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SHOCK & RESUSCITATION

237

dopamine because the latter depletes myocardial norepineph-

rine stores. Dosage typically ranges from 5–15 μg/kg per

minute. Increased urine output also may be achieved after

dobutamine administration because of increased renal perfu-

sion from elevated cardiac output. Infusion is begun at a rate

of 2–5 μg/kg per minute and titrated to the desired effect.

Maximal benefit is usually achieved at levels between 10 and

15 μg/kg per minute.

3. Alpha-adrenergic agents—Despite adequate volume

resuscitation and improved cardiac output, blood pressure

may remain depressed. Phenylephrine and norepinephrine

are two agents commonly used to increase systemic vascular

resistance.

Norepinephrine is the biosynthetic precursor of epineph-

rine, and as such posses both α- and β-adrenergic activity. In

low doses, its major effect is β-adrenergic. It increases cardiac

contractility, conduction velocity, and heart rate. At higher

doses, both α- and β-adrenergic effects occur, which include

peripheral vasoconstriction, increased cardiac contractility, car-

diac work, and stroke volume. Norepinephrine causes splanch-

nic vasoconstriction, which may lead to end-organ ischemia.

The drug is cleared rapidly from the plasma with a half-life of

approximately 2 minutes. Initial infusion rates are 0.5–1

μg/min. The usual maximum dose is 1 μg/kg per minute.

4. Vasopressin—Vasopressin (antidiuretic hormone) is nor-

mally released by the hypothalamus and produces vasocon-

striction of vascular smooth muscle in addition to its

antidiuretic effect on the renal collecting system. At low plasma

concentrations it causes vasodilation of the coronary, cerebral,

and pulmonary vessels. Vasopressin levels increase in early sep-

tic shock and later fall as sepsis worsens. When given in doses

of 0.01–0.04 units/min, vasopressin infusion increases serum

vasopressin levels and decreases the need for other vasopres-

sors. At this dose, urinary output may increase, and pulmonary

vascular resistance may decrease. Doses higher than 0.04

units/min can cause undesirable vasoconstrictive effects.

5. Vasodilators—Because decreased vascular resistance is

the primary cause of hypotension in septic shock, further

pharmacologic vasodilation is contraindicated. Occasionally,

severe myocardial depression is accompanied by an increase

in systemic vascular resistance. This preterminal event puts

further strain on the left ventricle and may cause complete

hemodynamic collapse. Judicious use of vasodilators such as

nitroprusside may be tried. Nitroglycerin is probably an infe-

rior choice because it also reduces preload.

E. Antimicrobial Agents—Identification of the source of

sepsis is imperative. If the offending tissue bed is not drained

or if bacteremia is not treated, outcome will be adversely

affected. Evaluation of the patient’s history is essential to deter-

mine likely sources. Once the probable origin has been identi-

fied, appropriate antimicrobial therapy can be instituted to

provide coverage for organisms commonly encountered. The

details of diagnosis and therapy of infections are presented in

Chapters 15 and 16. When a likely source cannot be identified,

empirical broad-spectrum therapy should be instituted with

drugs known to be effective against gram-positive, gram-

negative, and anaerobic organisms. In surgical patients who

have had abdominal procedures, enteric gram-negative and

anaerobic organisms are of particular concern. Attention must

be given to dosing in these patients because alterations in renal

function may affect degradation and because an expanded

plasma volume affects the volume of distribution and there-

fore the size of the loading dose that must be given.

F. Glycemic Control—Hyperglycemia is defined as a blood

glucose concentration of greater than 110 mg/dL and is com-

mon in critically ill patients. Multiple factors contribute to

hypergylcemia, including increased levels of stress hor-

mones, peripheral insulin resistance, drugs, and exogenous

dextrose infusion. Hyperglycemia has a number of detrimen-

tal effects, including decreased leukocyte adhesion, impaired

neutrophil chemotaxis, and phagocytosis. Hypergylcemia

also may be prothrombotic.

Rigid control of hyperglycemia has been shown to

improve outcome, likely by reducing the incidence of sepsis-

induced multiple-organ failure. Additionally, tight control

has been shown to reduce the length of stay in the ICU, atten-

uate the inflammatory response, decrease antibiotic use,

reduce the incidence and duration of critical-illness polyneu-

ropathy, and reduce the number of ventilator days.

Glucose control may be provided with either a glucose

concentration–dependent dose (“sliding scale”) or a con-

stant infusion for higher serum glucose levels. Typically, glu-

cose levels should remain below 130 mg/dL.

G. Corticosteroids—While older studies demonstrated no

benefit to the use of supraphysiologic doses of corticos-

teroids, more recent work has found that lower physiologic

doses for longer periods of time may be beneficial. Patients

should undergo a Cortrosyn stimulation test. After obtaining

blood for a baseline concentration of serum cortisol, 250 μg

Cortrosyn is given intravenously, and blood for a repeat

serum cortisol assay is collected 30–60 minutes later. If there

is concern that the patients is hypoadrenal, 4 mg dexametha-

sone can be given prior because it does not interfere with the

test. If the increase after Cortrosyn is less than 9 μg/dL, there

is insufficient adrenal reserve, and 50 mg hydrocortisone

should be given every 6 hours for 7 days. This should be sup-

plemented with fludrocortisone 50 μg orally every day. It is

likely that all patients should be started on replacement cor-

ticosteroid until the results of the stimulation study are

known, at which time supplementation can be withdrawn

from those who responded to the stimulation test.

H. Drotrecogin Alfa—Drotrecogin alfa is a glycoprotein ana-

logue of protein C that is activated by thrombin. Activated

protein C inhibits coagulation, increases fibrin breakdown,

and possibly inhibits the synthesis of TNF. A large clinical

study of drotrecogin alfa found a reduction in mortality from

30.8% in patients treated with placebo to 24.7% in those

treated with the drug. The most important adverse effect of

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238

the drug is bleeding, which occurred in 3.5% of those treated

with the drug compared with 2% treated with placebo.

