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C HAP TE R 24 / Heart Failure and Cardiogenic Shock 585

tion (cool and dry) as seen in patients with hypovolemia. Subset with patients with severe hypoxemia, hypercarbia, or metabolic
II describes the patient with pulmonary edema with an elevated acidosis, then endotracheal intubation may be required with me-
PAWP but without peripheral hypoperfusion (warm and wet), chanical ventilation. A PA catheter may be placed. Volume ex-
which may be seen in acute HF or decompensated chronic HF. pansion may be needed to restore adequate circulation to main-
Subset IV describes the patient with pulmonary edema with hy- tain a PAWP of 14 to 16 mm Hg. Vasopressor support should be
poperfusion (cold and wet), as seen in cardiogenic shock. 201 used only after preload is adequate to restore the blood pressure.
Assessment of tissue metabolism, which is determined by The choice of a particular vasopressor/inotropic agent depends on
mixed venous oxygen saturation, conventionally required sending the clinical circumstance (Table 24-14).
a PA blood sample to the laboratory for interpretation. Some PA Acute manifestations of HF can be either in the setting of a
catheters are designed with a fiberoptic photometric lumen, al- new onset or in patients with established chronic HF. It is critical
lowing for continuous monitoring of mixed venous oxygen satu- to establish the diagnosis and determine the hemodynamic status:
ration. Although PA catheters have been widely used for almost pulmonary congestion without peripheral hypoperfusion versus
40 years, there has been controversy because there are data to sug- shock/hypoperfusion (Fig. 24-19). The three major goals of treat-
gest increased mortality in critically ill patient who had PA ment of acute HF, acute decompensated chronic HF, and cardio-
lines. 202 Current consensus is that PA catheters are useful in set- genic shock are (1) to increase the oxygen supply to the my-
tings MI and cardiogenic shock. 1 ocardium; (2) to maximize the cardiac output; and (3) to decrease
the workload of the left ventricle.
Prognosis
Goal 1: Increase Oxygen Supply
The stages of shock depict a series of pathophysiologic changes to the Myocardium
that occur if medical and nursing interventions are delayed or in- Increased inspired oxygen concentrations, including the institu-
appropriate. The stages do not progress at the same speed in all tion of mechanical ventilation with positive end-expiratory pres-
patients. The length of time tissues are hypoxic is a major factor sure, may be required to maintain arterial blood gases within nor-
in determining the occurrence of complications. The initial and mal limits. Narcotic analgesics are used to control the patient’s
intermediate stages of shock are reversible with aggressive man- pain and aid in reducing myocardial oxygen demands.
agement. The irreversible stage is caused by cellular necrosis and Aggressive reperfusion of the coronary arteries can be under-
multiple organ failure. Thus, the chance of recovery in the irre- taken by invasive and noninvasive approaches, including percuta-
versible stage without permanent injury is low. In cardiogenic neous transluminal coronary angioplasty, atherectomy or stent
2
shock, patients with a CI less than 1.81 L/min per m have a 70% placement, use of adjunctive antiplatelet therapy, thrombolytic
mortality rate. 200 Patients with 2 less than 55% also have a therapy, and coronary artery bypass grafting, which were all asso-
high mortality rate. 190 ciated with lower in-hospital mortality rates than treatment with
standard medical therapy. 195 Studies suggest that immediate
Approach to Treatment revascularization with percutaneous coronary intervention,
which may include angioplasty, stent placement, and atherec-
The main goal of treatment of the metabolic defects produced by tomy, along with adjunctive antiplatelet therapy, improves out-
shock is the restoration of adequate tissue perfusion. 197 comes in patients with cardiogenic shock. 203 Improvement is
Initial general management for patients is placement of large- seen in wall motion in the infarct territory, with increased perfu-
bore venous catheters, and continuous monitoring of blood pres- sion of the infarct zone augmenting contraction of remote my-
sure, pulse oximetry, and ECG. If respiratory failure is imminent ocardium, possibly because of recruitment of collateral blood

Table 24-14 ■ VASOPRESSORS AND INOTROPES USED IN CARDIOGENIC SHOCK
Feature Dopamine Dobutamine Norepinephrine Epinephrine Phenylephrine Milrinone
Dosage (mcg/kg/min) 1–4 4–20 2.5–20 0.05–1 0.05–2 0.5–5 0.375–0.750
Receptor

0

0 0
1
0 0

0

0 0
2
Dopaminergic

0 0 0 0 0
Chronotropic (HR)

0
Inotropic (stroke

/

0
volume/cardiac output)
SVR (afterload) T cc TT cccc TTcc cccc TTT
Filling pressure (preload) T 4cc TT 4cc 4 4 TT
Comments Improves renal First-line agent Pure vasoconstrictor Increases MVO 2 , Purest Inotrope of choice
flow in low to improve CO, compared to supports BP vasoconstrictor in pulmonary
dose; first-line but may be dopamine hypertension
y
y
drug to arrhythmogenic
restore BP