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aa Step 3 World & MTB & cases > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Most common cause of death in the US

A

Coronary artery disease (CAD)

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2
Q

Does stress affect risk for CAD?

A

Stress is not a clear risk factor since it cannot be measured properly

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3
Q

Sxs that signal something other than CAD

A

Pleuritic pain - PE, pneumonia, pneumothorax
Positional pain- pericarditis
tenderness- costochondritis

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4
Q

Chest pain. pain also occurs in epigastric area and is associated with a sore throat, metallic bad taste and cough

A

GERD- administer PPI

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5
Q

Alcoholic patient with chest pain. Nausea, vomiting, and epigastric tenderness

A

Ddx- pancreatic

Check amylase and lipase levels.

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6
Q

Chest pain and right upper quadrant tenderness. mild fever

A

Cholecystitis, cholelithiasis

order ABD sonogram for gallstones

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7
Q

abnormal finding: S3 gallop

cadriovascular

A

rapid ventricular filling using diastole.rushing blood cause “splash” or S3

aka: dilated left ventricle

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8
Q

Abnormal finding: S4 gallop

cardio vascular

A

the sound of partial systole into a stiff or non compliant left ventricle. before s1

AKA: left ventricular hypertrophy

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9
Q

abnormal finding: JVD oe holosystolic murmur (MR)

A

cardio vascular piece of physical exam

Jugular vein exam is in chest not HEENT on CCS

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10
Q

abnormal finding: rales suggestive of CHF

A

piece of physical exam: chest

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11
Q

abnormal finding: dishes patient, SOB, clutching chest

A

piece of physical exam: general exam

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12
Q

abnormal finding: edema

A

physical exam includes: extremities

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13
Q

Ischemic-type chest pain. Next step in management?

A

BIT: EKG

but choose treatment first (if made to choose)

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14
Q

CK-MB and troponin

A

Most accurate test but not initial.

Best to detect a reinfarction a few days after initial infarction.

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15
Q

When to order stress test?

A

When case is not acute and initial EKG/enzyme tests do not establish the diagnosis.

Stress test is a way to increase the sensitivity of detection of CAD beyond EKG and enzymes.

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16
Q

Action of Troponin C

A

Binds to calcium to activate actin:myosin interaction

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17
Q

Action of Troponin T

A

Binds to Tropomyosin

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18
Q

Action of Troponin I

A

Inhibits actin:myosin interaction

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19
Q

When is dipyridamole or adenosine thallium stress test or dobutamine echo the answer?

A

Pt cannot exercise to target heart rate >85% of maximum.

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20
Q

63yo woman abnormal stress, reversible ischemia. No risk factors CAD. BNS?

A

Angiography is the next diagnostic for “reversible” ischemia, followed by bypass.

“Fixed” defects (unchanged between exercise and rest) are scars and require no angiogram

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21
Q

Sestamibi nuclear stress testing

A

Used in obese patients and those with large breasts because of its ability to penetrate tissue.

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22
Q

Use of Nuclear Ventriculogram (MUGA scan)

A

most accurate method to evaluate ejection fraction

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23
Q

Mechanism of Thallium

A

Isotopes picked up by the Na/K pump of the normal myocardium. Cardiac tissue alive and perfused= high uptake.

Decreased uptake: damaged tissue

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24
Q

LOS:5 post MI. most specific method for establishing the diagnosis of a new infection?

A

CK-MB

troponin will be elevated for 2 weeks LOS

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25
Q

Best initial treatment for ACS

A

Aspirin administered PO.

Instant effect on inhibiting platelets.

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26
Q

Mortality reduction of aspirin for ACS

A

Reduces 25% mortality of acute MI
Reduces 50% for “unstable angina”

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27
Q

Other treatments for ACS

A

-Clopidogrel or ticagrelor (Acute MI)
-Prasugrel (angioplasty)
-Nitrates and morphine (no effect on mortality)
-O2 if pt is hypoxic.

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28
Q

Mechanism of P2Y12 Antagonists

A

Clopidogrel, prasugrel, and ticagrelor block aggregation of platelets to each other by inhibiting ADP-induced activation of the P2Y12 receptor.

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29
Q

Prevention Tx angioplasty or stent

A

Clopidogrel, prasugrel, and ticagrelor
(inhibit ADP activation of platelets)

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30
Q

Time critical Tx that lowers mortality in STEMI

A

Angioplasty preformed within 90 minutes of arrival at ED (does not depress mortality for stable angina)

If angioplasty cannot be preformed: thrombolytics wishing 30min of arrival at ED.

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31
Q

Indication for thrombolytics

A

chest pain <12hrs
ST elevations >1 leads
New LBBB

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32
Q

Tx that lowers mortality in STEMI

A

Beta Blockers (not time critical)
(prioritize aspirin, thrombolytics and angioplasty)

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33
Q

Mortality reduction of ACEi/ARBs

A

Will only lower mortality if there is left ventricular dysfunction or systolic dysfunction.

