CHF Flashcards
epidemiology of CHF
effects 10% of men and 8% of women over 60yo
incidence on the rise, especially diagnosis 3mil visits/yr
5yr mortality after diagnosis is 50%
etiology of CHF
- CAD & HTN are most common
- cardiomyopathies - alcoholic, viral myocarditis, idiopathic, infiltrative, post partum
- valvular dz
- cardiotoxins - chemo, anabolic steroids
- arrhythmias, diabetes, and congenital heart disorders
- dz promotion - renal dz, NSAIDS, CCBs
s/s systolic left sided failure
fatigue
crackles/rales - small clicking, bubbling or rattling sounds in lungs
DOE
orthopnea
PND
Cheyne-Stokes respiration
diminished pulse pressure, cyanosis, JVD, S3 gallop, tachycardia, murmurs
what is cheyne-stokes respirations
apnea = hyperventilation = apnea
caused by diminshed sensitivity of resp center to arterial PCO2
what is diastolic (right sided) failure
disruption in diastolic filling or contractility of RV secondary to MI, obstructive outflow process (anatomical vs inc p ulm capillary wedge pressures resulting from L sided failure)
what is left sided failure CHF
LV remodeling secondary to MI, HTN, or obstructive outflow process
s/s of diastolic (right sided) failure
- peripheral pitting edema - may be on back or buttocks if sedentary
- GI tract congestion - decreased appetite, hepatomegaly,ascites
- JVD, prolonged L parasternal impulse with RV hypertrophy
DDX for CHF - cardiovascular
acute coronary syndrome valvular/septal rupture aortic dissection arrhythmia critical aortic stenosis endocarditis/myocarditis HTN crisis pericardial tamponade
DDX for CHF - pulm
COPD PE multilobar pneumo ARDS asthma
ddx for chf - other
acute renal failure iatrogenic volume overload post transfusion overload sepsis med non compliance new meds
w/u for CHF
(results are related to progression of dz)
- labs: CBC, CMP, UA, A1C, lipid panel, TSH, BNP, troponin
- EKG: LV hypertrophy, MI/prior MI (Q waves), arrhythmia/tachycardia
- ECHO: assess for LV/RV hypertrophy, wall motion abnormalitites, ejection fraction (>50% normal), valvular abnormalities***essential for DX, Tx, management
- CXR (see other flash card for findings)
what is BNP
vasodilatory protein released by stretched myocardium in response to increased ventricular filling pressures. attempts to offset the effects of neurohormonal activation by promoting diuresis, vasodilation and suppressing the renin-angiotensin system.
***>500 is diagnostic
definition of CHF
cardiac pumping capacity that is inadequate to meet the body’s metabolic demands
CHF tx
- treat reversible causes - HTN, DM, CAD, arrhythmias, structural
- diuretics
pharacology tx for CHF - diuretics
- diuretics: most effective agents for chronic symptomatic relief –thiazides for mild CHF
- HCTZ
- chlorthalidone
- loop diuretics - used for mod-severe HF - K+ sparing - hypo K, dehydration, hypouricemia due to diuretics (used in combo with thiazide or loop
pharm tx for CHF - ACE-I & ARBS
- ACE-I: 20% reduction in mortality, increased exercise tolerance
- ARBS: demonstrated improved mortality rates and symptom control when added to ACE?