Although the incidence of bleeding did not reach statistical

significance, the drug is contraindicated in patients with active

or recent bleeding or a high risk of bleeding, an epidural

catheter, or intracranial hemorrhage. It should be used cau-

tiously in those at risk for bleeding. Drotrecogin alfa is admin-

istered intravenously at a continuous dose of 24 μg/kg per

hour for 96 hours. No alteration in the dose is required for

those with renal or hepatic compromise. The drug’s cost is

approximately $8000 for a 4-day regimen in a 70-kg patient.

I. Transfusion—The traditional transfusion threshold of 10

mg/dL has been challenged by the finding that patients are

not adversely affected by withholding transfusion until

hemoglobin concentration drops to between 7 and 9 g/dL.

Further, there may be some advantage to lower hemoglobin

concentrations in patients older than age 55. Such data come

from broad groups of patients, and specific conclusions can-

not be drawn. It is likely, however, that more restrictive

thresholds are not harmful and actually may reduce mortal-

ity. The availability of recombinant human erythropoietin

may be a useful adjunct to reducing the need for transfusion

in critically ill patients.

J. Other Modalities—Septic patients require multimodality

support, including gastrointestinal and renal. To this end,

proper prophylaxis against gastric stress ulceration should be

provided with either H

-receptor blockade or proton pump

inhibitors. Additionally, renal function must be monitored

closely, and appropriate support with either hemofiltration

and/or dialysis should be provided. Adequate prophylaxis

against deep venous thrombosis includes either unfraction-

ated or low-molecular-weight heparin. The dose of some

low-molecular-weight heparins needs to be adjusted or with-

held in patients with renal failure. Lower extremity compres-

sion stockings are valuable adjuncts.

Current Controversies and Unresolved Issues

A. Fluid Resuscitation—The choice of fluid for the initial

and continued resuscitation of septic patients is widely

debated. Proponents of balanced salt solutions claim that pul-

monary dysfunction is not worsened by judicious administra-

tion guided by endpoints such as ventricular filling pressure

and cardiac output. Colloids increase the circulating plasma

volume more effectively than do crystalloids, but they are

expensive. When pulmonary microvascular permeability is

increased, colloids actually may worsen respiratory function

by increasing the osmotic gradient favoring translocation of

fluid into the alveolar and pulmonary interstitial spaces.

Activated protein C (Xigris) for severe sepsis. Med Lett Drugs Ther

2002;44:17–18. [PMID: 11856952]

Bernard GR et al: Efficacy and safety of recombinant human acti-

vated protein C for severe sepsis. N Engl J Med 2001;344:

699–709. [PMID: 11236773]

Dellinger RP et al: Surviving Sepsis Campaign guidelines for man-

agement of severe sepsis and shock. Crit Care Med

2008;36:296–327. [PMID: 18158437]

Holcroft JW, Robinson MK: Shock: identification and manage-

ment of shock states. In: Care of the Surgical Patient. Scientific

American, 1992.

Holmes CL et al: Physiology of vasopressin relevant to manage-

ment of septic shock. Chest 2001;120:989–1002. [PMID:

11555538]

Howell G, Tisherman SA: Management of sepsis. Surg Clin North

Am 2006;86:1523–39. [PMID: 17116461]

Mecher CM et al: Unaccounted anion in metabolic acidosis during

septic shock in humans. Crit Care Med 1991;19:705–11. [PMID:

2026034]

Opal SM, Cross AS: Clinical trials for severe sepsis. Infect Dis Clin

North Am 1999;13:285–97. [PMID: 10340167]

Sihler KC, Nathens AB: Management of severe sepsis in the surgi-

cal patient. Surg Clin North Am 2006;86:1457–81. [PMID:

17116457]

Smith AL: Treatment of septic shock with immunotherapy.

Pharmacotherapy 1998;18:565–80. [PMID: 9620107]

Snell RJ, Parillo JE: Cardiovascular dysfunction in septic shock.

Chest 1991;99:1000–9.

Suffredini A et al: The cardiovascular response of normal humans

to the administration of endotoxin. N Engl J Med 1989;321:

280–86. [PMID: 2664516]

Vincent JL, Preiser JC: Inotropic agents. New Horizons 1993;1:

137–44. [PMID: 7922387]

Vercueil A, Grocott MPW, Mythen MG: Physiology, pharmacology,

and rationale for colloid administration for the maintenance of

effective hemodynamic stability in critically ill patients.

Transfusion Med Rev 2005;19:93–109.

Vincent JL, Herwig G: Fluid resuscitation in sevre sepsis and septic

shock: An evidence-based review. Crit Care Med 2004;32:451–4.



Anaphylactic Shock & Anaphylactoid

Reactions

ESSENTIALS OF DIAGNOSIS



Cutaneous flushing, pruritus.



Abdominal distention, nausea, vomiting, diarrhea.



Airway obstruction owing to laryngeal edema.



Bronchospasm, bronchorrhea, pulmonary edema.



Tachycardia, syncope, hypotension.



Cardiovascular collapse.

General Considerations

Anaphylactic shock and anaphylactoid reactions are due to

the sudden release of preformed inflammatory mediators

from mast cells and basophils. After exposure to the offend-

ing stimulus, initial symptoms may appear within seconds to

minutes or may be delayed as long as 1 hour. Anaphylactic

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SHOCK & RESUSCITATION

239

shock is differentiated from anaphylactoid reactions in that

the former is a true anamnestic response in which a sensi-

tized individual comes in contact with an antigenic sub-

stance. This reaction stimulates membrane-bound IgE,

causing mast cells and basophils to release histamine and

PAF into the circulation. These mediators result in vasodila-

tion, bronchoconstriction, pruritus, bronchorrhea, platelet

aggregation, and increased vascular permeability. The latter

may lead to laryngeal edema that culminates in airway

obstruction. The frequency and outcome of anaphylactic

reactions are summarized in Table 11–6. Anaphylactoid reac-

tions occur when the offending agent causes the direct release

of these substances without mediation by IgE. This may

involve a number of pathways, including complement-

mediated reactions, nonimmunologic activation of mast

cells, and production of arachidonic acid mediators.

