Shock is a "circulatory collapse" characterized by inadequate blood flow and inability to maintain cellular perfusion of peripheral tissues. Shock as a syndrome is defined by a group of clinical signs arising from any of a number of causes and is usually associated with hypotension and oliguria. A life-threatening medical emergency, shock occurs in both sexes and all ages. Although prevalence is not well established, an estimated 71,000 hospitalized patients develop cardiogenic shock each year.

Cardiogenic shock:

• Myocardial ischemia or infarction, particularly if > 40% of left ventricular muscle mass is involved; most common cause of cardiogenic shock; can also occur with right ventricular failure
• Ruptured interventricular septum
• Ventricular aneurysm
• Prolonged cardiopulmonary bypass; myocardium may be stunned for hours to days
• Severe cardiomyopathy or myocarditis
• Arrhythmia
• Acute mitral or aortic regurgitation or acute ventricular septal defect 
• Aortic stenosis leading to decreased cardiac output and stroke volume 
• Prosthetic valve malfunction 
• Outflow obstruction—e.g., hypertrophic cardiomyopathy (IHSS) 

Extra cardiac obstructive shock:

• Pericardial tamponade—impairs ventricular diastolic filling causing decreased cardiac output, diminished stroke volume, and reduced preload
• Massive pulmonary embolism 
• Tension pneumothorax—diminishes venous return to the heart
• Severe pulmonary hypertension 

Hypovolemic shock :

• Acute hemorrhage due to trauma or preexisting disease (e.g., peptic ulcer or aortic aneurysm)
• Massive fluid depletion—e.g., severe vomiting or diarrhea; or extreme insensible losses as in the case of burns
• Diabetes insipidus

Distributive shock (tissue perfusion due to abnormal shunting of a normal or increased cardiac output):

• Bacteremic or septic shock
• Drug overdose
• Anaphylaxis 
• Neurogenic shock 
• Addisonian crisis

• Serious injury and trauma
• Cardiogenic disorders (e.g., acute myocardial infarction, cardiomyopathy)
• Surgery
• Bacteremia
• Hemorrhage
• Large volume loss from excessive diarrhea or vomitting
• Excess alcohol consumption
• Anemia
• Allergic reactions to medication(s)
• Drug overdose

• Low or unobtainable BP; often <60 mm Hg systolic in adults; regardless of absolute number, reduction of mean arterial pressure by 40 mm Hg also indicative of shock
• Lethargy, confusion, and somnolence
• Cold, moist, and often cyanotic and pale hands and feet
• Weak and/or rapid pulse
• Tachypnea and hyperventilation
• Oliguria
• Shaking chills, rapid temperature increase, warm flushed skin, hyperdynamic syndrome (septic shock)
• Engorged neck veins (cardiogenic and extra cardiac obstructive)
• Pulmonary congestion (cardiogenic)
• Gallop rhythm (cardiogenic)
• Systolic murmur (cardiogenic)—new
• Pulsus paradoxus—pericardial tamponade

Shock is an emergency that requires rapid evaluation based on "limited" history and physical signs and symptoms (e.g., cold and sweaty skin, weak and rapid pulse, irregular breathing, dry mouth, dilated pupils) and rapid initiation of treatment. Further diagnostic procedures (e.g., right heart catheterization) should determine cause and severity of shock. Specific diagnostic criteria include the following:

• Hypotension
• Tachycardia
• Diminished sensorium
• Oliguria

Also, listen for heart murmer, gallop rhythm, and pulmonary congestion (signs of cardiogenic shock). Distant heart sounds and presence of pulsus paradoxus suggest pericardial tamponade.

