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Cardiology Flashcards

1
Q

Cocaine associated chest pain
percentage with AMI

A

6%

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2
Q

Acute myocardial infarction

anatomic difference STEMI vs NSTEMI

prognosis STEMI vs NSTEMI

A

STEMI: trans mural infarction, full thickness of myocardium

NSTEMI: seven the cardio, partial wall thickness

prognosis similar

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3
Q

Acute myocardial infarction
percentage with normal EKG
significant Q wave

A

percentage with normal EKG: 4%
significant Q wave: 1 square wide, 1/3 of height of R wave

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4
Q

Differential diagnosis of ST segment elevation

A

–Acute MI

–Prinzmetal’s angina (vasospasm)

–Pericarditis

–Ventricular wall aneurysm

–Benign early repolarization

–Bundle branch block

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5
Q

Prinzmetal’s angina - EKG diagnostic pearl to distinguish from STEMI (1)

LV aneurysm: EKG diagnostic pearl to distinguish from STEMI (4)

A

Prinzmetal: Usually no reciprocal depression

LV aneurysm:

No reciprocal depression

Qwaves present

Look for old ECGs — no change

No serial changes

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6
Q

Posterior MI EKG description

A

Posterior MI (ST-depression with tall R-waves and upright Ts in V1-2)

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7
Q

Sgarbossa criteria - use and description (2)

A
  • ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
  • ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads (concordant with the QRS).
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8
Q
A

Possible isolated posterior MI

ST-depression + tall R-waves in V1-2 + upright Ts

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9
Q

Diagnosis

A

MI in setting of LBBB - Sgarbossa: concordance in aVL, V5-6

Scarbosa:

  • ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
  • ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads (concordant with the QRS).
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10
Q
A

concordance in V3

MI by Scarbosa

  • ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
  • ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads (concordant with the QRS).
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11
Q
A

STE in aVR à acute LMCA occlusion

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12
Q
A

deWinter T-waves acute LAD occlusion

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13
Q

Normalization of ischemia-related ST elevation

Early T wave inversions can be highly specific markers of reperfusion

accelerated idioventricular rhythm (rate 60-120) AIVR

A

Predictors of reperfusion in AMI

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14
Q
A

accelerated idioventricular rhythm (rate 60-120) AIVR

Benign after reperfusion, don’t supress

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15
Q

Troponin rise, peak and normalization

A

•Troponin

–3-6 hours (rises)

–12-24 hours (peaks)

–7-10 days (normalizes)

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16
Q

AMI oral meds

A

•Beta blocker (metoprolol) early IV discouraged

–Give within 24 hours orally but no rush

–Contraindications (asthma, CHF, bradycardia, hypotension; caution in RV MI)

•Addl. platelet inhibitors (in ED or cath lab)

–GP Ilb/IIIa receptor antags IV

–Clopidogrel, ticagrelor: can give oral load

–Prasugrel 60 mg oral load at cath; avoid if history of TIA or stroke

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17
Q

AMI thrombolytic therapy indications (3)

A

symptoms greater than 30 minutes, less than 12 hours

STEMI EKG criteria (STE 2 contig, posterior STEMI, LBBB + Scarbossa)

PCI would be > 90 minutes

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18
Q

absolute contraindications to thrombolytic therapy (6)

A
  • PCI immediately available
  • Active bleeding from any site
  • CVA within 6 months or hemorrhagic CVA at any time in the past
  • Intracranial or intraspinal surgery or trauma within 2 months
  • Intracranial or intraspinal neoplasm, aneurysm or AV malformation
  • Suspected aortic dissection
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19
Q

Early AMI arrhythmias with poor prognosis (5)

A

–2˚ Mobitz II (progress to 3˚)

–3˚ AV block from anterior MI

–Persistent sinus tach, SVT, A-fib

–New BBB, bifascicular block (RBBB (RBBB + hemiblock)

–Left posterior hemiblock (large infarct size)

•Increased risk of pump failure, mortality

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20
Q

AMI valve dysfunction

A

•Acute mitral regurgitation (usually due to ischemic dysfunction of papillary muscles)

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21
Q

chest pain, hypertension, JVD, lungs CTA

A

inferior STEMI with RV infarct

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22
Q

late complications of MI - weeks

systemic (1)

Pericardial and eponym

Myocardial (3) and tx

A

systemic (1): embolism of mural thrombus

Pericardial and eponym: pericarditis, Dressler’s syndrome if approximately 2 to 8 week timeframe

Myocardial (3) and tx: acute mitral regurgitation from papillary muscle rupture, LV free wall rupture, septal wall rupture (acute VSD with CHF)

