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Trials, Hemodynamics, CP Flashcards

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USMLE® Step 1 flashcards
1
Q

PARADIGM-HF Trial:

  • Clinical Question
  • Bottom Line
A
  • CQ –>
    • Among patients with HFrEF, does treatment with an angiotensin receptor-neprilysin inhibitor reduce CV mortality or HF hospitalizations when compared to ACE inhibitor therapy?
  • BL –>
    • Among patients with HFrEF, treatment with an angiotensin receptor-neprilysin inhibitor reduces CV mortality or HF hospitalization when compared to enalapril.
    • It is also associated with a reduction in all-cause mortality
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2
Q

PARADIGM-HF TRIAL:

What is neprilysin?

A
  • endopeptidase that breaks down vasoactive peptides (BNP, bradykinin, and adrenomedullin)
  • its inhibition may lead to:
    • reduced remodeling
    • vasoconstriction
    • renal sodium retention
    • –> improved outcomes in HFrEF
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3
Q

Paradigm-HF TRIAL:

  • What was the trial preceding the Paradigm-HF trial?
  • What was the major limitation of this trial and the target of the Paradigm-HF trial?
A
  • OVERTURE TRIAL (2002)
  • Increased rates of angioedema with omapatrilat (aminopeptidase P + ACE + neprilisyn) –> ARB + NI –> targeting multiple points in the pathophysiologic pathway and reducing angioedema
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4
Q

PARADIGM-HF TRIAL (2014):

  • Study design
  • Major inclusion criteria
  • Major outcome
  • Guideline generated from study
A
  • Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF)
  • Design:
    • Multicenter, prospective, randomized, comparative trial - N = 8,399 with median follow up of 27 months
  • Inclusion:
    • HFrEF (LVEF <40% and <35% were used at different points in the trial) + NYHA class II-IV symptoms randomized to ARNI vs. ACE.
  • Major outcome:
    • ARNI had a significant reduction in CV mortality (21.8% vs. 26.5%), all-cause mortality (17% vs. 19.8%), as well as each individual component –> trial stopped early.
  • Guideline:
    • In patients with NYHA Stage II-III HFrEF tolerating ACE inhibitor or ARB, replacement with ARNI is recommended to improve morbidity and mortality.
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5
Q

What are the aldosterone antagonist trials for HFrEF demonstrate mortality benefit and dictate the guidelines?

A
  • RALES (1999) - spironolactone
  • EPHESUS (2003) - eplerenone

**TOPCAT (2014) - spironolactone in HFpEF

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6
Q

What are the BB trials for HFrEF demonstrate mortality benefit and dictate the guidelines?

A
  • MERIT-HF (1999) - metoprolol succinate
  • CIBIS-II (1999) - bisoprolol
  • COPERNICUS (2002) - carvedilol
    • COMET (2003) - carvedilol > metoprolol tartrate
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7
Q

RE-LY Trial:

  • Clinical Question
  • Bottom Line
A

CQ –>

  • Among individuals with chronic atrial fibrillation, how does dabigatran compare to warfarin in terms of stroke risk and the risk of major bleeding?

BL –>

  • Compared to warfarin, high-dose dabigatran (20mg) reduces stroke risk without increasing the risk of major bleeding among patients with atrial fibrillation
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8
Q

RE-LY TRIAL:

What is dabigatran?

A
  • Pradaxa
  • Direct Thrombin inhibitor
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9
Q

RE-LY TRIAL:

  • Study design
  • Major inclusion criteria
  • Major outcome
  • Guideline generated from study
A
  • Dabigatran vs. warfarin in patients with atrial fibrillation - NEJM (2009)
    • Randomized Evaluation of Long-Term Anticoagulation (RE-LY)
  • Design:
    • Multicenter, parallel-group, randomized controlled trial, N=18,113, median follow up ~ 2 years
      • low-dose dabigatran
      • high-dose dabigatran
      • Warfarin
  • Inclusion:
    • Nonvalvular A-fib + moderate-high risk of thromboembolic stroke
  • Major outcome:
    • Reduced incidence of stroke compared with warfarin
  • Guideline:
    • Approved for storke prevention in A-fib (2014)
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10
Q

What are the two major axes of cardiac hemodynamic assessment?