Must be monitored closely and continuously in an intensive care setting:

• Arterial blood gas—likely to reveal a metabolic acidosis from lactate
• CBC, PT, PTT
• Blood chemistry (electrolytes including calcium, magnesium, and phosphorus, as low levels depress myocardial and respiratory function)
• In the case of septic shock—blood cultures, urinalysis, and urine cultures (if urine can be obtained), sputum cultures if any respiratory secretions

Cardiogenic and hypovolemic shock result in decreased tissue perfusion. Distributive shock results from decreased arterial pressure due to systemic vascular resistance. Recent studies indicate two modes of gene expression in stress (acute-phase and heat-shock response), which may be harmful in shock. Common findings include decreased arterial pressure and often multiple organ system failures. Specific findings per type of shock include the following:

Cardiogenic:

• Myocardial injury or necrosis
• Reduced systolic performance
• Low cardiac output

Hypovolemic:

• Reduced preload
• Low cardiac output

Distributive:

• Decreased systemic vascular resistance
• Myocardial dysfunction
• High or normal cardiac output
• Maldistribution of blood flow in microcirculation
• In the case of septic shock, cardiovascular decompensation is due to the organism itself, endotoxins, or exotoxins

Extra cardiac obstructive:

• Reduced filling pressure
• Low cardiac output

• Chest X ray to look for interstitial edema and thickening and loss of definition of pulmonary vasculature shadow, characteristic appearance of Kerley A and B lines
• Echocardiography to evaluate for valvular disease and vegetation, wall-motion abnormalities, LV function, and cardiomyopathy
• Coronary angiography may be warranted in the case of cardiogenic shock

• Electrocardiogram (ECG) to diagnose myocardial damage; help identify arrhythmias
• Right heart catheterization for hemodynamic assessment and monitoring therapy

Primary goals are to maintain mean arterial pressure (at least 60 mm Hg) and to ensure adequate perfusion and oxygen delivery. Initial first-aid therapy includes covering for warmth, raising legs to improve venous return, stopping hemorrhage, and CPR/ACLS if needed. Oxygen should be given via nasal cannula or mask. Once patient reaches intensive care, continuous ECG monitoring, careful monitoring of oxygenation, and right heart catheterization should be instituted. Mainstay therapy in the case of hypovolemic shock is volume repletion; in the case of hemorrhage, this should be done with packed RBCs; fluids also used for septic shock even if edematous.

• Ionotropic agents—dopamine, dobutamine, norepinephrine—intravenous to augment arterial pressure and cardiac output in cardiogenic shock
• Vasodilators—to decrease afterload and thereby decrease LV work in the case of cardiogenic shock
• Vasopressors often necessary for septic shock—e.g., dopamine, norepinephrine
• Corticosteroids (e.g., hydrocortisone, 2 to 10 gm IV) for anaphylactic shock; to stabilize patient, prevent recurrence, and block late-phase reactants
• Antimicrobials (septic shock)—initial broad-spectrum regimen to cover wide range of causative microorganisms in infections
• Morphine—serves as venodilator and to decrease anxiety
• Thromobolytic therapy should be considered in the case of myocardial infarction or pulmonary embolism

• Surgery may be necessary in cases such as valvular heart disease or ventricular septum rupture after myocardial infarction
• Emergency angioplasty or coronary bypass surgery may improve survival at 6 months in patients with acute myocardial infarction complicated by cardiogenic shock
• Placement of intra-aortic balloon pump may be necessary in the case of cardiogenic shock
• Emergency pulmonary embolectomy in the case of pulmonary embolism, particularly if thrombolytic therapy is contraindicated

While shock is a life-threatening condition requiring emergent attention and treatment, some CAM modalities may provide adjunctive care. Nutritional manipulation, for example, has demonstrated some protection against the deleterious effects of shock and improvement in outcome, including possible roles for:

• Omega 3 fatty acids
• L-acetyl carnitine
• Glutamine
• Coenzyme Q10
• N-acetylcysteine
• Nicotinamide
• Vitamin B12
• Vitamin C
• Vitamin E

See details in the respective subsections.