Reactions to nonsteroidal anti-inflammatory drugs

(NSAIDs) are particularly dangerous because NSAID inhibi-

tion of the cyclooxygenase pathway favors the formation of

lipoxygenase pathway mediators from arachidonic acid.

Some of these include leukotrienes C

(slow-reacting

substance of anaphylaxis), and B

. These leukotrienes and

their intermediate products (5-HETE and 5-HPETE)

increase vascular permeability and produce bronchocon-

striction. Leukotriene B

is an eosinophilic and neutrophilic

chemoattractant. If the cyclooxygenase pathway is activated

by the inciting agent, the production of prostaglandin D

furthers bronchoconstriction. The most common agents

causing anaphylactic shock and anaphylactoid reactions are

listed in Tables 11–7 and 11–8. Anaphylactoid reactions may

occur in up to 10% of patients. When an initial reaction

occurs after the infusion of radiocontrast agents, the risk of a

similar reaction on reexposure approaches 35%.

Clinical Features

A. Symptoms and Signs—The initial symptoms are often

complaints of pruritus and a sense of impending doom.

These can progress to overt signs over several seconds or may

be delayed for up to an hour. Respiratory symptoms may

start with complaints of a lump in the throat, progressing to

dyspnea, dysphonia, hoarseness, and cough. If pulmonary

edema develops as a result of increased capillary permeability,

dyspnea and cyanosis result. Cardiovascular findings begin

with symptoms of weakness and faintness that may be accom-

panied by palpitations. As shock progresses, tachycardia

Agent

Frequency of Events

Mild Severe

Deaths per Year

(USA)

Penicillin 0.5–1% 0.04% 400–800

Hymenoptera stings 0.5% 0.05% ≥100

Contrast media 5% 0.10% 250–1000

From Lavine SJ, Shelhamer JH: Anapyhlaxis. In: Critical Care.

Civetta JM, Raylor RW, Kirby RR (editors). Lippincott, 1992.

Table 11–6. Frequency of anaphylactic events and

deaths.

Haptens Foods Venoms

Beta-lactam antibiotics Nuts Stinging insects,

Sulfonamides Shellfish especially

Nitrofurantoin Buckwheat Hymenoptera,

Demeclocycline Egg white fire ants

Streptomycin Cottonseed Hormones

Vancomycin Milk Insulin

Local anesthetics Corn Adrenocortico-tropic

Others Potato hormone

Serum products Rice Thyroid-stimulating

Immune globulin Legumes hormone

Immunotherapy for allergic Citrus fruits Enzymes

diseases Chocolate Chymopapain

Heterologous serum Others L-Asparaginase

Miscellaneous

Seminal fluid

Others

Modified from Austen KF: Systemic anaphylaxis in man. JAMA

1965;192:108; and from Kaliner M: Anaphylaxis. NER Allergy

Proceedings 1984;5:324.

Table 11–7. Etiologic agents responsible for anaphylactic

shock.

Complement-mediated reactions

Blood

Serum

Plasma

Plasmanate (not albumin)

Immunoglobulins

Nonimmunologic mast cell activators

Opioids

Radiocontrast media

Dextrans

Neuromuscular blocking agents

Others

Arachidonic acid modulators

Nonsteroidal anti-inflammatory drugs

Tartrazine (possibly)

Idiopathic

Most common conclusion after thorough evaluation

Adapted from Kaliner M: Anaphylaxis. NER Allergy Proceedings

1984;5:324.

Table 11–8. Etiologic agents for anaphylactoid reactions.

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240

appears along with arrhythmias, conduction disturbances, and

myocardial ischemia. Cutaneous symptoms include flushing

and pruritus that progress to urticaria, angioedema, and

diaphoresis. Patients may complain of abdominal pain or

bloating, cramps, and nausea. These progress to emesis, diar-

rhea, and occasionally hematemesis and hematochezia.

Other signs include syncope, seizures, conjunctival injection,

lacrimation, rhinorrhea, and nasal congestion.

B. Laboratory Findings—An increased hematocrit is found

commonly as a result of hemoconcentration from vascular

permeability. Serum mast cell tryptase is usually elevated.

Differential Diagnosis

Several common disorders seen in the ICU may be confused

with anaphylactic shock and anaphylactoid reactions:

myocardial ischemia and infarction, cardiac arrhythmias,

hypovolemic shock, septic shock, pulmonary embolism, aspi-

ration of feedings, bronchitis, acute exacerbation of chronic

obstructive pulmonary disease (COPD), seizure disorder,

hypoglycemia, and cerebrovascular accidents. Relationship to

administration of medications, blood, and new intravenous

solutions should suggest the possibility of anaphylaxis.

Treatment

A. Airway—The first mandate is to ensure a secure airway. If

the patient was intubated prior to the reaction, one should

take care that the endotracheal or nasotracheal tube does not

become dislodged during resuscitation. If the patient was not

intubated, emergency airway control by bag and mask or

intubation probably will be necessary. It is far better to intu-

bate these patients before laryngeal edema develops because

subsequent intubation is extremely difficult. Some clinicians

recommend the use of inhaled racemic epinephrine (0.3 mL

in 3 mL of saline administered by nebulizer) if upper airway

compromise occurs because of edema. It is far safer to intu-

bate the patient.

B. Circulatory Support—Most patients who develop ana-

phylactic shock or an anaphylactoid reaction in the ICU will

already have intravenous access. However, this catheter may

be small and will not permit the administration of large vol-

umes of fluid over a short period of time. Large-bore peripheral

intravenous lines are mandatory for fluid and drug adminis-

tration. Do not attempt central line placement in a hypoten-

sive patient who is hypovolemic. Collapse of the large veins

normally used for central catheter placement increases the

risk of a life-threatening complication.

