Invasive mechanical ventilation is indicated when arterial oxygen
saturation cannot be maintained above 90% despite 100% oxygen per facemask.
Once the patient is intubated, sedation should be provided to alleviate anxiety and
discomfort while cautiously monitoring hemodynamic effects.
The arterial pressure must be increased to provide adequate coronary and systemic
perfusion to meet oxygen requirements. Some areas of ischemia in the infarct zone
may be depressed but viable, provided myocardial oxygen supply exceeds demand. If
the myocardial oxygen demands are not met, however, myocardial tissue necrosis
will expand into the area of ischemia. This results in further hemodynamic
impairment and initiates a vicious cycle that can lead to intractable pump failure and
irreversible shock. To be effective, treatment of cardiogenic shock should favorably
influence the balance between oxygen supply and demand in the ischemic zone.
Optimizing preload to improve CO and systemic perfusion is crucial, especially in
patients with RV infarction. In patients with severe LV impairment, increasing
intravascular volume can worsen pulmonary congestion. J.S. currently has signs of
pulmonary congestion and RV infarction is not evident; thus, a fluid challenge must
be administered cautiously or withheld until hemodynamic monitoring can be
Inotropic agents or vasopressors should be used to increase systemic BP and
reestablish coronary perfusion in patients with cardiogenic shock and hypotension.
However, vasoactive agents have risk because they can exacerbate ventricular
in ischemic myocardium. Therefore, the minimal dose
that will provide adequate perfusion pressure should be used. Achieving a MAP of
65 to 70 mm Hg is the immediate goal of therapy, but it should be adjusted based on
adequate perfusion (e.g., warm extremities, adequate urine output, improved mental
51 Elevation of the MAP to more than 80 mm Hg is unnecessary because
coronary blood flow is not significantly changed at this level, but energy expenditure
Correction of metabolic acidosis is best accomplished by treating the underlying
cause. Improving tissue perfusion by optimizing oxygen content and increasing CO
can eventually restore aerobic metabolism and eliminate lactic acid production. The
use of sodium bicarbonate to correct lactic acidosis in cardiogenic shock and other
critically ill patients is controversial. Sodium bicarbonate can have numerous
adverse effects, such as hypernatremia, paradoxical intracellular acidosis, and
hypercapnia; conclusive data on its efficacy are lacking. Bicarbonate therapy is
recommended only, if at all, when severe acidemia (pH below 7.2 or HCO3
Inotropic agents and vasoconstrictors can increase myocardial O2 and potentially
extend the area of necrosis in patients with infarct-induced cardiogenic shock.
Careful selection and titration of agents that will best preserve myocardium while
sustaining systemic arterial pressure and tissue perfusion is essential. Although
correction of volume deficits and early pharmacologic support may prevent the
extension of myocardial damage, it must be emphasized that exclusive use of these
measures does not improve survival. Therefore, drug therapy must be considered
only an interim maneuver to preserve myocardial and systemic integrity while further
therapeutic interventions and definitive therapy are being considered.
Cardiogenic shock after AMI occurs in only a small percentage of patients, but it
carries a high mortality rate. Reperfusion of the occluded artery is of paramount
importance in these patients. Two options are available for restoring patency of the
artery: thrombolytic therapy and revascularization (PCI or coronary artery bypass
grafting [CABG]) (see Chapter 13, Acute Coronary Syndrome).
Thrombolytic therapy in AMI may reduce the incidence of subsequent cardiogenic
shock, but its value may be limited in patients who have already experienced shock.
The effectiveness of thrombolysis is reduced in this setting, possibly because of
reduced delivery of the agent to the coronary artery thrombus as a result of
54 The use of an intra-aortic balloon pump (IABP) to augment coronary
artery blood flow may improve the efficacy of thrombolytic agents but has not been
Early revascularization with PCI or CABG is preferred in patients with
cardiogenic shock complicating AMI, irrespective of time delay.
trial, emergency revascularization, compared to immediate medical stabilization
(fibrinolysis and IABP), resulted in significantly lower mortality at 1 and 6 years in
patients with ST-elevation MI and cardiogenic shock.
positively correlated with time to revascularization from 0 to 8 hours, confirming that
revascularization should be performed as soon as possible. However, a survival
benefit for revascularization remains even as long as 54 hours after MI and 18 hours
53 Operator skill is also a consideration, and larger centers with
greater experience may have better outcomes than smaller centers. In settings in
which interventional cardiac procedures such as percutaneous transluminal coronary
angioplasty or stenting are not readily available, insertion of an IABP and
thrombolytic agents should not be delayed if indicated.