A
  • Volume status
    • “congestion” characterized as elevated LV filling pressure, often measured as elevated PCWP
  • Adequacy of perfusion
    • characterized by cardiac index
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11
Q

What does assessment of each axes guide in decision making:

  • volume status
  • adequacy of perfusion
A
  • Volume status
    • titration of diuretics
    • suitability for, and/or tolerability of BB’s
  • Adequacy of perfusion
    • need for inotropic agents and advanced therapies (LVAD, transplant)
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12
Q

What are the noninvasive modalities for assessing cardiac hemodynamics?

A
  • H&P
  • Biomarkers (BNP)
  • CXR
  • Impedance cardiography
  • Echo
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13
Q

What are the invasive modalities for assessing cardiac hemodynamics?

A
  • RHC
  • Implantable monitors
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14
Q

What are the invasive hemodynamic measurements obtained from RHC?

A
  • RA
  • RV
  • PA
  • PCWP (used as index of LV filling pressure and CO)
  • CO (via Fick or TD method)
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15
Q

What is the key parameter/measurement obtained in RHC?

A

PCWP

  • correlates well with left atrial pressure –> usually (in the absence of mitral stenosis) is equivalent to LVEDP
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16
Q

When is PCWP obtained during RHC?

A

after balloon inflation while balloon wedged in PA

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17
Q

What are the two waves forms that should be identified on PCWP pressure tracing?

What should be obtained simultaneously with these tracings?

A

PCWP pressure tracings:

  • A wave
  • V wave

EKG tracing to compare timing and recogniation of wave forms

18
Q

CVP waveform: -a wave

A

-atrial contraction -precedes S1 -EKG: correlates with the P wave -disappears with atrial fibrillation -prominent in patients with reduced RV compliance

19
Q

Where are Canon “a” waves seen

A
  • AV dissociation
    • RA contracts against a closed TV
20
Q

CVP waveform: -c wave

A

-Cusp of the TV, protruding backwards through the atrium as the RV contracts -EKG: Correlates with QRS

21
Q

CVP waveform: -x descent

A

-movement of the RV, descends as it contracts -downward movement –> decreases pressure in the RA -concurrent atrial diastolic relaxation, which further decreases the RA pressure -EKG: occurs before the T-wave

22
Q

CVP waveform: -v wave

A

-back pressure generated from blood filling the RA -EKG: occurs after the T-wave -Occurs just after S2 -Huge v-wave = TR *represents blood flowing back ouf of the contracting RV –> V wave would be most prominent wave, and RVSP (30 mmhg)

23
Q

CVP waveform: -y descent

A

-pressure decrease caused by the TV opening in early ventricular diastole -EKG: occurs just before the P wave -Loss of y descent = tamponade (restricted RV filling) or TS -Rapid y descent = pericardial constriction

24
Q

What are the five primary risk factors for increased risk of SCD/candidate for ICD therapy (primary prevention) in HCM?

A
  • FH of premature HCM-related death, particularly sudden death, in close or multiple relatives
  • Unexplained syncope, judged non-neurocardiogenic, particularly if recent, in young patients
  • NSVT on serial ambulatory EKGs, particularly when bursts are multiple, repettitive, or prolonged
  • Hypotensive or attenuated BP response to exercise
  • Extreme LV hypertrophy (LV wall thickness > 30mm)
25
Q

What are the two risk factors for increased risk of SCD/candidate for ICD therapy (secondary prevention) in HCM?

A
  • Prior cardiac arrest
  • Spontaneous, sustained VT
26
Q

OAT trial (2006)

  • Clinical Question
  • Bottom Line
A

CQ –>

  • Among stable, high risk patients presenting with subacute myocardial infarction (3-28 days prior) with poor or absent flow of the affected artery, does late PCI + optimal medical therapy reduce mortality, MI, or NYHA class IV HF symptoms when compared to optimal medical therapy?