1. Epinephrine—Drug therapy should begin with epineph-

rine (1:1000), 0.3–0.5 mL subcutaneously. The dose of epi-

nephrine may be repeated every 5–10 minutes as needed. If

the patient does not respond to the initial dose—or if severe

laryngospasm or frank cardiovascular collapse is present—

5–10 mL of epinephrine (1:10,000) may be administered

intravenously. If intravenous access is not available, either

0.5 mL of a 1:1000 dilution may be given intramuscularly or

10 mL of a 1:10,000 dilution may be instilled into the endo-

tracheal tube. When epinephrine is given intravenously,

severe tachycardia, myocardial ischemia, vasospasm, and

hypertension may result. Epinephrine decreases mediator

synthesis by increasing intracellular concentrations of cAMP.

Furthermore, it counteracts many of the deleterious effects of

the mediators of anaphylaxis.

2. Histamine antagonists—Histamine antagonists should

be administered as early as possible. Diphenhydramine

(1 mg/kg intravenously) and ranitidine (50 mg intravenously

over 5 minutes) are the preferred drugs. Cimetidine must be

used with extreme caution because rapid intravenous admin-

istration may result in hypotension or asystole.

3. Pressors—If hypotension persists after the repeated

administration of epinephrine and histamine antagonists,

aggressive fluid resuscitation is required. If this fails,

dopamine may be started at an initial dose of 5 μg/kg per

minute and increased until the dose reaches 20 μg/kg per

minute. A plateau effect occurs above this dose, requiring

that a second pressor be used if an adequate response has not

yet been achieved. Because of the extreme vasodilation, nor-

epinephrine should be started in the range of 3–4 μg/min

and titrated until a mean arterial pressure between 60 and

80 mm Hg is reached. The patient should be weaned from

pressors as quickly as possible.

C. Other Measures—Continued observation in the ICU is

indicated. An arterial catheter should be inserted for pressure

monitoring and to aid in securing blood gas samples for ven-

tilator management. In patients who remain unstable or who

require continuing pressor infusion, a pulmonary artery

catheter should be placed. Biphasic anaphylaxis may occur in

up to 25% of patients. Life-threatening reactions reappear

after an asymptomatic interval of up to 8 hours following

resuscitation. Hydrocortisone, 100–250 mg intravenously

every 6 hours, may help to prevent the late manifestations of

biphasic anaphylaxis. Steroids probably have no role in the

immediate treatment of acute anaphylaxis.

Patients who are receiving beta-blockers at the time of an

anaphylactic reaction may be resistant to the effects of

administered epinephrine. Atropine and glucagon may be

useful adjuncts to reverse the cardiac manifestations of

anaphylaxis in these patients.

Prognosis

The patient’s overall medical condition, the delay between

exposure to the antigen and the onset of anaphylaxis, and the

severity of symptoms all influence the outcome.

Anderson JA: Allergic reactions to drugs and biological agents.

JAMA 1992;268:2844–57. [PMID: 1433700]

Atkinson TP, Kaliner MA: Anaphylaxis. Med Clin North Am

1992;76:841–55. [PMID: 1614236]

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SHOCK & RESUSCITATION

241

Goust JM: Immediate hypersensitivity. Immunol Ser 1993;

58:343–59. [PMID: 8424982]

Levine SJ, Shelhamer JH: Anaphylaxis. In: Civetta JM, Taylor RW,

Kirby RR (eds), Critical Care. Philadelphia: Lippincott, 1992.

Levy JH, Levi R: Diagnosis and treatment of anaphylactic/

anaphylactoid reactions. Monogr Allergy 1992;30:145–55.

[PMID: 1280764]

Marone G, Stellato C: Activation of human mast cells and basophils

by general anesthetic agents. Monogr Allergy 1992;30:54–73.

Raper RF, Fisher MM: Profound reversible myocardial depression

after anaphylaxis. Lancet 1988;1:386–9. [PMID: 2893192]

White MV: The role of histamine in allergic disease. J Allergy Clin

Immunol 1990;86:599–605. [PMID: 1699987]



Neurogenic Shock

ESSENTIALS OF DIAGNOSIS



Preceded by trauma or spinal anesthesia.



Hypotension with tachycardia.



Cutaneous warmth and flushing in the denervated area.



Venous pooling.

General Considerations

Neurogenic shock is produced by loss of peripheral vasomo-

tor tone as a result of spinal cord injury, regional anesthesia,

or administration of autonomic blocking agents. Blood

becomes pooled in the periphery, venous return is decreased,

and cardiac output falls. If the level of interruption is below

the midthorax, the remaining adrenergic system above the

level of injury is activated, resulting in increased heart rate

and contractility. If the cardiac sympathetic outflow is

affected, bradycardia results. Blood pressure can decrease to

extremely low levels as blood pools peripherally in the

venous reservoir. All patients who have sustained spinal

trauma should be assumed to have hypovolemic shock from

associated injuries until proved otherwise.

Clinical Features

A. Symptoms and Signs—Patients may be alert and

responsive if head injuries are absent. Extremities are warm

above the level of injury and cool below. Blood pressure may

be extremely low, with a very rapid heart rate. Skeletal mus-

culature is affected after trauma. Loss of the peripheral

venous muscular pump may further decrease venous return.

Signs and symptoms of spinal cord injury and spinal shock

will be present.

B. Laboratory Findings—Laboratory studies are not helpful

in diagnosis. Because capillary permeability is normal,

plasma leaks do not occur. Prior to volume resuscitation,

hematocrit is usually normal.

C. Imaging Studies—Radiographs of the cervical, thoracic,

and lumbosacral spine are important to determine whether

fractures are present that may be unstable. These typically

will have been completed before the patient was admitted to

the ICU, but the intensivist must review the films so that

patient manipulations will not cause further spinal cord

injury. CT and MRI may be useful to determine whether

fragments within the spinal canal may be causing cord com-

pression. When present, they may be amenable to neurosur-

gical decompression.

Differential Diagnosis

Trauma patients considered for admission to a critical care

unit after spinal injury must have thorough surgical and neu-

rosurgical evaluation before transfer. The presence of con-

comitant hypovolemic shock from unrecognized bleeding

sites within the abdomen, chest, and extremities must be

excluded. Isolated head injury does not cause shock. Rather,

it may increase the blood pressure while slowing the heart

rate (Cushing’s reflex).

