cardiac outline.docx - Topical Outline Cardiac Review Ch....

Topical Outline Cardiac
Review Ch. 31 and Focus on Ch. 32, 33, 34, 36, 37 & Corresponding EKG text.
 Hypertension/Hypertensive Emergency: stages, causes, pathophysiology,
signs and symptoms complications, treatment, patient education
 CHF, Pulmonary edema: pathophysiology, complications, treatment,
medications, loop diuretic vs Potassium-sparing diuretic, patient education
 Pg. 281, Ch. 16, Hyperkalemia, Hypokalemia: causes, patho, EKG
appearance, complications, signs and symptoms, treatment
o Always check Magnesium level if Hypokalemia, may need to replace
Magnesium first in order to retain Potassium and replace potassium
efficiently/successfully.
o Remember when replacing Potassium IV, it burns regular peripheral veins-
may need to slow it down (the rate) or dilute with Normal Saline concurrently run
together. If in Central Line or PICC, ok to run at normal rate without diluting.
Hyperkalemia (high serum potassium) may result from impaired renal excretion, a shift of
potassium from ICF to ECF, a massive intake of potassium, or a combination of these factors
( Table 16-5 ). The most common cause of hyperkalemia is renal failure. Adrenal insufficiency
with a subsequent aldosterone deficiency leads to potassium retention. Factors that cause
potassium to move from ICF to ECF include acidosis, massive cell destruction (as in burn or
crush injury, tumor lysis, severe infections), and intense exercise. In metabolic acidosis,
potassium ions shift from ICF to ECF in exchange for hydrogen ions moving into the cell.
Digoxin-like drugs and β-adrenergic blockers (e.g., propranolol) can impair entry of potassium
into cells, resulting in a higher ECF potassium concentration. Several drugs, such as heparin,
potassium-sparing diuretics, angiotensin II receptor blockers (e.g., losartan), and angiotensin-
converting enzyme (ACE) inhibitors (e.g., lisinopril), can contribute to hyperkalemia by reducing
the kidney's ability to excrete potassium.
5
Clinical Manifestations
The increased potassium concentration outside the cell changes the normal ECF and ICF ratio, resulting in increased cell
excitability and changes in impulse transmission to the nerves and muscles. The most clinically significant problems are
the disturbances in cardiac conduction. The initial finding is tall, peaked T waves. As potassium increases, cardiac
depolarization decreases, leading to loss of P waves, a prolonged PR interval, ST segment depression, and widening QRS

complex ( Fig. 16-14 ). Heart block, ventricular fibrillation, or cardiac standstill may occur. Elevated potassium may cause
failure to capture in a patient who has a pacemaker.
The patient may experience fatigue, confusion, tetany, muscle cramps, paresthesias, and weakness. As potassium
increases, loss of muscle tone and weakness or paralysis of other skeletal muscles, including the respiratory muscles can
occur, leading to respiratory arrest. Abdominal cramping, vomiting, and diarrhea occur from hyperactivity of
gastrointestinal smooth muscles.