittent
friction rub, clear lungs; may have evidence of pericardial
effusion/tamponade; unlikely to have trop leak

64
Q

What are classic EKG changes
with Pericarditis?

A

PR depression (most specific), PR segment elevation (aVR), diffuse
STE, TW flattening followed by TW inversion

65
Q

What is the appropriate
treatment for Pericarditis?

A

Must get Echo to r/o pericardial effusion; NSAIDS, ± colchicine (↓
recurrent pericarditis)

66
Q

What are the classic clinical clues
for diagnosis of Myocarditis?

A

Dyspnea = most common sx, chest pain, viral prodrome, CHF sx (wet
lungs, edema), arrhythmias, unresolving sinus tachycardia; usually (+)
troponin; Echo usually with global hypokinesis and dilated chambers

67
Q

What are classic EKG changes
with Myocarditis?

A

Sinus tachycardia, non-specific STE; can be similar to pericarditis

68
Q

What is the appropriate
treatment for Myocarditis?

A

Supportive care, avoid early NSAIDs or steroids, ICU admit if
severe/CHF

69
Q

What are the most common
causes of Myocarditis?

A

Idiopathic (most common overall), Parvovirus (most common viral cause),
Chagas disease (most common worldwide)

70
Q

JVD, decreased heart sounds,
and hypotension

A

JVD, decreased heart sounds,
and hypotension

71
Q

What are the clinical features of
hypertensive emergency?

A

CNS: dizziness, n/v, confusion, weakness, encephalopathy, ICH, SAH,
CVA; Eyes: ocular hemorrhage, papilledema, vision loss; Heart: ACS,
Ao dissection, shock; Kidneys: hematuria, proteinuria, acute renal
failure

72
Q

Review the definitions of
Asymptomatic HTN, HTN
Urgency and HTN Emergency

A

Asymptomatic HTN: BP >140/90 without apparent symptoms; HTN
Urgency: BP >180/110 but WITHOUT signs of end organ dysfunction;
HTN Emergency: BP >180/110 WITH signs of end organ dysfunction

73
Q

Asymptomatic HTN: BP >140/90 without apparent symptoms; HTN
Urgency: BP >180/110 but WITHOUT signs of end organ dysfunction;
HTN Emergency: BP >180/110 WITH signs of end organ dysfunction

A

Asymptomatic: no workup needed (Cr = only screening test shown to
change mgmt for ITE), no treatment needed, restart home meds (if any),
refer to PMD; HTN Urgency: rule out end organ dysfunction (based on
sx), gradually lower BP over 1-2d with PO meds (restart home or HCTZ,
BB/CCB); HTN Emergency: if end organ dysfunction then goal 20-30%
BP reduction (Nicardipine, Esmolol, Labetalol, Nitroglycerin, etc. based
on sx)

74
Q

What are the JNC 8
recommendations for BP meds in
asmyptomatic HTN

A

NOT a requirement to start in ED, but recommended (esp. for boards).
Non-African-American: Thiazide, CCB, ACEI, ARB; African-American:
Thiazide, CCB; CKD: ACEI or ARB

75
Q

What medications are best to
lower BP in patients with severe
HTN and the following: Encephalopathy, Aortic
Dissection, Cocaine use,
pregnancy, ACS/CHF

A

Encephalopathy: Nicardipine; Aortic Dissection: Beta blockers FIRST
(Esmolol or labetalol to reduce rate & shear stress), ± Nitroprusside
AFTER rate reduction); Cocaine use: benzos and phentolamine (no
beta blockers); Pregnancy: IV Mg, Hydralazine, Labetalol
(preeclampsia); ACS/CHF: Nitroglycerin

76
Q

How should HTN be managed
for Ischemic and Hemorrhagic
Strokes?

