Shock Circulatory Disease

DESCRIPTION
Inadequate perfusion (oxygen supply) of tissues which results in organ dysfunction, cellular and organ damage and, if not corrected quickly, death of the patient. Classification of shock:
  • Hypovolemic shock - cardiac output is severely reduced due to loss of intravascular volume which results in reduced return of venous blood to the heart. Most often caused by blood loss.
  • Cardiogenic shock - cardiac output is severely reduced due to a loss of myocardial muscle function, valvular dysfunction, or arrhythmia. Most often caused by large myocardial infarctions.
  • Obstructive shock - cardiac output is severely reduced by vascular obstruction of venous return to the heart (vena cava syndrome), compression of the heart (pericardial tamponade, tension pneumothorax), or outflow from the heart (aortic dissection, pulmonary embolism)
  • Distributive shock - maldistribution of blood flow
  • Venous pooling (most often due to spinal shock or drug overdose) behaves much like hypovolemic shock; cardiac output severely reduced because blood is pooled in peripheral veins rather than being returned to the heart
  • High output or vasodilating shock (most often due to sepsis or septic-like states such as toxic shock) is unique in that cardiac output is normal or elevated, but not distributed appropriately, resulting in overperfusion of some tissues and underperfusion (to the point of critical ischemia) of other tissues
  • System(s) affected: Cardiovascular
  • Genetics: Unknown
  • Incidence/Prevalence in USA: N/A
  • Predominant age: All ages. Determined by underlying diseases causing shock. More frequent and less well tolerated in the elderly.
  • Predominant sex: Male = Female
SIGNS AND SYMPTOMS
  • Underlying disease:
    • Upper gastrointestinal (UGI) bleeding (ulcer pain, hematemesis, melena)
    • Sepsis (fever, chills, dysuria and/or costovertebral angle [CVA] tenderness with urinary tract infection)
    • Myocardial infarction (chest pain, diaphoresis, nausea, vomiting, S4 or S3 gallop, new heart murmur, rales due to pulmonary edema)
  • Underperfusion of organ systems:
    • Brain: confusion, anxiety, agitation, coma only if severe
    • Kidney: oliguria
    • Skin: peripheral cyanosis, sluggish capillary refill, mottling, coolness; may be overly perfused (flushed) in high output (septic) shock
    • GI: absence of bowel sounds
    • Circulation: thready pulses, tachycardia, hypotension (mean arterial pressure < 60 torr or systolic pressure < 90 torr or blood pressure > 40 torr less than usual blood pressure in chronic hypertension), secondary cardiac ischemia (ST depression) or heart failure may occur due to underperfusion of the heart during shock; jugular venous distention (JVD), pulsus paradoxus in pericardial tamponade
CAUSES
  • Hypovolemic shock
    • Blood loss due to trauma or gastrointestinal bleeding
    • Third space loss of plasma volume (pancreatitis, bowel obstruction, infarction, anaphylaxis)
    • Diarrhea (e.g., in cholera-like states)
    • Burns
  • Cardiogenic shock
    • Acute myocardial infarction (> 40% of LV mass)
    • Arrhythmia (heart block, ventricular tachycardia, atrial fibrillation with rapid ventricular response, etc.)
    • Acute valvular dysfunction (mitral valve due to papillary muscle rupture following inferior MI or chordal rupture; aortic or mitral valve due to bacterial endocarditis)
    • Ventricular septal rupture following anterior/septal MI
  • Obstructive shock
    • Pericardial tamponade
    • Inferior/superior vena caval obstruction, usually due to neoplasms
    • Aortic dissection
    • Massive pulmonary embolism
  • Distributive shock
    • Venous pooling – due to loss of venous tone caused by loss of sympathetic nervous system activity (acute spinal injury, general or spinal anesthesia, overdose of sedative drugs)
    • High output shock – due to sepsis, toxic shock, or anaphylaxis (once plasma volume normalized)
RISK FACTORS
Included with Causes
LABORATORY
  • Specific to shock
    • Elevated lactate (> 2 mmol/L) indicates anaerobic metabolism due to underperfusion of tissues
    • Reduced mixed venous PO2 (< 28 mm Hg) (< 3.7 kPa) obtained from the pulmonary artery indicates vigorous extraction of oxygen from tissues due to underperfusion
  • Underlying diseases responsible for shock
    • ECG, CPK (serial)
    • Chest x-ray
    • Arterial blood gases
    • Gram stain and culture of infected sites
    • Blood cultures
    • CBC (serial determination of Hgb/Hct in bleeding patients)