Treatment

A. Supportive Measures—A secure airway and adequate

intravenous access are urgent priorities. If intubation is

required and there is concern regarding the stability of the

cervical spine, fiberoptic or nasotracheal intubation may be

required. A diligent search must be made for other injuries in

trauma patients. When neurogenic shock arises from a spinal

anesthetic procedure in which the level of blockade has

become too high, intubation also may be necessary because

of compromise of the muscles of respiration.

Depending on the level of the injury, patients may have

loss of bladder function. A Foley catheter should be

inserted to decompress the bladder and aid in monitoring

urine output.

B. Fluid Resuscitation—Effective circulating blood volume

decreases dramatically because of venous pooling. Fluid

resuscitation is usually necessary and typically begins with

several liters of balanced salt solution. In some patients, this

may be all that is required to increase blood pressure.

C. Pharmacologic Support—If volume infusion fails to

restore the blood pressure, infusion of an alpha-adrenergic

agent is required to provide direct vasoconstriction. Either

phenylephrine or norepinephrine may be used. These drugs

are started in low doses and increased slowly until just suffi-

cient to restore blood pressure to a mean between 60 and

80 mm Hg. Weaning usually can be achieved fairly quickly, so

central venous or pulmonary artery catheterization is not

often required.

D. Surgery—If spinal cord transection is complete, the only

role for surgery is stabilization of vertebral fractures to pre-

vent further injury. If a foreign body is present, removal may

promote return of function if the cord is intact.

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242

E. Rehabilitation—After the acute stage has passed and the

patient has been stabilized, planning should be undertaken

to provide long-term care. This is the most difficult part of

the management of these patients. Demands on nursing and

support personnel are extreme in order to prevent pressure

ulcers and urinary and respiratory tract infections and to

provide nutritional support. Early consultation with a psy-

chiatrist is recommended to help the patient adjust to com-

plete and permanent loss of function.

CARDIAC SHOCK

Cardiac shock occurs when the heart fails to adequately

pump the blood volume presented to it. There are two gen-

eral categories: cardiogenic shock and cardiac compressive

shock. Cardiogenic shock develops when the heart loses its

ability to function as a pump. Cardiocompressive shock is

due to compression of the great veins and cardiac chambers,

restricting their normal filling and emptying.



Cardiogenic Shock

ESSENTIALS OF DIAGNOSIS



Decreased urine output.



Impaired mental function.



Cool extremities.



Distended neck veins.



Hypotension with evidence of peripheral and pul-

monary venous congestion.

General Considerations

Cardiogenic shock occurs most commonly either after

relentless progression of cardiac disease or after an acute

event such as myocardial infarction or rupture of a cardiac

valve or septum. These causes are summarized in Table 11–9.

The absolute amount of myocardium involved is probably

the most important prognostic factor. When more than 45%

of the left ventricular myocardium is necrotic, cardiogenic

shock becomes evident clinically.

Bradycardia and arrhythmias may underlie cardiogenic

shock. Heart rates less than about 50 beats/min may be inad-

equate to support cardiac output. Similarly, arrhythmias may

significantly alter cardiac filling patterns and prevent ade-

quate pumping.

A staging system has been developed for the classification

of cardiogenic shock that develops on a chronic basis.

A. Stage I (Compensated Hypotension)—The decreased

cardiac output and resulting hypotension invoke compensa-

tory mechanisms able to restore blood pressure and tissue

blood flow to normal levels. These reflexes are mediated by

the arterial baroreceptors, which increase the systemic vascu-

lar resistance.

B. Stage II (Decompensated Hypotension)—Cardiac

output falls below that which enables the peripheral vascula-

ture to maintain blood pressure by vasoconstriction. Blood

pressure and tissue perfusion fall.

C. Stage III (Irreversible Shock)—Profound reduction in

flow activates ischemic mediators such as the complement

cascade. Membrane injury develops that further aggravates

the ischemic insult. Irreversible myocardial and peripheral

tissue damage occur.

Clinical Features

A. Symptoms and Signs—When cardiogenic shock occurs

as a result of an acute event, pain may be a prominent find-

ing. Details of diagnosis and management of acute myocar-

dial infarction are presented in Chapter 22. When shock is an

acute exacerbation of a relentless process or the result of

another disease, symptoms may be less pronounced.

Physical examination will reveal signs consistent with the

underlying pathophysiologic mechanism of decreased car-

diac output and absolute hypervolemia. Blood pressure is

less than 90 mm Hg. The heart rate may be extremely high

and exceed the maximum aerobic limit (230––the patient’s

age in years). When decompensation occurs, bradycardia

usually develops. Neck veins are distended, and pulsations

frequently can be observed more than 4 cm above the clavi-

cle with the patient in the semierect position. Peripherally,

the extremities are cool, reflecting inadequate perfusion.

Abdominal examination may reveal a congested and dis-

tended liver that is tender to palpation. Rales are detected on

auscultation of the lungs in a patient who has a normal right

ventricle. With biventricular failure or pulmonary hyperten-

sion, pulmonary auscultation may be normal. Cardiac exam-

ination typically reveals a third heart sound, and there may

be a murmur characteristic of valvular disease.

B. Hemodynamic Effects—Virtually all patients with car-

diogenic shock will require a pulmonary artery catheter for

monitoring and evaluation of the response to therapy. The

Nonmechanical Causes Mechanical Causes

Acute myocardial infarction

Low cardiac output syndromes

Right ventricular infarction

End-stage cardiomyopathy

Rupture of septum or free wall

Mitral or aortic insufficiency

Papillary muscle rupture or

dysfunction

Critical aortic stenosis

Pericardial tamponade

From Farmer JA: Cardiogenic Shock. In: Critical Care. Civetta JM,

Taylor RW, Kirby RR (editors). Lippincott, 1992.

Table 11–9. Causes of cardiogenic shock.

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SHOCK & RESUSCITATION

243

usual findings are elevation of central venous and pul-

monary capillary wedge pressures and a cardiac index less

than about 1.8 L/min/m

C. Laboratory Findings—If acute myocardial infarction is

the precipitating cause, elevated cardiac bands of creatine

kinase will be observed. Plasma drug levels of medications

the patient has been receiving should be measured to deter-

mine whether they are in the toxic or subtherapeutic ranges.

