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The Physiology of Shock

Unit 8 / week 1

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R.E.B, 4MedStudents.com, 2003

What is Shock?
Shock is any condition in which the circulatory system is

unable to provide adequate circulation to the vital body organs such as the brain,heart and lungs. As a result of a decrease in the blood pressure. Shock is usually accompanied by renal failure, as a normal compensatory mechanism, because the blood flow to the kidney is decreased to keep enough blood for the vital organs.
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Increase heart rate as a result of the baroreflex:

Shock will decrease the volume of blood pumped from the heart and the blood flow to the brain. That will activate the baroreceptors in the carotid bodies to increase HR trying to supply enough blood to the vital organs.

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Pale skin:
As a result of vasoconstriction of the peripheral vessels, because the skin is the least priority tissue for blood flow

3. Cold and clammy skin : As a result of vasoconstriction.

Shock decreases the skin surface temperature as a result of vasodilatation, which will increase the internal body temperature. Because the skin plays a major role in controlling body temperature, as it will help in exchanging heat with the external environment. There are two mechanisms to get red of the excess heat:
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Hyperventilation ( Minimal effect in humans) Vasodilatation of the vessels Flush ( Increase blood flow to the skin) BP Real shock

Some of the signs and symptoms of shock include:

Confusion or lack of alertness Loss of consciousness Sweating A weak pulse Rapid breathing Decreased or no urine output Cool hands and feet

Precipitating cause of shock Circulating blood volume Cardiac output Hypotension & perfusion tissue

Baroreceptors stimulated Sympathetic stimulation & cardiovascular system Heart rate; contractility Cardiac Output Anteriolar constriction Blood Pressure Venous constriction Venous return

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a. Compensatory stage- the blood pressure

remains w/in normal limit. Vasoconstriction, increased heart rate, & increased contractility of the heart contribute to maintaining adequate cardiac output. This results from stimulation of the sympathetic nervous system & subsequent release of catecholamines (epinephrine & norepinephrine). It displays the often described fight or flight response.
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b. Irreversible Stage ( refractory )- represents

the point along the shock continuum at w/c organ damage is so severe that the pt. does not respond to treatment and cannot survive.
c. Progressive stage- the mechanisms that

regulate BP can no longer compensate & the MAP falls below normal limits, w/ an average systolic blood pressure of less than 90 mmHg.
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CLINICAL FINDINGS IN STAGES OF SHOCK

FINDINGS BP COMPENSATOR PROGRESSIVE Y Normal Systolic <80-90 mmHg IRREVERSIBLE Requires mechanical or pharmacological support Erratic or systole Requires intubation Jaundice Anuric, requires dialysis Unconscious Profound acidosis

HR Respiratory status Skin Urinary Output Mentation

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>100bpm >20cpm

>150bpm Rapid, shallow respirations; crackles Mottled, petechiae 0.5mL/kg/hr Lethargy Metabolic acidosis

Cold, clammy Decreased Confusion Respiratory alkalosis

Acid-base balance

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Shock

Hypovolemic

Cardiogenic

Distributive

Neurogenic

Anaphylactic

Septic

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 Hypovolemic shock- characterized by a

decreased intravascular volume. Body fluid is contained in the intracellular and extracellular compartments. Intracellular fluid accounts for about two thirds of the total body water. The extracellular body fluid is found in one of two compartments; intravascular (inside blood vessels) or interstitial (surrounding tissues). The volume of interstitial fluid is about three to four times that of intravascular fluid. Hypovolemic shock occurs when there is a reduction in intravascular volume of 15% to 25%. This would represent a loss of 750 to 1,300 mL of blood in a 70-kg(154-lbs) person.

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Decreased blood volume Decreased venous return Decreased stroke volume Decreased cardiac output Decreased tissue perfussion
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RISK FACTORS FOR HYPOVOLEMIC SHOCK

External: Fluid losses Fluid Shifts
Trauma Hemorrhage Surgery Vomiting Diarrhea Diuresis Diabetes Insipidus

Internal:

Burns Ascites Peritonitis Dehydration

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Restore intravascular volume to reverse

the sequence of leading to inadequate tissue perfusion Redistribute fluid volume Correct the underlying cause of the fluid loss as quickly as possible

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FLUID REPLACEMENT IN SHOCK FLUIDS Crystalloids 0.9% NaCl( NSS ) ADVANTAGES Widely available, inexpensive DISADVANTAGES

Requires large volume of infusion; can cause pulmonary edema Lactated Ringers Requires large volume Lactate ion helps buffer of infusion; can cause Hypertonic Saline( 3%, metabolic acidosis PE 5%, 7.5% ) Small volume needed Danger of to restore intravascular hypernatremia volume Colloids Albumin ( 5%, 25% ) Dextran ( 40, 70- )

