Page 610 - Cardiac Nursing

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586 PA R T I V / Pathophysiology and Management of Heart Disease
Establish diagnosis
Determine hemodynamic status
■ Figure 24-19 Algorithm for establishing the diag-
Congestion Shock/congestion nosis of acute heart failure/acute decompensation of
SBP≥ 80-90mm Hg, dyspnea SBP≤ 80mm Hg, cool extremities chronic heart failure with pulmonary congestion versus
Orthopnea, edema Change in renal output cardiogenic shock with hypoperfusion and pulmonary
"Warm and wet" "Cold and wet" congestion. General management principles for each
diagnosis are listed. SBP, systolic blood pressure; IV, in-
travenous, IABP, intra-aortic balloon pump. (Adapted
Management: Management: from Lyengar, S., Hass, G., & Young, J. [2006]. Acute
heart failure. In E. J. Topol [3rd ed.], Textbook of car-
IV loop diuretics Single agent or combination of
IV nesiritide vasopressors/inotropes diovascular medicine [pp. 1845–1898]. Philadelphia:
Other preload/afterload reducers Supplemental oxygen Lippincott Williams & Wilkins.)
Supplemental oxygen Hemodynamic monitoring in CCU/ICU
Telemetry or observation unit Mechanical support
flow. Reperfusion therapy with thrombolytic agents has de- between 14 and 18 mm Hg. However, fluid loading must be
creased the occurrence of cardiogenic shock in patients with per- abandoned when the increase in filling pressure occurs without
sistent ST-segment elevation MI, but thrombolytic therapy for increase in cardiac output.
patients in whom shock has already developed is disappointing Unlike patients with acute HF, patients with chronic HF are
and may be attributed to low perfusion pressure. 195 For hospitals usually using chronic pharmacologic therapy (i.e., diuretic, ACE-
without revascularization capability, early thrombolytic therapy I, -blocker, and digitalis). Treatment of acute episodes in these
along with intra-aortic balloon pumping followed by immediate two scenarios are similar, with the exception of the higher inci-
transfer for percutaneous coronary intervention or coronary ar- dence of reparable lesions in acute HF (e.g., acute occlusion of
tery bypass grafting may be appropriate. 204 There are data to major coronary artery, ruptured chordae tendineae). 205 The For-
support favorable outcomes for patients undergoing emergent rester subsets (see Fig. 6-18) can be used as guidelines for these pa-
coronary artery bypass grafting. 192 tients in pulmonary edema (warm and wet). 201 In subset II, the
goal of therapy is to reduce the PAWP below a level that causes
Goal 2: Maximize Cardiac Output pulmonary congestion but above a level that causes a deleterious
Because the cardiac output is already compromised, arrhythmias, reduction in cardiac output by the Starling mechanism. There are
which occur as a result of ischemia, acid–base alterations, or MI, several options because diuretics, peripheral vasodilators, and in-
can cause a further decline in cardiac output. Electrolyte abnor- otropic agents all reduce PAWP (Tables 24-14 and 24-15). The
malities should be corrected, because hypokalemia and hypo- management strategy for the patient in acute cardiogenic pul-
magnesemia predispose to ventricular arrhythmias. Antiarrhyth- monary edema is outlined in Display 24-2.
mic agents, pacing, or cardioversion may be used to maintain a An intravenous diuretic such as furosemide is administered
stable heart rhythm. Volume loading is undertaken with caution when symptoms of pulmonary edema occur. Nesiritide (BNP)
and in the presence of adequate hemodynamic monitoring. Op- represents a recent drug class for acute decompensated HF. Nesir-
timal preload (LV end-diastolic pressure or PAWP) ranges itide affords a unique combination of hemodynamic effects as a
Table 24-15 ■ PRELOAD- AND AFTERLOAD-REDUCING AGENTS FOR ACUTE/DECOMPENSATED HEART FAILURE
Drug Dosing Advantages Disadvantages
Nitroglycerin Sublingual: 0.4 mg (or 1 to 2 sprays) at
Effect on coronary vasculature Hypotension; drug tolerance; inadequate afterload
5-minute intervals intravenous: 0.4 g/ and in myocardial ischemia reduction in catastrophic disorders (e.g., acute valve
kg/min initially; increase as needed infarction insufficiency)
Nitroprusside Intravenous: 0.1 g/kg/min initially; Powerful afterload reducer Hypotension; infusion needs to be watched closely;
increase as needed less favorable effects on coronary vasculature and
myocardial ischemia; thiocyanate or cyanide toxicity
during high-dose or prolonged infusion;
particularly in renal failure
Nesiritide Intravenous: bolus of 2 g/kg, followed by Useful afterload reducer and Hypotension; has been linked to progressive renal
0.01 g/kg/min infusion; may rebolus diuretic; use in acute dysfunction; not to be used in patients in
1 g/kg 1, and increase infusion up to decompensated heart failure cardiogenic shock, moderate renal dysfunction or
maximum, which is 0.03 g/kg/min systolic BP 90 mm Hg