Shock

Shock

• Clinical syndrome characterized by a systematic imbalance between oxygen supply and demand.

• Results in a state of inadequate blood flow to body organs and tissues, causing life-threatening cellular dysfunction

Cellular Homeostasis and Hemodynamics • A cardiac output sufficient to meet bodily

requirements• An uncompromised vascular system, in

which the vessels have a diameter sufficient to allow unimpeded blood flow and have a good tone (the ability to constrict or dilate to maintain normal pressure)

• A volume of blood sufficient to fill the circulatory system, and a blood pressure adequate to maintain blood flow

• Tissues that are able to extract and use the oxygen delivered through the capillaries

Stroke volume (SV)• Amount of blood pumped into the aorta with each

contraction of the left ventricle• SV= ESP - EDP

Cardiac Output (CO)• Amount of blood pumped per minute into the

aorta by the left ventricle• CO= SV x HR

Mean Arterial Pressure (MAP)MAP= CO x SVR

Pathophysiology

Stage 1: Early, Reversible, and Compensatory Shock

• MAP falls 10 to 15mmHg below normal levels

• Circulating bloodvolume is reduced by 25% to 35% (1000ml or more)

• Stimulation of the sympathetic nervous system

• Renin-angiotensin response• Adrenocorticotropic hormone (ACTH)• Anti-diuretic hormone (ADH)

• Stage 2: Intermediate or Progressive Shock

• ↓ in MAP of 20mmHg or more

• Fluid loss of 35 to 50% (1800 to 2500ml of fluid)

• Aerobic to anaerobic metabolism

• Stage 3: Refractory or Reversible shock

• Irreversible stage

• Tissue anoxia: generalized and cellular death

• Death of cells → death of tissues → death of organs → death of the body

Multisystem Effects of ShockCardiovascular

• Early• No change

• Progressive• Slightly ↑ BP• Slowly rising HR• Sinus tachycardia• Thready pulse

• Late• MAP <60mmHg• Steadily ↓ BP• Steadily ↓ C/O• Imperceptible pulsesT

• Respiratory• ↑ respiratory rate• Respiratory acidosis• Potential Complication

• ARDS• Gastrointestinal

• Early• ↓ GI motility

• Late• Paralytic ileus• Ulceration of GI

mucosa• Potential

Complication• Bowel necrosis

Hepatic• Early

• ↑ glucose production• Progressive

• ↓ glucose production= hypoglycemia

• ↓ lactic acid conversion= metabolic acidosis

• Progressive Complication• Destroyed Kupffer cells=

systematic bacterial infections Integumentary

• Pallor (skin,lips, oral mucosa, nail beds, conjunctiva)

• Cool.moist skin• Late

• Edema

Neurologic• ↓ condition• ↓ sympathetic activity• ↓ consciousness

• Early• Restlessness, apathy

• Progressive• Lethargy

• Late• Coma

Urinary• ↓ renal perfusion• ↓ GFR

• Late• Oliguria

• Potential Complications• Acute tubular necrosis• Kidney failure

Diagnostic Tests

• Blood hemoglobin and hematocrit• Arterial Blood Gases (ABGs)• Serum electrolytes• Blood urea nitrogen (BUN)• Blood cultures• White blood cell count and

differential• Serum cardiac enzymes• Central venous pressure

Types of Shock

Hypovolemic Shock

• Most common type of shock and often occurs simultaneously with other types

• ↓ in intravascular volume of 15% or more

• The venous blood returning to the heart ↓ and ventricular filling drops

• Result: stroke volume, cardiac output, and blood pressure (↓)

Cause

• Loss of blood volume from Hemorrhage• Loss of intravascular fluid from the skin due to injuries

such as burns• Loss of blood volume Severe Dehydration • Loss of body fluid from GI system due to persistent and

severe vomiting or diarrhea or continuous nasogastric suctioning

• Renal losses of fluid• Conditions causing fluid shifting • Third spacing

Assessment Findings System/ Assessment Initial Stage Compensatory and

Progressive stagesIrreversible Stage

Blood Pressure normal to slightly ↓ Hypotension Severe hypotension

Pulse slightly ↑ from baseline Rapid, thready Very rapid, weak

Respirations Normal (baseline) Increased Repid, shallow;crackles and wheezes

Skin Cool, pale (in periphery, moist

Cool, pale (includes trunk); poor skin turgor with fluid loss, edematous

with fluid shift

Cool, pale, mottled cyanosis

Mental status Alert and oriented Restless, anxious, confused, or agitated

Disoriented, lethargic, comatose

Urine output Slight  ↓ Oliguria (less than 30ml/hour)