A routine chemistry panel is required to evaluate K

and

HCO

–

. Serum lactate may be elevated when shock has been

prolonged. Hematocrit and hemoglobin should be deter-

mined to evaluate the need for transfusion.

D. Imaging Studies—Chest radiography often will reveal a

pattern of pulmonary edema. Radionuclide ventriculogra-

phy may be helpful in evaluating ventricular ejection frac-

tion. Echocardiography is also useful in the evaluation of

valvular and ventricular function. If pericardial tamponade

is suspected, echocardiography is the examination of choice

to establish that diagnosis.

Differential Diagnosis

Cardiogenic shock should be suspected in patients with

chronic myocardial disease who experience a sudden wors-

ening of symptoms. Acute myocardial infarction may be

complicated by ventricular septal rupture, papillary muscle

rupture, and papillary muscle dysfunction, which can lead to

cardiogenic shock. Constrictive pericarditis and rupture of a

cardiac ventricular aneurysm may lead to cardiac compres-

sive shock. Rupture of an abdominal aortic aneurysm in a

patient with coronary artery disease may cause diagnostic

confusion. Abdominal pain owing to rupture of the

aneurysm may simulate the pain of acute myocardial infarc-

tion. Electrocardiography typically reveals myocardial

ischemia. The absence of distended neck veins is the critical

distinguishing feature. Myocardial contusion after blunt

trauma may cause severe cardiogenic shock.

Treatment

A. General Measures—Patient comfort and relief of anxi-

ety should be addressed immediately. Opioids not only

relieve pain and provide sedation—but they also block

adrenergic discharge and lessen cardiac stress. Intravenous

morphine should be given starting with a bolus of 2–4 mg.

Dosing should be titrated to both subjective response and

effect on blood pressure. Because morphine is a vasodilator,

it may decrease right ventricular filling and adversely affect

blood pressure in a hypovolemic patient. An arterial catheter

and a pulmonary artery flotation catheter usually are

mandatory to manage these patients effectively.

When cardiogenic shock is the result of acute myocardial

infarction, early efforts should be directed at controlling the

infarct size. An imbalance between oxygen delivery and

increased oxygen consumption prompted by changes in

heart rate, blood pressure, and contractility may extend the

size of the infarction. If therapy is begun within 3 hours of

myocardial infarction, the incidence of cardiogenic shock is

4%. However, if therapy is delayed, cardiogenic shock occurs

in up to 13% of patients. Intravenous nitroglycerin and beta-

blockers are the main features of early treatment.

Nitroglycerin reduces right ventricular preload and

decreases left ventricular afterload. The reduction in after-

load decreases end-diastolic pressure and reduces wall stress

and myocardial oxygen consumption. Furthermore, it dilates

epicardial vessels and may improve oxygen delivery to

ischemic areas. The early use of nitroglycerin both decreases

infarct size and reduces early mortality. The possibility of

right ventricular infarction and pericardial tamponade must

be excluded before therapy with nitroglycerin is begun.

Beta-blockers decrease myocardial oxygen demand,

antagonize circulating catechols, and have antiarrhythmic

activity. A particular benefit may accrue when beta-blockers

are combined with thrombolytic agents. Beta-blockers are

best started within 2 hours of infarction. Calcium channel

blockers also have been investigated for this purpose but have

failed to demonstrate efficacy in acute situations. The mor-

tality rate may be increased if calcium channel blockers are

used in patients with pulmonary edema.

B. Resuscitation—Although cardiogenic shock may occur

in patients with whole body fluid overload, they may be

effectively hypovolemic. If PCWP is less than 10–12 mm Hg,

balanced salt solution should be administered in an attempt

to increase filling pressures. Cardiac output should be meas-

ured after each change of 2–3 mm Hg in PCWP. Filling pres-

sures near 20 mm Hg may be required before cardiac output

increases.

If laboratory studies reveal that the patient is hypoxemic,

supplemental oxygen should be provided. Oxygen delivery

should be maximized by ensuring complete arterial hemo-

globin saturation. Intubation with PEEP may be required to

accomplish this when pulmonary edema is present. Judicious

use of PEEP is required because it adversely affects ventricu-

lar preload and cardiac output.

C. Pharmacologic Support—Once volume status has been

optimized, support of the failing myocardium is often neces-

sary. Inotropes, vasodilators, and diuretics all may be used.

1. Inotropes—

a. Dobutamine—Dobutamine is the inotropic drug of

choice for the management of congestive heart failure and

cardiogenic shock. It is a β

-adrenergic agonist that has min-

imum chronotropic and peripheral vasoconstrictive effects.

It has a significant advantage over dopamine in that it does

not cause the release of norepinephrine. Furthermore, it does

not require the presence of norepinephrine at the nerve ter-

minals for effect. Because of its minimum chronotropic

effect, dobutamine can improve ventricular performance

without significantly increasing myocardial oxygen demand.

Dobutamine’s greatest potential is realized in patients with

reduced cardiac indices and increased filling pressures.



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244

Because it is a vasodilator, dobutamine reduces filling pres-

sures and wall tensions in patients with dilated ventricles.

This permits better myocardial nutrient flow during diastole.

A recent study found a 33% improvement in cardiac index, a

decrease in systemic vascular resistance, and no change in

heart rate or systemic blood pressure when dobutamine was

given in doses that averaged 8.5 μg/kg per minute. The drug

may be given in doses up to 40 μg/kg per minute without sig-

nificantly increasing heart rate. When three-vessel coronary

artery disease is present, dobutamine may create a steal and

direct blood away from ischemic areas.

b. Dopamine—The effects of dopamine depend on the

dose administered. In lower doses (<4 μg/kg per minute),

dopamine increases renal blood flow by stimulating

dopaminergic (D

) receptors in the kidney and causes

peripheral vasodilation through D

receptors that inhibit the

release of norepinephrine. At intermediate dosages (5–10

μg/kg per minute), dopamine improves cardiac function and

increases blood pressure without elevating myocardial oxy-

gen consumption. Systemic vascular resistance is usually not

increased. At higher doses (>10 μg/kg per minute),

dopamine elevates systemic vascular resistance by stimulat-

ing alpha-adrenergic receptors and heart rate by stimulating

beta-adrenergic receptors. A recent study found that an aver-

age dose of 17 μg/kg per minute was needed to optimize

coronary perfusion pressure in a group of patients that

developed cardiogenic shock after myocardial infarction.

