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Nurs 211 Gail L Lupica PhD, RN, CNE
SHOCK Nurs 211 Gail L Lupica PhD, RN, CNE
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SHOCK Failure of the circulatory system to maintain adequate perfusion of vital organs. キ Without adequate perfusion, oxygenation of cells is compromised, and anaerobic metabolism will take place. キ The by-product of anaerobic metabolism is lactic acid. A metabolic acidosis ensues. Also, when there is inadequate tissue perfusion, waste products of cellular metabolism accumulate (CO2). Remember what ph our body cells function best at? When acidosis occurs, and ph levels fall below 7.35 for an extended period. Cell & organ death occur. Shock can be divided into three major classifications: i. Hypovolemic ii. Cardiogenic iii. Distributive = septic, anaphylactic & neurogenic STAGES OF SHOCK 1. Compensatory Stage/Early Compensation Stage A decrease in cardiac output sets this stage into motion. Compensatory mechanisms kick in to maintain BP and perfusion. HOW? 1. Autonomic Nervous System (ANS) 2. Renin Angiotensin Aldosterone System (RAA) 1) Autonomic Nervous System Falling BP is sensed by the “presso receptors” in the carotids and aortic arch. Signals are sent to the terminal nerve plates to release norepinephrine & to the adrenal medulla to release norepinephrine & epinephrine. What effect will these catecholamines have on: キ vasculature? キ HR? キ Contractility? キ Blood flow to the myocardium and the brain? A decrease in ph and an increase in PCO2 is sensed by “chemo receptors” in the carotids and aortic arch. Signals are transmitted to the Respiratory center in the medulla to increase the rate and depth of ventilation. 2. Renin Angiotensin Aldosterone System. Decreased blood flow to the kidney is sensed by the juxtaglomerular receptor. In turn rennin (a hormone) is released. Renin reacts with Angiotensinogen (from the liver) and produces Angiotensin I. Angiotensin I is converted to Angiotensin II (by a converting enzyme in the lung) Angiotensin II is a potent vasoconstrictor. BP is raised! It also stimulates Aldosterone release from the Adrenal cortex (which causes reabsorption of Na+ and water. This will increase circulating fluid volume, and therefore raise blood pressure) In addition ADH is released from posterior pituitary because of signals received from hypothalamus to hold on to body water (to maintain BP) Critical Thinking *Let’s look at the patient in this stage of shock. 1. Will his respiratory rate be increased or decreased? Why? What effect will this response have on the ABG initially? 2. Will he be hypotensive, normotensive, or hypertensive? 3. Will his urine output be maintained? Why or why not? 4. What will the appearance of his skin be? 5. Will his blood sugar be affected? Why, Why not? 2. Progressive/Decompensation Stage Compensatory Mechanisms are no longer able to compensate for decreased cardiac output. Massive organ hypoperfusion develops. How are organ systems adversely affected? キ Respiratory system. Hypoperfusion to pulmonary capillary bed caused alveolar cells to become ischemic & unable to produce surfactant. Alveoli collapse. => ARDS developes ( We will discuss this later). Bradykinins are released (a vasoactive polypeptide) which produce vasodilation and increased capillary permeability, contributing the progression of ARDS. キ Cardiovascular system. Cardiac dysrhythmias develops due to the acidosis that develops In addition myocardial depressant factor (also a vasoactive polypeptide) is released which further diminishes CO. キ Disseminated Intravascular Coagulation can develop. キ Renal System. Hypoperfusion to the kidney could eventually result in tubular necrosis and renal shutdown. (Urinary output is a direct determinant of circulation and blood flow through the vital organs. キ Hepatic System o Hepatic failure o An impaired ability to detoxify キ Neurological System キ Could see changes in the patient level of consciousness キ GI System. o Reduced blood flow through the intestines during shock results in the movement of normal GI flora into the bloodstream. Patients in shock are much more susceptible to sepsis. 3. Refractory Stage/Progressive Stage Body is refractory to all therapeutic measures. It is irreversible Multiple organ failure develops Death is imminent. SHOCK Failure of the circulatory system to maintain adequate perfusion of vital organs.
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What’s perfusion anyway?
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Perfusion Yes! Blood flow!
So in the shock state there is NOT delivery of the oxygen, electrolytes, proteins, fluids, and hormones….that your cells need
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NO PERFUSION? キ Without adequate perfusion, oxygenation is compromised, and anaerobic metabolism will take place.
