MANAGEMENT OF PATIENTSWITH COMPLICATIONS

FROM HEART DISEASE

• Also known as Congestive Heart Failure (CHF)

• This refers to the inability of the heart to pump

an adequate supply of blood to meet the
metabolic needs of the body

• A syndrome of systemic or pulmonary

circulatory congestion caused by decreased
myocardial contractility resulting to inadequate 4 factors affecting hemodynamic condition
cardiac output to meet oxygen demands
1. Heart rate
Common types: 2. Stroke volume
a. Preload
a. Left-sided heart failure (Respiratory)
b. Afterload
b. Right-sided heart failure (Circulatory) c. Contractility
3. Vasoactivity
Etiology: 4. Cardiac output

• Decreased myocardial contractility due to CAD, Preload

MI, cardiomyopathy
• Valvular heart disease, hypertensive heart
disease, dysrhythmias, cor pulmonale,
pericardial tamponade, pericarditis, other
systemic conditions
- Volume of blood in ventricles at end of diastole.
- Increased in preload may indicate:
a. Hypervolemia
b. Regurgitation of cardiac valves
c. Heart failure

Pathophysiology: Afterload

• Systolic HF: Decreased amount of blood from - Resistance in left ventricle must overcome to
the ventricle – stimulates sympathetic nervous circulate blood.
system – release of epinephrine and - Increased in afterload may indicate:
norepinephrine – further heart muscle damage a. Hypertension
– decreased renal perfusion – Renin secretion – b. Vasoconstriction
Angiotensin I production – ACE in the lumen – - Increased afterload, increased cardiac workload
Angiotensin II – causes vasoconstriction and
aldosterone production – fluid retention – Heart Failure
increases heart’s workload – ventricular
Signs and Symptoms:
hypertrophy without capillary blood supply –
myocardial ischemia General:

• Diastolic HF: Increased workload – cardiac
hypertrophy – decreased blood in the ventricles
– causes decreased cardiac output
- Pale, cyanotic skin (with decreased perfusion to
extremities)
- Dependent edema (with increased venous
pressure)

- Deceased activity tolerance

Cardiovascular: b. Class II: Slight limitation in ADL’s, no symptoms
at rest, positive symptoms in increased
- Apical impulse, enlarged and left lateral activities (Good Prognosis)
displacement (with cardiac enlargement)
c. Class III: marked limitations in ADL’s,
- Third heart sound (S3) comfortable at rest but symptoms present in
- Murmurs (with valvular dysfunction) less than ordinary activities (Fair Prognosis)

- Tachycardia d. Class IV: symptoms are present at rest (Fair

Prognosis)
- Increased jugular venous distention (JVD)
Left sided Heart failure
Cerebrovascular:
• Left ventricular damage usually due to MI,
- Lightheadness hypertension, ischemic heart disease, aortic
valve disease or mitral stenosis
- Dizziness
• Left ventricular damage causes blood to back up
- Confusion
through the atrium into the pulmonary veins
Gastrointestinal: which results to pulmonary congestion

- Nausea and anorexia • Diminished blood flow will result to decreased

blood flow to the brain, kidneys and other
- Enlarged, pulsatile liver tissues

- Ascites Pathophysiology:

- Hepatojugular test, increased (with increased • Left ventricular failure→ pump failure→ back up
right ventricular filling pressure) of blood into the pulmonary veins → increased
pulmonary capillary pressure → pulmonary
Renal:
congestion
- Decreased urinary frequency during the day
• Left ventricular failure → decreased cardiac
- Nocturia output → decreased perfusion to the brain,
kidney and other tissues → oliguria, dizziness
Respiratory:
Predisposing Factors
- Dyspnea on exertion
-1. 90% is mitral valve stenosis due to
- Orthopnea
a. RHD – inflammation of mitral valve due to
- Paroxysmal nocturnal dyspnea invasion of Group A beta-hemolytic
streptococcus
- Bilateral crackles that do not clear with cough
- Formation of aschoff bodies in the mitral
New York Heart Association’s Classification of Heart
valve
Failure:
- Common among children (throat infection)
a. Class I: ordinary physical activity does not cause
chest pain and fatigue, no pulmonary - ASO Titer (Anti streptolysin O titer)
congestion, asymptomatic, no limitations in the
activity of daily living (ADL’s) (Good Prognosis) - Penicillin
 - Aspirin 14. Nocturia – sleeping cardiac workload decreased,
improving renal perfusion, which then leads to frequent
b. Aging urination at
Predisposing Factors: Night.
2. Myocardial Infarction Left-Sided Heart Failure (CHOP):
3. Ischemic heart disease C- Cough
4. Hypertension H- Hemoptysis
5. Aortic valve stenosis O- Orthopnea
Signs and Symptoms P- Pulmonary Congestion (crackles/ rales)
1. Dyspnea