Drugs that may alter lab results: N/A
Disorders that may alter lab results: N/A

PATHOLOGICAL FINDINGS
N/A
SPECIAL TESTS
  • Certain tests are essential to making correct and prompt diagnosis in order to dictate specific therapy of disease states producing shock. For example:
  • Endoscopy/Radioisotope bleeding scans - enable localization of ongoing bleeding which may direct surgical intervention. The endoscopist may intervene directly via the endoscope (e.g., injection of sclerosants into varices or ulcers).
  • Echocardiograms - may detect and/or quantify pericardial effusions in shock due to pericardial tamponade. Pericardiocentesis can then be performed under echocardiographic guidance. Also useful for detection of valvular failure.
  • Lung scans and/or pulmonary arteriography - for the detection of massive pulmonary embolism.
  • Pulmonary artery (Swan-Ganz) catheterization - for serial measurement of cardiac output, central venous, pulmonary arterial, and pulmonary arterial occlusion pressures (left atrial pressure) and vascular resistance. Mixed venous blood gases can be drawn from the catheter. Indicated when the etiology of shock is uncertain, in cardiogenic and septic shock, or when initial therapy of shock fails to provide for rapid correction of perfusion failure.
IMAGING
See Special Tests
DIAGNOSTIC PROCEDURES
See Special Tests
APPROPRIATE HEALTH CARE
  • Emergency room or intensive or coronary care unit
  • Continuous electrocardiographic monitoring with frequent assessment of blood pressure, respiratory status, and urine output
GENERAL MEASURES
  • Therapy must proceed quickly before extensive damage to vital organs occurs. Therapy is directed simultaneously to correct both the deficit in tissue perfusion and the underlying disease causing shock (see Associated conditions).
  • Maintain SaO2 > 95% with supplemental oxygen. Intubate and mechanically ventilate patient if patient cannot be oxygenated with 100% oxygen or has markedly increased breathing effort (excessive oxygen cost of breathing).
  • Maintain pH above 7.3 (but less than 7.5) to preserve vascular responsiveness to endogenous or exogenous catecholamines.
  • Correct plasma volume deficits rapidly by volume expanders consisting of isotonic saline (0.9% Ns or Ringer's lactate) with or without colloid (albumin 5% or hydroxyethyl starch 6%).
  • Packed red blood cell transfusion to correct or prevent anemia. Hgb maintained at or above 10 grams/dL.
  • Administer coagulation factors (fresh frozen plasma, cryoprecipitate) and platelets if coagulopathy (prolonged PT, PTT, or platelet count < 50,000) is present in a patient who is bleeding.
  • Tachyarrhythmias (other than sinus tachycardia) should be promptly corrected by electrocardioversion. Transvenous pacemakers should be placed to correct bradyrhythmias.
  • Vasopressors (see Medications) to correct hypotension or low cardiac output due to myocardial failure or hypotension due to low vascular resistance.
  • End points of resuscitation: adequate blood pressure (> 60 mm Hg [8.0 kPa] mean or > 90 mm Hg [12.0 kPa] systolic or within 40 mm Hg [5.32 kPa] of patient's normal blood pressure). Patient is awake/alert, urine output adequate, heart rate < 100, warm skin with brisk capillary refill, bowel sounds present. Lactate < 2 mmol/L, mixed venous PO2 > 30 mm Hg.
SURGICAL MEASURES

N/A

ACTIVITY

None

DIET

N/A

PATIENT EDUCATION

N/A

PREVENTION/AVOIDANCE

Shock is best avoided by prompt recognition and treatment of underlying diseases which cause shock (e.g., early antibiotic therapy for infections)

POSSIBLE COMPLICATIONS
  • Multiple organs may be damaged by underperfusion during shock
  • Acute tubular necrosis
  • Ischemic hepatitis
  • Ischemic bowel
  • Disseminated intravascular coagulopathy
  • Adult respiratory distress syndrome (ARDS)
  • Encephalopathy and/or cerebrovascular accident
EXPECTED COURSE AND PROGNOSIS
  • Mortality is determined by a complex interaction of primary disease causing shock, age, coexisting chronic disease, and shock severity as marked by the number of acute organ system failures that follow shock
  • Best outcome (> 90% survival) in young patient with transient shock due to trauma or gastrointestinal blood loss without chronic irreversible illnesses
  • Poor outcome (> 90% mortality) in elderly patient with septic shock, underlying chronic liver disease, who develops acute renal failure, ARDS, and coagulopathy
ASSOCIATED CONDITIONS
  • Gastrointestinal blood loss: may require endoscopic or surgical intervention if bleeding doesn't spontaneously cease, e.g., electrocoagulation or injecting sclerosant for bleeding peptic ulcers, sclerotherapy in esophageal varices
  • Sepsis: empiric antibiotic therapy, antibodies against gram negative antigens
  • Cardiogenic shock: therapy should help reduce cardiac ischemia (oxygen, nitrates) and accomplish rapid reperfusion of injured, but potentially viable, myocardium (thrombolysis with fibrinolytic agents, balloon angioplasty of stenotic vessels or surgical bypass grafting) A balloon pump may temporize by providing improved coronary blood flow during and following diagnostic testing and revascularization therapy. If shock is due to acute failure of the mitral or aortic valve, surgical valve replacement may be lifesaving.
  • Pulmonary embolism
  • Cardiac tamponade
AGE-RELATED FACTORS

Pediatric: N/A
Geriatric: N/A
Others: N/A

PREGNANCY

N/A

OTHER NOTES

N/A

ABBREVIATIONS

N/A

Clinical Investigations

ROLE OF HOMOEOPATHY

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