Module 8/9 - Heart Failure Flashcards
Risk Factors for HF *
CAD
HTN
valvular disease
asymptomatic LV dysfunction
alcoholism /cardiotoxic drugs
smoking
diabetes
obesity and HLD
African American - esp women
Neurohormonal Responses *
renin-angiotensin-aldosterone system
(RAAS)
Perfusion to the kidneys decrease
- increased levels of angiotensin II and aldosterone
- angiotensin II causes arteriole vasoconstriction (increased afterload)
- aldosterone causes Na and water retention (increased preload)
- increased release of ADH from post. pituitary
- further an and water retention
- release of endothelin = vasoconstriction
Neurohormonal Response *
Ventricular Remodeling
decrease perfusion to kidneys
change in ventricular size, geometry and function as a result of years of toxic neurohormonal stimulation
- hypertrophy of myocytes
- large abnormal cells that don’t contract efficiently
- dilation and hypertrophy of ventricle
- reshaping of LV from football to basketball shape
HFrEF *
systolic heart failure (left)
- aka when your heart muscle has decreased ability to contract
- LV wont empty properly
caused by dilated cardiomyopathy from increased afterload (HTN) and preload (Valvular Dx)
EF < 40 and decreased CO
almost always associated with diastolic dysfunction as well
Manifestations of HF *
- tachycardia early sign
- dyspnea early sign
- low BP, S3, S4, shift of PMI
- peripheral hypoperfusion (cool skin, pallor, cyanosis) chest pain
- crackles, tachypnea, cough, orthopnea
- increased BUN/Cr, (renal insufficiency)
- progression leads to s/s of RVF, weight loss, low grade temp, malnutrition, confusion, cardiomegaly
Usual Respiratory Progression in HF *
- exertional dyspnea (progressive)
- orthopnea
- paroxysmal noctural dyspnea
- dyspnea at rest
- acute pulmonary edema
Signs and Symptoms of Fluid Overload (signs of early decompensations) *
dyspnea
orthopnea
PND
worsening new edema
worsening new ascites/anascara
worsening new weight gain
known sodium indescretion
fluid indiscretion
S3 gallop
JVD
worsening new systolic murmur
crackles/cxr infiltrates
Na < 137
Signs and Symptoms of Worsening HF (Signs of Decompensation) *
dyspnea
orthopnea
PND
worsening cough
RUQ pain/tenderness
decreased exercise tolerance
therapy noncompliance
worse new fatigue
nausea/anorexia
decrease heart rate variability
afib/flutter
recent flu-like symptoms
ICD firing
changing irregular ventricular rate
ACE for HFrEF *
MAKE SURE THEY ARE ON ACE (or ARB if cant tolerate)
- both are RAAS inhibitors
inhibit angiotensin II
- inhibits vasoconstriction
- inhibits stimulation of aldosterone secretion
- prevents breakdown of bradykinen (vasodilate)
reduces death, hosp., improves symptoms
use in all patients with HFrEF
use at recommended doses
ARBs for HFrEF *
alternative to ACE
- intolerance to cough
- do not inhibit bradykinin breakdown
directly block effect of angiotensin II at receptor level
still can develop angioedema
patient education
- ARBs are typically used for individuals who cannot tolerate ACE’s often due to cough
ARNI for HFrEF *
ENTRESTO: angiotensin receptor neprilysin inhibitor
- DO NOT USE WITHIN 36 HOURS OF LAST DOSE OF ACE DUE TO RISK OF ANGIOEDEMA
For patient on low dose ACE/ARB
- start on 25/26mg BID
For patient on high dose ACE/ARB
- start on 49/51mg BID
May increase in 2-4 weeks up to 79/103mg BID
Med Rec of HFrEF *
Class I: ACE (preferred) or ARB
Class II: ACE or ARB + BB (bisoprolol, metoprolol, carvedilol)
NYHA Class II - IV ACE/ARB
BB for HFrEF *
BB are recommended for all HFrEF in combo with RAAS inhibitor
bisoprolol metoprolol cavedilol
Block beta-adrenergic receptors
- decrease SNS activity, decreases workload of heart
- leads to reduced cardiac remodeling, slowing progression of disease
- titrate to target dose
DO NOT STOP ABRUPTLY (BB should be tapered, physical activity should be limited during this taper period)
Ivabradine for HFrEF *
Class II or II or stable chronic heart failure with: 1. LVEF< 35%
2. sinus rhythm with resting HR of >70
3. remain symptomatic on max doses of BB or who cannot tolerate BB
- Reduces hospitalized but not morality
- Selectively inhibits the pacemaker current in SA node
- *** Reduces HR with minimal effect on BP
(but hypotension and bradycardia are contraindications) - S/E: bradycardia, afib, phosphenes
Treat Symptoms and Comorbidities in HFpEF *
Definitive pharm therapy has not been identified in HFpEF
- treated cautiously with diuretics plus mgmt of comorbid (ie: afib, COPD, HTN, obesity, apnea)
- treatment of hypertension may slow progression; consider BB ACE ARB
==== ARB may reduce hospitalization
** ACC/AHA RECS COMBINED ENDURANCE AND RESISTANCE TRAINING TO IMPROVE EXERCISE CAPACITY, PHYSICAL FUNCTIONING, and DIASTOLIC FUNCTION
