Shock

Relationship of Shock, SIRS, and MODS

Fig. 65-1

Shock
Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism Imbalance in supply/demand for O2 and nutrients Adequate blood flow to the tissues and cells requires;
Adequate cardiac pump Effective vasculature or circulatory system Sufficient blood volume

Physiologic responses to shock

Hypoperfusion of tissues Hypermetabolism Activation of the inflammatory responses (activation of SNS)

Normal cellular function

Energy metabolism Occurs in the cell; breakdown of nutrients and stored as ATP
Aerobic Yields greater amounts of ATP/e of glucose More efficient and effective Anaerobic Results in accumulation of toxic products and lactic acid

Pathophysiology
Cellular changes;
Lack of adequate blood supple decreased nutrient and oxygen --- cells use anaerobic metabolism decreased yields of energy and an acidotic environment normal function ceases Cells swells Cellular membrane become more permeable Uncontrolled fluid and electrolyte transfer Na-K punp becomes impaired Cellular structures damaged (mitochondria) Cellular death Increased blood glucose levels

 Vascular responses Local regulatory mechanisms react to decreased oxygen AUTOREGULATION stimulates vasodilation or vasoconstriction

 BP regulation
Blood volume Cardiac pump Vasculature MAP = CO x Vascular Resistance
Tissue and organ perfusion depend on MAP, or the average pressure at which the blood moves through the vasculature MAP of more than 65 mmHg should be maintained to ensure adequate tissue

perfusion

Causative Factors of decreased blood supply -- cellular metabolsim

Shock
Classification of Shock Low Blood Flow Shock Cardiogenic shock Hypovolemic shock Maldistribution of Blood Flow Shock

Neurogenic shock
Anaphylactic shock Septic shock

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
Systolic or diastolic dysfunction Compromised cardiac output (CO)

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
When affecting the right side, pulmonary circulation is compromised

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
MI Cardiomyopathies Severe systemic/pulmonary HTN Blunt cardiac injury Severe myocardial depression from sepsis

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
Diastolic dysfunction Impaired ability of either ventricle to fill during diastole Decreased stroke volume

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
Early manifestations Tachycardia Hypotension Narrowed pulse pressure Increased SVR Increased myocardial O2 consumption

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
PE findings Tachypnea Pulmonary congestion Crackles

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
Increase in pulmonary artery wedge pressure and pulmonary vascular resistance

Classification of Shock
Low Blood Flow Shock (Cardiogenic)
S/S of peripheral hypoperfusion Renal blood flow Urine output Anxiety/delirium with impaired cerebral blood flow

Classification of Shock
Hypovolemic Shock
Loss of intravascular fluid volume Either absolute or relative volume loss

Classification of Shock
Hypovolemic Shock
Absolute hypovolemia Hemorrhage GI loss Fistula drainage Diuresis

Classification of Shock
Hypovolemic Shock
Relative hypovolemia Fluid moves out of vascular space into extravascular space (third spacing)

Pathophysiology of Hypovolemic Shock

Fig. 65-03

Classification of Shock
Hypovolemic Shock
Size of vascular compartment unchanged Decreased venous return to heart Decreased preload, SV, and CO Impaired cellular metabolism

Classification of Shock
Hypovolemic Shock
Response to acute volume loss depends on: Age Injury Health

Classification of Shock
Hypovolemic Shock
If loss greater than 30%, blood volume must be replaced

Classification of Shock
Neurogenic Shock
Occurs after spinal cord injury at T5 or above Results in massive vasodilation leading to pooling of blood in vessels

Pathophysiology of Neurogenic Shock

Classification of Shock
Neurogenic Shock
Manifestations of hypotension and bradycardia Hypothalamic dysfunction is characteristic Temperature dysregulation Can begin 30 minutes after injury and last days to weeks

Classification of Shock
Anaphylactic Shock
Acute, life-threatening hypersensitivity reaction Massive vasodilation Release of mediators Increased capillary permeability

Classification of Shock
Anaphylactic Shock
Can lead to respiratory distress and circulatory failure Sudden onset of S/S Anxiety Confusion Sense of impending doom

Classification of Shock
Septic Shock
Systemic inflammatory response to infection Presence of sepsis with hypotension despite fluid resuscitation with presence of abnormal tissue perfusion

Classification of Shock
Septic Shock
Leading cause of death in noncoronary ICUs Primary causative organisms Gram-negative and grampositive bacteria Endotoxin stimulates inflammatory responses

Pathophysiology of Septic Shock

Fig. 65-5

Classification of Shock
Septic Shock
Increased coagulation and inflammation Decreased fibrinolysis Formation of microthrombi Obstruction of microvasculature