BL –>

  • Among stable, high risk patients presenting with subacute myocardial infarction (3-28 days prior) with poor or absent flow of the affected artery, late PCI + OMT does not reduce mortality, MI, or NYHA class IV HF symptoms when compared to OMT alone.
27
Q

OAT trial (2006)

  • Study design
  • Major inclusion criteria
  • Major outcome
  • Guideline generated from study
A
  • Coronary Intervention for Persistent Occlusion after MI - NEJM 2006
    • “Occluded Artery Trial” (OAT)
  • Design:
    • Multinational, multicenter, randomized controlled trial - N = 2,166 with mean follow up of 2.9 years
  • Inclusion:
    • Recent MI (3-28 days) –> PCI (< 24 hours) + OMT vs. OMT alone
  • Major outcome:
    • No significant difference in the primary outcome (composite of all-cause mortality, MI, NYHA class IV HF)
      • Guideline:
    • Delayed PCI >24 hours after STEMI
      • May be considered as part of an invasive strategy in stable patients if there is a significant stenosis in a patient infarct artery (IIb).
28
Q

What is the open artery hypothesis?

A
  • suggests reperfusion of the infarct-related artery salvages myocardium and preserves LV function, thereby increasing survival
29
Q

What two trials supported the open artery hypothesis in acute MI (as well as many others)?

A
  • ISIS-2 (1988)
  • GUSTO (1993)

**many others

30
Q

What is the anacrotic notch?

A
  • notch in hemodynamic monitoring that falls on the upstroke and represents a sudden decrease in the rate of acceleration of pressure
  • usually present in AS
31
Q

What is the difference in measurement pressure measurment between catheter and Echo?

A
  • Cath measures peak-to-peak pressure gradients from LVOT-Aortic outflow tract
    • Cath has tendency to underestimate pressure difference
    • Pressure recovery when some pressure is reconstituted in ascending aorta
  • Echo measures pressure gradient difference between LVOT and EROA
    • greatest pressure drop seen at EROA
32
Q
A
  • Right atrial enlargement
  • Left atrial enlargement
  • NSR
  • Dual-chamber pacemaker (DDD), normally functioning
    • PM in DDD mode paces and senses in both the atrium and the ventricle, and inhibits itself from firing if intrinsic atrial or ventricular activity is recognized
  • Paced morphology consistent with biventricular pacing/cardiac resyncchronization
    • Dual ventricular pacing spikes, typically occurring within 80 msec of each other, resulting from two separate pacing leads (one in the RV and the other placed epicardially via the coronary sinus)
    • May result in a paced RBBB QRS morphology if the epicardial lead is being activated first (usually standard RV apical pacing results in a paced LBBB QRS morphology)
33
Q

EKG findings:

  • Dual-chamber pacemaker (DDD), normally functioning
A

PM in DDD mode paces and senses in both the atrium and the ventricle, and inhibits itself from firing if intrinsic atrial or ventricular activity is recognized

34
Q

EKG findings:

  • Paced morphology consistent with biventricular pacing/cardiac resyncchronization
A
  • Dual ventricular pacing spikes, typically occurring within 80 msec of each other, resulting from two separate pacing leads (one in the RV and the other placed epicardially via the coronary sinus)
  • May result in a paced RBBB QRS morphology if the epicardial lead is being activated first (usually standard RV apical pacing results in a paced LBBB QRS morphology)
35
Q

What are the 3 most common causes of constrictive pericarditis?

A
  • Radiation
  • Idiopathic
  • Post-cardiac surgery
36
Q

What are the presenting signs/symptoms of constrictive pericarditis?

A
  • Fatigue
  • Exertional dyspnea
  • Abdominal distention, early satiety
  • Dramatic systemic venous congestion (peripheral edema, ascites, pulsatile hepatomegaly, JVD, pleural effusions (rare))
37
Q

What are the hallmark findings of constricitive pericarditis on jugular venous/RA tracing?

A
  • Prominent X and Y descents
    • especially during inspiration (Kussmaul’s sign)
38
Q
A

Constrictive pericarditis

  • rapid X and Y descents
  • Kussmauls sign
39
Q

What causes the dramatic X and Y descents in constrictive pericarditis?

A

exaggerated longitudinal annular motion and prominent early ventricular filling

40
Q

What are the 2D Echo/Doppler findings in constrictive pericarditis?

A
  • Respiratory variation in mitral inflow ( > 25% drop during inspiration)
  • Hepatic vein flow reversal during expiration
  • Septal “bounce” or “notch” (2D or M mode) which correlates to the time of pericardial knock on exam
    • must be distinguished from other septal motion abnormalities (pacing or LBBB)

Medical (69 decks)

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