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CCFP EM > Cardiovasc > Flashcards

Cardiovasc Flashcards

1
Q

Two main pathophysiology of peripheral artery disease

A

atherosclerotic PAD and Buerger dz, describe both: pg 70

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2
Q

what is Buerger dz?

A

thromboangiitis obliterans, “caludication in young smoker”, more common in males/Middle East/Asian, pg 70

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3
Q

exam findings PAD

A

Muscle atrophy, shiny or scaly skin, evidence of poor wound healing, digital ulcerations, lots of hair follicles, diminished pulses, slowed capillary refill

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4
Q

vascular vs neurgenic claudication

A

GO!

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5
Q

Leriche Syndrome triad?

A

Bilateral hip claudication, erectile dysfunction, absent femoral pulses equals aortoiliac occlusive disease

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6
Q

What ABI is diagnostic of PAD? When does claudicatin start? When do rest symptoms start? Descrie ABI

A

< 0.9, < 0.6, <0.25, cuff and doppler “ankle to arm”

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7
Q

what is only effective therapy for beurger?

A

smoking cessation

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8
Q

3 layers or arteries

A

tunica: intima, media, adventitia

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9
Q

most common sites of arterieal aneusrysms

A
  1. abdo aorta (AAA)
  2. popliteal
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10
Q

pathophys of true and pseudo aneurysms, differentiate from a dissection

A

True aneurysm: constant shear stress weekends the tunica media leading to dilation/ ballooning of all three layers. This shear stress is generally caused by atheros sclerosis and its risk factors.

Pseudo aneurysm: trauma to the vessel wall results in disruption of the intima and the media and communicates with a pseudo aneurysm which is usually a thin wall of tunica adventitia or other surrounding tissue

this is different from a dissection where the tunica intima is disrupted and blood is in a false lumen between the media and the intima

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11
Q

where do AAA most commonly happen?

A

below renal arteries or inferior SMA

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12
Q

most common location of AAA rupture?

A

retroperitoneal

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13
Q

what size defines AAA, when is surgery indicated for non-ruptured AAA?

A

> 3 cm =AAA, if >5 cm in females, 5.5 cm in males

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14
Q

RF for AAA

A

1st degree relative with same, CAD, PAD, age greater than 65 , , smoking history

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15
Q

symptoms of rapidly expanding/ruptured AAA

A

Abdominal, back or flank pain. Nausea slash vomiting. Syncope or hypertension

Rarely, can also rupture into GI tract leading to GIB or can rupture into IVC and cause AV fistula leading to CHF

** if pt has aortic graft and GIB, need to think AAA

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16
Q

exam finding AAA

A

pulsatile mass, abdo pain, peritonitis, hypotension/shock

if retroperitoneal rupture can tamponade which may have normal vitals. look for cullen/grey-turner sign

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17
Q

ddx of AAA

A

Renal colic, muscular back pain, pancreatitis, mesenteric ischaemia, diverticulitis, biliary disease, appendicitis . Rarely, GI bleed or congestive heart failure.

Can also present like a ACS due to hypo perfused coronary is especially impatient with predisposing CAD

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18
Q

what is endoleak?

A

complication of AAA graft repair. blood gets between graft and aneurysm and aneurysm can continue to grow +/- rupture

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19
Q

complications of AAA graft repair

A

Acute complications include vascular injury to renal, or mesenteric arteries.

Chronic complications include infection, thrombosis, migration, aortaenteric fistula, pseudo aneurysm at anastamosis site or endo leak

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20
Q

what defines thoracic aortic aneurysm

A

TAA > 4.5 cm, often an incidental finding

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21
Q

symptoms of thoracic aortic aneurysm

A

same as AAA, asymptomatic unless ruptures or rapidly expanding or mass effect

if ruptured: chest or back pain, can have hoarsness, cough, wheeze d/t RLN compression

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22
Q

Tx of thoracic aortic aneurysm

A

similar to dissection: aggressive BP/HR control, pain control, surgical consult STAT

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23
Q

Stanford Classification of Aortic Dissection

A

A: ascending (or both)
B: descending

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24
Q

RF for aortic dissection

A

Hypertension, advanced age, connective tissue disease, congenital heart disease, giant seller arteritis, family history, stimulant abuse, iatrogenic [ catheterization or surgery]

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25
Q

complication of dissection

A

if proximal: MI, aortic regurg, tampondae,

if distal: stroke like symptoms, limb/organ ischemia

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26
Q

chest pain and neuro symptoms, think?