Oxidative stress has been implicated as a contributor to the development of shock (e.g., cardiogenic shock from myocardial ischemia as well as septic shock from bacterial endotoxins). Several studies have suggested that treatment with antioxidants and free radical scavengers may have protective effects against developing these shock syndromes. See subsections entitled Coenzyme Q10, Vitamin C, and Vitamin E for more information.

Arginine, Omega-3 Fatty Acids, and Nucleotide Supplement

Nutritional supplementation has been examined for benefits in the correction or inhibition of inflammation and metabolic derangements that accompany shock. A prospective, randomized, double-blind, controlled study of 32 patients with severe multiple trauma compared possible benefits from a nutritional formulation containing arginine, omega-3 fatty acids, and nucleotides with those from an isonitrogenous isocaloric control diet. Although no significant difference was seen in mortality or hospital stay (the sample size was too small to test for these parameters adequately), patients in the test group developed significantly less systemic inflammatory response syndrome (SIRS), a condition that can induce multiple organ failure (MOF). SIRS is defined according to criteria determined at the Society of Critical Medicine Consensus Conference and is related to body temperature, heart rate, respiratory rate, WBC count, and band formation of WBCs. The authors conclude that critically ill patients due to trauma and other causes may benefit from the addition of arginine, omega-3 fatty acids, and ribonucleotides to enteral nutrition (Weimann et al. 1998).

An earlier, prospective, randomized study of critically injured patients compared a standard diet and an experimental diet supplemented with arginine, omega-3 fatty acids, and trace elements. Over time, the group on the experimental diet showed a trend toward normal levels of immune mediators (e.g., tumor necrosis factor and prostaglandin E2) in comparison with patients on the standard diet (Mendez et al. 1996).

Omega-3 vs. Omega-6 Fatty Acids

Animal studies investigating the role of essential fatty acids in the clinical outcomes from shock show positive benefits from omega-3 essential fatty acids and negative outcomes associated with omega-6 essential fatty acids. These data are consistent with other scientific information suggesting that omega-3 essential fatty acids are anti-inflammatory while omega-6 essential fatty acids are pro-inflammatory. Perinatal supplementation with omega-3 polyunsaturated fatty acids significantly decreased mortality from endotoxic shock in newborn rats (Farolan et al. 1996). Guinea pigs fed an intravenous diet containing black currant oil (rich in omega-6 gamma linolenic acid—namely, 20% GLA) showed no improvement in resistance to shock; in fact, they exhibited a more rapid onset of metabolic acidosis and increased mortality compared with guinea pigs getting soy supplementation (0% GLA) (Hirschberg et al. 1990). The results of these two animal trials suggest that a diet rich in omega-3 essential fatty acids compared with omega-6 fatty acids may prove protective against the deleterious effects of septic shock following exposure to the endotoxin—i.e., a potential prophylactic use. Diets in the United States and some other industrialized countries tend to be high in omega-6 fatty acids and low in omega-3.

Carnitine

A multi-center, double-blind clinical study of 115 patients with septic, cardiac, or traumatic shock investigated the effects of acetyl-L-carnitine infused for 12 hours after a single intravenous bolus. Clinical improvements were seen in patients with all three conditions (Gasparetto et al. 1991):

• Cardiogeneic shock -- heart rate decreased to normal values; oxygen saturation improved; right atrial pressure diminished
• Septic shock -- systolic arterial pressure increased; oxygen saturation improved
• Traumatic shock -- right arterial and mean arterial pressures improved

Intravenous administration of L-carnitine may also prevent cardiogenic shock in patients suffering from acute myocardial infarction. An open pilot study of 27 patients hospitalized with acute MI evaluated the effects of standard treatment, an intravenous bolus of L-carnitine, and subsequent continuous infusion of the supplement. According to hemodynamic measurements (via Swan-Ganz catheter), blood-gas analysis, and biochemical parameters, L-carnitine had a beneficial effect (Corbucci and Loche 1993). The supplement appeared to:

• Oppose the metabolic derangements induced by acute ischemia
• Protect cardiac function
• Improve outcome of acute MI

