Heart Failure Flashcards
Complex Syndrome Acute or chronic Leads to drop in cardiac output CO=HRxSV Compensatory mechanisms activated Pulmonary edema Cardiogenic pulmonary edema (wet lungs)
Overview of Heart Failure
Mechanisms activated to compensate -When heart begins to fail *Primary compensatory mechanisms -Frank-Starling mechanism -Neuroendocrine responses by Renin-RAAS, and Sympathetic Nervous System -Mycardial hypertrophy No minimal cardiac reserve Activity intolerance when client at rest
Pathophysiology and Etiology of HF
Ability for heart to pump stronger. Alpha (squeeze) & stimulation of Beta, increased HR, increase work load of Heart. The increase preload by Systemic better pump until a certain point.
-Elasticity of heart gone
Frank-Starling mechanism
Over grow heart. Suppy from coronary arteries. HT. Silent Killer. Heart is enlarged
Myocardial hypertrophy
*Systolic vs. Diastolic Failure; during rest stage; trouble with stiff ventricles; various reasons
*Left-sided vs. Right-sided Failure
*Low output vs. high-output failure; heart working OT. If HR goes to fast doesn’t have time to fill. decreased CO
*Acute vs. Chronic Failure; pulm. embolism (acute) blockage longterm
*
Classifications of HF
- Ischemic Heart disease; heart not perfusing well. BP not high enough
- Cardiomyopathies; reasons for Heart failure prob. with tissue itself. Fatty tissues (4th level)
- Hypertension
- Congenital, valvular heart diseases
- Incidence, prevalence increase with age
- African Americans more than Whites
Etiology of HF
- CAD, hypertension
- Family hx
- Cardiotoxic drugs
- Smoking
- Obesity
- Alcohol abuse
- Diabetes mellitus
Risk Factors for HF
4 to 8 L
Cardiac output/min
-Fatigue, activity intolerance
-Dizziness, syncope, dyspnea, S3
Lefty Larry; SOB
Hear crackles
Flash pulmonary edema; treat with LMNOP
skinny ankles, but lungs filled with fluid
**Paroxysmal nocturnal dyspnea
Left-sided Heart Failure
Lasix; fluid off
Morphine; reduce anxiety. vasodilate
Nitroglycerin; vasodilate; fluid off lungs; blood to heart
Oxygen; (Really 1st)
Position; HOB High Fowler’s. Pulmonary dilators; pressure low; pressures med, increase BP if low
LMNOP; Flash pulmonary edema; Left-sided HF
Edema in feet, legs, sacrum Anorexia, nausea RUQ pain Righty Rachel; 3 lbs/5lbs in a week or above pressure line SVC elevated. CVP elevated Peripheral edema; left has to pump with fluid. increase left heart over worked. NOT SOB Right side not pumping well Fluid to Sup Venaccava Flow Liver congestion systemic circulation congestion. Put legs up!; to pee out more Weigh everyday. Over 5 lbs call Dr! Nocturia
Right-sided Heart Failure
- Hepatomegaly, splenomegaly
- Impaired liver function
- Dysrhythmias
- Acute pulmonary edema
- Renal insufficiency; BUN, Cr increase; if heart is not perfusing well, will affect kidneys
- Pleural Effusions
Complications of HF
Main goals of care:
- Slow progression; catch early
- Reduce cardiac workload
Collaboration of HF
Class I: No abnormal symptoms with activity
Class II: Symptoms with normal activity
Class III: Marked limitation due to symptoms with less than ordinary activity
Class IV: Symptoms at rest and severe limitation in functional activity
Clinical Classifications of Heart Failure
Below 40%
Ejection Fraction in trouble
B-Type natriuretic peptide; heart stretched
Serum electrolytes
Urinalysis, BUN, serum Creatinine
Liver function tests
Thyroid function tests; hypothyroid does to heart-weakens the heart. assoc. with A fib
ABG’s
CXR
ECG; irreg. rhythms
Echocardiogram/EKG; soundwaves/ultrasound of heart. est. ejection fraction % of volume that pumps out.