A

Ischemic Strokes: permissive HTN to protect penumbra up to 220/120
BUT reduce to <185/110 if considering tPA; Hemorrhagic: varied
guidelines for BP control (good goal SBP 140 or MAP < 130), use CCBs
to prevent vasospasm (PO Nimodipine = classic for boards)

77
Q

What are potential non-cardiac
causes of syncope?

A

Aortic (Aortic dissection, ruptured AAA), neurologic (CVA, SAH, sz),
bleeds (RP bleed, ruptured ecoptic or AAA, GI bleed), orthostatic
(meds), reflex (vasovagal)

78
Q

What is the differential for
potential life-threatening cardiac
causes of syncope?

A

Dysrhythmias (VT), structural abnormalities (HOCM, critical aortic
stenosis), electrical abnormalities (Brugada, WPW, Prolonged QT,
arrhythmogenic right ventricular dysplasia), others (PE, MI); Screen all
EKGs for these findings

79
Q

What minimum workup should be
completed on young female
patients with syncope

A

Pregnancy test (ruptured ectopic may only present with syncope)

80
Q

How is near syncope treated
differently than syncope?

A

They aren’t, they have the same causes and should be worked up the
same way

81
Q

What is the overall most common
cause of syncope?

A

Idiopathic (40-50%) > Vasovagal (~20%)

82
Q

What factors make someone with
syncope “high risk” requiring
admission and significant
workup?

A

San Francisco Syncope Rule: CHESS - Admit patients with CHF, Hct <
30, EKG that is abnormal, Shortness of Breath or Systolic BP < 90, as
they are high risk for serious outcomes. Other high risk features: family
history of sudden death, syncope with exertion, structural heart disease.

83
Q

What EKG changes may be
seen in a patient with Wolff-
Parkinson-White?

A

Slurred upstroke of QRS (delta wave), wide QRS (QRS > 120ms), short
PR interval (most common, PR < 120ms)

84
Q

What EKG changes may be
seen in a patient with Brugada
Syndrome?

A

Pseudo-RBBB, STE V1-3 (types: coved/downsloping STE followed by
TWI, or “saddle-back” STE)

85
Q

What EKG changes may be
seen in a patient with Long QT?

A

End of T wave > 1/2 R to R interval

86
Q

What EKG changes may be
seen in a patient with
Arrhythmogenic Right Ventricular
Dysplasia?

A

Epsilon wave (postive notch at end of QRS)

87
Q

What is the underlying pathology
in Arrhythmogenic Right
Ventricular Displasia?

A

Genetic abnormality, autosomal dominant, causes fibro-fatty infiltrate in
RV (best seen on Cardiac MRI) that causes arrhythmogenic focus in RV
(30% with epsilon wave) and predisposes for fatal arrhythmias; Rxantiarrhythmics,
AICD

88
Q

What EKG changes may be
seen in a patient with
Hypertrophic Obstructive
Cardiomyopathy (HOCM)?

A

LVH, LARGE voltages (tall QRS), deep/narrow Q waves (“needle-like”)
in lateral (I, aVL, V5-6) and inferior (II, III, aVF) leads

89
Q

What patients are higher risk for
Aortic Dissection?

A

Prolonged HTN, connective tissue disease (e.g. Marfan syndrome); also
pregnancy, congenital heart disease, trauma

90
Q

What are the classic clinical clues
for diagnosis of Aortic
Dissection?

A

Acute onset severe pain radiating in direction of propogation (neck/arms
vs back/abdomen); chest pain (most common) + something else = TAD;
HTN = most common risk factor AND exam finding; can be associated
with any sx linked to sequelae of dissection including new murmur, MI,
CHF, renal insufficiency, mesenteric ischemia, new neuro deficits. Note
BP can be high, low or normal

91
Q

What is the most common XR
finding in acute aortic
dissection?

A

Mediastinal widening

92
Q

What is the appropriate
management and treatment of a
patient with suspected Aortic
Dissection?