A

Aortic Dissection

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27
Q

D-Dimer and CXR in dissection?

A

dimer: 90% sens, poorly specific
CXR abn in 85%, however CTA by far the best test

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28
Q

Initial TX of Dissection:

A

pain control, SBP 100-120, HR <60
-labetalol, esmolol can then add nitroprusside prn

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29
Q

target time to re-vascularization after acute peripheral artery occlusion

A

4-6 hrs before limb ischemia requiring amputation, can also cause death

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30
Q

acute artery occlusion pathphys

A

either embolic or thrombotic, embolic (usually from LV in pt with MI) is worse b/c it is so acute there is no collateral blood flow. thrombotic likely has collateral flow bc atherscleoriss occurs at site pg 78

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31
Q

6 P’s of limb ischemia

A

pallor, pulselessness, pain out of proportion, paralysis, poikilothermic, paresthesia

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32
Q

treatment of acute peripheral artery occlusion

A

Heparin! then surgical tx depends on whether embolic or thrombotic.

diagnosis is clinical, can get CTA to confirm

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33
Q

RF for VTE

A

Trauma, travel, hypercoagulable state, hormone replacement, family history, IVDU, age over 60, malignancy, birth control, obesity, pregnant, recent surgery, smoking, immobilization, sickness… DVT is biggest risk for PE

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34
Q

Homans Sign?

A

Pain in calf or posterior knee with passive dorsiflexion of foot…. looks for DVT

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35
Q

3 complications of DVT

A

PE, chronic vebous insufficieny, SVC sydrome (with upper extremity clot), postphlbetic syndrome

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36
Q

2 severe manifestations of DVT

A

Phlegmasia cerulean dolens = painful blue leg –> massive clot, causes massive edema to venous insufficieny

phlegmasia alba dolens= painful whit leg, massive venous clot causes arterial spasm

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37
Q

W/U of DVT

A

Wells 2 or less = dimer
wells 3 or more = u/s

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38
Q

timeframe of surgery/trauma that confers biggest VTE risk?

A

within last 4 weeks

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39
Q

PE wells: 2-tier model?

A

wells 4 or less = dimer
wells 5 or more = CTA

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40
Q

2 cxr findings in PE

A

Hamptom hump, Westermark sign (rare)

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41
Q

when to use PERC

A

in a patient with low pretest probability

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42
Q

indications for thrombolysis in PE

A

hypotension (SBP <90 for >15 minutes or SBP 60 pts below baseline), severe hypoxemia, cardiac arrest, evidence of right heart strain

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43
Q

RBBB ECG findings?

A

QRS > 0.12, rSR’ in V1, slurred S in V6 and discordant T waves

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44
Q

LBBB ECG findings

A

QRS > 0.12 s, big S wave in V1, monophasic or notched R in lateral (somtimes looks like M), discordant T waves

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45
Q

conduction path in BBB

A

through opposite side of heart

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46
Q

Can RBBB and LBBB occur in healthy heart?

A

RBBB can but usually not, LBBB cannot

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47
Q

causes of RBBB

A

acute or chronic rt heart strain ( pulm HTN, PE, COPD, cardiomyopathy)

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48
Q

Causes of LBBB (same as fasicular blocks)

A

HTN, valve dz, IHD, cardiomyopathy, myocarditis, CHD, post cardiac sx

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49
Q

what are bifasciular blocks? what to do for them?

A

LBBB (according to some, but maybe not)
,RBBB + LAFB (manifested as LAD)
RBBB+LPFB (manifested as RAD)
temporary then permanent pacing if symptomatic brady (syncope etc)

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50
Q

LAFB and LPFB ECG findings:

A

normal QRS for both:
LAFB: big S in inf leads, R in Lat leads
LPFB: big R in inf leads big S in lat leads

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51
Q

RVH causes?

A

anything increasing rt sided pressures chronically eg Pulmonic stenosis, pulm HTN, chronic PE,

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52
Q

LVH ECG findings?