2. Paroxysmal nocturnal dyspnea – client awakened at

night due to DOB (sudden attacks of Orthopnea at
night)

3. Orthopnea – use 2 – 3 pillows when sleeping or place

in high fowlers

4. Productive cough with blood tinged sputum (severe

pulmonary edema)

5. Frothy salivation

Signs and Symptoms

Diagnostic Procedure
6. Cyanosis
1. Chest x-ray – reveals cardiomegaly
7. Rales/Crackles (bi-basilar lobes that do not clear w/
coughing) 2. PAP (pulmonary arterial pressure) – measures
pressure in right ventricle or cardiac status
8. Bronchial wheezing
PCWP (pulmonary capillary wedge pressure) – measures
9. Pulsus Alternans – weak pulse followed by strong end systolic and dyastolic pressure
bounding pulse
- both are increased
10. PMI is displaced laterally due to cardiomegaly
- done by cardiac catheterization (insertion of
Signs and Symptoms swan ganz catheter)

11. There is anorexia and generalized body malaise 3. Echocardiography – enlarged heart chamber
(cardiomyopathy), dependent on extent of heart failure
12. S3 – ventricular gallop
4. ABG – reveals PO2 is decreased (hypoxemia), PCO2 is
13. Oliguria – blood flow to the kidney decreases,
increased (respiratory acidosis)
causing decreased perfusion and reduce urine output.
(Daytime)
Diagnostic tests: 3. Ascites

• Chest X-ray: cardiac hypertrophy, vascular 4. Weight gain

congestion
5. Hepatosplenomegaly
• 2D echocardiography: increased size of cardiac
chamber 6. Jaundice

• ECG: cardiac hypertrophy 7. Pruritus (albumin)

• ABG: decreased PaO2; increased PaCO2 8. Anorexia

• Pulse oximeter: decreased SaO2 9. Esophageal varices

• Pulse arterial pressure (PAP) and Pulmonary Right-Sided Heart Failure (HEAD):
capillary wedge pressure (PCWP): increased H- Hepatomegaly
RIGHT sided Heart failure E- Edema (Bipedal)
• Weakened right ventricle is unable to pump A- Ascites
blood into the pulmonary system; systemic
venous congestion occurs as pressure builds up D- Distended Neck Vein

• Caused by left sided heart failure, right

ventricular infarction, atherosclerotic heart
disease, COPD, pulmonic stenosis, pulmonary
embolism

Pathophysiology:

• Right ventricular failure → blood pooling in the

venous circulation → increased hydrostatic
pressure → peripheral edema

• Right ventricular failure → blood pooling →

venous congestion in the kidney, liver and GIT

Predisposing Factors
Diagnostic Procedures
1. Tricuspid valve stenosis
1. Chest x-ray – reveals cardiomegaly
2. Pulmonary embolism
2. Central venous pressure (CVP)
3. Related to COPD
- Measure pressure in right atrium (4 – 10 cm of water)
4. Pulmonic valve stenosis
- CVP fluid status measure
5. Left sided heart failure
- If CVP is less than 4 cm of water hypovolemic shock
Signs and Symptoms (venous congestion)
- Do the fluid challenge (increase IV flow rate)
1. Neck/jugular vein distension
- If CVP is more than 10 cm of water hypervolemic shock
2. Pitting edema (lower extremities)
- Administer loop diuretics as ordered 9. Assist in bloodless phlebotomy – rotating tourniquet,
rotated clockwise every 15 minutes to promote
- When reading CVP patient should be flat on bed decrease venous return
- Upon insertion place client in Trendelenburg position 10. Provide client health teaching and discharge
to promote ventricular filling and prevent pulmonary planning
embolism
Prevent complications
3. Echocardiography – reveals enlarged heart chambers
(cardiomyopathy) a.Arrhythmia

4. Liver enzymes – SGPT and SGOT is increased b.Shock

Goal: increase cardiac contractility thereby increasing c. Right ventricular hypertrophy

cardiac output (3 – 6 L/min)
d. MI
1. Enforce CBR
e. Thrombophlebitis
2. Administer medications as ordered
a. Dietary modification
a. Cardiac glycosides - Dilated cardiomyopathy
b. Strict compliance to medications
b. Digoxin (Lanoxin) (increases cardiac contraction but
lowers the pulse rate) MANAGEMENT OF Heart failure

