Shock and Multiple Organ Dysfunction Syndrome

SHOCK

• Inadequate perfusion at the tissue level, leading to a decreased supply of oxygen and nutrients needed to maintain the body's metabolic needs.

• Referred to as “The reversible stage of dying.”

SHOCK Classifications

• Hypovolemic

• Cardiogenic

• Obstructive

• Distributive

SHOCK Compensatory Mechanisms

Vascular Response

• Sympathetic stimulation

• Baroreceptor inhibition

• Arteriole constriction

• Increased peripheral resistance

• Increased Blood Pressure

• Venous vasoconstriction

• Increased venous return to the right atrium (RA)

• Total

Cerebral Response

• The primary goal of the body is to maintain perfusion of the heart, brain, and kidneys.

• Preferential perfusion is given to the heart, brain, and kidneys.

• Compromised perfusion of other organs.

• Sympathetic stimulation has little effect on cerebral and coronary arteries.

• Cerebral ischemia occurs when BP < 50 mmHg.

• Manifestations include agitation, confusion, and altered level of consciousness (LOC).

Renal Response

• Renal ischemia triggers the following:

  • Renin release

  • Angiotensin I production

  • Lungs convert Angiotensin I to Angiotensin II via angiotensin-converting enzyme (ACE).

  • Angiotensin II causes vasoconstriction and stimulates sympathetic activity.

  • Aldosterone release, leading to Na+ and H2O retention.

Adrenal Response

• Release of catecholamines from the adrenal medulla.

• Results in tachycardia and anxiety.

• Compensatory rise in diastolic blood pressure (DBP).

Hepatic Response

• Glycogenolysis is activated by epinephrine.

• Hepatic ischemia may occur.

Pulmonary Response

• Tachypnea to maintain acid-base balance and increase oxygen supply.

• Metabolic acidosis due to anaerobic metabolism.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)

• Upsets the balance between pro-inflammatory and anti-inflammatory processes.

• A normally localized process becomes systemic.

• Release of mediators leads to:

  • Increased permeability of the endothelial wall.

  • Fluid shifts out of intravascular spaces.

  • Depletion of intravascular volume, resulting in relative hypovolemia.

PERIPHERAL VENOUS LACTATE LEVEL

• Lactate is a marker for cellular hypoxia.

• Serial lactate measures help assess response to therapy.

• Normal lactate level: less than 2.0 mmol/L.

• A level above 4.0 mmol/L is associated with an increased mortality rate.

• Ensure the tourniquet is not on for more than 2 minutes when drawing the blood sample.

STAGES OF SHOCK

• Stage I: Initiation

• Stage II: Compensatory

• Stage III: Progressive

• Stage IV: Refractory

STAGES OF SHOCK—STAGE I: INITIATION

• Hypoperfusion: inadequate delivery or extraction of oxygen.

• No obvious clinical signs.

• Early and reversible.

STAGES OF SHOCK—STAGE II: COMPENSATORY

• Sustained reduction in tissue perfusion.

• Initiation of compensatory mechanisms:

  • Neural: baroreceptors and chemoreceptors

  • Endocrine: ACTH and ADH

  • Chemical: low oxygen tension, hyperventilation, and respiratory alkalosis

STAGES OF SHOCK—STAGE III: PROGRESSIVE

• Failure of compensatory mechanisms.

• Profound cardiovascular effects:

  • Increased hypoperfusion

  • Vasoconstriction:

    • Extremity ischemia

    • Cellular hypoxia

    • Lactic acid production

    • Failure of the Na^+/K^+ pump

  • Increased capillary hydrostatic pressure

  • Intravascular fluid shifts:

    • Interstitial edema

    • Decreased circulating intravascular volume

  • Decreased coronary perfusion:

    • Myocardial depressant factor released

    • Decreased myocardial contractility

STAGES OF SHOCK—STAGE IV: REFRACTORY

• Prolonged inadequate tissue perfusion.

• Unresponsive to therapy.

• Contributes to multiple organ dysfunction and death.

• Thrombi in microcirculation.

• Metabolic acidosis.

• Vasomotor failure.

• Decreased coronary perfusion leading to decreased myocardial contractility.

• Tissue ischemia.