ASSESSMENT BY HEMODYNAMIC PROFILE
CASE 17-3, QUESTION 2: Cardiac catheterization reveals an acute occlusion of the proximal left
been stable at 50 mL/hour. His current hemodynamic profile is as follows:
PA pressure (S/D), 41/24 mm Hg
What is your assessment of J.S.’s clinicalstatus and hemodynamics?
Clinically, J.S. has signs of hypoperfusion manifested by low urine output; mottled,
cool skin; and metabolic acidosis. His decreased SvO2 shows that he has impaired
perfusion owing to his low ḊO2
. Evaluation of his hemodynamics will help
determine a potential cause for his hypoperfusion and assist with the decision about
appropriate therapeutic interventions to prevent his condition from worsening to
serious organ dysfunction and death.
Possible causes of shock in cardiac surgery patients include blood loss, excessive
vasodilation from medications or cardiopulmonary bypass-induced inflammation,
cardiac ischemia-reperfusion injury, valvular dysfunction, tamponade, heart failure,
or perioperative MI. Another concern is “stunning” of the myocardium caused by
surgical trauma, which can take hours to days to resolve.
Hypovolemia should always be evaluated first when assessing hemodynamic
profiles. Using vasopressor or inotropic agents in the setting of hypovolemia is rarely
effective and could cause further hypotension or serious adverse effects (e.g., cardiac
arrhythmias). Also, correction of hypovolemia is relatively straightforward and can
be accomplished rapidly. Most patients require no more than 2 to 3 L of crystalloid
after cardiac surgery, especially once rewarming is complete. J.S.’s tachycardia, low
urine output, low BP, and low CO could indicate volume depletion. However, his
Hct is adequate, and he has an elevated CVP, PAP, and PCWP, suggesting that he is
Excessive vasodilation is also unlikely in J.S., given that his calculated SVR
(afterload) is above normal range. Cardiac tamponade should always be considered
after cardiac surgery, and it is usually manifested by very high CVP, PCWP, and PA
pressures, with significant decreases in CO and BP. Diminished or muffled heart
sounds and an inappropriately fluctuating BP with respirations (pulsus paradoxus)
will usually accompany an equalization of diastolic pressures during cardiac
tamponade. J.S.’s CVP and PCWP are not as high as would be expected in
pericardial tamponade, and his chest tube output has remained consistent, suggesting
that blood is not accumulating.
Based on this hemodynamic profile, it appears that J.S. is in shock because of
acute HF, most likely from postoperative myocardial dysfunction, although he should
also be evaluated for myocardial ischemia or infarction and to rule out early cardiac
tamponade. This evaluation should not delay the initiation of therapy.
Patients with cardiogenic shock from an acute event (such as an MI) are usually
more critical than patients who have an acute exacerbation of chronic HF. Patients
with HF have compensated with time for the increases in preload and reduced CO,
but patients such as J.S. have not had time to develop compensatory mechanisms. His
severely depressed CO should be treated immediately to prevent further
CASE 17-3, QUESTION 3: The chest radiograph shows moderate pulmonary edema, and rales were heard
on auscultation. His ABG measurements on mechanical ventilation with 50% inspired oxygen are pH 7.3,
− 18 mEq/L. Tamponade is not evident on the radiograph. The
How would these choices affect J.S.’s ventricular function?
Fluid Challenge (Increase Preload)
Augmentation of preload with a fluid challenge to improve CO is the first option.
However, J.S. has signs of pulmonary edema on chest radiograph, PCWP is 24 mm
is 90 mm Hg on 50% inspired oxygen. Increasing the PCWP above 18
mm Hg usually does not result in further benefit.
57,58 Therefore, giving volume might
increase the pulmonary vascular hydrostatic pressure and worsen his pulmonary
edema. If a fluid challenge is attempted to enhance preload, 250 to 500 mL of NS
solution should be given over 20 to 30 minutes while continuously monitoring the
hemodynamic profile and for volume overload. If the PCWP rises but the CO does
not improve, fluid challenges should be discontinued. Elevating the preload without
appreciably improving CO increases LV wall tension, which is a major determinant
; consequently, myocardial ischemia could develop. Although J.S.
has signs of pulmonary edema, diuretics to reduce his volume overload can be
detrimental to his CO and BP and should not be used until J.S.’s hemodynamics and
signs of hypoperfusion have improved.