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34
Q

HMG CoA protocol for CAD/ACS

A

give HMGCoA to all patients with CAD or ACS.
regardless of LDL level, EKG, troponin or CK-MB level.

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35
Q

Greatest single efficacy in lowering mortality in STEMI?

A

Angioplasty or PCI or Thrombolytics (unless contraindicated)

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36
Q

Mechanism of thrombolytics

A

Thrombolytics activate plasminogen into plasmin. Plasmin cleave fibrin strands into D-dimers.

Plasmin can only cleave fibrin prior to stabilization by factor XIII

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37
Q

Mechanism of BBlockers in MI

A

Prevents ventricular aTrrhythmia brought on by ischemia. Slower heart rate ^ time for artery perfusion. Increased left ventricular filling time increases both SV and CO

BB are anti-arrhythmic and anti-ischemic

38
Q

72yo man. Chest pain 1hr. EKG: ST elevation leads V2-V4. Aspirin given.

most likely benefit patient?

A

Angioplasty will lower the risk of mortality most.

give metoprolol before sending home

39
Q

ACS Tx that always lower mortality

A

Aspirin
Thrombolytics
Primary Angioplasty
Metoprolol
Statins
P2Y12 inhibitors

40
Q

ACS Tx that only lower mortality in certain conditions

A

ACEi/ ARBs- low ejection fraction
Heparin- ST depression

41
Q

ACS Tx that do not lower mortality

A

Oxygen
morphine
nitrates
CCBs
Lidocaine
Amiodarone

42
Q

Pacemaker for acute MI

A

Third-degree AV Block
Second degree AV Block (Mobitz II)
Bifascicular block
New LBBB
Symptomatic Bardycardia

43
Q

Aspirin Allergy Alternative

A

-grel (P2Y12)

44
Q

Intolerance to Beta Blockers
-reaction
-alternative

A

Alternative: Verapamil or Diltiazem (CCB)

BB intolerance: Reactive Airway, cocaine - induced chest pain, coronary vasospasm

45
Q

Prasugrel vs Clopidogrel

A

Prasugrel has grater efficacy but it increases bleeding in >75yo and <60kg

46
Q

Sxs MI complication

A

All complications of MI lead to hypotension

47
Q

Management of MI complication:
Cardiogenic Shock

A

Dx: Echo, Swan-Ganz (right heart), catheter

Tx: ACEi, urgent revasularization

48
Q

Management of MI complication:
Valve Rupture

A

Dx: Echo

Tx: ACEi, nitroprusside, intra-aortic ballon as a bridge to therapy

49
Q

Management of MI complication:
Septal Rupture

A

Dx: Echo, right heart catheter showing a step up in saturation from the right atrium to the right ventricle.

Tx: ACEi, Nitroprusside and urgent surgery

50
Q

Management of MI complication:
Myocardial wall rupture

A

Dx: Echo

Tx: Pericardiocentesis, urgent cardiac repair

51
Q

Management of MI complication:
Sinus Bradycardia

A

Dx: EKG

Tx: Atropine, followed by pacemaker if there are still symptoms

52
Q

Management of MI complication:
Third-degree (complete) heart block

A

Dx: EKG, con “a” waves

Tx: Atropine and pacemaker even if symptoms resolve

53
Q

Management of MI complication:
right ventricular infarction

A

Dx: EKG showing right ventricular leads

Tx: Fluid loading

54
Q

Mechanism of septal rupture systolic murmur

A

Left ventricular pressure is grater than right ventricular pressure. Left to right shunt go oxygenated blood.

SaO2 increased RV compared to RA

55
Q

Post MI wait for sexual activity

A

can resume sex within several days if there are no further symptoms of chest pain or dyspnea.

56
Q

Management of Non- STEMI

A

-No thrombolytic use
-Heparin use routinely (LMWH > IV unfractionated)
-Glycoprotein IIb/ IIIa inhibitors lower mortality sp. with angioplasty

57
Q

54yo Man. PMHx DM HTN. Substernal Chest Pain radiates Left Arm. Previously with exercise now on rest. EKG normal. Troponin elevated. Aspirin, O2, nitrates give. Most likely benefit?

A

LMW Heparin (Shown to lower mortality in NSTEMI)
GPIIb/IIIa
Angioplasty/ PCI

58
Q

GPIIb/IIIa inhibitors

A

GPIIb/IIIa work best in combination with angioplasty and stent.

epitibatide
tirofiban
abciximab (doesnt benefit STEMI)

59
Q

Mechanism of Heparin

A

Potentiates the effect of antithrombin.

antithrombin inhibits almost every step of clothing cascade. does not work with antithrombin deficiency. (only prevents new clots)

60
Q

Chronic CAD Further Management

A

Aspirin & Metoprolol
Nitrates for angina pain (no benefit for mortality)
ACEi/ARBs (only for stable cases with CHF, systolic dysfunction, low ejection fraction)

61
Q

Can initiate without doing angiography

A

Aspirin + metoprolol
Nitrates (pain)
ACEi/ARBs (low ejection fraction)
GPIIb/IIIa
Statins
Ranolazine (if pain persists)

62
Q

Indications for CABG

A

Angiography needed to determine use of CABG

-three coronary vessels >70% stenosis
-Left main coronary artery stenosis >50-70%
-2 vessels in a diabetic
-2 or 3 vessels with low ejection fraction

63
Q

Main difference between saphenous vein graft and internal mammary artery graft?

