Heart Failure

Question 1

Heart Failure: Definition

Answer 1

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

Question 2

Heart Failure: Stats

Answer 2

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

Question 3

Risk Factors of HF

Answer 3

CAD
risk increases with age
HTN increases risk of failure 3x
Smoking
DM
Obesity
Hyperlipidemia

Question 4

Precipitating Factors of HF

Answer 4

arrhythmias
stress-physical and emotional
anemia
thyroid dysfunction
pulmonary disease
endo-, peri-, myocarditis
fluid retention
new cardiac conditions can cause heart failure

Question 5

Systolic Failure:

Answer 5

most common cause of HF

inability to pump blood

decreased LV ejection fraction (normal is 50-70%)

Question 6

Systolic Failure: Causes

Answer 6

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)

Question 7

Diastolic Failure:

Answer 7

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)

Question 8

Mixed Failure:

Answer 8

mix of systolic and diastolic failure

dilated cardiomyopathy (DCM) - biventricular failure - both are dilated

hypertropic cardiomyopathy

Question 9

1st Compensatory Mechanism

Answer 9

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)

Question 10

2nd Compensatory Mechanism

Answer 10

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)

Question 11

3rd Compensatory Mechanism

Answer 11

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

Question 12

LVF - S/O

Answer 12

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

Question 13

LVF - Acute Pulmonary Edema

Answer 13

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)

Question 14

LVF - Acute Pulmonary Edema Symptoms

Answer 14

Agitation
Skin cool and clammy
Severe Dyspnea
Orthopnea
Cough, frothy blood-tinged sputum
Pallor-cyanosis
Tachycardia
Tachypnea (>30/min)
Moist crackles

Question 15

RVF - S/O

Answer 15

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

Question 16

RVF - Edema

Answer 16

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

Question 17

RVF and Skin

Answer 17

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

Question 18

Acute vs. Chronic HF

Answer 18

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

Question 19

Diagnostic Tests

Answer 19

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)

Question 20

HF Tx

Answer 20

UNLOAD FAST

• upright position
• nitrates
• lasix
• oxygen
• ACE Inhibitors
• Digoxin
• Fluids (decrease)
• Afterload (decrease
• Sodium Restriction
• Test (Dig level, ABGs, Potassium level)

Question 21

Acute HF and Pulmonary Edema: Plans/Interventions

Answer 21

1. 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+
2. 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)
3. 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
4. Improve Gas Exchange/ Oxygenation: morphine decreases O2 demand, 02: 2-5LPM via NC or higher level of O2 delivery.
5. 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)
6. Decrease Anxiety: morphine

Question 22

Chronic HF: Plan/Interventions

Answer 22

Need to tx underlying cause, contributing factors, maximize CO, prevent and alleviate Sx

Refer for CHN f/u care at home

1. O2 therapy: may require home O2 to decrease dyspnea and fatigue
   - monitor w/ oximetry, go in for ABGs
2. Adequate rest: conserve energy, decrease O2 demand, limit activities an have rest periods
3. 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)
4. Nutritional Therapy: teach low salt foods (use of flavor enhancers instead), fluid restriction for sever HF or HF with renal disease, DASH diet
5. Daily Weights: detect fluid retention and worsening HF or exacerbation (same time each day in same clothing)
6. Cardiac Resynchronization - coordinates ventricular contraction if failure d/t arrhythmias
7. Cardiac Transplants
8. Ventricular Assist Devices (VADs) - support for up to 2 years
9. 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.