Diagnostic Tests for Heart Failure
Parameters Monitoring devices Risks assoc. with hemodynamic monitoring Intra-arterial pressure monitoring Venous pressure monitoring Pulmonary artery pressure monitoring
Hemodynamic Monitoring HF
Angiotensin-converting enzyme (ACE) inhibitors; (pril)
decrease afterload. decrease workload on heart. decrease preload. Does cause cough in patients.
Decreases Angten. II. Decreases vasoconstriction. Decreases Fluid Vol. Decreases Na and H2O
Angiotensin-converting enzyme (ACE) inhibitors
Pharm Therapy for HF
Angiotensin II receptor blockers; (Sartans)
blocks vasoconstriction. Blocks Aldosterone. release.
Angiotensin II receptor blockers;
Pharm therapy for HF
Beta-blockers; blocks beta1. decreases HR, decreases contractility, decreases workload on heart, vasoDilation. [Beta2 can cause vasoconstriction. bronchodilation]
careful giving to patients with pulmonary constriction issues. Diabetes lungers
Beta-blockers1
Pharm therapy for HF
Diuretics; decrease preload. Lasix
Vasodilators
Digitalis, digoxin; pos inotropic agent. increases contractility, more Ca in heart muscle. increase power of pump. (check K levels, K low worry digtoxicity)
Antidysrhythmics; heart irritable, overloaded (irreg. rhythms)
Pharmacologic therapies cont. for HF
Sodium-restricted diet; Na goes H2O goes
Fluid restriction; only if fluid overloaded.
Exercise intolerance; optimize ability to move.
-moderate, progressive activity program.
Nutrition and Activity for HF patients
*Circulatory assistance;
-Intra-aortic balloon pump; temp measure balloon on stick. catheter in groin. inflats/deflats
-Left-ventricular assist device
*Cardiac transplantation; intune to complications
-Cardiac tamponade; fluid in pericardial sac. (fluid in sac);Heart hardly pumps; Chest tubes in perisac.
-Nursing care for transplant;
bleeding precautions
chest tube care
assess for cardiac tamponade
treat atrial dysrhythmias
treat hypothermia
assess and treat infections, rejection
Surgery for HF patients
- Cardiomyoplasty; stimulate muscle, helps contract.
- Ventricular reduction; piece of muscle out hopes of decreasing preload.
Other surgical procedures for HF patients
- Hawthorn; increase healthy elasticity of arterial vessels.
* Coenzyme Q10, Mg, thiamine; mitochondrial cellular structure of heart
Complementary and Alternative Therapy of HF patients
Chronic heart failure is terminal disease.
-unless cardiac transplant
Advance directives
Hospice; if no treatment options
End-of-life care for HF patients
- **Teach clients about coronary heart disease; education Na/fluid restriction. cessation of smoking. HT, diabetes mellitus management
- *Discuss risk factors for coronary heart disease, ways to reduce
- Health Hx
Nursing Process for HF
Health Promotion -Instruct about CAD -Reduction of risk factors -Hypertension -Diabetes management Assessment -health hx -physical examination
Nursing Assessment for HF
Decreased Cardiac Output
Excess Fluid Volume
Activity Intolerance
Deficient knowledge r/t low-sodium diet
Nursing Diagnosis for HF
Client will: -Describe purpose of medication -Report symptoms -Maintain adequate oxygenation -Maintain adequate tissue perfusion -Meet body's nutritional needs Pt. knows how to take pulse. **look for weight gain, low pulse, etc.
Planning for HF
Monitor vitals, ox sat Monitor BNP levels Auscultate heart and breath sounds Admin supplemental oxygen Admin medications Encourage rest
Implementation: Maintain Cardiac Output
Heart Failure
Assess Respiratory status/airway Monitor I & O Record abdominal girth Measure hemodynamic parameters Restrict fluids ***Weight gain best indicator of FVE
Implementation: Monitor Fluid Volume
Heart Failure
Organize rest periods between activities
Assist with ADL’s as needed
Plan progressive activities
Provide written, verbal instructions about activity after discharge
Implementation: Monitor Activity
Heart Failure
Discuss rationale for sodium restrictions
Consult with dietician
Implementation: Provide Low-Sodium Diet
Heart Failure
Describe meds Describe symptoms to report Explains importance of daily weights Chooses appropriate low-sodium foods Modifies routine for adequate rest periods
Evaluation: The client
- Documentation of discharge instructions in 6 areas: medication management, low-sodium diet, activity and exercise, signs and symptoms of worsening condition, weight monitoring, and when to contact a healthcare provider.