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Metabolic acidosis The by-product of anaerobic metabolism is lactic acid. A metabolic acidosis ensues. Also, when there is inadequate tissue perfusion, waste products of cellular metabolism accumulate (CO2).
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Remember what ph our body cells function best at? 7.35 - 7.45
Remember what ph our body cells function best at?
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Acidosis leads to cell death.
When acidosis occurs, and ph level fall below 7.35 for an extended period. Cell & then organ death occur.
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Shock Classifications
Shock can be divided into three major classifications:
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Shock Classifications
1. Hypovolemic (low blood flow) 2. Cardiogenic (low blood flow) 3. Distributive = septic, anaphylactic & neurogenic (maldistribution of blood flow) 4. Obstructive (cardiac fx by non-cardiac factors) More about them later
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The Three Stages of Shock
JUST A FRAMEWORK FOR DISCUSSING CLIENT MANIFESTATIONS THAT OCCUR ON A CONTINUUM Initial Non- progressive (Compensatory) Progressive Refractory (Final)
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Initial Stage Patient may NOT have any clinical manifestations of . Tissue perfusion. Lack of oxygen is occurring at the cellular level May have a in MAP mmHG HR will .
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NON- progressive Stage (Compensatory)
Compensatory mechanisms kick in to maintain BP and perfusion. (A diminishing CO sets this in motion.) MAP falls 10-15mmHg HOW is that done?
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NON- progressive Stage (Compensatory)
1. Autonomic Nervous System (ANS) 2. Renin Angiotensin Aldosterone System (RAA)
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NON- progressive Stage (Compensatory)
Autonomic Nervous System “presso receptors” in the carotids and aortic arch sense a falling BP. Signals are sent in order to release norepinephrine & epinephrine.
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NON- progressive Stage (Compensatory)
Autonomic Nervous System What effect will these catecholamines have on: vasculature? HR? Contractility? Blood flow to the myocardium and the brain?
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NON- progressive Stage (Compensatory)
Autonomic Nervous System A decrease in ph (due to lactic acidosis & hypoventilation) is sensed by “chemo receptors” (chemo=chemical receptors) in the carotids and aortic arch. Signals are transmitted to the Respiratory center in the medulla. What effect does this have?
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NON- progressive Stage (Compensatory)
Renin Angiotensin Aldosterone System
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NON- progressive Stage (Compensatory)
Decreased blood flow to the kidney is sensed by the juxtaglomerular receptor. In turn renin (a hormone) is released. Renin reacts with Angiotensinogen (from the liver) and produces Angiotensin I. Angiotensin I is converted to Angiotensin II (by a converting enzyme in the lung) Angiotensin II is a potent vasoconstrictor. BP is raised!
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NON- progressive Stage (Compensatory)
Renin Angiotensin Aldosterone System It also stimulates Aldosterone release from the Adrenal cortex (which causes reabsorption of Na+ and water. This will increase circulating fluid volume, and therefore raise blood pressure) In addition ADH is released from posterior pituitary because of signals received from hypothalamus to hold on to body water (to maintain BP)
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NON- progressive Stage (Compensatory)????
Critical Thinking ?? ?? ?? ?? ?? ?? ?? ?? ?? NON- progressive Stage (Compensatory)????
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???????? NON- progressive Stage (Compensatory)????
Will his respiratory rate be increased or decreased? Why? What effect will this response have on the ABG initially? Will he be hypotensive, normotensive, or hypertensive? Why? Will his urine output be maintained? Why or why not?
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???NON- progressive Stage (Compensatory)???????
What will the appearance of his skin be? Why? Will his blood sugar be affected? Why, Why not?
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Progressive Compensatory Mechanisms are no longer able to compensate for decreased cardiac output. MAP falls > 20-mmHg Massive organ hypoperfusion develops. What would that look like?
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Progressive How are organ systems adversely affected?
Respiratory system. Hypoperfusion to pulmonary capillary bed caused alveolar cells to become ischemic & unable to produce surfactant. Cardiovascular system (Heme) Disseminated Intravascular Coagulation
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Progressive How are organ systems adversely affected?
Renal System. (acute tubular necrosis Hepatic System An impaired ability to detoxify Neurological System GI System.*********************************
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Refractory (Final) Body is refractory to all therapeutic measures.
It is irreversible Death is imminent.
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