Heart Failure Flashcards
Heart Failure: Definition
the inability of the heart to pump enough blood to meet the metabolic needs of the body (determined as O2 consumption)
not a disease but a clinical syndrome characterized by:
- volume overload
- inadequate tissue perfusion
- poor exercise tolerance
- decreased BP, decreased CO
- arrhythmias
which leads to tissue hypoperfusion followed by pulmonary and systemic congestion
Heart Failure: Stats
5 million people, 650,000 new cases/year
while rates of other CV disease are decreasing, heart failure has been increasing steadily since 1975 due to increased survival rate after MIs
affects both men and women but there is a higher mortality in women
death rates increase in african americans
leading cause of hospitalization in those over 65yo
Risk Factors of HF
CAD risk increases with age HTN increases risk of failure 3x Smoking DM Obesity Hyperlipidemia
Precipitating Factors of HF
arrhythmias stress-physical and emotional anemia thyroid dysfunction pulmonary disease endo-, peri-, myocarditis fluid retention new cardiac conditions can cause heart failure
Systolic Failure:
most common cause of HF
inability to pump blood
decreased LV ejection fraction (normal is 50-70%)
Systolic Failure: Causes
Impaired contractile function - MI
increased afterload - from HTN (the harder heart has to work to overcome afterload, heart can get floppy)
cardiomyopathy and mechanical abnormalities (like defective valves)
Diastolic Failure:
impaired ability of ventricles to fill during diastole which means decreased stroke volume characterized by:
- high filling pressure, pulmonary and systemic vascular congestion
- LV hypertrophy from chronic HTN, aortic stenosis, hypertrophic caridomyopathy
(walls of heart get thickened due to having to work hard against resistance)
Mixed Failure:
mix of systolic and diastolic failure
dilated cardiomyopathy (DCM) - biventricular failure - both are dilated
hypertropic cardiomyopathy
1st Compensatory Mechanism
SNS - triggered by decreased CO
- causes increased HR, contractility, PV vasoconstriction which leads to increased CO
- problem: increased need for O2 by heart muscle so vasoconstriction increases preload and afterload (heart is already overloaded)
2nd Compensatory Mechanism
Neurohormonal: decreased CO = decreased renal perfusion which causes:
- kidneys to produce renin
- adrenal cortex produces aldosterone (cause Na+ and water retention and vasoconstriction = leads to increased afterload which increases BP)
- posterior pituitary produce ADH (water reabsorption which increases blood volume which means increase in preload)
3rd Compensatory Mechanism
Cardiac Compensation
- dilation: enlargement of chambers of heart (stretching of ht muscle fibers cause: increase contraction, increase CO, increase BP, increase perfusion but fibers become overstretched causing decreased ability to contract leading to decreased CO)
- hypertrophy: response to over and strain (SVR) increasing cardiac wall and muscle mass (increase CO and perfusion but has poor contractility which eventually leads to decrease CO)
- ventricular remodeling: hypertrophy of cardiac myocytes leading to increased ventricular mass, change in shape, impaired contractility leading to decrease CO and perfusion
LVF - S/O
Leads to pulmonary congestion and respiratory Sx:
- dyspnea
- tachycardia
- orthopnea
- PND (paroxysmal nocturnal dyspnea - very anxiety producing)
- cough
Displacement of PMI S3 or S5 heart sounds Tachycardia Cerebral hypoxia Fatigue Muscle Weakness
LVF - Acute Pulmonary Edema
Medical Emergency
- increase capillary pressure in lungs pushes fluid into the interstitum and then into the alveoli, bronchioles, and bronchi
- death can result d/t suffocation (lungs are filled with fluid)
LVF - Acute Pulmonary Edema Symptoms
Agitation Skin cool and clammy Severe Dyspnea Orthopnea Cough, frothy blood-tinged sputum Pallor-cyanosis Tachycardia Tachypnea (>30/min) Moist crackles
RVF - S/O
Leads to peripheral edema and venous congestion of organs
Sx:
- hepatomegaly
- abd pain
- cardiac cirrhosis (sx = ascites, jaundice)
- anorexia, nausea, bloating d/t congestion of GI tract leads to decreased caloric intake
- weight gain (from fluid)
- increased nocturia
- dependent edema
- JVD
RVF - Edema
Dependent edema is an early Sx of RVF
- symmetrical
- if ambulatory, edema begins in feet and progresses up, worse at the end of the day, decreases after night’s rest
