Heart Failure Flashcards
Heart Failure
Complex clinical syndrome that can result from any cardiac disorder that impairs the ability of the ventricle to deliver adequate blood to tissues
Left sided failure
Blood not pumped adequately from left ventricle to the peripheral circulation and accumulates in the ventricle.
Portion of fluid backs up into the pulmonary alveoli, developing pulmonary edema, causing
Shortness of breath,
Dyspnea on exertion
A third heart sound
Right sided failure
Blood not pumped from right ventricle. The fluid portion backs up throughout the body (veins liver legs bowel) Systemic edema Peripheral edema Jugular vein distention
Diastolic dysfunction
Inability for ventricles to fill with blood during diastole (ventricular relaxation)
Stiffness in ventricular walls due to hypertension, aortic stenosis, diabetes, myocardial infarction and cardiac ischemia.
Normal or slight Reduced left ventricular ejection fraction LVEF> 50%
HF symptoms
Increased diastolic filling pressure
Systolic dysfunction
Impaired degree of ventricular contraction
Decrease inotropy
Decrease stroke volume
Lower than normal Ejection fraction < 40%
Drugs promoting Na retention
Androgens Corticosteroids Diazoxide Estrogen Licorice Li Carbonate NSAIDs
Drugs producing Osmotic Effect
Albumin Glucose Mannitol Saline Urea
Drugs reducing contractility
Anti arrhythmic B Blockers 1st gen Ca channel blockers Direct Cardiotoxins (Doxorubicin, ethanol, cocaine, amphetamines) TCAs
Drug Ranking system for HF
Size of Treatment effect:
Class I : Benefit»_space;> Risk
Class IIa : Benefit»_space; Risk
Class IIb : Benefit >= Risk
Class III : Benefit < Risk
Certainty of treatment effect:
Level A : multiple popular evaluated
Level B : Limited population evaluated
Level C : Very Limited Population
HF Patients class Stage A
Patient: risk of developing HF , No structural or functional abnormalities, no sign symptoms
Goals: treat Hypertension, stop smoking, treat lipid disorders
Encourage exercise, discourage alcohol, control metabolic syndrome
Drugs: ACEIs or ARBs in appropriate Patients
HF Patients class Stage B
Structural heart change
No symptom
Goals: same as A
Drugs: ACE , ARBs , B blockers
Inolant defibrillator in selective patients
HF Patients class Stage C
Structural change
Symptoms present
Treat htn Stop smoking & alcohol Exercise Treat lipid disorder and metabolic syndrome Dietry salt restrictions
Diuretics
ACEIs
B Blockers
In selective patients Ald antagonist Arbs Digitalis Hydralazine Biventricular pacing Implantable de fibrilator
HF Patients class Stage D
Patients with refractory HF who require special intervention
Goals Same as A B C
Decision concerning appropriate level of care
Palliative care Heart transplant Chronic inotropes Permanent mechanical support Experimental surgery or drugs
Compensation mechanism
Sympathetic stimulation (epinephrine)
Hormonal stimulation (renin angiotensin aldosterone system)
Cardiac hypertrophy
Frank starling mech
Over time these mechanism work harder and harder causing more harm to the heart and exhausting themselves
Afterload
Tension in ventricular muscles during contractions to overcome pressure in aorta or pulmonary artery
Preload
Force exerted on ventricular muscle at tye end of diastole determines the degree of muscle stretch
Signs and symptoms of Heart Failure
Dyspnea
Dry wheezing cough
Exertional fatigue
Nocturia
Rales indicate movement of air through fluid filled passages
Tachycardia
S3 ventricular Gallop (rapid filling of ventricle early in diastole)
S4 aterial Gallop (increased resistance to sudden forceful ejection of atrial blood in late diastole
Diagnostic test in HF
Cardiomegaly by chest radiography, ECG, echocardiography, radionuclide ventriculography
Arm to tongue circulation time
Transudative pleural effusion by radiography
LFT increase ALT
Checking Natriuretic peptides
Moderate Na restriction
2 to 4g / day
ACE inhibitor
Can cause angio-edema in Less than 1% patients
B blockers
Metoprolol
Bisoprolol
Carvedilol
Life saving
Nitroprusside
Nitropress
0.3 to 10mcg/kg/min
Long term use causes Thiocyanate toxicity
Nesiritide
Binds to Natriuretic Peptide receptor results in increase production of cGMP in target tissues which causes vasodilation
Digoxin lanoxin side effects
Hypokalemia causes digoxin increases effect
Hypercalcemia increase digoxin activity
Hypermagnesemia decreses digoxin activity
Digoxin normal serum level : 0.8 to 1.0ng/ml
Dose : 0.125 to 0.25 mg daily tablet
Digoxin toxicity
Anorexia Fatigue Headache Malaise Nausea vomiting Mental confusion Altered visual perception (blurring, yellow halo) Cardiac effect such as Premature vent cont SA AV block Atrial tachycardia
Digoxin toxicity treatment
Discontinue digitalis
Discontinue any K sparring diuretic
If Hypokalemia — give K supplement unless patient has AV block
Treat arrhythmia with Lidocaine 100 mg bolus followed by infusion at 2 to 4 mg/min
Cholestyramine (Questran) bind to digitalis preventing Its re Absorption
Digoxin immune FAB digifab . 1 vial 40 mg will bind with 0.5mg of digitalis.
Inamrinone
Non glycoside, non sympathomimetic inotrope
Positive inotropic effect
Vasodilating Effect
Inhibits phosphodiesterase located in cardiac cells, increases cAMP
Used for refractory patients
IV 0.75 mg/kg over 2 to 3 min followed by maintenance at 5 to 10 mg/kg/min
Inamrinone precautions
Unstable in dextrose Given in saline (careful in HF Patients) Monitoring for hypotension Thrombocytopenia Ventricular tachy
