Heart Failure Flashcards
Major cause of mortality and morbidity in the US
Over 5 million Americans currently
African Americans are twice as likely to develop
550,000 cases each year
heart failure
broadly describe heart failure
Heart pump actually fails
The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs
Results in decreased CO
causes of HF
Cardiac defect: Myocardial infarction Valve deficiency Defect outside the heart: Coronary artery disease Pulmonary hypertension Diabetes
decrease C.O., increased pressure in lungs, DOE, cough, inc. PCWP
Most heart failure begins with failure of this ventricle and progresses to failure of both
left sided heart failure
backs up from Left, to body, edema, organ congestion, inc. CVP
High output heart failure – caused by increased metabolic needs, septicemia, anemia and hyperthyroidism
right sided heart failure
treatments for HF
O2, meds: diuretics, vasodilators, ACE & Beta blocker, digoxin
Monitor wt gain & activity level
HF can result from:
Ischemic heart disease, MI 1/3 of all MI patients Chronic HTN 75% of cases Valve disease Third most common cause Cardiomyopathy Myocarditis Rheumatoid arthritis, Lupus erythematosis Substance abuse
pathophysiology of HF
Decreased tissue perfusion from poor cardiac output and pulmonary congestion occurs r/t increased pressure in the pulmonary vessels
two types of left HF
Systolic heart failure
Diastolic Heart Failure
cardiac output is decreased, fluid backs up into the pulmonary system
forward failure
Heart can’t contract forcefully to eject enough blood (decreased ejection fraction to <40%), What can cause this??
Preload increases and afterload increases because of peripheral resistance from compensatory mechanisms
Tissue perfusion diminishes and blood accumulates
Forward failure-
systolic heart failure
Preserved LV function
Left ventricle can’t relax during diastole becomes stiff
Prevents the ventricle from filling with enough blood to maintain the cardiac output
Ejection fraction is >40%, becomes stiffer with time
Usually the result of chronic HTN
diastolic heart failure
Caused by left ventricular failure, right ventricular MI or pulmonary hypertension
RV can not empty, increased volume and pressure develops in the venous system, peripheral edema results
right sided heart failure
AHA Stages of Heart Failure
Class 1 NYHA- high risk for developing heart failure
Class II NYHA- cardiac structural abnormalities or remodeling who have not developed HF symptoms
Class III NYHA- current or prior symptoms of heart failure
Class IV NYHA- refractory end-stage heart failure
describe stimulation of sympathetic NS as a compensatory mechanism
Catecholamines, epinephrine and norepinephrine to increase HR and BP- immediate response
Increasing HR causes a decrease in fill time increase preload
Increased SV increased stretch and Hypertrophy
Arterial vasoconstriction occurs to maintain BP and low C.O. increased afterloadLV overworks and SV may decline
Reduced blood flow to the kidneys causes the RAAS system to activate vasoconstriction and water and sodium retention
Preload and afterload increase
Angiotensin II ventricular remodeling myocyte contractile dysfunction (can’t contract)
RAAS system (compensatory mechanism)
Immune response r/t heart cell injury Cytokines, TNF and interleukins IL-1 and 6, these contribute to ventricular remodeling Natriuretic Peptides (neurohormones) promote vasodilation and diuresis through Na loss in the kidneys BNP B-type natriuretic peptide released by the ventricles when fluid overload, levels raise dramatically ADH (vasopressin) levels and Endothelin levels also rise in response to low fluid output and stretch of myocardial fibers worsening HF
chemical response (compensatory mechanism)
specific questions to ask regarding signs/symptoms of heart failure
FACES: Fatigue Activity intolerance Chest congestion Edema Shortness of breath
visual inspection of assessment
Altered LOC Respiratory distress JVD, how do you measure this?? Cyanosis Peripheral edema Tachypnea with minimal exertion
palpation during assessment
Enlarged, laterally displaced PMI
Thrill may be felt along left sternal border
Palpate abdomen
Ascites
Hepatomegaly
Check for presence of edema in lower extremities
Check peripheral pulses
Check for lower extremity cyanosis
Note ADL’s, can they climb stairs, how far can they walk?