Anuria

Other Thirst, ↓ capillary refill time Marked thirst, acidosis, hyperkalemia, ↓

capillary refill time, ↓ or absent peripheral pulses

Loss of reflexes, ↓ or absent peripheral pulses

Oxygenation• Provide supplemental O2• Monitor SvO2 or ScvO2

Circulation• Restore fluid volume• Rapid fluid replacement using two

large-bone (14-16 gauge) peripheral IVs

• Endpoint of fluid resuscitation:• CVP 15mmHg• PAWP 10-12 mmHg

Collaborative Care

Supportive Therapies• Correct the cause• Use warmed fluids

• Medicines such as dopamine, dobutamine, epinephrine, and nor epinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart (cardiac output).

Swan-Ganz

Catheter

Cardiogenic Shock

• Occurs when the heart’s pumping ability is compromised to the point that it cannot maintain cardiac output and adequate tissue perfusion

Causes• Myocardial infarction• Cardiac tamponade• Restrictive pericarditis• Cardiac arrest• Dysrhythmia• Pathologic changes in the valves• Cardiomyopathies• Complications from cardiac surgery• Electrolyte imbalances• Drugs• Head injuries causing damage to the

cardioregulatory center

Assesment findings• Blood pressure: hypotension

• Pulse: rapid, thready; distention of veins of hands and neck

• Repirations: increased, labored; crackles and wheezes; pulmonary edema

• Skin: pale, cyanotic, cold, moist

• Mental Status: restless, anxious, lethargic progressing to comatose

• Urine output: oliguria to anuria

• Other: dependent edema; ↑ CVP, ↑ pulmonary capillary wedge pressure; arrhytmias

Collaborative Care

Oxygenation

• Provide supplemental O2

• Intubation/ mechanical ventilation, if necessary

• Monitor SvO2 or ScvO2

Circulation

• Restore blood flow with thrombolytics, angioplasty with stenting, emergent coronary revascularization

• Reduce workload of the heart with circulatory assist devices

Drug therapies

• Nitrates

• Inotropes

• Diuretics

• B-Adrenergic blockers

Supportive Therapies

• Correct dysrhythmias

Meningococcal septic shock with adrenal apoplexy

• Sepsis leading to distributive shock occurs when organisms are present in the blood. This form of shock is most commonly called septic shock

• Common organisms causing sepsis include gram-negative bacteria (Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumonia) and gram positive bacteria (Staphylococcus and Streptococcus)

• Through the activity of white blood vessels, the reactions start inflammatory and immune events known as the systemic inflammatory response syndrome (SIRS)

• These toxin-host actions activate complement, cause small clots to form within the capillaries of vital organs, increase capillary leakiness, injure cells (esp. endothelial cells of blood vessels), and increase cell metabolism

• Septic shock occurs when large amounts of toxins and endotoxins produced by bacteria are released into the blood, causing a whole-body inflammatory reaction.

• These substances react with blood vessels and cell membranes.

• These toxin-host actions activate complement, cause small clots to form within the capillaries of vital organs, increase capillary leakiness, injure cells (esp. endothelial cells of blood vessels), and increase cell metabolism.

• Damage to endothelial cells reduces anticlotting actions and triggers the formation of small clots. Metabolism becomes anaerobic because of decreased MAP, clot formation in capillaries, poor cell uptake of oxygen

Capillary leak syndrome

• Capillary leak syndrome leading to distributive shock occurs when fluid shifts from the blood to the interstitial space. Such shifts are caused by increased size of capillary pores loss of plasma osmolarity, increased hydrostatic pressure in the blood.

• Capillary leak syndrome leading to distributive shock occurs when fluid shifts from the blood to the interstitial space.

• Such shifts are caused by increased size of capillary pores loss of plasma osmolarity, increased hydrostatic pressure in the blood.

