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SHOC K
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A complex clinical syndrome that may occur at any time and in any place. Inadequate blood flow to body organs and tissue causing lifethreatening cellular dysfunction. A syndrome not an illness nor a disease. A syndrome in which there is circulation perfusion compromise. tissue perfusion. Their is a cellular anoxia, if not prevented leads to tissue death. Homeostasis just to restore the patency of the blood. Inadequate tissue perfusion. Oxygen in the blood. Serious life threatening condition.

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Classificatio n

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Shock is commonly divided into three major classifications: SHOCK

1. HYPOVOLEMIC

2. CARDIOGENIC

3. DISTRIBUTIVE

Hemorrhage Anaphylactic Burns Neurogenic Dehydration

MI Obstructive condition other causes Septic

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1. Hypovolemia
Reduced

intravascular blood volume causing circulatory dysfunction and inadequate tissue perfusion resulting from loss of blood, plasma, or fluids. loss of fluid in our body. life threatening.

Massive

Potentially

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Pathophysiology
CAUSES:

Hemorrhage Burns Dehydration ( as from excessive perspiration, severe diarrhea, protracted vomiting, diabetes insipidus, diuresis, or inadequate fluid intake)

When fluid is lost from the intravascular space ( venous return to the heart is reduced )

This decreases ventricular filling ( which leads to a drop in stroke volume.)

Cardiac output falls (causing reduced perfusion to tissues and organs.)

Tissue anoxia prompts a shift in cellular metabolism from aerobic to anaerobic pathways.

This produces an accumulation of lactic acid, resulting in metabolic acidosis.

HYPOVOLEMIA

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ASSESSMENT

FINDINGS

Preexisting disorders or conditions that reduced blood volume, such as GI hemorrhage, trauma, and severe diarrhea and vomiting. Some anginal pain in patients with cardiac disease ( because of decreased myocardial perfusion and oxygenation.) Physical symptoms consistent with reduced

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TREATMENT

In severe cases, an intra-aortic balloon pump, ventricular assist device, or pneumatic anti shock garment ( rare, only when unstable fractures involved) Oxygen administration Bleeding control by direct application of pressure and related measures Possible parenteral nutrition or tube feedings Bed rest Prompt and vigorous blood and fluid replacement Positive inotropes Possibly diuretics Possible surgery to correct underlying problem

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NURSING

MANAGEMENT

Check for a patient airway and adequate circulation. ( if blood pressure and heart rate are absent, start cardiopulmonary resuscitation. Obtain type and cross match as ordered. Administer prescribed I.V solutions or blood products. Insert an indwelling urinary catheter. Administer prescribed oxygen. Provide emotional support to the patient and his family. Used modified Trendelenburgs position. Monitor Vital signs and peripheral pulses Cardiac rhythm

Coagulation studies for signs of impending coagulopathy Complete blood count and electrolyte measurements Arterial blood gas level Intake and output Hemodynamics

Monitor the patient for such complications as:

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2. CARDIOGENIC SHOCK

condition of diminished cardiac output that severely impairs tissue perfusion ( myocardial damage of more than 40% of the left ventricle most common) of the heart to pump blood adequately to meet oxygenation needs of the body. lethal form of shock.

Failure

Most

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pathophysiology

Left ventricular dysfunction initiates as series of compensatory mechanisms that attempt to increase cardiac output.

Initial

Decreased myocardial contractility

Decreased stroke volume

Decreased left ventricular emptying

Increased heart rate

Left ventricular dilation and back up of blood Increased preload

Decreased coronary artery perfusion and collateral blood flow. Myocardial Hypoxia

Pulmonary Congestion

Decreased cardiac output

Compensation

Decompensation and DEATH

CAUSES
Acute mitral or aortic insufficiency End- stage cardiomyopathy Myocardial infarction (MI);myocardial damage of more than 40% of the left ventricle most common Myocardial Ischemia Myocarditis Papillary muscle dysfunction Ventricular aneurysm Ventricular septal defect

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ASSESSMENT FINDINGS
Determination of existing disorder, such as MI or cadiomyopathy that severely decreases left ventricular function. Anginal pain Urine output less than 20ml/hr Pale, cold, clammy skin Decreased sensorium Rapid, shallow respirations Rapid, thready pulse Mean arterial pressure of less than 60 mm Hg in adults Gallop rhythm, faint heart sounds, and possibly, a holosystolic murmur

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TEST RESULTS
Serum enzyme measurements show elevated levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine amino transferase. Troponin level is elevated. Cardiac catherterization and echocardiography may reveal other conditions that can lead to pump dysfunction and failure ( cardiac tamponade, papillary muscle infarct or rupture, ventricular septal rupture, pulmonary emboli, venous pooling, and hypovolemia) Pulmonary artery pressure monitoring reveals increased pulmonary artery pressure and pulmonary artery wedge pressure, reflecting an increase in left ventricular end-diastolic pressure (preload) and heightened resistance to left ventricular emptying (afterload) caused by ineffective pumping and increased peripheral vascular resistance. Invasive arterial pressure monitoring shows systolic arterial pressure less than 80mm Hg ,caused by impaired ventricular ejection. Arterial blood gas (ABG) analysis may show metabolic and respiratory acidosis and hypoxia. Electrocardiography demonstrates possible evidence of acute MI , ischemia, or ventricular aneurysm.

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TREATMENT

Intra aortic balloon pump (IABP) Vasopressors, inotropics, and vasoconstrictors Oxygen Osmotic diuretics Vasodilators Analgesics, sedatives Bed rest Possible parenteral nutrition or tube feedings Possible ventricular assist device Possible heart transplant.

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NURSING INTERVENTION
Administer prescribed oxygen Follow IABP protocols and policies. ( When a patient is receiving treatment with an IABP, sitting position higher than 45 degrees (including for chest x-rays) because the balloon may tear through the aorta and cause immediate death. Monitor the patient continuously for cardiac arrhythmias. Monitor ABG levels (acid-base balance) and pulse oximetry. Evaluate complete blood count and electrolyte levels. Obtain vital signs and peripheral pulses. Monitor hemodynamic parameters. Measure and record urine output every hour from indwelling catheter, and fluid intake. Monitor heart and breath sounds. Evaluate LOC Be alert to adverse responses to drug therapy Plan care to allow frequent rest periods, and provide as much privacy as possible. Provide explanations and reassurance for the patient and his family as appropriate. Prepare the patient and his family for a possibly fatal outcome , and help them find effective coping strategies. Monitor the patient for possible multiple organ dysfunction.

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3. Distributive shock

v v

Problem is in vascular area Is due to changes in blood vessel tone that increase the size of the vascular space without an increase in the circulating blood volume. also called as Vasogenic Shock

Distributive Shock is divided into three types :

Anaphylactic Shock Neurogenic Shock Septic Shock