Tx -> Hemodynamic support, IABP, OR

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23
Q

high-output heart failure causes (5)

A

–Thyrotoxicosis

–Anemia

–A-V fistula

–Paget’s disease of the bone

–Beriberi

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24
Q

ssystolic dysfunction leads to high levels of (2) which in turn leads to (1)

A

renin and anngiotensin, high afterload

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25
heart failure afterload reduction: 3 preload reduction: 3 hypotension management: 2
afterload reduction: nitroglycerin, ACE inhibitor, nitroprusside preload reduction: nitrates, diuretics, and nesiritdie hypotension management: dobutamine, IABP
26
Endocarditis risk factors, less known (two) valves affected, relative hierarchy most common infective agent for IVDA and prosthetic valves
Endocarditis risk factors, less known (two): mitral valve prolapse, pacemaker valves affected, relative hierarchy: –Mitral \> aortic \> tricuspid (IVDA) \> pulmonic most common infective agent for IVDA and prosthetic valves: staph aureus
27
Endocarditis most common pathogen for acute and subacute forms left-sided (2) right-sided (3)
Common pathogen: staph aureus and strep viridans respectively left-sided (2): –S. viridans, S. aureus right-sided (3): –S. aureus, S. pneumoniae, gram negatives
28
Endocarditis, most common pathogens prosthetic valve, early: aesthetic valve, late:
prosthetic valve, early: •S. epidermidis, S. aureus aesthetic valve, late: •S. viridans, Serratia, Pseudomonas
29
Endocarditis, cutaneous stigmata (4)
–Osler nodes: tender nodules on the tips of the fingers and toes (Osler = Ow!) –Janeway lesions: nontender, hemorrhagic plaques on the palms and soles –Roth spots: retinal hemorrhages with central clearing –Petechiae and splinter hemorrhages
30
Endocarditis treatment antibiotics x or y + z; add this for prosthetic valves
•penicillins or vancomycin, and add aminoglycoside –Add rifampin for prosthetic valves
31
Endocarditis, indications for prophylaxis
High-risk cardiac conditions + dental procedure –Prosthetic cardiac valve –History of infective endocarditis –Congenital heart disease (CHD) –Cardiac transplantation recipients with cardiac valvular disease
32
Endocarditis, prophylaxis medication, PCN all alternative PO and IV
33
Aortic stenosis contraindicated medications
Nitrates and vasodilators
34
Aortic regurgitation acute and chronic etiologies (2 each)
–Acute: endocarditis, dissection –Chronic: RHD; also seen with Marfan’s syndrome
35
Mitral valve stenosis Associated arrhythmias
•atrial tachyarrhythmias
36
Etiology of chronic mitral regurgitation (4)
•Etiology of chronic MR –MVP –Dilated cardiomyopathy –RHD –Mitral annulus calcification
37
Medical management of mitral regurgitation acute (2) chronic (3)
•Medical management of acute MR –Afterload reduction –IABP to temporize until surgery •Medical management of chronic MR –Symptomatic treatment of CHF –Treatment of A-fib –Endocarditis prophylaxis (s/p replacement)
38
Mitral valve prolapse Symptoms (4) Complications (2) Endocarditis proph?
•Symptoms –Chest pain (atypical) –Dyspnea –Anxiety –Palpitations (increased incidence of SVT) complications: rare, arrhythmias, thromboembolic disease, rare endocarditis prophylaxis: no; anticoagulation and beta blockers as needed
39
Cardiomyopathy types (3)
•Three types –Dilated cardiomyopathy –Hypertrophic cardiomyopathy –Restrictive cardiomyopathy
40
Dilated cardiomyopathy etiologies (8)
–Idiopathic (most common) –Alcohol –Peripartum –Viral (myocarditis) –End-stage CAD –Sarcoidosis –Amyloidosis –Hypothyroidism
41
Hypertrophic cardiomyopathy ``` etiology mechanical pathophysiology (2) ```
* Often familial autosomal dominant * Asymmetric thickening of septum causing two problems –Noncompliant ventricle with decreased diastolic filling –Dynamic obstruction of LV outflow (with mitral valve leaflets blocking outflow tract) Leads to: –Exertional syncope –Sudden death –Cardiac ischemia –Dysrhythmias
42
Hypertrophic cardiomyopathy murmur louder with murmur decreased with
murmur louder with: decreased preload (hypovolemia, standing, Valsalva) murmur decreased with: increased afterload (squatting, Trendelenburg, handgrip, volume expansion)
43