Conditions predisposing to sepsis-induced Distributive shock (Septic Shock)• Malnutrition• Immunosuppresion• Large, open wounds• Mucous membrane fissures in prolonged contact with

bloody or drainage-soaked packing

• Gastrointestinal ischemia• Loss of GI integrity• Exposure to invasive procedures• Malignancy• Over 85 years of age• Infection with resistant microorganisms• Receiving cancer chemotherapy

Medical Management

• Specimens of blood, sputum, urine, wound drainage, and invasive catheter tips are collected for culture using aseptic technique

• Crystalloids, colloids, and blood products may be administered to increase the intravascular volume

Medication

• A third-generation cephalosporin plus an aminoglycoside

Nursing management

• All invasive procedures must be carried out with aseptic technique after careful hand hygiene.

• Additionally, intravenous lines, arterial and venous puncture sites, surgical incisions, traumatic wounds, urinary catheters, and pressure ulcers are monitored for signs of infection in all patients.

• Elevated body temperature (hyperthermia) is common with sepsis and raises the patient’s metabolic rate and oxygen consumption.

• Fever is one of the body’s natural mechanisms forfighting infections. Thus, an elevated temperature may not be treated unless it reaches dangerous levels (more than 40°C [104°F]) or unless the patient is uncomfortable.

• Efforts may be made to reduce the temperature by administering acetaminophen or applying hypothermia blankets

• Because of decreased perfusion to the kidneys and liver, serum concentrations of antibiotic agents that are normally cleared by these organs may increase and produce toxic effects

• Therefore, the nurse monitors blood levels (antibiotic agent, BUN, creatinine, white blood count

Distributive shock

• It is by a loss sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, increased blood vessel permeability (capillary leak).

• All these factors can decrease mean arterial pressure(MAP) and may be started by nerve changes (neural-induced) or the presence of chemicals (chemical-induced).

Neural-Induced Distributive Shock

•  Neural-induced loss of MAP occurs when sympathetic nerve impulses controlling blood vessel smooth muscles are decreased and the smooth muscles of blood vessel relax, causing vasodilation.

• This blood vessel dilation can be a normal local response to injury, but shock results when the vasolidation is widespread or systemic.

Risk factors

• Pain• Anesthesia• Stress• Spinal cord injury• Head trauma

Chemical-Induced distributive Shock

• Chemical-induced distributive shock has three common origins: anaphylaxis, sepsis, capillary leak syndrome. Chemical-induced distributive shock occurs when certain chemicals or foreign substances within the blood and blood vessels start widespread changes in blood vessel walls.

• Exogenous• Endogenous

Risk factors

• Anaphylaxis• Sepsis• Capillary leak• Burns• Extensive trauma• Hepatic dysfunction• Hypoproteinemia

Obstructive Shock

• It is caused by problems that impair the ability of the normal heart muscle to pump effectively.

• The heart itself is normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. 

Risk factors

• Cardiac tamponade• Arterial stenosis• Pulmonary embolus• Pulmonary hypertension• Constrictive pericarditis• Thoracic tumors• Tension pnemothorax

•Vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation.

•Sympathetic stimulation causes vascular smooth muscle to constrict.

•Parasympathetic stimulation causes the vascular smooth muscle to relax or dilate.

• Blood volume is adequate, because the vasculature is dilated, the blood volume is displaced, producing a hypotensive (low BP)state.

• In adequate BP result insufficient perfusion of tissues and cells that is common to all shock states.

Neurogenic Shock can caused by

• Spinal cord injury

• Spinal anesthesia or nervous system damage

• Lack of glucose

• BP and heart rate increase

• Dry skin rather than cool • Moist skin seen in hypovolemic shock• Bradycardia rather than tachycardia

• The stabilization of spinal cord injury or proper positioning of the patient

• Elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock when the patient receives spinal or epidural anesthesia.

• Applying elastic cpmpression stocking and elevating the foot of the bed may minimize pooling of blood in the legs

• The nurse should check the lower extremity pain, redness, tenderness and warmth of the calves

• Occurs rapidly and life is threatening • Occurs in patients already exposed to an antigen and

who have developed antibodies

Caused by

• Severe allergic reaction

• Removing the causative antigen (discontinuing an antibiotic agent)

• Epinephrine is given for its vasoconstriction action• Diphenhydramine (Benadryl)• Albuterol (Proventil)

• Asses for all allergies or previous reactions to antigens (medications, blood products, foods contrast agents, latex).

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