Vasodilators (Preload and Afterload Reduction)
A peripheral venodilator will decrease pulmonary venous congestion by reducing
preload (CVP and PCWP) and pulmonary vascular hydrostatic pressure. With
myocardial ischemia, a reduction of the LV filling pressure may improve
subendocardial blood flow, reduce the myocardial wall tension, and reduce the LV
radius. The resultant decrease in myocardial O2 will help prevent further
depression of cardiac function.
In patients with LV failure, arterial resistance is also elevated because of a reflex
increase in sympathetic tone in response to a fall in systemic arterial pressure. In LV
failure, CO is inversely related to resistance to outflow from the LV. Lowering an
elevated SVR (afterload) will decrease resistance to ventricular ejection and shift
the ventricular function curve up and to the left, depending on whether an arterial,
venous, or mixed vasodilator is used, thereby improving cardiac performance at a
lower filling pressure (Fig. 17-4).
J.S. appears to have LV failure with elevations in PCWP and SVR. Vasodilator
therapy in this setting will likely improve his CO and, therefore, increase the ḊO2
the tissues and prevent organ dysfunction. The major risk of vasodilator therapy in
J.S., however, is further reduction of an already low MAP. Although the reduction in
BP may be offset by an increase in CO, a significant drop in arterial BP could occur,
which could decrease perfusion to vital organ systems and exacerbate myocardial
ischemia by reducing coronary perfusion pressure. Vasodilator therapy should be
reserved for situations of LV failure with elevations in PCWP and SVR and a SBP
A rapid-acting inotropic agent also can be used to increase myocardial contractility
if the CO remains low or inadequate with signs of tissue hypoperfusion after
optimization of the volume status.
1 This intervention shifts the ventricular function
curve upward and slightly to the left (Fig. 17-4). The disadvantage of this
intervention is that improved CO is accompanied by increased myocardial oxygen
demand. Depending on the agent selected, three of the determinants of myocardial
O2 could be elevated: HR, contractility, and ventricular wall tension. Therefore,
inotropic support is directed at establishing or maintaining a reasonable arterial
pressure and ensuring adequate tissue perfusion by improving the CO.
Figure 17-4 Ventricular function curve for J.S. PCWP, pulmonary capillary wedge pressure.
In summary, the most appropriate therapeutic intervention for J.S. at this time
would be inotropic support. The PCWP is elevated, suggesting that the preload has
been maximized; therefore, fluid may worsen J.S.’s pulmonary edema. Although
J.S.’s SVR is elevated (1,570 dyne·s·cm−5
), his BP is low; therefore, initial use of a
peripheral vasodilator could jeopardize perfusion. Thus, an acceptable initial
therapeutic intervention to improve CO and tissue perfusion is inotropic support.
After a reasonable BP has been established, addition of a peripheral vasodilator
could be considered to further enhance CO if needed, and diuretics added to reduce
CASE 17-3, QUESTION 4: Which inotropic agent is the best choice for J.S.?
Dopamine, a precursor of norepinephrine, has inotropic, chronotropic, and
vasoactive properties, all of which are dose dependent (Table 17-7). The distinct
ranges noted for dopamine activity are generalizations; responses noted in clinical
practice will be patient specific. At less than 5 mcg/kg/minute, dopamine stimulates
dopaminergic receptors primarily in the splanchnic, renal, and coronary vascular
beds. The effect on dopaminergic receptors is not blocked by β-blockers, but is
antagonized by dopaminergic-blocking agents such as the butyrophenones and
phenothiazines. Depending on the clinical state of the patient, low dosages of
dopamine may slightly increase myocardial contractility, but it usually will not alter
At 5 to 10 mcg/kg/minute, the improved cardiac performance produced by
dopamine is through direct stimulation of β1
-adrenergic receptors and indirectly
through release of norepinephrine from nerve terminals. Increased β1
receptor stimulation increases SV (inotropic effect), HR (chronotropic effect), and
consequently CO. These cardiac effects can be blocked by β-blockers. As infusion
rates increase above 5 mcg/kg/minute, the α-adrenergic receptors are activated. At
this dosage, the vasoactive effects on peripheral blood vessels are unpredictable and
depend on the net effect of β1
-adrenergic stimulation, α-adrenergic stimulation, and
reflex mechanisms. MAP and PCWP usually will rise. The increased HR, along with
the elevated PCWP in J.S., could adversely affect the myocardial oxygen supply to
demand ratio. However, it is hoped the increase in coronary blood flow (caused by
the rise in arterial pressure) and the decrease in LV chamber size (associated with
the increase in contractility) would tend to offset the increase in myocardial oxygen
Inotropic Agents and Vasopressors
Receptor Sensitivity Pharmacologic Effect
>10 mcg/kg/minute ++ ++++ +++ ++ + ++++
c <0.1 mcg/kg/minute + ++++ +++ + + ++++
>2 mcg/kg/minute ++++ ++ + 0 ++++ ++
aDobutamine, milrinone, and epinephrine have more inotropic effect than dopamine.
