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MED233 Cardiovascular > PMT, Johnston - Heart Failure > Flashcards

PMT, Johnston - Heart Failure Flashcards

1
Q

Definition of HF

A

Inability of heart to meet metabolic demands of the body.

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2
Q

4 main causes of LV filling insufficiency, leading to HF.

A 
Restriction/obstruction to vent filling:
RV infarct
Constrictive pericarditis
MS
Atrial myxoma
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3
Q

Goal of ACC/AHA

A

ID patients at risk for developing HF.

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4
Q

**ACC/AHA Stages of evolution of HF

A

A) High risk. Without structural heart disease and s/s of HF - i.e. HTN, DM, CAD, etc.
B) Asymptomatic, but has structural disease (LV-dysf) - i.e. prior event/MI, LVH, etc.
C) Currently or prior symptoms of HF. Has structural disease - i.e. structural dz and dyspnea, fatigue, reduced exercise.
D) Pts with REFRATORY HF requiring specialized interventions - i.e. s/s at rest despite max therapy.

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5
Q

NYHA Functional Classification

A

Class 1 - Asymptomatic
Class 2 - No s/s at rest. Exertional s/s with ordinary activity.
Class 3 - No s/s at rest. S/s with minimal activity
Class 4 - Rest s/s

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6
Q

What do 60-75% of people with HF have?

A

Have CAD - IHD. Most common cause of LV systolic dysfunction.

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7
Q

What five specific causes of HF can be seen with echo?

A

1) Hypertensive HD (concentric)
2) IHD
3) Hypertrophic HD (septal thickening)
4) Infiltrative HD (amyloid etc.)
5) Primary valvular disease

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8
Q

Acute v. chronic HF

A

Acute - MR, AI, toxins, rupture papillary m., acute MI

Chronic - slowly progresses, edema/wt gain, multivalvular dilated cardiomyopathy

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9
Q

s/s of Systolic HF

A

weak, fatigued, reduced exercise tolerance

PULM problems - DOE, orthopnea, paroxysmal nocturnal dyspnea

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10
Q

s/s of Diastolic HF

A

SOB, DOE, pulmonary edema

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11
Q

Diastolic dysfunction (impaired vent relaxation) can propagate/contribute to what three things?

A

Acute ischemia
Myocardial fibrosis
Amyloidosis

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12
Q

What is Low Output HF?

A

IHD, HTN
Dilated cardiomyopathy, valvular, pericardial disease.
Low CO.

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13
Q

What is High Output HF?

A

hyperthyroid, anemia, preg, AV fistula, beriberi

High CO, low EF.

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14
Q

What is Right Sided HF v. Left Sided HF?

A
  • Right = RV affected. Pulmonary HTN dt pulm embolus, edema, hepatomegaly, venous distention.
  • Left = LV overload. AS, MI. Dyspnea, orthopnea due to pulmonary congestion.
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15
Q

What are the compensatory neurohumoral responses to HF?

A

SNS upreg, RAS upreg, Cytokine activation, altered renal physiology, LV remodeling.

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16
Q

Seven precipitating causes of HF?

A
  • Noncompliance with diet (Na, calories, caffeine).
  • Noncompliance with meds ($$, AE)
  • Taking meds that worsen decompensated HF
  • Infection
  • Anemia
  • Thyroxicosis/Pregnancy
  • Arrhythmia
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17
Q

What meds worsen decompensated HF?

What is the only AV block you can give BB?

A
  • CCB, BB, NSAID, antiarrhythmics

- DO NOT give if more than 1st degree AV block

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18
Q

Why does a tachy arrhythmia provoke chest pain?

A
  • Tachy shortens diastole, leading to ischemia.
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19
Q

What three things indicate AS?

A

Angina, syncope, dyspnea

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20
Q

S/s of HF

A
  • Most common: dysnpea
  • ***S3 gallop = 11-fold inc. likelihood of HF
  • ***crackles
  • ***new murmur
  • ***JVD
  • Pulmonary symptoms
  • Paroxysmal Nocturnal Dyspnea = 2-fold inc. likelihood of HF
  • Orthopnea
  • Pulm edema, wheezing, dec. breath sounds
  • Percussion pleural effusions
  • Hematomegalia
  • LV Failure
  • RV Failure*
21
Q

S/s of RV failure

A

Peripheral/sacral edema, heaptomegalia, asictes, increased JVD, HJR

22
Q

How much below the sternal angle is the R atrium?

A

R atrium is 4 cm below sternal angle

23
Q

Is unilateral or bilateral edema associated with HF? What else?

A

Bilateral edema!

Caused by heart, liver, lung, or venous stasis/insufficiency until proven otherwise.

24
Q

What do presence of S3 gallop and Paroxysmal Nocturnal Dyspnea indicate - how much to they increase likelihood of this?

A
  • *S3 gallop = 11-fold inc. likelihood of HF

* *PND = 2-fold inc. likelihood of HF

25
Q

What do echos show?

A

wall motion (ischemic), muscle thickness, pericardial effusions

26
Q

If person is more than 65yo is in HF with Afib, what do you always check?

A

thyroid

27
Q

DDx of HF - mimics of HF.