A

internal mammary artery graft remains open for 10 years.

Vein grafts start to become occluded after 5 years.

no difference in need for medications

64
Q

Hyperlipidemia management standards

A

Statins- every patient with CAD abd strike. Most DM. Definitely the choice for >7.5% 10 year mortality.

Proprotein convertase subtilisin Kexin type 9 (PCSK9) inhibitor (no known mortality benefit)

65
Q

Goal of Hyperlipidemia TX in CAD and diabetes

A

LDL <70mg/dL

66
Q

CAD equivalents that require a statin for any level of LDL

A

PAD
Aortic Disease
Carotid Disease
Cerebrovascular Disease

67
Q

Rick Factors in lipid management

A

-Tobacco use (cigarette smoking))
-HTN (>140/90 or on BP meds)
- Low HDL cholesterol (<40mg/dL)
-Fx early coronary heart disease (Fm <65, Male <55)
-Age (males> 45, females >55)

68
Q

Statin liver toxicity

A

Liver Toxicity
Raised transaminases
(check LFTs)

Rhabdomyolysis (less common)
(check CPK)

69
Q

mechanism of PCSK9 inhibitor

A

injectable medications which block the clearance of LDL by the liver from the blood.

works well in familial hypercholestolemia

70
Q

PCSK9 inhibitor medications

A

Evolocumab and alirocumab

71
Q

Erectile dysfunction post MI

A

cause: anxiety.
BB is mcc of medication related ED, Anxiety is the MCC of post infarction MI

72
Q

ED post MI. going to start sildenafil.

First stop?

A

Nitrates

contraindicated with sildenafil.

together can cause severe hypotension

73
Q

CHF symptoms

A

SOB
Edema
Rales on Lung
Ascities
JVD
S3 gallop
Orthopnea
Paroxysmal nocturnal dyspnea
Fatigue

74
Q

Mechanism of rales

A

increased hydrostatic pressure develops in pulmonary capillaries from left heart pressure overload.

Transudation of liquid into alveoli.
During inhalation alveoli “pop” open

75
Q

Worst manifestation of CHF

A

pulmonary edema (clinical diagnosis for CHF)

76
Q

First step in management in pulmonary edema

A

more important than diagnostic tests is to remove volume from vascular system (thus from the lungs)

77
Q

Sxs pulmonary edema

A

SOB
rales
S3
orthopnea

78
Q

Pulmonary edema on CCS

A

move the clock forward no more than 15-30min at a time for all acutely unstable ICU or ED patients.

order:
CXR,
EKG,
Oximeter
Echo
Initial Therapy (O2, Furosemide, nitrates, morphine)

79
Q

Mechanism of carvedilol

A

B1 B2 and A1 receptor antagonist

anti-arrhythmic, anti-ischemic and antihypertensive

80
Q

Pulmonary edema on CXR

A

pulmonary vascular congestion
cephalization of flow
effusion
cardiomegaly

81
Q

Pulmonary edema on EKG

A

Sinus Tachycardia
Atrial and ventricular arrhythmia

82
Q

Pulmonary edema on Oximeter or ABG

A

Hypoxia
Respiratory Alkalosis

83
Q

Pulmonary edema on echo

A

Distinguishes systolic from diastolic dysfunction

84
Q

63yoW acute severe SOB, rales present, S3 gallop and orthopnea. Next Step?

A

Oxygen, Furosemide, nitrates and morphine.

mainstay treatment no mortality benefit.

If no response- positive inotrope

85
Q

Mechanism of “cephalization” of flow

A

Bases of Bottom of the lungs are generally more “full” of blood because of gravity. Fluid build up fills the vessels from the bottom to the top (head/ cephalization).

86
Q

Mechanism of Dobutamine, Inamrinone, and Milrinone

A

Phosphodiesterase inhibitors. Increase contractility, decrease after load.

Dobutamine less effective if Pt on BB

87
Q

Mechanism of respiratory alkalosis in CHF

A

Fluid overload –> hypoxia –> hyperventilation –> decreased pCO2 –> alkalosis

hypoxia causes respiratory alkalosis

88
Q

TX: Acute CHF

A

Preload reduction to control acute symptoms

if no response- positive inotrope.

Never use DIGOXIN for acute (slows CHF

89
Q

TX: chronic CHF

A

Echocardiogram once stabilized to establish systolic vs diastolic dysfunction

90
Q

Tx: CHF systolic dysfunction

A

ACEi/ ARBs & Beta Blockers

Digoxin
Mineralocorticoid receptor antagonist

if counterindicated or if not responding : Hydralazine + nitrates

91
Q
A

aa Step 3 World & MTB & cases (13 decks)

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