HYPOVOLEMIC SHOCK

Clinical Presentation

• SKIN: Pale, waxen, ashen, cool, mottled

• NECK VEINS: Collapsed

• CAPILLARY REFILL: >3 seconds

• PULSES: Weak & thready

• AFTERLOAD (SVR): Increased

• PRELOAD (RAP): Decreased

• CO: Decreased

• COMPENSATED: MAP Normal

• DECOMPENSATED: MAP Decreased

Treatment

• ABC’s first

• Identify & control the source of the fluid/blood loss

• VOLUME, VOLUME, VOLUME!!!

• Vasopressors should be avoided until replacement of the volume loss is well under way

• DEHYDRATION: Electrolyte solution, i.e., Lactated Ringer's (LR)

• HEMORRHAGE >1000-1250 cc blood loss:

  • 3 cc of crystalloid for every 1 cc of blood loss

  • OR

  • 1 cc of colloid (blood products, albumin, etc.) for every 1 cc blood loss

• < 1500 cc blood loss:

  • Crystalloid plus blood components

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)

• Widespread systemic inflammatory response.

• Associated with diverse disorders:

  • Infection

  • Trauma

  • Shock

  • Pancreatitis

  • Ischemia

• Most frequently associated with sepsis

SEPTIC SHOCK

• Viral, Bacterial: Gram - or Gram +, Fungal

• Predisposing factors:

  • Elderly

  • Immunocompromised

  • Invasive procedures, indwelling catheters

  • Neonates

  • Alcoholics

  • Diabetics

• As a bacterial endotoxin enters the body, normally protective inflammatory processes spiral out of control

• Macrophages produce cytokines causing vessel dilation and increased permeability leading to occlusion of microvasculature and Generalized ischemia.

• Dilated intravascular compartment & “Leaky” vascular compartment leads to:

  • Hypotension

  • Tachypnea, respiratory alkalosis

  • Tachycardia

  • Warm, flushed skin, hyperthermia

  • Altered LOC

  • Polyuria

  • Increased WBC’s

  • Hyperglycemia

HYPERDYNAMIC PHASE : Hemodynamics

• MAP: Normal or decreased

  • Initially, MAP may be normal due to compensatory mechanisms, but as vasodilation progresses, it tends to decrease.

• AFTERLOAD (SVR): Decreased

  • Systemic vascular resistance decreases due to the release of inflammatory mediators causing vasodilation.

• PRELOAD (RAP): Normal or decreased

  • Right atrial pressure can be normal or decreased, influenced by fluid shifts and venous dilation.

• CO: Increased

  • Cardiac output is typically elevated in the hyperdynamic phase as the heart attempts to compensate for reduced SVR and maintain tissue perfusion.

HYPODYNAMIC PHASE CLINICAL PRESENTATION

• Hypotension

  • прогрессирует, несмотря на fluid resuscitation.

• Tachycardia

  • Heart rate increases to compensate for decreased blood pressure and cardiac output.

• Tachypnea

  • Increased respiratory rate due to metabolic acidosis and hypoxemia.

• Metabolic Acidosis

  • Anaerobic metabolism leads to lactic acid production.

• Cool, pale skin

  • Vasoconstriction and decreased perfusion result in cool and pale skin, especially in the extremities.

• Hypothermia

  • Body temperature may decrease due to impaired thermoregulation and decreased metabolic rate.

• Worsening LOC

  • Decreased cerebral perfusion leads to confusion, disorientation, and reduced responsiveness.

• Decreased WBC’s

  • Leukopenia may occur due to exhaustion of WBC reserves or increased margination and sequestration of WBCs in the microvasculature.

• Oliguria

  • Kidney function declines due to decreased renal perfusion, resulting in reduced urine output.

• Hypoglycemia

  • Glucose consumption by tissues exceeds glucose production, leading to hypoglycemia.

HYPODYNAMIC PHASE : Hemodynamics

• MAP: Decreased

  • Mean arterial pressure is reduced due to progressive vasodilation, myocardial depression, and hyp

Vasopressors

• Dopamine

• Dobutamine

• Epinephrine

• Phenylephrine

• Norepinephrine

Treatment

• Antibiotic therapy

• Removal of septic focus when possible

• Cooling measures for T > 102 o F

• Glucocorticoids to reduce inflammatory response (controversial)

ANAPHYLACTIC SHOCK

• Circulatory failure related to biochemical abnormalities secondary to a systemic allergic reaction.

• Exposure to allergen leads to the production of IgE antibodies, resulting in the release of biochemical mediators.

• Leaky vascular compartment, Vasodilation, and Massive 3rd space fluid shifting occur.

• Angioedema.