- Assessment of Left ventricular function (%ejection fraction)
- Use of an ACE-I or ARB in patients with left ventricular dysfunction. (EF less than 40%) [ventricular remodeling of the heart]
- Smoking cessation advice and counseling.
All 6 areas have to be met.
The Joint Commission on Accreditation of Healthcare organizations (JCAHO)
Wont’ pay if patients keep coming back. must educate patients. Poor measures
a condition in which the heart is unable to pump enough blood into circulation to meet the body’s needs.
-inability to pump is commonly due to the inability of the heart to fill with enough blood or the inability of the heart to pump with enough force to meet the metabolic demands. (or combo of the two)
Heart Failure
Long term effect of coronary heart disease and MI when left ventricular damage is extensive enough to impair cardiac output.
-Can be acute or chronic
_Usually from MI, which results from coronary heart disease & myocardial ischemia. or primary cardiac muscle disorder.
-
HF
an abnormal accumulation of fluid in the interstitial tissue and alveoli of the lung.
-both cardiac and noncardiac disorders can cause pulmonary edema
-medical emergency;
drowning in the fluid in the alveolar and interstitial pulmonary spaces. Acute or gradual. progressing to severe respiratory distress. immediate treatment necessary.
Pulmonary Edema
the loss of effective compensation
-Cardiogenic pulmonary edema, is a sign of severe cardiac decompensation.
decompensation
Mech. pumping action of cardiac muscle propels the blood it receives to the pulmonary and systemic vascular systems for reoxygenation and delivery to the tissues
Pathophysiology HF
is the amount of blood pumped from the ventricles in 1 min. -Used to assess cardiac performance, esp. left ventricular function. ***Effective CO depends on adequate functional muscle mass and the ability of the ventricles 2 work together.
CO
is the ability of the heart to increase CO to meet metabolic demands.
*Ventricular damage decrease cardiac reserve
Cardiac Reserve
HR affects cardiac output by controlling the # of ventricular contractions per min.
-influenced by the autonomic nervous system, catecholamines and thyroid hormones.
CO=HRxSV (stroke volume)
the volume of blood in the ventricles @ end diastole (just before contraction)
Preload
End-diastolic Volume depends on the amount of blood returning to the ventricles and on the distensibility or stiffness of the ventricles (compliance)
venous return
the force needed to eject blood into the circulation.
afterload
(increased systemic resistance) increases afterload, impairing stroke volume and increase myocardial wok.
HTN
is the natural ability of cardiac muscle fibers to shorten during systole.
-necessary to overcome arterial pressures and eject blood during systole.
Contractility
is the % of blood in the ventricle that is ejected during systole
-normal ejection is 50-70%
Ejection Fraction
- The Frank-Starling mechanism
2.Neuroendocrine responses, including activation of the SNS and the Renin angiotensin system (RAS)
3 Myocardial hypertrophy
Failing heart-mechanisms are activated
intially stimulates aortic baroreceptors, which in turn stimulates the SNS
- stimulation of SNS produces both cardiac and vascular responses; release of norepinephrine.
- Norepinephrine increase HR and contractility by stimulating cardiac beta-receptors.
Decreased Cardiac Output
Norepinephrine causes arterial and venous vasoconstriction, increase venous return to the heart.
- Increase venous return, increase ventricular filling and myocardial stretch, increase the force of contraction.
- Overstretching the muscles fibers past their physiological limit; ineffective contraction.
-the greater the stretch of cardiac muscle fibers, the greater the force of contraction. Increase contractile force leading to increase CO
~Increased myocardial oxygen demands
~limited by overstretching
- Frank-Starling Mechanism (Failing Heart-mechanisms are activiated)
Decrease CO stimulants the SNS and Catecholamine release
~increase HR, BP & Contractility. Increase vascular resistance. Increase venous return complications.
~Increase vascular resistance.
*tachycardia, with decreased filling time and decrease CO, Increase myocardial work and o2 demand.
