Question

Mrs. E., a 70-year-old Hispanic woman, was admitted to the medical unit with complaints of increasing dyspnea on exertion.

Subjective Data

·     Had a severe MI at 58 years of age

·     Has experienced increasing dyspnea on exertion during the last 2 years

·     Recently had a respiratory tract infection, frequent cough, and edema in legs 2 weeks ago

·     Cannot walk two blocks without getting short of breath

·     Has to sleep with head elevated on three pillows

·     Does not always remember to take medication

Objective Data

Physical Examination

·     In respiratory distress, use of accessory muscles, respiratory rate 36 breaths/min

·     Heart murmur

·     Moist crackles in both lungs

·     Cyanotic lips and extremities

·     Skin cool and diaphoretic

Diagnostic Studies

·     Chest x-ray results: cardiomegaly with right and left ventricular hypertrophy; fluid in lower lung fields

Collaborative Care

·     Digoxin 0.25 mg PO qd

·     Furosemide (Lasix) 40 mg IV bid

·     Potassium 40 mEq PO bid

·     Enalapril (Vasotec) 5 mg PO qd

·     2 g sodium diet

·     Oxygen 6 L/min

·     Daily weights

·     Daily 12-lead ECG, cardiac enzymes q8hr x 3

Critical Thinking Questions

1.    Explain the pathophysiology of Mrs. E.’s heart disease and include the RAAS system.

Answer 1

Myocardial Infarction ( MI)

Necrosis of Heart muscles caused by an interruption to the supply of blood to the heart often as a result of Coronary Thrombosis. The main cause of Myocardial Infarction is ischemia.

Pathophysiology of Mrs. E's heart disease:

Myocardial Infarction (previous history, may be due to Hypertension, Ischemic heart disease or Diabetes Mellitus)

? ( leads to)

Formation of scar tissue on Myocardium as a result of inflammation.

?

Left ventricle have to work hard to pump the blood and the work load increases

?

Muscle tissues of the left ventricle thickens or size of the chamber enlarges

?

Loss of elasticity of the left ventricular muscles

?

Failure to fill and pump the blood

?

Inability to pump the blood throughout the body( heary failure)/

compress the blood vessels in the heart chambers may lead to reduced blood supply to the heart muscles.

?

Abnormal heart rhythm, stroke, ischemia.

Pathophysiology of developing Right ventricular hypertrophy :

Left ventricular hypertrophy may cause left side heart failure, as the left ventricle is unable to pump the blood efficiently. Because of the inability to pump the blood, the blood backs up in left atrium and in the lungs. It cause fluid retention in the pulmonary veins and lung fields. This blood and fluid back up in the lungs leads to breathing difficulty, crackles in lungs and  the failure of right side of the heart , as the right ventricle is unable to pump the blood to the pulmonary arteries for oxygenating the blood. This inturn leads to the Venous stasis throughout the body, resulting in swelling especially in legs.

RAAS system in heart failure:

Renin Angiotensin Aldosterone System( RASS) serves as a compensatory mechanism during the condition of decreased cardiac output or heart failure .

When there is decreased cardiac output, and renal supply reduces , kidney releases Renin. This hormone helps to convert Angiotensinogen to convert Angiotensin I , this inturn leads to the formation of Angiotensin II. Angiotensin II is a vasoconstrictor and it increases the blood pressure by increasing Peripheral Vascular resistance . It also stimulate Aldosterone release. Aldosterone increases Sodium and water retention in the body. Actually RASS system is meant for protecting the body when there is decreased cardiac output. But during this condition it actually worsen the condition and helps in the progress of heart failure by increasing Blood pressure , water and sodium retention, thus increases pulmonary oedema, swelling in the legs etc. Due to pulmonary edema, there will not be proper gas exchange and oxygen supply to the tissues. This leads to cyanotic lips and extremities.