Hypertrophic cardiomyopathy treatment (3) + contraindication
Treatment: ## Footnote –Avoid exertion (worsens obstruction and leads to arrhythmias) –Negative inotropes (beta blockers, calcium channel blockers) to decrease obstruction –Never use digoxin or positive inotropes (increased obstruction) –Surgical myomectomy
44
Hypertrophic cardiomyopathy with large amplitude QRS complexes, deep, narrow Qs
45
Pericarditis less common etiologies (4)
–Connective tissue disease –Neoplasm –Uremia –Radiation
46
Features –Chest pain ________ with inspiration and swallowing –Pain ________ on sitting up, bending forward - Rub\_\_\_\_\_\_\_\_ on sitting up, bending forward
–Chest pain increases with inspiration and swallowing –Relief on sitting up, bending forward (and may hear the rub better in this position) –Rub (increased by leaning forward)
47
Pericarditis four stages of EKG changes
–Stage 1: Diffuse ST elevation (does not correspond to coronary artery distribution) & PR segment depression –Stage 2: ST-segments and PR return to baseline –Stage 3: T wave inversions –Stage 4: Normalization of EKG
48
Pericarditis treatment (2)
ASA, NSAIDs, colchicine
49
Pulsus paradoxus Definition
Fall in systolic blood pressure greater than 10 during inspiration
50
Pericardial Tamponade ECHO findings (2)
•ECHO findings –Effusion –RV diastolic collapse (specific for tamponade)
51
Myocarditis etiologies (4)
–Idiopathic –Infectious (usually viral, especially coxsackie B virus) –Chemotherapy –Connective tissue disease
52
Hypertensive emergency therapeutic goal
–rapid reduction in BP (reduce MAP 30%)
53
Hypertensive emergency agent choices for CNS (non-ischemic stroke), ischemic stroke, pregnancy induced
•CNS: encephalopathy, hemorrhagic CVA –Nitroprusside –Labetalol •Ischemic stroke –Hypertension usually resolves within hours •Transient and cerebroprotective –Treatment: observe, labetalol, nicardipine •Pregnancy-induced hypertension, eclampsia –Hydralazine –Labetalol –Magnesium sulfate for seizures
54
55
Hypertensive emergency agent choices for cardiac ischemia/CHF, aortic dissection
cardiac ischemia/CHF: nitroglycerin, nitroprusside/Nicardipine if severe aortic dissection: BB (esmolol, labetalol, propranolol), then nitroprusside or nicardipine
56
Hypertensive emergency agent choices for catecholamine crisis (pheochromocytoma, cocaine, MAOI)
–Alpha plus beta blocker is best –Do not use beta blocker alone (avoid unopposed alpha effect) –Labetalol plus phentolamine (alpha blocker)
57
Hypertensive emergency medications nitroprusside mechanism half-life use with avoid in
mechanism: arterial and venous dilation half-life: minutes use with: beta-blocker to blunt reflex tachycardia avoid in: pregnancy and renal patients due to cyanide metabolite
58
Hypertensive emergency medications labetalol mechanism contraindications (3)
Mechanism: beta greater than alpha blocker contraindications: bronchospasm, CHF, AV blocks
59
Hypertensive emergency medications fenoldopam mechanism benefits
mechanism: dopamine agonist, no alpha or beta affects benefits: may increase renal blood flow and sodium excretion
60
Hydralazine mechanism side effects, acute and chronic
mechanism: arteriolar vasodilator side effects, acute and chronic: reflex tachycardia, lupus Lake syndrome
61
Aortic dissection less common risk factors (four)
* Collagen vascular disorders such as Marfan’s * Pregnancy (especially third trimester) * Bicuspid aortic valve * Aortic coarctation * Chest trauma, iatrogenic (cardiac catheterization)
62
Aortic dissection Stanford classification
–Type A: any dissection which involves ascending aorta (surgical treatment) –Type B: descending aorta only (primarily medical management)
63
Aortic dissection best test
Best tests: TEE alternatives: CT first-line MRI alternative
64
Aortic dissection treatment (3)
–Beta blockers, then nitroprusside for both types –Stanford A: requires surgery –Stanford B: 1/3 will require surgery for complics.
65
AAA location, majority elective repair \> \*\*\* cm
location, majority: infra renal elective repair \> 5 cm
66
Acute limb ischemia timing, embolus versus thrombus
timing, embolus versus thrombus: symbolic usually much more acute, thrombus most likely secondary to severe underlying atherosclerosis
67