Exertional Dyspnea, Orthopnea and PND (paroxysmal nocturnal dyspnea),
auscultation during assessment
S3, why would they have this? Mitral murmur Holosystolic Heard best at apex Radiating to axilla Cardiac rhythm irregularities A fib / PVC / ventricular tachycardia / v fib Crackles, wheezes, decreased breath sounds Cough may be present Indicative of pulmonary edema
clinical manifestations of left sided failure
Decreased Cardiac Output: Fatigue Weakness Oliguria in day and nocturia at night Angina Confusion Dizziness/tachycardia Weak pulses and cool extremities Pulmonary Congestion: Hacking cough, worse at night Dyspnea/breathlessness/tachypnea Crackles/wheezes Frothy pink sputum S3 and S4 gallop
clinical manifestations in right sided failure
Systemic Congestion JVD Enlarged liver and spleen Anorexia and nausea, why?? Dependent edema Distended abdomen Swollen hands and fingers Polyuria at night Weight gain Increased BP at first from volume, then decreased BP from output
diagnostic testing for HF
ECG, CXR, CBC, UA, serum creatine, albumin, electrolytes
Secreted by the ventricular tissue in the heart when ventricular volume and pressure is increased
Sensitive indicator
Can be positive for heart failure when CXR does not indicate a problem
B-type Natriuretic peptide
Best tool for diagnosing HF
Looks at the pumping action or ejection fraction of the heart muscles
echocardiogram
congestive heart failure treatment and interventions
UNLOAD FAST
Upright position, Nitrates, Lasix, Oxygen, ACE Inhibitors, Digoxin
Fluids (decreased), Afterload (decreased), Sodium restriction, Test (digoxin level, ABGs, K level)
standard med therapy for heart failure
Standard medication therapy is ACE inhibitors and ARBS
Block the effects of Angiotensin II receptors decrease in arterial resistance and decreased blood pressure
ARBS
Suppress Renin Angiotensin System prevents conversion of Angiotensin I to Angiotensin II arterial dilation and increased stroke volume
ACE Inhibitors
Both ACEI s and ARBs block
aldosterone which causes patients to lose sodium which in turn will cause the client to lose sodium and water and retain potassium…MONITOR FOR Hyperkalemia!!
drugs that Increase the force of myocardial contraction
Positive inotropic drugs
drugs that increase heart rate
Positive chronotropic drugs
drugs that Accelerate cardiac conduction
Positive dromotropic drugs
all the potential drug therapy for HF
ACE inhibitors Angiotensin II receptor blockers Beta blockers Aldosterone antagonists B-type natriuretic peptides Phosphodiesterase inhibitors Cardiac glycosides
Prevent sodium and water resorption by inhibiting aldosterone secretion
Diuresis results, which decreases preload, or the left ventricular end-volume, and the work of the heart
ACE Inhibitors
examples of ace inhibitors
lisinopril, enalapril, fosinopril, quinapril, captopril, ramipril, trandolapril, and perindopril
Potent vasodilators; decrease systemic vascular resistance (afterload)
Angiotensin II Receptor Blockers (ARBs)
examples of ARBs
valsartan (Diovan), candesartan (Atacand), eprosartan (Teveten), irbesartan (Avapro), telmisartan (Micardis), olmesartan (Benicar), and losartan (Cozaar)
work by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system
Reduced heart rate, delayed AV node conduction, reduced myocardial contractility, and decreased myocardial automaticity result
beta blockers
examples of beta blockers
metoprolol, carvedilol (Coreg)
Potassium-sparing diuretic
Also acts as an aldosterone antagonist, which has been shown to reduce the symptoms of heart failure
spironolactone (Aldactone)
Selective aldosterone blocker
treats HF
eplerenone (Inspra)
First drug approved for a specific ethnic group, namely African Americans
treats HF
hydralazine/isosorbide dinitrate (BiDil)
Beta1-selective vasoactive adrenergic drug
Structurally similar to dopamine
dobutamine
Used in the intensive care setting as a final effort to treat severe, life-threatening heart failure, often in combination with several other cardiostimulatory medications
nesiritide (Natrecor)
B-type Natriuretic Peptides:Mechanism of Action
Effects include diuresis (urinary fluid loss), natriuresis (urinary sodium loss), and vasodilation
Vasodilating effects on both arteries and veins
Indirectly increases cardiac output
Suppresses renin-angiotensin system
B-type Natriuretic Peptides:Adverse Effects
Hypotension
Dysrhythmia
Headache
Abdominal pain
Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation
Phosphodiesterase Inhibitors
indications of Phosphodiesterase Inhibitors
Short-term management of heart failure
Given when patient does not respond to treatment with digoxin, diuretics, and/or vasodilators
AHA and ACC advise against long-term infusions
adverse effects of milrinone
Dysrhythmia Hypotension Angina (chest pain) Hypokalemia Tremor Thrombocytopenia
No longer used as first-line treatment
Originally obtained from Digitalis plant, foxglove
Digoxin is the prototype
Used in heart failure and to control ventricular response to atrial fibrillation or flutter
Increase myocardial contractility
Cardiac Glycosides
effects of cardiac glycosides
Increased force and velocity of myocardial contraction (without an increase in oxygen consumption)
Reduced heart rate
Decreased automaticity at SA node, decreased AV nodal conduction, and other effects
Increased stroke volume
Reduction in heart size during diastole
Decrease in venous BP and vein engorgement
Increase in coronary circulation
Promotion of diuresis because of improved blood circulation
Palliation of exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis
effects of cardiac glycosides