A

HR and BP control to decrease shear stress (Esmolol followed by
Nitroprusside, or Labetalol), control pain, T&C x 10-15; if unstable
consult cards/thoracic surgery with dispo to OR, consider bedside echo;
if stable get CTA aortogram; NEVER send unstable patient to CT

93
Q

What is the difference between
Type A and Type B aortic
dissections?

A

Type A: Ascending Aorta, managed surgically; Type B: Descending
Aorta, usually managed medically

94
Q

What patients are higher risk for
Ruptured AAA?

A

Disease of arteriosclerosis (all the same risk factors): age > 60, males,
family history, HTN, HL, smoking, CAD, connective tissue disease

95
Q

Most common presentation for
unruptured AAA?

A

Asymptomatic

96
Q

What are the classic clinical clues
for diagnosis of Ruptured AAA?

A

Cooper’s triad: sudden abdominal/flank pain + pulsatile abdominal mass
+ hypotension; Others: peripheral ischemia, syncope, sudden death

97
Q

What size AAA is higher risk for
rupture?

A

> 3cm is pathological, >5.0cm is high risk and requires surgery

98
Q

What is the appropriate
management and treatment of a
patient with suspected Ruptured
AAA?

A

Bedside US to eval for AAA, possible free fluid (though bleeding may
be retroperitoneal), T&C x 10-15, emergent vascular surgery consult
with dispo to OR ASAP; DO NOT send unstable patient to CT scan

99
Q

History of repaired AAA with
massive GI bleed

A

Aortoenteric fistula

100
Q

Dx and Tx of Acute Arterial
Occlusion

A

Look for medical problems related to thromboemboli (Afib = most
common embolic cause, MI, or endocarditis); 6 P’s: pain (out of
proportion to exam), pallor, pulselessness, poikilothermia, paresthesias,
or paralysis; Dx: CT angio vs duplex US; emergent vascular surgery
consultation; Rx: heparin vs thrombolysis vs embolectomy

101
Q

How sensitive is Homan’s sign for
DVT?

A

Homans (pain in the calf on dorsiflexion of ankle while the knee is fuly
extended) has 50% sensitivity

102
Q

What are risk factors for DVT?

A

Classic triad (Virchow’s): stasis, + hypercoagulability + endothelial
damage; acquired (persistent): age, active cancer, hx DVT/PE,
antiphospholipid Ab; acquired (transient): recent surgery or major
trauma, pregnancy, OCPs/HRT, paralysis/immobilized (3d within last
4wks); inherited- ATIII deficiency, Protein C/S deficiency, Factor V
Leiden; exam- tender vein or distended superficial veins, unilateral calf
swelling >3cm, unilateral pitting edema

103
Q

What is the appropropriate
workup for patients with clinical
symptoms and low versus high
risk of DVT?

A

Low risk: d-dimer ok; Moderate-high risk: d-dimer & duplex US (alt CT
venography); if high risk may require serial dopplers & whole leg US

104
Q

What is the appropriate
management of isolated calf
DVT?

A

Anticoagulation not required unless within 5cm of popliteal vein (ASA
otherwise); repeat ultrasound (in 2-5d) to r/o propogation. This is only
true for low risk pts w/ transient risk factors (such as recent travel).

105
Q

What are considered distal veins
in the evaluation of a DVT?

A

Anything in the calf - infrapopliteal veins: posterior tibial, peroneal,
anterior tibial. If a pt is low risk (e.g. NOT obese or prothormobic for any
reason) and has a transient risk factor (e.g. recent travel, prolonged
immobilization, ect …) distal DVTs can be monitored w/ repeat US and
no anticoagulation.

106
Q

Review the definitions and EKG
changes of 1st, 2nd, and 3rd
degree AV Block

A

1st: PR >200 and otherwise normal; 2nd: Mobitz Type I (Wenckebachincreasing
PR interval then dropped beat), Mobitz Type II (stable long
PR, then sudden, non-conducted PR → dropped beat); 3rd: P waves
entirely dissociated from QRS

107
Q

What types of heart block
typically require pacemaker
placement?