Carnitine may also ameliorate the response of cachexia from sepsis and other causes, as suggested by a controlled animal study. Cachexia, a complication of septic shock, is accompanied by:

• Protein wasting
• Lipogenesis
• Reduced fatty acid oxidation
• Hypertriglyceridemia

Carnitine supplements administered in the feed of rats with cachexia from septic shock had a normalizing effect on lipid metabolism compared with controls. The authors of this trial propose that the improvement in metabolism in cachectic animals may contribute to reduction in mortality rate seen in earlier studies of septic rats supplemented with carnitine (Winter et al. 1995).

Coenzyme Q10

Coenzyme Q10 (CoQ10) is a lipophilic antioxidant that has been shown to protect cellular and subcellular membranes from lipid peroxidation. A small controlled canine study evaluated the effects of CoQ10 against hemorrhagic shock. Pretreatment with CoQ10 before induction of hemorrhagic shock moderated the accumulation of lactate and metabolic acidosis and was responsible for returning catecholamine levels to baseline more quickly than in the control group. Histamine levels, chemical mediators that may be reduced during hemorrhagic shock, were found to be higher in the treatment group; the author to speculates that the maintenance of normal histamine levels by CoQ10 (Yamada 1990):

• Prevents vasoconstriction
• Supports microcirculatory blood flow
• Promotes survival by maintaining histamine levels

Other studies of endotoxic shock have reported that CoQ10 pretreatment improves pulmonary function by decreasing histamine levels. When considering these results and the present findings, the author proposes that CoQ10 administration has protective effects in both hemorrhagic and endotoxic shock and it works by different mechanisms in the two related but distinct clinical circumstances. The beneficial effects of CoQ10 in each type of shock are dependent on factors in addition to the impact of the supplement on histamine levels in the respective clinical settings (Yamada 1990).

A similar study that evaluated the effects of CoQ10 on puppies with induced septic shock showed the following beneficial changes (Lelli et al. 1993):

• Improvement in cardiovascular hemodynamics including enhanced cardiac output and improved mean arterial pressure
• Inhibition of free radical-mediated lipid peroxidation.
• Prevention of early hypotension

Glutamine

The addition of glutamine to parenteral nutrition may have the following beneftits:

• Preservation of the integrity of the gut
• Maintenance of mucosal weight and villous height
• Possible prevention of bacterial translocation and septic complications
• Decreased mortality among critically ill patients

Glutamine is thought to be a safe adjunctive therapy without significant side effects (Felbinger et al. 1999).

Nicotinamide

At least two animal studies have suggested a protective effect from nicotinamide (the biologically active amide of niacin or vitamin B₃; also called niacinamide) following exposure to bacterial endotoxin (LeClaire et al. 1996; Zingarelli et al. 1996). The significant results seen in the treatment group compared to controls include:

• Improved survival
• Reduced hypotensive response

The authors suggest that benefits are conferred by:

• Reduction of cytokine activity
• Protection from nitric oxide mediated vascular failure

Vitamin B12

Animal studies suggest that hydroxycobalamin (vitamin B12) may attenuate the hypotensive response to E. coli endotoxin through mechanisms similar to those conferred by nicotinamide (see previous subsection of this title) (Greenberg et al. 1995).

Vitamin C

Reactive oxygen species (ROS) production from phagocytes, such as superoxide anions, has been implicated as contributing to the high mortality rate from septic shock. Administration of ascorbic acid to in vitro macrophages taken from mice suffering from endotoxic shock reduced adherence, ingestion, and superoxide production by the phagocytes. The authors speculate that this may ultimately translate into vitamin C attenuating the severity of septic shock (Victor et al. 2000). More research is needed.