Goal of Treatment:
- Increase force of cardiac contraction
• Eliminate or reduce any etiologic contributory
- If heart rate is decreased do not give
factors
c. Loop Diuretics Lasix (Furosemide) peak 1-2 hrs,
duration 6-8 hrs (monitor for hyperkalemia) • Reduce workload of the heart by decreasing
preloads and afterloads
d. Bronchodilators aminophylline
Medical Management:
e. Narcotic analgesics Morphine Sulfate
• Sodium and fluid restriction; weight reduction;
f. Vasodilators Nitroglycerine less than 2-3g of sodium per day

g. Anti Arrhythmic Lidocaine (Xylocane) • Avoidance of alcohol and smoking

3. Administer oxygen inhalation with high inflow, 3 – 4 • Oxygen therapy depending on the client’s
L/min, delivered via nasal cannula condition

4. High fowler‘s position • PTCA, CABG, Pacemakers, Valvular Replacement

5. Monitor strictly vital signs, intake and output and ECG Pharmacology:
tracing
Major types of drugs used to treat CHF:
6. Measure abdominal girth daily and notify physician
a. Inotropic – affects cardiac contractility
7. Provide a dietary intake of low sodium, cholesterol
and caffeine b. Chronotropic – affects heart rate

8. Provide meticulous skin care

 c. Dromotropic – affects conduction velocity of
the AV node and rate of electrical impulses in
the heart

Vasodilators: decreases blood pressure with pooling of

blood in the veins; decreases preload and after load

ACE inhibitors: decreases after load; decreases blood

volume Nursing intervention:
ARB: lowers blood pressure and systemic vascular 1. Monitor and assess client’s respiratory status,
resistance provide ventilation, ABG, vital signs, weight
monitoring, MIO
Diuretics
2. Increase cardiac output: VS, ECG
Beta stimulators: increases myocardial contraction
(positive inotropic effect) 3. Provide rest
Beta blockers: decreases myocardial contraction 4. Prevent complications such as hypokalemia and
hypomagnesemia
Cardiotonic drugs: increases myocardial contractility
5. Reduce/eliminate edema
Hydralazine: lowers systemic vascular resistance,
decreases left ventricular afterload 6. Skin care
Isosorbide Dinitrate: vasodilation, decreases preload 7. Low salt diet
Digitalis: increases myocardial contraction, improves ACUTE HEART FAILURE (pulmonary edema)
contractility
• Condition of rapid fluid accumulation in the
Anti-coagulants extravascular lung spaces
Calcium Channel Blockers • Medical emergency that usually results from
left sided heart failure

• Capillary pressure within the lungs is too much.

Fluid pours from the blood into the alveoli,
bronchi and bronchioles

Etiology:

• MI, LSCHF, circulatory overload, smoke

inhalation or embolism, pulmonary infections,
CVA, head trauma, substance abuse

Pathophysiology:

• Pulmonary capillaries become filled with blood

→ increase in hydrostatic pressure → capillaries
cannot hold the hydrostatic pressure → fluid
leaks out to the adjacent alveoli → fluid in the
lungs → atelectasis → severe hypoxia
Clinical Manifestations: • Aminophylline: relieve bronchospasm and
increase output
• Restlessness, Fear, Anxiety
• Vasodilators: nitroglycerin; dilate vessels
• DOB, Dyspnea
Pharmacology:
• Cyanotic nailbeds
• Dobutamine: beta-adrenergic receptor
• Ashen skin stimulant, increases cardiac contractility and
• Cold and moist hands heart rate, to be administered after/with
digitalis, beta-blockers or calcium channel
• Incessant coughing blockers

• Depressed O2 sat • Milrinone: decreases cardiac pre load and after

load by delaying the release of calcium from
• Frothy, Blood-tinged Sputum
intracellular reservoir
• Tachycardia
• Nesiritide: causes vasodilation and suppresses
• Elevated CVP neurohormones (renin, aldosterone,
norepinephrine)
Diagnostic Tests:
Nursing Intervention:
• Chest X-ray: vascular congestion of the lung
fields(butterfly appearance) 1. Monitor VS and hemodynamics

• CVP and PCWP: elevated 2. Provide ventilation; intubation; high

concentration O2 (40-60%)
• ABG: decreased PaO2 and increased PaCO2
3. MIO
• Pulse oximetry: decreased SaO2
4. Positioning
Goal of Medical Management:
5. Health teaching
• Improvement of ventricular function
6. Diet: low sodium, low cholesterol, potassium
• Increase respiratory exchange rich

Medical Management: 7. Rotating tourniquets, phlebotomy

• Oxygenation – Positive End Expiratory Pressure Emergency management:cardiopulmonary

(PEEP) Resuscitation

Pharmacology: Resuscitation consists of the following steps:

• Morphine sulfate(2-5mg): induce vasodilation 1. Airway: maintaining an open airway

• Cardiac glycoside: digitalis to increase cardiac 2. Breathing: providing artificial ventilation by rescue
output breathing

• Diuretics: furosemide, excretion of sodium and 3. Circulation: promoting artificial circulation by

water external cardiac compression

4. Defibrillation: restoring the heartbeat