Dopamine at such high levels increases myocardial oxygen

demand, produces tachycardia, and may limit renal perfusion.

It should be used with caution in patients with cardiogenic

shock because it may adversely influence the balance of

myocardial oxygen delivery and consumption.

c. Digoxin—Although digitalis preparations have modest

inotropic effects, they are probably of little importance in the

treatment of cardiogenic shock except for the treatment of

atrial fibrillation with rapid ventricular response. Small

intravenous doses of digoxin may improve diastolic filling

time and increase cardiac output in these situations.

d. Isoproterenol—This agent causes tachycardia, increased

myocardial contractility, and decreased peripheral vascular

resistance through its stimulation of both α

and β

receptors.

Myocardial oxygen consumption is increased dramatically.

Although isoproterenol increases coronary blood flow, it actu-

ally may shunt blood away from ischemic areas and increase

the infarct size. Highly restricted indications include the pres-

ence of bradycardia and severe aortic valvular insufficiency.

Intravenous administration is started at a dose of 0.01 μg/kg

per minute and increased until the desired effect is obtained.

e. Norepinephrine—Norepinephrine has both alpha- and

beta-adrenergic effects. At low doses, it causes beta stimula-

tion of the heart and increases blood pressure and cardiac

output. At higher doses, it primarily affects the alpha-

adrenergic receptors and supports blood pressure by increas-

ing systemic vascular resistance. At higher doses it also tends

to produce tachycardia, arrhythmias, and peripheral visceral

ischemia. Norepinephrine should be used with extreme caution

because at higher doses it increases left ventricular afterload

and may worsen myocardial ischemia. If cardiogenic shock

proves resistant to both dobutamine and dopamine, norepi-

nephrine may be started at doses of 1–2 μg/min and

increased until blood pressure increases. Of particular con-

cern are the visceral and renal vasoconstrictive effects that

may produce end-organ ischemia in the face of apparently

satisfactory blood pressure.

f. Other agents—Amrinone is a weak inotrope that increases

contractility independently of the catechol pathways. Although

its exact mechanism of action is not known, it increases intra-

cellular cAMP and calcium concentrations. The increased

cAMP concentration in smooth muscle decreases peripheral

and pulmonary vascular resistance and dilates coronary arter-

ies. Amrinone increases stroke volume without increasing heart

rate. The usual loading dose is 0.75 mg/kg over 3–5 minutes,

followed by a second bolus 30 minutes later. The boluses are

followed by a continuous intravenous infusion of 5–10 μg/kg

per minute. The total daily dose should not exceed 10 mg/kg.

After the bolus is given, effects are seen within several minutes.

Glucagon increases cardiac contractility and decreases

peripheral vascular resistance. The onset of action is

extremely rapid. A test dose of 4–6 mg should be given intra-

venously to determine whether any effect is produced. If suc-

cessful, this is followed by a constant infusion of 4–12 mg/h.

The agent appears to be useful for the treatment of cardio-

genic shock and left ventricular failure. It probably merits

consideration in patients who have failed to respond to other

agents or when dysrhythmias develop. It may be helpful when

left ventricular dysfunction is a result of treatment with beta-

blockers. Hyperglycemia is a side effect of the drug.

2. Vasodilators—Vasodilators are used to lower left ven-

tricular afterload, which decreases myocardial oxygen con-

sumption. Their use is limited by their hypotensive effect,

which may compound the difficulties associated with

peripheral oxygen delivery.

a. Nitroprusside—Nitroprusside decreases both afterload

and preload. When nitroprusside is used optimally, the

increase in left ventricular ejection fraction partially offsets

the decrease in systemic vascular resistance. Therapy begins

with a dose of 5–10 μg/min and is advanced in increments of

2.5–5 μg/min every 10 minutes until an increase in cardiac

output is noted. The dose should be reduced if systolic blood

pressure falls below 90 mm Hg. Nitroprusside may produce

an intracoronary steal that may aggravate areas of ischemia.

The drug is metabolized to cyanide and subsequently to thio-

cyanate. Doses above 3 μg/min may lead to toxicity, especially

when the drug is used for more than 3 days. Free cyanide ions

combine with cytochromes, leading to anaerobic metabolism

and increased lactate levels. This results in a metabolic acido-

sis that eventually culminates in confusion, hyperreflexia,

and coma. Thiocyanate levels should be monitored and not

permitted to rise above 10 mg/dL. Prophylactic infusion of

hydroxocobalamin may avert toxicity by combining with

cyanide to form cyanocobalamin.

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SHOCK & RESUSCITATION

245

b. Nitroglycerin—Nitroglycerin is a nitrate derivative

whose greatest effect is preload reduction, which reflexly

decreases left ventricular filling. It has the additional advan-

tage of dilating the coronary vasculature and is the drug of

choice when cardiogenic shock is due to ischemia.

Nitroglycerin is also effective in the treatment of acute valvu-

lar incompetence. Care must be exercised to ensure that

patients are not hypovolemic prior to its administration

because the increased venous capacity will decrease venous

return and further lower the cardiac output. The normal

starting dose is 10 μg/min, which can be increased by 10 μg/min

every 5–10 minutes to a total dose of 50–100 μg/min. Doses

as high as 400 μg/min can be tolerated for several days.

D. Other Modalities—The management of acute myocar-

dial infarction is discussed in Chapter 22. Newer modalities

available to improve cardiac function after infarction include

thrombolytic therapy, percutaneous angioplasty, balloon

pumping, and left ventricular assist devices. Emergency

coronary artery bypass grafting is an option for patients who

fail to respond to other forms of treatment.