- Neuroendrocrine response (Failing Heart-mechanisms are activiated)
- Increase cardiac workload causes myocardial muscle to hypertrophy and ventricles to dilate. (physiology)
- Increase contractile force to maintain CO (effects on body)
- Increase myocardial O2 demand; cellular enlargement.(complications)
- Ventricular hypertrophy (Failing Heart-mechanisms are activated)
Ventricle fails to contract adequately to eject a sufficient volume of blood into the arterial system.
-affected by loss of myocardial cells as a result of ischemia and infarction, cardiomyopathy, or inflammation.
systolic failure
when the heart can not completely relax in diastolic, disrupting normal filling. Passive diastolic filling decrease, increase the importance of atrial contraction to preload.
-decrease ventricular compliance caused by hypertropic and cellular changes and and impaired relaxation of the heart muscle.
Diastolic Failure
coronary heart disease
hypertension
Left-sided HF
restrict blood flow to lungs, acute or chronic pulmonary disease
right-sided HF
hypermetabolic states
Require increase CO to maintainblood flow and O2 to the tissues. If increase blood flow cannot meet O2 demands of the tissue, compensatory mechanisms are activated to further increase CO, which in turn increases O2 demand.
-
High Output Failure
Decreased CO;
weakness
fatigue
decreased exercise tolerance
Manifestation of Systolic Failure
Ventricle fails to contract adequately to eject a sufficient volume of blood into the arterial system.
-affected by loss of myocardial cells as a result of ischemia and infarction, cardiomyopathy, or inflammation.
systolic failure
when the heart can not completely relax in diastolic, disrupting normal filling. Passive diastolic filling decrease, increase the importance of atrial contraction to preload.
-decrease ventricular compliance caused by hypertropic and cellular changes and and impaired relaxation of the heart muscle.
Diastolic Failure
coronary heart disease
hypertension
Left-sided HF
restrict blood flow to lungs, acute or chronic pulmonary disease
right-sided HF
frightening condition in which the client awakes @ night acutely SOB.
- edema from day reabsorbs causing fluid overload and pulmonary congestion.
- Severe HF may cause dyspnea @ rest and with activity signifying little or no cardiac reserve.
- Both S3 and S4 maybe heard.
Paroxysmal nocturnal dyspnea
Decreased CO;
weakness
fatigue
decreased exercise tolerance
Manifestation of Systolic Failure
SOB tachypnea respiratory crackles in left ventricle distended neck vein liver enlargement anorexia and nausea (if right ventricle is affected)
Manifestation of Diastolic Failure
Fatigue and activity intolerance
Dizziness and syncope from decrease CO
Manifestation of Left-sided Failure
Causes dyspnea, SOB & cough
May develop orthopnea
difficulty breathing when supine
cyanosis; impaired gas exchange maybe noted
crackles (rales) and wheezes @ bases
-S3 gallop maybe present (reflects hearts attempt to fill an already distended ventricle).
Pulmonary congestion
Edema develops feet and legs (scrum if client is bed-ridden)
Congestion of gastrointestinal tract vessels causes anorexia and nausea.
Right upper quadrant pain. (liver engorgement)
-Neck Veins distend & become viable (even when upright) b/c increase venous pressure
-Decrease in CO cause increase in Na & H2O causing weight gain; further increase pressure in capillaries. Resulting in edema.
Nocturia; voiding 2 or more times a night. develops when edema reabsorbs while supine
Manifestation of Right-Sided Failure
tachypnea paroxysmal nocturnal dyspnea labored respirations cough productive of frothy, pink sputum dyspnea crackles, wheezes orthopnea
Manifestations of Pulmonary Edema; respiratory
tachycardia cool, clammy skin hypotension hypoxemaia, severe can cause confusion/lethargy cyanosis ventricular gallop
Cardiovascular
restlessness
feeling of impending doom
anxiety
neurological
Levels have been shown to positively correlate with pressures in the left ventricle and the pulmonary vascular system.
BNP
study of forces involved in blood circulation
-assess cardiovascular function in the client who is critically ill or unstable.
goals; evaluate cardiac and circulatory function and the response to intervention.
hemodynamics
desirable 70 to 90 mmHg perfusion severely jeopardized at MAP’s @ 50 or below, Greater than 105 mmHg indicates hypertension or vasoconstriction.
Mean arterial pressure (MAP)
Labs needed to evaluate renal function
BUN, CR, urinalysis
compression of the heart
Cardiac tamponade