Epinephrine may vasodilate at low dosages, vasoconstrict at high dosages.
eCardiac output unchanged or may decline because of vagal reflex responses that slow the heart.
fHighly variable, titrate to desired MAP
receptors to cause vasoconstriction in the periphery.
peripheral vascular vasodilation.
At doses greater than 10 mcg/kg/minute, dopamine primarily stimulates peripheral
α-adrenergic receptors. SVR increases, splanchnic and renal blood flow decreases,
and LV filling pressure is raised. Cardiac irritability is a potential complication, and
is increased. The increase in SVR limits CO; thus,
infusion rates should be limited to less than 15 mcg/kg/minute in patients with
In a recent trial of 1,679 patients with shock, who were randomized to dopamine
or norepinephrine for blood pressure support, there was no significant difference in
the primary outcome of 28-day mortality.
60 However, patients receiving dopamine
had more arrhythmic events and a prespecified subgroup analysis showed an
increased mortality rate in 280 patients with cardiogenic shock. Although these
findings may have been because of chance and randomization was not stratified, these
findings warrant consideration before selecting dopamine for J.S. and highlight the
need for more studies comparing catecholamines in cardiogenic shock.
Dobutamine, a synthetic catecholamine, is a potent positive inotropic agent with
dose-dependent but predominant direct β1
adrenergic effects. With greater β2
dobutamine reduces systemic and pulmonary vascular resistance. The reduction in
SVR may be caused by a reflex decrease in vasoconstriction secondary to enhanced
CO. Unlike dopamine, dobutamine does not release endogenous norepinephrine or
stimulate renal dopaminergic receptors.
Studies assessing dobutamine in cardiac failure demonstrate consistent increases
in CO and SV, with reductions in PCWP and SVR. The reduction in filling pressures,
as indicated by a lowered PCWP, results in a decrease in LV wall tension and
. Consequently, coronary perfusion pressure and myocardial oxygen
Compared with dopamine, dobutamine has equal or greater inotropic action.
Dobutamine lowers PCWP and SVR with increasing doses, whereas dopamine may
increase PCWP and SVR with increasing doses.
62 The effect on HR is variable;
however, evidence suggests that dobutamine is less chronotropic than dopamine at
lower infusion rates. In the clinical setting, dobutamine may be preferred in patients
with depressed CO, elevated PCWP, and increased SVR with mild hypotension
(SBP above 70 mm Hg) and no signs or symptoms of shock. The increase in CO may
not be sufficient to raise the BP in a patient who initially is moderately to severely
hypotensive (SBP below 70 mm Hg) or with signs or symptoms of shock. Dopamine
may be recommended in patients with mild hypotension and symptoms of shock,
norepinephrine is reserved for patients with a SBP below 70 mm Hg.
recent concerns of increased mortality with dopamine monotherapy in patients with
cardiogenic shock, the combination of dopamine or norepinephrine with dobutamine
may be preferred in patients with depressed CO, normal or moderately elevated
PCWP, and moderate or severe hypotension.
Similar to dopamine and dobutamine, epinephrine has dose-dependent hemodynamic
effects (Table 17-7). At lower infusion ranges (less than 0.1 mcg/kg/minute)
-adrenergic receptors, causing increases in HR and
contractility. As the dose increases, more α1
-receptor stimulation occurs, resulting in
vasoconstriction and corresponding increases in SVR.
The favorable hemodynamic effects (increased CO and BP) make low-dose
epinephrine an attractive option for J.S.; however, epinephrine can induce
hyperglycemia through gluconeogenesis and has been shown to increase lactate
levels compared with other vasopressors and inotropic agents.
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