A

2nd degree (Mobitz Type II) and 3rd degree

108
Q

What is the appropropriate
treatment for unstable
bradycardia?

A

Atropine (may help if narrow QRS); Others: Dopamine, Epinephrine,
Isoproterenol; Unstable: transcutaneous pacing (± transvenous pacing);
Definitive Rx: permanent pacemaker

109
Q

Review the general steps for
transcutaneous pacing

A

Sedate/pain control if able, place pacer pads, turn on pacing function,
set rate 70-80, increase voltage until capture noted

110
Q

Review the general steps for
transvenous pacing

A

Place IJ or SC cortis, introduce catheter and inflate balloon, set pacer at
80 bpm and voltage to 20 mA, advance catheter to RV (will show LBBB
pattern), deflate balloon, secure and decrease voltage to lowest setting
with continued capture. Preferred sites: RIJ and left subclavian

111
Q

Treatment for arrhythma and
unstable patient

A

Electricity

112
Q

DDX for narrow complex
tachyarrhythmia WITH P waves;
Treatment for stable patient

A

Sinus tach, AFlutter, MAT; Treat underlying problem If present, and
control rate with AV nodal blockers (and shock if unstable!)

113
Q

DDX for narrow complex
tachyarrhythmia WITHOUT P
waves; Treatment for stable
patient

A

AF, SVT, AVNRT, orthodromic AVRT; Treat with Adenosine or AV
nodal blockers (and shock if instable!)

114
Q

Differential for wide complex
tachyarrhythmia without P
waves; Treatment for stable
patient

A

VT (VF possible but likely unstable pt), SVT with BBB, Antidromic AVRT
(e.g. WPW); Rx: Procainamide or Amiodarone; AVOID AV nodal
blockers; Unstable- shock!

115
Q

EKG with chaotic P waves,
irregularly irregular rhythm

A

Atrial Fibrillation; Rx- CCB or BB

116
Q

EKG with “sawtooth” symmetrical
P waves, regularly irregular
rhythm

A

Atrial Flutter; Rx- CCB or BB

117
Q

EKG with multiple types of P
waves, irregularly irregular rhythm

A

Multifocal Atrial Tachycardia; 2/2 pulmonary disease (COPD = most
common cause); Rx- CCB or BB

118
Q

EKG with regular tachycardia
and narrow QRS

A

AV nodal reentrant tachycardia (AVNRT) or Orthodromic Atrioventricular
Reentrant Tachycardia (AVRT); Rx- Adenosine (first line), consider BB or
CCB, shock (cardioversion)

119
Q

EKG with regular tachycardia
and wide QRS

A

Antidromic Atrioventricular Reentrant Tachycardia (AVRT) OR Ventricular
Tachycardia; Rx- Procainamide vs Amiodarone, consider Mag (shock if
unstable); Avoid AV nodal blockers in these patients

120
Q

What is the difference between
Orthodromic and Antidromic
Atrioventricular Reentrant
Tachycardia (AVRT)?

A

Reentry circuit with accessory pathway (WPW- Bundle of Kent);
Orthodromic travels anterograde down AV node and back up accessory
pathway resulting in regular and narrow QRS complex (looks like SVT);
Antidromic travels anterograde down accessory pathway and back up
AV node (retrograde) resulting in regular and wide QRS complex (looks
like VT). Tx antidromic w. Procainamide.

121
Q

What is the appropriate
management of a patient with
tachydysrhythmia and suspected
WPW?

A

Procainamide or Amiodarone if stable; Shock if unstable; AVOID AV
nodal blockers. If any signs of WPW (delta wave, short PR) or borderline
wide QRS, presume WPW and avoid AVNBs

122
Q

EKG with multiple chaotic
ventricular foci that are wide and
irregular

A

Ventricular Fibrillation; shock (defibrillate)

123
Q

What BP measurements define
Stage I and Stage II HTN?