Prognosis

Fulminant cardiogenic shock continues to carry a mortality

rate of 90% when only pharmacologic therapy is used.

Application of percutaneous transluminal coronary angio-

plasty, left ventricular assist devices, and early surgical revas-

cularization may help to improve this outcome.

Farmer JA: Cardiogenic shock. In: Civetta JM, Taylor RW, Kirby RR

(eds), Critical Care. Philadelphia: Lippincott, 1992.

Handler CE: Cardiogenic shock. Postgrad Med J 1985;61:705–12.

[PMID: 3898054]

Holcroft JW, Wisner DH: Shock and acute pulmonary failure in

surgical patients. In: Way LW (ed), Current Surgical Diagnosis &

Treatment, 9th ed. Stanford, CT: Appleton & Lange, 1991.

Mueller HS: Inotropic agents in the treatment of cardiogenic

shock. World J Surg 1985;9:3–10. [PMID: 3885584]



Cardiac Compressive Shock

ESSENTIALS OF DIAGNOSIS



Hypotension with tachycardia.



Oliguria.



Mental status changes.



Distended neck veins.

General Considerations

Cardiac compressive shock is a low-output state that occurs

when the heart or great veins are compressed. Compression

either impedes the return of blood to the heart or prevents

effective pumping action of the heart itself. Pericardial tam-

ponade is due to fluid within the pericardial sac that con-

stricts the cardiac chambers and prevents them from filling

properly. This may occur acutely after penetrating trauma

with laceration of a coronary artery, or it may be progressive

with chronic diseases such as uremia and connective tissue

disorders. Distention of the abdomen with elevation of the

diaphragm compresses the heart and may produce a form of

shock. PEEP used with mechanical ventilation increases the

intrathoracic pressure, which both collapses the superior and

inferior venae cavae and reduces the transmural pressure

gradient, thereby decreasing cardiac filling. In similar fash-

ion, tension pneumothorax increases the intrathoracic pres-

sure and decreases venous return.

Clinical Features

A. Symptoms and Signs—Signs associated with poor

peripheral perfusion such as hypotension, tachycardia, cool

extremities, oliguria, and altered mental status are usually

present. The presence of distended neck veins is central to the

diagnosis, although they may be absent if the patient is hypo-

volemic. When tension pneumothorax is the cause, hyperres-

onance is noted on thoracic percussion, breath sounds are

absent on the affected side, and the mediastinum is shifted

away from the involved chest. Displacement of the trachea in

association with distended neck veins is pathognomonic of

tension pneumothorax. For patients who are breathing spon-

taneously, inspiration increases the degree of venous disten-

tion (Kussmaul’s sign). Paradoxic pulse also may occur with

spontaneous breathing and consists of a decrease in systolic

pressure of more than 10 mm Hg with inspiration.

When cardiac compressive shock occurs after injury, pen-

etrating trauma to the chest is usually present. Pericardial

tamponade is uncommon after blunt injuries. Patients

admitted for exacerbations of chronic disease often have a

history of pericardial effusion. When mechanical ventilation

is used, cardiac compressive shock occurs because (1) the

inflated lungs compress the superior and inferior venae

cavae, (2) the right atrium and ventricle are compressed, and

(3) expansion of the lungs compresses the pulmonary vascu-

lature and increases the resistance to right ventricular ejec-

tion. Hypotension and tachycardia worsen in these patients

as PEEP is increased. The correlation between the two may

not be apparent at first, although careful examination of the

patient’s flowsheet will reveal changes in hemodynamics that

correspond to ventilator manipulations.

B. Hemodynamic Monitoring—Central venous pressure is

increased, as are pulmonary artery and pulmonary capillary

wedge pressures. Equalization of central venous pressure,

pulmonary artery, and pulmonary capillary wedge pressures

strongly suggests pericardial tamponade.

C. Imaging Studies—Upright posteroanterior chest radi-

ographs may show an enlarged cardiac shadow, but this is

nonspecific. If tension pneumothorax is suspected, treatment



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246

must not be delayed while x-rays are obtained. If an inciden-

tal chest radiograph is available, it will reveal hyperlucency of

one or both hemithoraces with displacement of the mediasti-

nal structures to the contralateral side. Transesophageal two-

dimensional echocardiography is very sensitive and can be

used to establish the diagnosis in nonemergent situations.

Treatment of suspected decompensated traumatic pericar-

dial tamponade should never be postponed while awaiting

imaging studies.

Differential Diagnosis

Primary cardiogenic shock without compression presents

the major differential dilemma because both types present

with low cardiac output and high venous pressure. An acute

myocardial infarction or progressive deterioration in a criti-

cally ill patient suggests cardiogenic shock. Most patients

who develop tension pneumothorax or pericardial tampon-

ade after injury will have had the diagnosis established and

therapy instituted before arrival in the critical care unit.

Missed injuries occur occasionally and must be differentiated

from traumatic air embolism to the coronary arteries. The

latter usually causes severe dysrhythmias and a rapid down-

hill course.

Treatment

A. Fluid Resuscitation—Rapid fluid infusion may tran-

siently compensate for the decrease in ventricular filling.

Central venous pressure cannot be used to guide such infu-

sion because central venous pressure always will be elevated

prior to the administration of fluid.

B. Operative Treatment—Surgical decompression of the

offending site is indicated. For tension pneumothorax,

immediate insertion of a large-bore intravenous catheter into

the affected hemithorax will rapidly release the increased

pressure. After pulse and blood pressure return to normal,

this small catheter can be replaced with a larger tube thora-

costomy connected to a chest evacuation device. Placement

of the smaller catheter never should be delayed pending pro-

curement and placement of a more definitive thoracostomy

tube. If cardiac compression is due to gastric distention,

placement of a nasogastric tube may be helpful. When dis-

tention is due to other causes, surgical exploration is usually

warranted. Pericardial decompression should be performed

for pericardial tamponade. Reduction of ventilatory pres-

sures and augmentation of the circulating blood volume, if

possible, usually correct compression resulting from the use

of PEEP.