A

left axis,
S in v1 + R in V5 > 35 mm or R in aVL > 11mm

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53
Q

ECG signs of rt sided heart strain?

A

inverted Ts in V1-3

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53
Q

RVH ECG findings?

A

-Right axis deviation
-Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
-Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
-QRS duration < 120ms (i.e. changes not due to RBBB).

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54
Q

ECG findings in hyperK, and at what levels

A

6.5-7.5 –> Tall peaked T’s (EARLIEST), PR prolongation
7.5-8 –> P wave flattens, QRS widens
>9.0 –> sine wave, anticipate arrest

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55
Q

ECG findings of hypokalemia

A

flattening of T wave (earliest), U wave following T wave, ST depression, PR prolongation

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56
Q

hypercalcemia ECG

A

short QT, depressed and short ST

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57
Q

hypocalcemia ECG

A

long QT

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58
Q

dig effect vs dig toxicity on ECG

A

dig effect = common in dig users (not indicative of toxicity) = depressed ST, short QT, flat T, prominent U AKA similar to hypo K
dig toxic: any arrythmia –> PVC, a fib, AVB,

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59
Q

hypothermia ECG

A

everything prolongs and J wave (aka Osborn wave)
defn hypothermia = T < 35, biggest risk of arrhythmia < 30.

progressino is often : sinus brady –> afib –> Vfib

60
Q

SACPE (aka flash pulm edema, aka severe hypertensive HF) features?

A

-Rapid onset of respiratory distress (e.g., usually within <6 hours).
-Marked tachypnea and dyspnea.
-Hypoxemia.
-Hypertension (generally SBP>160 mm and/or MAP>120 mm).(31327485, 29776826)
-Diffuse rales on auscultation.
-Pink, frothy sputum may be seen.
-Clinical features of sympathetic activation:
Diaphoresis, pallor, appearing extremely unwell.
Tachycardia.
Agitation.
Patients may have a history of recurrent episodes of SCAPE.

61
Q

mortality of HF

A

50% die in 5 yrs of dx

62
Q

precipitants of AHF

A

non-adherence (meds or excessive fluid/salt), renal failure, drugs (meth, cocaine, etoh), HTN, IHD, iatrogenic (meds)

63
Q

6 phenotypes of AHF

A

SCAPE, cardiogenic shock, pulm edema, acute on chronic, high-output, right sided

My approach: Is it SCAPE? Is it cardiogenic shock? or is it “regular” HF

if regular: what is BP, what TX can they tolerate, what Tx do they need, what Tx are they on already.

if SCAPE: bipap or cpap and nitro, these usually reduce BP if not add something else

cardiogenic shock:
- Optimize oxygenation with NIPPV
-Optimize blood pressure with vasopressors (eg. norepinephrine) to maintain cardiac/end-organ perfusion targeting a MAP of 65-80
Optimize contractility with ionotropes (eg. dobutamine, milrinone)
-Optimize volume status (crystalloid or diuretics)

** norepi 1st!!, most inotropes are vasodilators, so can worsen things if pressor not on board.

64
Q

indications of bipap in AHF

A

hypoxia, tachypnea/resp distress, pulm edema

65
Q

5 types of cardiomyopathy –> names, pathophys, some causes

this means structural or functinoal dz in the absence of CAD, HTN, valve dz

A
  1. dilated, myocyt death leading to chamber dilation and systolic dysfunction, 40% are genetic rest are d/t drugs (cocaine, etoh), myocarditis (NOT ISCHEMIA) etc, presenet like Lt sided HF
  2. resitrictive (leat common), infiltrates that impair fillin and cause diastolic dysfunction, systolic function retained, eg amyloid, sarcoid, hemochromatosis,
  3. hypertrophic –> often autosomal dom (ask about famhx SCD), causes asymetric LV thickening, will lead to LV outflow tract obstruction (aka HOCM)
  4. ARVC(H) –> auto dom, common in italy, right ventricular dysplasia, leading to ventricular arrythmias
  5. unclassified (eg takutsubos LV dysfunctino caused by stress hormones/microvasc spasm) –>mimics stemi (HAS ST ELEVATION AND ELEVATED TROP) but has normal angiocath. treat like ACS, can only diagnose after normal cath
66
Q

when to consider restrictive cardiomyopathy

A

pt with HF and no cardiomegaly and no systolic dysfunction (eg preserved EF)