CLINICAL PRESENTATION

• Altered LOC

• Warm/flushed skin (Ashen in later stages)

• Edema of subcutaneous or mucus tissues

• Itching, hives

• Tachycardia, Weak, thready pulse

• Laryngeal edema

• Dyspnea, Stridor, Wheezing, Lower airway obstruction, Retractions, Pulmonary Edema

• N/V/D, abdominal cramping

Hemodynamics

• MAP: Decreased

• AFTERLOAD (SVR): Decreased

• PRELOAD (RAP): Decreased

• CO: Normal or decreased

Treatment

• ABC’S

• Epinephrine 3-5 cc of 1:10,000 IV push

• EpiPen (outside of hospital setting)

• Crystalloids or albumin

• Vasopressors for persistent hypotension

NEUROGENIC SHOCK

• Initiated by damage to and/or dysfunction of the sympathetic nervous system.

• Produced by spinal cord damage or pharmacological blockade of the sympathetic nervous system at the level of T-6 or higher.

• Interruption of vasoconstrictor or cardioaccelerator impulses

CLINICAL PRESENTATION

• Massive vasodilation

• Pooling of blood in peripheral circulation, leading to relative hypovolemia

• Altered LOC

• Warm, pink, dry skin

• Bradycardia

• Normal or weak pulses

• Hypoventilation or apnea

• Poikilothermy

Hemodynamics

• MAP: Decreased

• AFTERLOAD (SVR): Decreased

• PRELOAD (RAP): Decreased

• CO: Normal or decreased

Treatment

• ABC’s

• Crystalloids

• Elevation of lower extremities

• Control of severe symptomatic bradycardias

CARDIOGENIC SHOCK

• Heart unable to generate sufficient CO, Mortality 80-100%!

• May occur in association with normal or elevated CO

• Tachydysrhythmias & Bradydysrhythmias

• Myocardial depression due to electrolyte imbalances, hypoxemia, drugs, etc.

• Mechanical defects

• Major surgery or trauma

• AMI

CLINICAL PRESENTATION

• Altered LOC

• Pale, cool, clammy skin

• Tachycardia + Ectopics / Bradydysrhythmias associated with AMI

• Weak and/or muffled heart sounds

• Distended neck veins

• Displacement of the PMI downwards & to the left

• Dyspnea, tachypnea

• Oliguria

• “Wet” breath sounds

• Metabolic acidosis

Hemodynamics

• MAP: Decreased

• AFTERLOAD (SVR): Normal or increased

• PRELOAD (RAP): Normal or increased

• CO: Decreased

Treatment

• ABC’s

• Pain relief

• Control of rhythm disturbances

• Fluid challenge guided by hemodynamics

• Afterload reduction

• Inotropic support

• IABP

• LVAD

OBSTRUCTIVE SHOCK

• Tension Pneumothorax

• Pericardial Tamponade

• Pulmonary Embolism

Treatment

• ABC’s

• Treat the underlying cause!!!

MULTIPLE ORGAN DYSFUNCTION SYNDROME

• Progressive dysfunction of two or more organ systems

• Most common causes:

  • Sepsis

  • Septic shock

• Can occur after any severe injury or illness

• Mortality rates:

  • 45% to 55% failure of two organ systems

  • 80% with three or more

  • 100% with three or more for more than 4 days

Clinical manifestations

• Tachypnea/hypoxemia

• Petechiae/bleeding

• Jaundice

• Abdominal distention

• Oliguria to anuria

• Tachycardia

• Hypotension

• Change in level of consciousness

Management

• Control infection with Antibiotics

• Provide adequate tissue oxygenation:

  • Maintain 88% to 92% arterial oxygen saturation

  • Maintain hemoglobin above 7 to 9 g/dL

• Restore intravascular volume:

  • Aggressive fluid resuscitation with Isotonic crystalloids

• Support organ function

SHOCK NURSING INTERVENTIONS

• Maintain oxygenation/ventilation: Priority!

  • Maintain airway with Airway adjuncts, suctioning, and chest physiotherapy

  • Administer supplemental oxygen

  • Proper positioning with Head of bed elevation to promote ventilation

• Nutritional support via early enteral feedings

• Skin integrity:

  • Decreased perfusion precipitates injury, so Meticulous skin care is essential

  • Frequent turning

  • Lotions

  • Pressure-relieving devices

• Psychological support:

  • Identify the impact of illness and Provide frequent information

  • Address life-sustaining therapies/end of life concerns