CHF 2 Flashcards
causes of acute decompensated heart failure
- increased preload (accounts for most symptoms):
-increased sodium intake → fluid retention
-increased fluid intake
-noncompliance with diuretics
-change in meds
-IV fluids
-increased sympathetic stimulation - increased afterload (reduces SV):
-medical noncompliance
-increased sodium intake → increased BP
-increased sympathetic stimulation - decreased contractility
treatment strategy of acute decompensated heart failure - overview
*improve symptoms, particularly breathing (decreasing preload):
-DIURETICS → get rid of excess fluid
-nitroglycerin to lower venous pressures and reduce pulmonary edema
*increase cardiac output (decrease afterload and/or increase contractility):
-increase blood flow to kidneys to help urinate off excess fluid
-decrease sympathetic & neurohormonal activity
-reduce systemic vascular resistance
afterload graph in heart failure
*mild CHF: stroke volume starts to become impacted by higher blood pressure much more quickly than normal heart
*severe CHF: stroke volume is reduced even in the normal range
warm & wet CHF: treatment strategies
*DIURETICS (furosemide)
*VASODILATORS (nitroprusside, nitroglycerin, nesiritide)
cold & dry CHF: treatment strategies
*INOTROPIC DRUGS (dobutamine, milrinone)
cold & wet CHF: treatment strategies
*MECHANICAL SUPPORT
*vasodilators/diuretics, inotropic drugs?
heart failure results from:
*decreased compliance
*decreased contractility
*increased preload
*increased afterload
diuresis for treatment of heart failure
*diuresis decreases preload and decreases left atrial pressure → decreased LV EDP → symptom improvement
*examples of diuretics: furosemide, bumetanide
nitroglycerin for treatment of heart failure
*nitroglycerin decreases preload by venodilation → decreased left atrial pressure → decreased LV EDP → symptom improvement
decreasing afterload to treat heart failure
*ACE inhibitors (-opril), ARBs (-sartan), hydralazine, and nitroprusside are all medications that can be used to DECREASE AFTERLOAD
*decreased afterload → decreased LV ESV → INCREASED STROKE VOLUME
*a decrease in afterload shifts the Frank-Starling curve up, which means for a given LV volume, there is a higher stroke volume
inotropic therapy for treating heart failure
*dobutamine & milrinone are medications that can be used to INCREASE INOTROPY
*increased inotropy → decreased LV ESV → INCREASED STROKE VOLUME
*an increase in inotropy shifts the Frank-Starling curve up, which means for a given LV volume, there is a higher stroke volume
beta blockers for treatment of heart failure
*in acute CHF, beta blockers are usually not started as they may transiently make the volume status worse
*if someone is on them already, they are often continued at a lower dose
*recall: beta blockers end in “-lol”
long-term goals for treatment of chronic CHF
- prevent progression of disease
- prevent morbidity (hospitalization, functional class)
- prevent mortality
note - we start treatment in those with stage B CHF
stage B CHF long-term treatment
*ACE inhibitors or ARBs
*beta blockers
*sodium-glucose transport inhibitors (SGLT-2i)
stage C CHF long-term treatment
*stage B treatment (ACE inhibitor/ARB, beta blocker, SGLT-2i) PLUS:
-aldosterone antagonist
-hydralazine nitrates
-CR + ICD
stage D CHF long-term treatment
*consider LVAD/transplant
life-prolonging medical therapy for chronic CHF
*ARB + neprilysin inhibitors, ACE inhibitors or ARBs
*beta blockers
*aldosterone antagonists (class III or class IV)
*sodium-glucose cotransporter-2 inhibitor
note - the combination of hydralazine & isosorbide nitrate is recommended for African-Americans with class III-IV HF in addition
which calcium channel blocker should we avoid in CHF
*avoid verapamil (non-dihydropyridine CCB blocker) b/c it limits contractility
implantable cardiac defibrillators (ICDs) for chronic CHF
*a specific type of pacemaker that is implanted near the heart to automatically defibrillate life-threatening heart rhythms
*used in patients in heart failure with reduced ejection fraction
*shocks the patient if they go into a ventricular dysrhythmia
what is the most important risk factor for sudden cardiac death (SCD)
*LV EJECTION FRACTION (esp if LVEF < 30%)
ICD class I recommendations
*ischemic cardiomyopathy who are at least 40 days post-MI with an LVEF of 35% or less
*non-ischemic (chronic) ~ 6 months with an LVEF of 35% or less
*high risk of SCA due to genetic disorders such as long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular dysplasia (ARVD)
cardiac resynchronization therapy (CRT)
*electrophysiologist threads an electrical wire through the coronary sinus to the LV free wall and plug it into the LV through one of the cardiac veins
*ensures that you are pacing the septum and the free wall to coordinate the 2 walls of the ventricle
*in patients with a left bundle branch block (QRS > 150 ms) and class II-IV heart failure with a reduced LV EF < 35%, CRT may improve LV function by pacing LV free wall
CRT class I recommendations
*refractory LV dysfunction with a LV ejection fraction less than 35% with class II-IV heart failure
*left bundle branch block greater than 150 ms