- recumbent - presacral progresses to genital region, and mid thighs
Anasarca (generalized edema) = late Sx of RVF
Weight gain of more than 5lbs in 2-3 days or dependent edema indicates exacerbation of HF
RVF and Skin
skin is dusky
low extremities are shiny
decreased or absent hair growth
brown or brawny skin pigment of ankles and lower legs d/t chronic swelling
Acute vs. Chronic HF
Acute: sudden onset (i.e. MI)
Chronic: gradual onset (i.e. HTN)
-see a progression of compensatory mechanisms: decreased contractility, neurohormonal activation, increased preload and afterload, then remodeling
Acute on Chronic: acute exacerbation in patient with chronic HF
Diagnostic Tests
help determine underlying cause:
- B-type natriuretic peptide (BNP): hormone secreted from ventricles in response to overload (aka increased stretching of ventricles). Worsening of failure = increase in BNP (normal level =0-100, can see levels into 1,000’s)
- Echocardiogram: heart chamber size, function, EF
- Chest x-ray: size of heart, pulmonary and venous congestion
- Blood work: CMP (tells us how kidneys and liver are functioning and give electrolyte values), CBC with Diff, Lipids, TSH, Troponin, Lactic Acid, D-dimer
- ABG: early heart failure and pulmonary edema may lead to respiratory alkalosis d/t hyperventilation, as progresses leads to acidosis
- ECG: may help determine cause of failure (arrhythmia, MI, LV dysfunction)
HF Tx
UNLOAD FAST
- upright position
- nitrates
- lasix
- oxygen
- ACE Inhibitors
- Digoxin
- Fluids (decrease)
- Afterload (decrease
- Sodium Restriction
- Test (Dig level, ABGs, Potassium level)
Acute HF and Pulmonary Edema: Plans/Interventions
- Decrease Intravascular Volume: decrease blood volume which decreases preload and afterload
- IV loop diuretics (lasix): decrease volume = decrease venous return, LV more efficient = increase CO, decrease pulmonary pressure = improved gas exchange, monitor K+ - Decrease Venous Return (Preload): decrease amount of blood returning to LV during diastole
- pt in high fowlers with legs dangling (increases breathing capacity aka ventilation)
- IV Nitro (vasodilator): peripheral and coronary arteries dilate (increases myocardial O2 and decreases blood return to heart) - Decrease Afterload
- IV Nitroprusside - potent vasodilator (decrease preload and afterload, DOC for pulmonary edema)
- IV morphine: dilates pulmonary and systemic vessels which decreases ventricular effort, decreases anxiety - Improve Gas Exchange/ Oxygenation: morphine decreases O2 demand, 02: 2-5LPM via NC or higher level of O2 delivery.
- Improve Cardiac Function:
- Inotropic drugs digitalis (digoxin): increase LV function by increasing contractility w/o increasing O2 consumption
- monitor digoxin toxicity (anorexia, N/V, discolored vision - yellow) normal digoxin level = 0.5-2 (blood test) - Decrease Anxiety: morphine
Chronic HF: Plan/Interventions
Need to tx underlying cause, contributing factors, maximize CO, prevent and alleviate Sx
Refer for CHN f/u care at home
- O2 therapy: may require home O2 to decrease dyspnea and fatigue
- monitor w/ oximetry, go in for ABGs - Adequate rest: conserve energy, decrease O2 demand, limit activities an have rest periods
- Medications at home:
- ACEI: decrease SVR = increase CO, decrease aldosterone effects
- Diuretics: Loop = K spending, Spironolactone = K sparing
- Inotropic drugs = digoxin (check HR and do not give if below 60bpm), report visual changes
- Vasodilator drugs: increase venous capacity, increase ventricular function, decrease heart size (just by volume not structurally), decrease neurohormonal response
- beta blockers: decrease SNS effects, increase dose slowly (teach pt about SE = vertigo and edema) - Nutritional Therapy: teach low salt foods (use of flavor enhancers instead), fluid restriction for sever HF or HF with renal disease, DASH diet
- Daily Weights: detect fluid retention and worsening HF or exacerbation (same time each day in same clothing)
- Cardiac Resynchronization - coordinates ventricular contraction if failure d/t arrhythmias
- Cardiac Transplants
- Ventricular Assist Devices (VADs) - support for up to 2 years
- Home health care with pt seen at least weekly to monitor: weight gain, VS, lung sounds, meds, fluid restrictions, food in home (sodium), tolerance to activity level, then communicate with HCP.