Acute limb ischemia treatment (4)
–Vascular surgery consultation! –Heparin (unless worried dissection/AAA) –Embolectomy –Bypass for atherosclerotic disease
68
Virhow's triad what and the significance
Risk factors for VTE ## Footnote –Stasis –Hypercoagulability –Endothelial damage
69
Phlegmasia cerulea dolens and phlegmasia alba dolens what?
–Uncommon, severe presentation of DVT –Massive iliofemoral DVT –Acute, severe, massive swelling –Cyanotic, congested extremity (cerulea) –Pale (alba) if arterial spasm causes “milk leg” –Increased compartment pressure, ischemia –May require surgery for compartment syndrome
70
EKG changes, hyperkalemia (5)
Flat P wave –Peaked T waves –Wide QRS –Prolonged QT (due to hypoCa) and PR –Eventual sine wave and Vfib Arrs: –Bradydysrhythmias and AV blocks –Tachydysrhythmias
71
EKG changes, hypokalemia (4)
–PVCs –U waves –Prolonged QT –ST segment depression
72
73
Hypercalcemia
74
Hypocalcemia
75
Electrolyte abnormalities that prolong the QT interval
– Hypokalemia – Hypocalcemia – Hypomagnesemia
76
Torsade de Pointes treatment (4)
–Magnesium (will shorten QT interval) –Overdrive pacing –Isoproterenol –Cardioversion/defibrillation –Magnesium infusion for prophylaxis after conversion Do not use procainamide or amiodarone
77
This condition and other associated findings
Osborne wave (J) of hypothermia Prolonged intervals - Sinus bradycardia - +/- muscle tremor artifact - Slow a. fib - V. fib / asystole
78
EKG abnormality and description
Digoxin effect ## Footnote –T wave depression –ST downsloping (Salvador Dali moustache) –QT shortened
79
Digoxin arrhythmias at toxic levels (5)
–PVCs (most common dysrhythmia) –Sinus and AV node blocks –AV dissociation –SVT (especially with blocks) –Sinus bradycardia
80
TCA EKG (5)
* Sinus tachycardia (most common) * Prolonged QT * Right axis deviation * QRS width \> 100 ms * Conduction blocks
81
Multifocal atrial tachycardia Description (2) Tx (maybe) avoid
–At least 3 different P wave morphologies –Variable PR intervals –Associated with –Treat underlying condition MgSO4 may be helpful; no shocks
82
Multifocal atrial tachycardia
83
WPW Treatment caveats: wide complex and afib
wide complex: treat as VF afib: procainamide or cardioversion, NO AV nodal blockade (can potentiate conduction down the accessory pathway)
84
WPW with a fib and variable conduction down accessory pathway
85
Ventricular tachycardia preferred drug hierarchy Rate criteria
procainamide \> amiodarone \> lidocaine rate greater than 120, usually greater than 150
86
Accelerated idioventricular rhythm what underlying cause treatment
what: wide complex regular rhythm rate 40 to 120 underlying cause: seen during reperfusion after ischemia treatment: observation, atrial pacing if slow and hypotensive
87
Accelerated idioventricular rhythm
88
2nd° block Mobitz 1: associated disease, tx (2) Mobitz 2: associated disease, associated EKG finding, complication, treatment
Mobitz 1: inferior MI, atropine, occasionally transcutaneous spacing Mobitz 2: anterior MI, associated with bundle branch block, progression to complete heart block, pacemaker
89
2nd degreee Mobitz 1
90
2nd degreee Mobitz 2
91
Third-degree block treatment caveat
Narrow complex may not need treatment, transient wide complex, pacemaker
92
Brugada etiology of sudden death genetics racial epidemiology treatment
etiology of sudden death: V. fib genetics: autosomal dominant racial epidemiology: Southeast Asian male treatment: implantable defibrillator
93
Diagnosis EKG description
Brugada * Pseudo-RBBB pattern * ST elevations in V1 and V2
94
Always assume wide complex tachycardia on the boards is
Ventricular tachycardia
95
LLSA articles tips bystander hands only CPR \> Standard CPR Post cardiac arrest hyperoxia? Temperature? PCI?
bystander hands only CPR \>\> Standard CPR Post cardiac arrest hyperoxia? bad Temperature? hypothermia PCI? good for all STEMI, likely NSTEMI as well
96
Alteplase/thrombolytics in STEMI - absolute contraindications (9)
Any PMH ICH, brain tumor, aneurysm, suspected dissection, active bleeding, bleeding, bleeding disorder 3 wks: CPR 6 wks: trauma/surgery, bleeding 3 mo: stroke 6 mo: Head trauma/brain surgery

EM Board exam (18 decks)

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