Vitamin E

In a controlled study comparing elderly men with younger subjects, administration of a daily dose of 200 mg of vitamin E for 3 months decreased lymphocyte adherence (initially very high) and stimulated lymphoproliferation; each of these processes may be disturbed in the course of aging. Ingestion of vitamin E appeared to restore immune balance in the older male subjects (De la Fuente and Victor 2000). It is unclear what exact conclusions can be drawn in terms of the clinical application for vitamin E supplementation in the case of shock. One implied suggestion is that older men who use this antioxidant may be protecting their immune system and, thereby, may be less susceptible to the damaging effects of bacterial endotoxins at the time of exposure—i.e., a prophylactic use.

N-acetylcysteine

N-acetylcysteine (NAC), administered to mice with septic shock secondary to bacterial endotoxin, decreased lymphocytic adherence and increased chemotaxis compared with mice not given the supplement. The authors conclude from the animal study that NAC seems to preserve adequate immune function against imbalances such as those caused by endotoxic shock (De la Fuente and Victor 2000). Following further research in humans, there may be an adjunctive role for NAC supplementation following endotoxin exposure and development of septic shock.

The immunomodulatory effects of plant-based medicines may be beneficial in the treatment of systemic septic shock. An Ayurvedic formula was evaluated in a controlled animal study investigating septic shock; the formula contains:

• Tinospora cordifolia (Tamarisk) 
• Withania somnifera (Ashwagandha) 
• Phyllanthus emblica (Indian gooseberry)
• Ocimum sanctum (Sweet basil)

All of the mice were administered lethal doses of E. coli and development of bacteremia was reduced in the treatment group. The authors conclude that the protective effect of this Ayurvedic herbal formula may be due to indirect enhancement of antimicrobial defenses as well as direct enhancement of macrophage response (Mitra et al. 1999).

A series of new herbal preparations based on Traditional Chinese Medicine were evaluated for their ability to improve outcomes in 183 cases of septic shock. Injections of the following herbs which regulate the flow of qi, appeared to promote blood circulation and enhance the body's resistance to circulatory collapse: 

• Kangjue tongma
• Yiqi jiuyin
• Yiqi huiyang 

Injections were also reported to significantly improve mortality in the treatment group (4.4%) as compared to controls (23.0%). Blood pressure was stabilized, renal blood flow was enhanced, and blood viscosity was lowered. An additional animal study of the remedies reported reduced lipid peroxidation and stabilization of cellular membranes (Jin et al. 1995).

Scientific investigations of homeopathic remedies for the treatment of shock specifically have not been conducted. The remedy Aconite, however, is frequently used by homeopathic doctors for acute, emergent conditions which might include shock (Jack 1986)

In rabbits with induced hemorrhagic shock, electroacupuncture of Neiguan (P 6) (Song et al. 1993):

• Raised blood pressure
• Protected cardiac pump function
• Normalized serum levels of angiotensin II, atrial natriuretic peptide, serotonin, and thromboxane B2

While the most common adverse events related to acupuncture are forgotten needles, near syncope, and needle pain, there have been rare case reports of acupuncture producing serious side effects including one mortality secondary to septic shock (Ernst and White 2000). Nonfatal cardiac tamponade is extremely rare, but has been reported to follow acupuncture treatments in at least three cases (Kirchgatterer et al. 2000).

Hospitalization including admission to an intensive care unit is critical with careful monitoring of the following:

• Continuous cardiac monitoring and serial 12-lead ECGs
• Arterial BP
• Ventricular filling pressure via right heart catheterization
• Urine flow
• Arterial blood pH
• Body temperature
• Overall clinical status

• Treatment of related disorders may reduce risk
• Avoid allergens to prevent anaphylactic shock; carry epinephrine pen

• Damage to organs, including kidney, brain, liver
• Cardiac arrest
• Respiratory arrest
• Death

Outcome depends on immediate and proper treatment in most cases. Cure may occur with early diagnosis and treatment. However, all causes of shock have very high rates of morbidity and mortality. Immediate treatment for anaphylactic shock usually results in complete recovery. Mortality in elderly patients due to septic shock is particularly high.

Childbirth is a risk factor for shock.

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