A

1) **Pulmonary Problems - PE, asthma, pneumonia
2) **Cirrhosis - ascites, edema
3) Renal - edema
4) Venous insufficiency - edema

28
Q

Can HF exhibit hyper or hyponatremia?

A

Dilutional HYPONATREMIA, edema, retaining water

29
Q

Treatment of HF - non pharmacologic.

A
  • Quit smoking
  • If overweight - dec. caloric intake
  • 2gm Na diet
  • Fluid restriction
  • Isotonic activity
  • Avoid alcohol
  • Tx hyperlipidemia, HTN, diabetes
30
Q

Admit when?

A
  • Acute myocardial ischemia
  • Severe respiratory distress
  • Hypoxia
  • Hypotension
  • Cardiogenic shock
  • Anasarca
  • Syncope
  • HF refractory to oral meds
31
Q

Five basic steps to HF tx.

A
  1. Make correct dx - exclude mimics of HF
  2. Determine etiology of heart disease
  3. Determine precipitating factors
  4. Understand pathophysiology of HF
  5. Understand MOA of pharmacological therapy.
32
Q

Equation for Cardiac Output.

Stroke volume is modulated by what?

A

CO = SV x HR

SV modulated by preload, afterload, contractility

33
Q

Conventional tx of acuteHF (3)

A

1) Diuretics - educe fluid vol
2) Vasodilators - decrease preload and/or afterload
3) Inotropes - augment contractility

34
Q

ACEi (-pril)

A
  • Use for all systolic HF, reduced EF and symptoms of HF
  • Give it to lower mortality and inc. EF.
  • Caution use - renal insufficiency (Cr >2.5mg) or K >5mEq/l)
  • Level of evidence - A
  • NYHA - all classes
  • Lowers mortality.
  • CI - pregnancy or previous angioedema (or bilateral RAS)
  • SE - cough
35
Q

ARB (-sartan)

A

Comparable to ACEi, but not more efefctive. Don’t give if pt had angioedema from ACEi.

Blocs AT1 = Increase myocardial fibrosis, NE, vasoconstriction, endothelin.

36
Q

BB (-olol)

A
  • Use for all STABLE patients with s/s of HF, reduced EF.
  • Give it to improve LVEF, slows progression of disease, improves cardiac performance and sx of HF.
  • Level of Evidence: A
  • NYHA Class II and III
  • CI - don’t use in unstable pt
  • Lowers mortality in chronic systolic HF and dilated cardiomyopathy.
  • Hemodynamic effects
37
Q

Diuretics (LOH=ide, DT=metolazone/thiazide, Late DT=spironolactone)

A

Use to relieve pulmonary s/s by reducing preload to increase cardiac funciton. Natriuresis.
Caution - increases risk of arrhythmias without K sparing

38
Q

Digitalis - what is it and what is it used for?

What does it do for survival?

A

Used for afib to slow vent rate.
Does not improve survival!
Improves QoL.
MOA: Ionotropic by inc. contractility by inc. intracellular Ca.

39
Q

Ionotropes

Best to use?

A 
Increase contractility (use for shock).
**dobutamine** and dopamine.
40
Q

Hydralazine best used for what race?

A

African American - they don’t use NO well. Hydralazine is an NO enhancer.

41
Q

CCB:
Do they prolong survival?
What class?

A

No
Class3
Use for HF associated with reduced EF.

42
Q

OMM techniques

A

Lymphatics
Rib raising
Diaphragmatic doming
Effleurage, petrissage

43
Q

Classification of Recommendations of Therapy

Classes

A

Class I = best = evidence and agreement of 3+ benefit
Class II = conflicting evidence/divergent of opinion. 2+ or 1+ benefit.
Class III = evidence and agreement that tx is NOT EFFECTIVE. 0 benefit.

44
Q

Classification of Recommendations of Therapy

Level of Evidence

A 
A = best = multiple randomized trials with multiple populations
B = single randomized trial in a limited population
C = expert opinion consensus or case studies or very limited population evaluation
45
Q

Hemodynamics of BB

A
  • Decrease HR
  • Antiarrhythmic properties
  • Anti ischemic
  • Blunts SNS effects of NE
  • Reverse remodeling
46
Q

Spironolactone

A
  • Use in addition to ACE, BB, diuretic, dig).
  • Caution - Watch K is GFR less than 30cc/min or Cr more than 1.6mg/dl.
  • Level of Evidence: B
  • MOA: antagonizes aldosterone.
47
Q

What are three ionotropes and what do they do?

A
  • Dobutamine - Stimulates Beta1 and Beta2 receptors.
  • Milrinone - ionotropic vasodilator, inhibits phosphodiesterase.
  • Dopamine stimulates B1, higher doses stim alphaReceptors. SHORT TERM USE.
48
Q

What do hydralazne and isosorbide dinitrate do, respectively?

H + ID + ? + ? = ?

A

Hydralazine = arterial vasodilation, reduces afterload and SVR.
Isosorbide dinitrate = vasodilator to dec. preload and increase CO by reducing venous return.

H + ID + Diuretics + dig = reduce mortality, increase EF, increase exercise tolerance.

MED233 Cardiovascular (18 decks)

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