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Hetastarch

Rapidly expands blood Expensive,; requires volume human donors; limited supply; can cause heart failure Synthetic plasma Interferes w/ platelet expander aggregation; not recommended for hemorrhagic shock

 Primary prevention of shock is an essential focus of nursing

intervention. Hypovolemic shock can be prevented in some instances by closely monitoring patients who are at risk for fluid deficits & assisting w/ fluid replacement before intravascular volume is depleted. In other circumstances, hypovolemic shock cannot be prevented, and nursing care focuses on assisting w/ treatment targeted its cause & restoring intravascular volume. General nursing measures include ensuring safe administration of prescribed fluids & medications & documenting their administration of prescribed fluids and medications & documenting their administration & effects. Another important nursing role is monitoring for signs of complications & side effects of treatment & reporting these signs early in treatment.
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Cardiogenic shock occurs when the hearts

ability to contract & to pump blood is impaired & the supply of oxygen is inadequate for the heart & tissues. The causes of cardiogenic shock are known as either coronary or noncoronary. Coronary is more common than noncoronary & is seen most often in patients w/ MI.

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RISK FACTORS FOR CARDIOGENIC SHOCK

Coronary Factors coronary Factors

Myocardial Infarction Cardiomyopathies Valvular damage Cardiac tamponade Dysrhythmias

Non-

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Decreased cardiac contractility Decreased stroke volume & cardiac output

Pulmonar y congestio n

Decreased systemic tissue perfusion

Decreased coronary artery perfusion

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Limit further myocardial damage &

preserve the healthy myocardium Improve the cardiac function by increasing cardiac contractility, decreasing ventricular afterload

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Preventing cardiogenic shock Monitoring hemodynamic status Administering medications & intavenous fluids Maintaining intra-aortic balloon

counterpulsation Enhancing safety & comfort

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Vasodilation Maldistribution of blood volume Decreased venous return Decreased stroke volume Decreased cardiac output Decreased tissue perfusion

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Distributive shock ( Circulatory shock ) occurs

when blood volume is abnormally displaced in the vasculature. Classifications: Septic shock Neurogenic shock Anaphylactic shock

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 Septic shock is the most common of

circulatory shock & is caused by widespread infection. Neurogenic shock occurs as a result of sympathetic tone & can be caused by spinal cord injury, spinal anesthesia, or nervous system damage. It can result from the depressant action of medications or lack of glucose. Anaphylactic shock is caused by a severe allergic reaction when a patient who has already produced antibodies to a foreign substance( antigen ) develops a systemic antigen-antibody reaction.
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RISK FACTORS FOR CIRCULATORY SHOCK Septic Shock Anaphylactic Shock

Immunosuppression sensitivity Extremes of age (<1 yr & >65 yr ) reaction Malnourishment allergy Chronic illness sensitivity Invasive procedures

Penicillin Transfusion Bee sting Latex

Neurogenic Shock

Spinal cord injury Spinal anesthesia Depressant actions of medications Glucose deficiency

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VASOACTIVE AGENTS USED IN TREATING SHOCK

MEDICATION DESIRED ACTION IN SHOCK DISADVANTAGE

Sympathomimetics Improve contractility, Increase oxygen Amrinone(Inocor) increase stroke volume, demand of the heart Dobutamine(Dobutrex) increase cardiac output Dopamine(Intropine) Epinephrine(Adrenalin) Milrinone(Primacor) Vasodilators Nytroglycerine(Tridil) Nitroprusside(Nipride) Rduce preload & Cause hypotension afterload, reduce oxygen demand of heart Increase afterload, thereby increasing cardiac workload; compromise perfusion to skin, kidneys, lungs , GI tract

Vasoconstrictors Increase BP by Norepinephrine(Levophe vasonstriction d) Phenylephrine(NeoSynephrine) Vasopressin(Pitressin)

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o Biochemical radiators- messenger substances

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that may be released by a cell to create an action at that site or be carried by the bloodstream to a distant site before being activated; also called cytokines. o Cardiogenic shock- states that resulting from impairment or failure of the myocardium. o Colloids- intravenous solutions that contain molecules that are too large to pass through capillary membranes. o Crystalloids- electrolyte solutions that move freely between the intravascular compartment and interstitial spaces.

o Hypovolemic shock- states that resulting from

o
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decreased intravascular volume due to fluid loss. Neurogenic shock- states resulting from loss of sympathetic tone causing relative hypovolemia. Septic shock- circulatory shock state resulting from overwhelming infection causing relative hypovolemia. Shock- physiologic state in w/c there is in adequate blood flow o tissues & cells of the body. Systemic inflammatory response syndrome(SIRS)- overwhelming inflammatory response in the