67
Q

ECG finding for ARVC

A

T-wave inversion in V1,V2, V3 AND EPSILON WAVE (EXACT OPPO OF DELTA, AKA DOWN SLOPING AND ON OTHER SIDE OF QRS)

68
Q

ECG finding for Brugada

A

coved or DOWN sloping ST segments in V1-2

69
Q

ECG finding for HCM

A

dagger-like q waves in lateral and inferior, LVH criteria

70
Q

ECG finding for WPW

A

delta wave (upsloping QRS)

71
Q

Who presents atypically with ACS?

A

Women, diabetics, elderly, racial minorities, psych pts, altered mental status

72
Q

Immediately life threatening CP causes?

A

PE, esophageal rupture, tension pneumo, mi, aortic dissection, cardiac tamponde
Also consider pma, pericarditis/myocarditis

73
Q

Non ACS causes of elevated trop

A

Cardiac contusion, cardiac procedures, acute or chronic HF, dissection, aortic valve dz, HCM, arrhythmia, PE, pump htn, myocarditis, resp failure, burns, sepsis, among others

74
Q

Most common cause of myocarditis in developed vs worldwide

A

Viral illness
Chagas disease

75
Q

Common viral triggers for myocarditis

A

Cocksackie virus
Adenovirus
Covid
Hep B and C
HIV

76
Q

Bacterial causes of myocarditis

A

Strep
Mycoplasma
Diphtheria
Lyme (borrelia burgdoferi)
Mycobacterium

77
Q

Myocarditis symptoms

A

Flu like symptoms, CP, new chf ,
Syncope

78
Q

Two sensitive, but not specific blood tests in myocarditis

A

Trop, Crp

79
Q

General causes of myocarditis

A

Virus
Bact
Fungi
Parasite eg chagas
Tox eg pcn, sulfas, cocaine
Autoimmune eg Kawasaki, sarcoidosis, SLE

80
Q

Mgmt of myocarditis

A

Subclinical -> trend trop
Stable —> ace, BB, MRA
Unstable—> inotropes, balloon pump, ecmo etc

81
Q

Complications of myocarditis

A

Sudden death
Dilated cardiomyopathy
Heart failure
Mural thrombus
Dysrhythmia

82
Q

Echo in myocarditis

A

Dilated chambers
Global or focal hypokinesis
Note mri: is helpful too

83
Q

three principal presentations of unstable angina

A

rest angina, new-onset angina, increasing angina

84
Q

describe coronary artery anatomy

A

tintins 334

85
Q

what %age of ACS has cc other than CP?

A

47%!

86
Q

new systolic murmur in ACS could mean?

A

papillary muscle rupture and resultant mitral regurg

87
Q

time frame for ECG upon presentation for any ?ACS

A

< 10 mins

88
Q

next step in inferior STEMI?

A

rt sided leads, get lead V4R looking for rt ventricular infarct

right sided ECG - put precordial leads in mirror image on right sie, can usually leave V1,2 in place an just get v3-6R, alternatively, just get V4R as it is most useful.

89
Q

anatomical localisation of ST elevation?

A

Anteroseptal = LAD, V1-V4
Anterolateral = Cx V1-V6, aVL, 1
Inferior = RCA 2, 3, aVF
Posterior = Cx or PDA (off RCA), posterior ECG –> V7-9 elevation.

90
Q

STEMI minimum criteria:

A

≥ 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years

≥ 1.5 mm ST elevation in V2-3 in women

≥ 1 mm ST elevation in other leads

New LBBB (LBBB should be considered new unless there is evidence otherwise)

** note recirpocal changes are not required, but certainly make it more likely (ie help differentiate benign early repol most prominent in v2-5)

91
Q

posterior lead placement?

A

v7, 8, 9 get wrapped around left chest wall –> different from right sided placement

92
Q

inferoir wall MI can result from damage to which to vessels

A

LCx or right main

if ST elevation in 3>2, predicts right main

if inferior with any lateral lead STE (v6, 1, aVL) more likely LCx

93
Q

STE in aVR > v1 suggests?