A

Stage I HTN: systolic 140-159 mmHg or diastolic 90-99 mmHg; Stage II
HTN: systolic >160 mmHg or diastolic >100 mmHg

124
Q

What EKG findings suggest
Ventricular Aneurysm?

A

Persistent STE > 2wks after known MI (and lack of reciprocal changes),
most often in precordial leads (V3-5); Others: Q or QS waves, T waves
small relative to QRS, reciprocal changes absent

125
Q

What is “Holiday Heart
Syndrome” and how should it be
treated?

A

Typically atrial arrhythmia (Afib) after excessive ETOH intake; Rxobservation
(if stable), typically self-resolves within 48hr

126
Q

What EKG findings confirm a
diagnosis of Ventricular
Tachycardia?

A

AV dissociation, QRS > 120, HR > 100, fusion beats & capture beats (both help distinguish from SVT)

127
Q

What is the most common cause
of Cor Pulmonale?

A

Cor Pulmonale = R heart failure 2/2 respiratory disease; COPD = most
common CHRONIC cause; PE = most common ACUTE cause; otherspulm
fibrosis, ILD, pulmonary HTN, sleep apnea

128
Q

What are contraindications for
Coumadin with known AFib?

A

Alcoholism, recent trauma or surgery, respiratory bleeding, active GI
bleeding, GU bleeding, ICH, or significant risk of falls

129
Q

Review CHA2DS2VASc scoring
to determine need for
anticoagulation with AFib

A

CHF (1), HTN (1),Age ≥75 (2), DM (1), Stroke (2), Female (1); Rx- Low
risk (0)- ASA or none, intermediate risk (1)- consider AC, high risk (≥ 2)-
start AC

130
Q

How are vitals assessed on a
patient with an LVAD?

A

Blood pumped by machine from LV to aorta, no pulse will be present,
need to check with BP cufff to obtain MAP (goal 70-80)

131
Q

Pt with an LVAD and elevated
LDH?

A

Think pump thrombosis. Thrombosis leads to hemolysis which then
leads to elevated LDH. LDH levels are typically > 1000

132
Q

What is the most common site for
infection in a LVAD?

A

Drive line, followed by pump pocket

133
Q

What characterization of chest
pain is most consistent with a
cardiac cause?

A

Radiation of pain down to Right arm > radiation down both arms >
radiation down Left arm

134
Q

What is the path of electrical
conduction during a normal
cardiac cycle?

A

SA node → R atrium → AV node → Bundle of His → Bundle branches
→ Purkinje fibers

135
Q

What are the most appropriate
locations for central line
placement prior to transvenous
pacing?

A

Right IJ (preferred), L Subclavian (these offer the most direct routes to
the heart)

136
Q

What happens when a magnet is
placed over an AICD?

A

It disables defibrillation and switches to pacing mode; should be done if
pt is receiving inappropriate shocks. Note all AICDs are also
pacemakers (on XR AICDs have a thicker wire in the distal lead)

137
Q

What is oversensing in a
pacemaker?

A

When a pacemaker interprets signal noise as native heart beats and
does not generate a paced beat. Tx: place magnet over the
pacemaker to switch it back to pacer mode. This will present as an
individual with a pacemaker that is bradycardic and symptomatic and
w/o pacer spikes on the ekg.

138
Q

What is the appropriate
managment of a patient with an
AICD with unstable VT?

A

Immediate electrical cardioversion for AICD/pacemaker malfunction

139
Q

What medication decreases
mortality after an MI?

A

Aspirin

140
Q

With cardiac arrest, what drugs
can be given to adult and
pediatric patients by ET tube?

A

NAVEL (adults): Narcan, Atropine, Vasopressin, Epinephrine, Lidocaine
LANE (peds): all except vasopressin

ITE (18 decks)

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