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vascular bed results in circulatory failure and oxygen and nutrient deprivation of tissues
Hyperventilation leads to respiratory alkalosis Vasoconstriction Tachycardia Fluid shifts intracellular to extracellular to maintain circulating blood volume
Impaired metabolism tissue anoxia leads to anaerobic metabolism causing lactic acid buildup, resulting in metabolic acidosis Impaired organ function
Kidney: decreased perfusion can result in renal failure Lung: shock lung (ARDS)
Increased sympathetic response Increased renin-angiotensin activation Increase Decrese catecholamines respiratory and rate cortisol increase to -increase HR, BP, cardiac contractility -increase reabsorption of sodium and to water provide more oxygen glucose saturation for metabolism and delivery Leads toto increase in cardiac output - Leads increase in preload and decrease urine output
In the second stage of shock, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits. Patients are clinically hypotensive; -systolic BP of less than 90 mm Hg - or a decrease in systolic BP of 40 mm Hg from baseline
The irreversible (or refractory) stage of shock represents the point along the shock continuum at which organ damage is so severe that the patient does not respond to treatment and cannot survive.
Characteristic
Decreased circulating blood volume
Causes
Blood loss Plasma loss (e.g. burns) Fluid loss (e.g. excessive vomiting or diarrhea)
Characteristic
Failure of the heart to pump properly
Causes
Myocardial Infarction Congestive Heart Failure Cardiac arrhythmias Pericardial tamponade Tension pneumothorax
Cause
Release of bacterial toxins that act directly on the blood vessels producing massive vasodilation and pooling of blood; results most frequently from gram-negative septicemia
Characteristic
Failure of arteriolar resistance, leading to massive vasodilation and pooling of blood
Exposure to unpleasant circumstances Vasomotor depression Extreme pain Head injury Spinal cord injury
Characteristic
Massive vasodilation resulting from allergic reaction causing release of histamine and related substances
a. Skin
1. Cool, pale, moist in hypovolemic and cardiogenic shock 2. Warm, dry, pink in septic and neurogenic shock
b. Pulse
1. Tachycardia, due to increased sympathetic stimulation 2. Weak and thready
c. Blood pressure
1. Early stage: may be normal due to compensatory mechanisms 2. Later stage: systolic and diastolic BP drops
d. Respiration
- rapid and shallow due to tissue anoxia and excessive amounts of CO2
e. Level of consciousness
- Restlessness and apprehension, progressing to coma
f. Urinary output
- decreases due to impaired renal perfusion
g. Temperature:
- decreases in severe shock (except in septic shock)
A. Maintain patent airways and adequate ventilation B. Promote restoration of blood volume; administer fluid and blood replacement as ordered C. Administer drugs as ordered D. Minimize factors contributing to shock
-positioning, promote rest, relieve
(vs, i&o,
F. Provide psychologic support: reassure client to relieve apprehension and keep family advised
Medication Inotropic Agents Dobutamine (Dobutrex) Dopamine (Intropin) Epinephrine (Adrenalin) Milrinone (Primacor) Vasodilators Nitroglycerin (Tridil) Nitroprusside (Nipride)
Desired Action in Shock Improve contractility, increase stroke volume, increase cardiac output
Cause hypotension
Vasopressor Agents Increase blood pressure Norepinephrine (Levophed) by vasoconstriction Dopamine (Intropin) Phenylephrine (NeoSynephrine) Vasopressin (Pitressin)
Increase afterload, thereby increasing cardiac workload; compromise perfusion to skin, kidneys, lungs, gastrointestinal tract