A

LAD occlusion (strangely)

94
Q

what is wellens syndrome?

A

T wave abn (usually deep T wave inversion in V2-3), indicative of critical LAD stenosis

T wave abn often resolve when pain goes away, check ECGs when in pain and pain free

95
Q

de winter T wave?

A

upsloping ST depresiion with peaked T in precordial leads –> anterior MI/STEMI equivalent

96
Q

LBBB in ? ACS

A

look for concordant STE or STD (both suggest infarct) use sgarbossa and assume its new unless documented otherwise

97
Q

how long is trop + after MI

A

usually at least 10 days

98
Q

NSTEMI ED cocktail

A

ASA, ticag or plavix, enox or fonda SC

99
Q

STEMI cocktail

A

depends on reperfusion strategy, go through both

100
Q

time to needle goal for lytics?
time to balloon for PCI?

A

30 mins
90-120 mins

101
Q

indication for lytics

A

<6-12 hrs of symptoms onset, >=1mm STE in 2 or more contiguous leads and no CI

102
Q

list CI to lytics

A

tints 346

103
Q

failure rate of lytics in STEMI

A

40-50%

104
Q

when to start BB after STEMI?NSTEMI

A

start PO (not IV) within 24 hrs, if no CI (HF, brady, hypotension, etc)

105
Q

suspect posterior MI when

A

inferior or lateral ischemia, OR when big ST depression in V1-3 (can flip it upside and it looks like posterior ECG, get the post though and look for STE in v7-9

isoloated poterior is rare, (3-11%), but if posterior MI along with either inferior or lateral, suggests greater damage/ higher M&M

106
Q

ae of MI

A

acute: CHF, cariod genic shock, dysrhymia (any really), wall rupture, papillayr muscle rupture, pericarditis

longer term: LV thrombus, LV aneurysm, pleuropericarditis (Dressler syndrome)

107
Q

Dressler syndomre?

A

pleuropericarditis, presents with CP and fever 2-10 weeks post MI, tx is NSAIDs and steroids

108
Q

causes of pericarditis?

A

idiopathic (80%), infectious (mostly viral), then meds, autoimmnue dz, dressler’s, uremia, malignancy, trauma

109
Q

ECG changes, 4 stages of pericarditis,

A

1 (first hours-days): PR depression, diffuse STE
2. PR and ST normalize, then T waves flatten
3. diffuse t wave inversion
4. back to normal

110
Q

is pericarditis made better leaning forward or backwards

A

Better leaning forward!

111
Q

most specific finding for pericarditis

A

PR depression

112
Q

complications of pericarditis

A

tamponade
constrictive pericarditis

113
Q

etiologies of pericardial effusion

A

malignancy, trauma, post infection, radiation, post cardiac Sx, pericarditis, renal failure

114
Q

Becks triad for tamponde

A

hypotension, muffled HS, JVD

115
Q

what does electrical alternans signify

A

pericardial EFFUSION

116
Q

effusion vs tamponade

A

effusion: fluid in sac, generally develops slowky
tamponade= generally develop quicker, hemodynamic compromise from effusion, RV collapses during diastole (seen on echo)

117
Q

finding in tamponade

A

electrical alternans, low voltage QRS, kaussmaul sign, palsus parodoxus >10 mmhg, narrow pulse pressure, pericardial friction rub

118
Q

types of hypertensive emergency

A

head to toe: PRES (aka hypertensive encephalopathy), ICH,, aortic dissection, MI, pulm edema, HELLP, acute renal failure, retinopathy

119
Q

immediate mgmt of HTN emergency?

A

reduce MAP 10-20% in 30-60 mins or to DBP of about 110

can cause ischemia if reduction >20% dt relative hypotension.

120
Q

some meds for HTN emergencies

A

labetalol/esmolol/hydralazine,

esmolol onset 60 sec, offset 10-20mins. bolus 250-500mcg/kg ( probs 250?) then infusion.

121
Q

HTN urgency?

A

controversial. >180/110, but best Tx is oral meds, if no end organ damage, no need to tx IV.

can use captopril or losartan,

if on acei/ARB, can add HCTZ/increase dose, add beta blocker etc.

