Flashcards in PMT, Johnston - Heart Failure Deck (48):
Definition of HF
Inability of heart to meet metabolic demands of the body.
4 main causes of LV filling insufficiency, leading to HF.
Restriction/obstruction to vent filling:
Goal of ACC/AHA
ID patients at risk for developing HF.
**ACC/AHA Stages of evolution of HF
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.
NYHA Functional Classification
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
What do 60-75% of people with HF have?
Have CAD - IHD. Most common cause of LV systolic dysfunction.
What five specific causes of HF can be seen with echo?
1) Hypertensive HD (concentric)
3) Hypertrophic HD (septal thickening)
4) Infiltrative HD (amyloid etc.)
5) Primary valvular disease
Acute v. chronic HF
Acute - MR, AI, toxins, rupture papillary m., acute MI
Chronic - slowly progresses, edema/wt gain, multivalvular dilated cardiomyopathy
s/s of Systolic HF
weak, fatigued, reduced exercise tolerance
PULM problems - DOE, orthopnea, paroxysmal nocturnal dyspnea
s/s of Diastolic HF
SOB, DOE, pulmonary edema
Diastolic dysfunction (impaired vent relaxation) can propagate/contribute to what three things?
What is Low Output HF?
Dilated cardiomyopathy, valvular, pericardial disease.
What is High Output HF?
hyperthyroid, anemia, preg, AV fistula, beriberi
High CO, low EF.
What is Right Sided HF v. Left Sided HF?
- Right = RV affected. Pulmonary HTN dt pulm embolus, edema, hepatomegaly, venous distention.
- Left = LV overload. AS, MI. Dyspnea, orthopnea due to pulmonary congestion.
What are the compensatory neurohumoral responses to HF?
SNS upreg, RAS upreg, Cytokine activation, altered renal physiology, LV remodeling.
Seven precipitating causes of HF?
- Noncompliance with diet (Na, calories, caffeine).
- Noncompliance with meds ($$, AE)
- Taking meds that worsen decompensated HF
What meds worsen decompensated HF?
What is the only AV block you can give BB?
- CCB, BB, NSAID, antiarrhythmics
- DO NOT give if more than 1st degree AV block
Why does a tachy arrhythmia provoke chest pain?
- Tachy shortens diastole, leading to ischemia.
What three things indicate AS?
Angina, syncope, dyspnea
S/s of HF
- Most common: dysnpea
- ***S3 gallop = 11-fold inc. likelihood of HF
- ***new murmur
- Pulmonary symptoms
- Paroxysmal Nocturnal Dyspnea = 2-fold inc. likelihood of HF
- Pulm edema, wheezing, dec. breath sounds
- Percussion pleural effusions
- LV Failure
- RV Failure*
S/s of RV failure
Peripheral/sacral edema, heaptomegalia, asictes, increased JVD, HJR
How much below the sternal angle is the R atrium?
R atrium is 4 cm below sternal angle
Is unilateral or bilateral edema associated with HF? What else?
Caused by heart, liver, lung, or venous stasis/insufficiency until proven otherwise.
What do presence of S3 gallop and Paroxysmal Nocturnal Dyspnea indicate - how much to they increase likelihood of this?
**S3 gallop = 11-fold inc. likelihood of HF
**PND = 2-fold inc. likelihood of HF
What do echos show?
wall motion (ischemic), muscle thickness, pericardial effusions
If person is more than 65yo is in HF with Afib, what do you always check?
DDx of HF - mimics of HF.
1) **Pulmonary Problems - PE, asthma, pneumonia
2) **Cirrhosis - ascites, edema
3) Renal - edema
4) Venous insufficiency - edema
Can HF exhibit hyper or hyponatremia?
Dilutional HYPONATREMIA, edema, retaining water
Treatment of HF - non pharmacologic.
- Quit smoking
- If overweight - dec. caloric intake
- 2gm Na diet
- Fluid restriction
- Isotonic activity
- Avoid alcohol
- Tx hyperlipidemia, HTN, diabetes
- Acute myocardial ischemia
- Severe respiratory distress
- Cardiogenic shock
- HF refractory to oral meds
Five basic steps to HF tx.
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.
Equation for Cardiac Output.
Stroke volume is modulated by what?
CO = SV x HR
SV modulated by preload, afterload, contractility
Conventional tx of acuteHF (3)
1) Diuretics - educe fluid vol
2) Vasodilators - decrease preload and/or afterload
3) Inotropes - augment contractility
- 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
Comparable to ACEi, but not more efefctive. Don't give if pt had angioedema from ACEi.
Blocs AT1 = Increase myocardial fibrosis, NE, vasoconstriction, endothelin.
- 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**
Diuretics (LOH=ide, DT=metolazone/thiazide, Late DT=spironolactone)
Use to relieve pulmonary s/s by reducing preload to increase cardiac funciton. Natriuresis.
Caution - increases risk of arrhythmias without K sparing
Digitalis - what is it and what is it used for?
What does it do for survival?
Used for afib to slow vent rate.
Does not improve survival!
MOA: Ionotropic by inc. contractility by inc. intracellular Ca.
Best to use?
Increase contractility (use for shock).
**dobutamine** and dopamine.
Hydralazine best used for what race?
African American - they don't use NO well. Hydralazine is an NO enhancer.
Do they prolong survival?
Use for HF associated with reduced EF.
Classification of Recommendations of Therapy
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.
Classification of Recommendations of Therapy
Level of Evidence
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
Hemodynamics of BB
- Decrease HR
- Antiarrhythmic properties
- Anti ischemic
- Blunts SNS effects of NE
- Reverse remodeling
- 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.
What are three ionotropes and what do they do?
- **Dobutamine** - Stimulates Beta1 and Beta2 receptors.
- Milrinone - ionotropic vasodilator, inhibits phosphodiesterase.
- Dopamine stimulates B1, higher doses stim alphaReceptors. SHORT TERM USE.