pharm tx for CHF - beta blockers
- beta blockers: strongly recommended if symptoms are stable; carvedilol preferred
pharm tx for CHF - digitalis
digitalis: increased myocardial contractility, increases mortality due to arrhythmias and MI
list pharm options for tx CHF
1. diuretics (K+sparing drugs) 2. ACE-I 3. ARBS 4. beta blockers 5. digitalis 6. vasodilators
pharm tx for CHF - vasodilators
- vasodilators - improves SOB but no improvement in limiting advancing HF
- generally reserved for inability to tolerate other meds or failure to control symptoms
* *Nitrates - mostly venodilation, some arterial dilation at higher doses ex. nitroglycerin: most useful in acute exacerbations IC or transdermal
* *Hydralazine - mostly arteriolar dilation. ARB preferred
what would you tx CHF pt if rate is not controlled or if Afib is present
anticoagulation and amiodarone
non pharm tx of CHF
- defibrillator: HF+cardiomyopathy +EF
new/future tx of CHF
- Ivabradine - selective sinus node inhibitor, rate control
- Ranolazine - antischemic agent, inhibit the late sodium current in myocytes
- tolvaptan/conivaptan: vasopressin receptor antagonists, anti-hyponatremia
- sildenafil - decreases pulm vascular resistance
- serelaxin - is a recombinant form hormone relaxin which is naturally occurring hormone that is elevated in pregnancy, increase cardiac output, arterial compliance and renal blood flow
what is acute decompensated failure
- symptoms
- causes
pulmonary edema
- acute or subacute worsening dyspnea
- causes: acute MI, arrhythmia, infection, med/dietary noncompliance, sepsis, DIC, transfusion rxns
acute decompensated failure - PE/labs
- PE: hypoxia anxious or somulent, distress, diaphoresis, cyanosis, frothy cough, edema, rales (bases to apices)
- labs: increased BNP, troponin, or creatine (digoxin/INR if appropriate)
acute decompensated failure - imaging
EKG: acute MI, arrhythmia, low coltage (pericardial effusion)
CXR: increased interstitial markings, butterfly pattern, cardiomegaly
bedside ultrasound: assess for b-lines, wall motion, abnormalities
CXR findings in CHF
- bat wing sign = alveolar edema
- kerley b lines: interstitial pulmonary edema - they are thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs (diaphragmatic corners)
- pleural effusion
- cardiomegaly
- prominent upper lobe vessles
tx for acute decompensated failure
- sitting upright, oxygen, IV access, consider foley
- morphine IV - vasodilator, reduces anxiety
- diuretic IV - intravascular fluid reduction (lasix)
- nitrates - vasodilator, reduces BP and LV filling pressures
- support ventilation - CPAP better than BiPAP
- endotracheal intubation - indicated for severe distress or decreased mentation
what is CPAP vs BiPAP
CPAP - continuous positive airway pressure - improves pulm compliance, reduces work of breathing/preload/afterload
BiPAP - biphasic positive airway pressure - inspiratory and expiratory assitance
discharge planning for CHF
factors that may contribute to prolonged admission or re-admission
- prior hospitalization during adulthood
- arterial pH1.3
- hemoglobin levels -
heart failure pathophys
- myocardial injury (loss of functioning cardiac muscle or disruption of forces (MI, HTN, valves))
- reduced CO
- decreased carotid barorecptor stimulation, decr renal perfusion
- activation of SNS, RAAS
- increase HR and inotropy/myocardial toxicity
- vasoconstriction incr. afterload/hemodynamic alterations (increase afterload and preload) - negative remodeling = worsened LV function
- symptomatic pts
cardiorenal syndrome CHF pathophys -
poorly function heart:
1. systolic dysfunction (poor CO) = renal hypoperfusion occurs
2. activation of the RAAS
3. increased blood volume and vasoconstriction which activates sympathetic nervous system = venous congestion, vasoconstriction, hypertrophy, apaptosis, and fibrosis of cardiomyocytes and renal tubular cells
4. diastolic dysfunction = fluid overload = increased central venous pressure resulting in renal vascular congestion with poor renal perfusion
Poorly functioning kidneys:
1. electrolyte abnormalities resulting in :
-impaired renal K excretion
-reduced calcium absorption in GI
-kidneys not producing EPO needed for RBC production resulting in anemia and increasing cardiac workload
staging of CHF - ACC/AHA
A: high risk for developing CHF, no structural disorder of heart
B: structural disorder of heart, never developed s/s of CHF
3.C: past or current symptoms of CHF, symptoms associated with underlying heart dz
D: end stage dz, requires specialized treatment strategies
staging of CHF - NYHA
I: no limitation of physical activity
II: slight limitation of physical activity, comfortable at rest
III: marked limitation of physical activity, comfortable at rest
-IIIa:no dyspnea at rest
-IIIb: recent dyspnea at rest
IV: inability to carry on any physical activity w/o discomfort, symptoms present at rest