122
Q
A
123
Q

Most common valve lesion

A

Mitral prolapse

124
Q

Complications of LVH

A

LVH -> Dec cardiac output -> dilated cardiomyopathy -> can lead to CHF, arrhythmias, sudden death, (also can drop SBP)

125
Q

When is aortic stenosis symptomatic, classic triad?

A

70% stenosis, angina, syncope, CHF

126
Q

Aortic stenosis: causes, murmur

A

Calcific valve degen (>65), bicuspid valve (<65)
Crescendo decrescendo systolic

127
Q

Management considerations for aortic stenosis

A

Gentle diuresis, cautious fluid, rule out ACS, ?prophylaxis for IE, IABP which can bridge to definitive tx
Avoid preload and afterload reducers (no nitro)

128
Q

Causes of acute aortic regurg? Mgmt of acute aortic regurg? Presents like?

A

IE, aortic dissection, trauma
Mgmt: surgical emergency, need aggressive after load reduction
Presents like pulmonary edema, CV collapse

129
Q

Mitral stenosis causes,,, most common and a few other causes

A

Rheumatic dz (common)
Atrial myxoma, congenital abn, calcific valve degen

130
Q

valve indicaitons for IABP

A

Acute AS, MR, BUT NOT acute AR

131
Q

acute MR tx:

A

surgical emergency IABP as bridge, afterload reduction and tx of pulm edema

132
Q

what other valve dz does MVP cause

A

MR

133
Q

2 broad categories of prosthetic valves

A

mechanical and bioprosthetic

134
Q

complications of prosthetic valves:

A

failure, thrombosis +/- systemic embolization, paravavular leak, endocarditis

135
Q

RF for IE

A

CHD, rheumatic dz, IVDU, prosthetic valves, pacemaker

136
Q

most common causative organisms in IE

A

Staph and strep

137
Q

what are HACEK organisms

A

difficult to isolate bugs that can cause IE in immunocomp pts
Hemophilus, actinobacillus, Cardiobacterium, Eikenlla, Kingella

138
Q

Rt sided endo, think?

A

IVDU

139
Q

duke criteria for IE

A

2 major findings, 1 major and 3 minor or 5 minor findings = IE

major: 2 or more + BCx, major echo findings

minor: fever, minor echo findings, RF, embolic dz, immunologic phenomeneeon (osler’s nodes osler = ouch), 1 + BCx

140
Q

exam findings in IE

A

murmur, immuno: osler’s roths spots
vasc: splinter hemm, Janeway lesions, signs of emboli

141
Q

categories of syncope

A

First rule out catastrophic bleeds: subarachnoid hemorrhage, ectopic pregnancy, massive GI bleed, ruptured AAA (USUALLY THESE HAVE OTHER symptoms)

-Reflex syncope – vasovagal, carotid sinus syndrome, situational
-Orthostatic syncope – drug induced, volume depletion, neurogenic
-Cardiovascular syncope – mechanical (PE, tamponade, aortic stenosis), dysrhythmias

142
Q

clues for cardiac syncope

A

-Cardiovascular risk factors
-Structural heart disease (especially HCM, aortic stenosis)
-Pacemaker
-Sudden syncope with no prodrome
-Exertional syncope
-Prodrome that includes palpitations, shortness of breath or chest pain
-Associated facial injury (including dental injury, eye glasses damage, tip of tongue bite)
-Family history of unexplained sudden death, drowning or single MVC <50 years of age
-Aortic stenosis murmur – high mortality rate in patients with critical aortic stenosis and syncope

143
Q

seizure vs syncope 10:20 rule

A

<10 myoclonic jerks = syncope, >20 seizure, between ?

144
Q

what %age of pts with seizure have post ictal state

A

96% usually 5-30 mins

145
Q

7 step approach to syncope ECG

A

tachy/brady, bifasciular blocks, WPW, HCM, ARVC brugada, long qt

146
Q

drugs that commonly cause syncope

A

Erectile dysfunction medications, antihypertensive, beta blockers, cardiac glycosides, diuretics, antiarrhythmics, anti psychotics, antiparkinson drugs, antidepressants common nitrates, alcohol, cocaine

147
Q

4 tips to distinguish SVT from VT

A

These suggest VT:
Fusion beats
Capture beats
Precordial concordance
Av dissociation

CCFP EM (20 decks)

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