Page 184 - Cardiac Nursing

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160 PA R T II / Physiologic and Pathologic Responses

Long-standing hypokalemia is associated with selective my- mentation or angiotensin-converting enzyme inhibitors or used by
ocardial cell necrosis. As discussed in Chapter 27, selective my- people who have any degree of renal impairment. 50,51,53,54 Nonselec-
ocardial cell necrosis is associated with sudden cardiac death. tive -adrenergic blockers promote the development of hyperkalemia
by blocking catecholamine action at 2 receptors that normally stim-
Vascular Effects of Hypokalemia. In addition to the mul- 49,56
ulates potassium entry into cells. The hyperkalemic effect of
tiple cardiac effects discussed previously, hypokalemia has vascular
3
effects. Postural hypotension often occurs in hypokalemia, most -blockade is especially pronounced during exercise, which has
relevance to treadmill stress testing, and is enhanced in people who
likely caused by impaired smooth muscle function. 48,56,57
take digitalis. Administration of either unfractionated or
Classic studies indicate that chronic potassium depletion in
44
humans impairs vasodilation during strenuous exercise. The re- low-molecular-weight heparin, even in low-dose therapy, decreases
the synthesis of aldosterone; hyperkalemia is likely to occur in he-
sulting impaired muscle blood flow decreases oxygen delivery and 48,58
parinized individuals who have even mild renal insufficiency. A
contributes to the rhabdomyolysis that occurs with whole-body
potassium depletion. 45–47 massive digitalis overdose causes hyperkalemia by allowing intracellu-
lar potassium to leak into the extracellular fluid and impairing its
movement back into cells. 52
Hyperkalemia
Another cardiovascular-related source of hyperkalemia is mas-
Hyperkalemia, an increased plasma potassium concentration, re-
sive blood transfusion. While blood is stored, potassium ions leak
sults from increased potassium intake, shift of potassium ions
from the erythrocytes into the plasma. The longer the storage time,
from the cells to the extracellular fluid, decreased potassium ex- 59,60
1
cretion, or any combination of these factors. Examples of specific the greater the potassium load contained in a unit of blood. A
classic study indicates that if the blood has been in storage for more
etiologic factors in each of these categories are listed in Table 7-8.
than 3 days, rewarming the blood before administration causes
Hyperkalemia may occur during hemorrhagic or hypovolemic 61
only minimal return of potassium to the cells. Individuals re-
shock and during cardiopulmonary resuscitation.
ceiving more than 7 or 8 units of stored blood within a few hours
Several medications commonly administered to individuals
with cardiac disease may cause hyperkalemia. 48 Angiotensin- are considered at high risk for severe hyperkalemia; however, fatal
hyperkalemia has occurred with transfusion of fewer units, espe-
converting enzyme inhibitors such as captopril and enalapril, an- 60,62
cially when they are administered rapidly.
giotensin II receptor blockers such as losartan, selective aldosterone
Hyperkalemia may be manifested clinically by intestinal cramp-
blockers such as eplerenone, and direct renin inhibitors such as
ing and diarrhea, skeletal muscle weakness, flaccid paralysis, cardiac
aliskiren decrease the release of aldosterone. Aldosterone normally fa-
arrhythmias, and cardiac arrest. The cardiac effects of hyperkalemia
cilitates renal excretion of potassium. When these drugs decrease the
availability of aldosterone, hyperkalemia may occur. 49–52 The potas- are potentially fatal; they are discussed in the next section.
sium-sparing diuretics spironolactone, triamterene, and amiloride
Cardiac Effects of Hyperkalemia. Hyperkalemia alters
may cause hyperkalemia, especially if given with potassium supple-
myocardial cell function in several ways. When the plasma potas-
sium concentration increases, the extracellular/intracellular potas-
sium concentration ratio increases. Consequently, the resting
membrane potential of cardiac cells becomes partially depolarized
Table 7-8 ■ CAUSES OF HYPERKALEMIA 48
(hypopolarized). Initially, the partial depolarization of resting
Category Clinical Examples cardiac cells increases their excitability because the resting poten-
tial is close to threshold potential (see Chapter 16). As the extra-
Increased potassium intake Excessive IV potassium
Insufficiently mixed KCl in flexible cellular potassium concentration increases, however, the cardiac
plastic IV bag cells depolarize to the extent that they cannot repolarize. Cells in
Massive transfusion of blood stored longer this state are nonexcitable; no further contractile activity occurs.

than 3 days (K leaves red blood cells) The ability of hyperkalemia to cause asystolic cardiac arrest is ex-
Large doses of IV potassium penicillin ploited by using potassium as a cardioplegic agent during cardiac

G (contains 1.6 mEq K /million units) 63
Large oral intake only if decreased renal surgery.
excretion Other effects of hyperkalemia include decreased duration of
Potassium shift out of cells Acidosis due to mineral acids (not organic the action potential at all heart rates and increased rate of repolar-
acids like ketoacids) ization, the latter due to increased permeability of the cardiac cell
Insulin deficiency 32
Massive cell death (crushing injuries, membrane to potassium efflux. Hyperkalemia lengthens the ef-
burns, cytotoxic drugs) fective refractory period of atrial muscle and slows diastolic depo-
Large digitalis overdose larization of pacemaker cells, two antiarrhythmic effects. Cardiac
Familial periodic paralysis cells vary in their sensitivity to the effects of hyperkalemia. Atrial
Decreased potassium excretion Oliguria cells are more sensitive than ventricular cells; the conduction sys-
Extracellular fluid volume depletion 48
Oliguric renal failure tem is the last to be affected.
Decreased aldosterone from any cause As the plasma potassium increases, the rate of rise of the action
(Addison disease, chronic heparin potential decreases. Slow upstroke velocity decreases cell-to-cell
administration, lead poisoning, ACE in- conduction velocity (see Chapter 16). Hyperkalemia decreases
hibitors, angiotensin II receptor antago-
nists, selective aldosterone blockers, conduction velocity at all levels of the conduction system: atrial,
48,52
direct renin inhibitors) atrioventricular nodal, and intraventricular. In severe hyper-
Potassium-sparing diuretics kalemia, intraventricular conduction may be completely inhib-
ited. Bundle-branch block or, less frequently, complete heart
IV, intravenous; ACE, angiotensin-converting enzyme. block may occur. 42,64