Classification of Shock
Septic Shock
Decreased SVR Compensatory CO Hypotension Tachypnea Temperature dysregulation

Classification of Shock
Septic Shock
Decreased urine output Altered neurologic status GI dysfunction Respiratory failure is common

Stages of Shock
Initial Stage Compensatory Stage Progressive Stage Refractory Stage (Irreversible)

Stages of Shock
Initial May not be clinically apparent Metabolism changes from aerobic to anaerobic Lactic acid accumulates

Stages of Shock
Initial Lactic acid must be removed by blood and broken down by liver Requires unavailable O2

Stages of Shock
Compensatory Stage Attempt homeostasis Baroreceptors in carotid and aortic bodies activate SNS in response to decreased BP Vasoconstriction while blood to vital organs maintained

Compensatory Stage of Shock

Fig. 65-06

Fig. 65-6

Stages of Shock
Compensatory Stage Decreased blood to kidneys activates renin-angiotensin system Increased venous return to heart, CO, and BP

Stages of Shock
Compensatory Stage Impaired GI motility Risk for paralytic ileus Cool, clammy skin from blood Except septic patient who is warm and flushed

Stages of Shock
Compensatory Stage Shunting blood from lungs = physiologic dead space Decreased arterial O2 levels Compensatory breathing SNS stimulation increases myocardium O2 demand

Stages of Shock
Compensatory Stage If perfusion deficit corrected, patient recovers with no residual sequelae If deficit not corrected, patient enters progressive stage

Stages of Shock
Progressive Stage Begins when compensatory mechanisms fail Aggressive interventions to prevent multi-organ dysfunction syndrome

Progressive Stage of Shock

Fig. 65-07

Fig. 65-7

Stages of Shock
Progressive Stage Hallmarks of decreased cellular perfusion and altered capillary permeability: Leakage of protein into interstitial space Increased systemic interstitial edema

Stages of Shock
Progressive Stage Anasarca Fluid leakage affects solid organs and peripheral tissues Decreased blood flow to pulmonary capillaries

Stages of Shock
Progressive Stage Movement of fluid from pulmonary vasculature to interstitium Pulmonary edema Bronchoconstriction Decreased residual capacity

Stages of Shock
Progressive Stage
Fluid moves into alveoli Impaired gas exchange Decreased compliance Worsening if V/Q mismatch Tachypnea Crackles

Stages of Shock
Progressive Stage
CO begins to fall Decreased peripheral perfusion Increased capillary permeability Weak peripheral pulses Ischemia of distal extremities

Stages of Shock
Progressive Stage
Myocardial dysfunction results in: Arrhythmias Ischemia MI End result is complete deterioration of cardiovascular system

Stages of Shock
Progressive Stage
Mucosal barrier of GI system becomes ischemic Ulcers Bleeding Translocation of bacteria Decreased ability to absorb nutrients

Stages of Shock
Progressive Stage
Liver fails to metabolize drugs and wastes Jaundice Elevated enzymes Loss of immune function Risk for DIC and significant bleeding from many orifices

Stages of Shock
Refractory Stage Exacerbation of anaerobic metabolism Accumulation of lactic acid Increased capillary permeability

Refractory Stage of Shock

Fig. 65-08

Fig. 65-8

Stages of Shock
Refractory Stage Hypotension and tachycardia worsen Decreased coronary blood flow Cerebral ischemia Hypoxemia

Stages of Shock
Refractory Stage Failure of one organ system affects others Recovery unlikely

Diagnostic Studies
No single study to determine

Elevation of lactate
Thorough PE and PMH

Diagnostic Studies
ECG X-ray Pulse oximetry Hemodynamic monitoring

Collaborative Care
Identification of risk for shock

Integration of PE, PMH, and clinical findings to diagnose

Collaborative Care
Interventions to control or eliminate cause of decreased perfusion Protection of organs from dysfunction

Collaborative Care
Provision of multisystem care Ensure patent airway Optimize O2 delivery Blood transfusion

Collaborative Care
Pulmonary catheter to measure venous O2 saturation Fluid replacement Crystalloids and colloids Warm fluids for hypothermia

Collaborative Care
Indwelling catheter Serial BP Vasopressor agents for persistent hypotension Assessment of organ perfusion

Collaborative Care
Vasodilator therapy Enteral feedings Enhance perfusion of GI tract Prevent bacterial translocation

Nursing Assessment
ABCs

Tissue perfusion

Nursing Assessment
Brief history Events leading to shock Onset and duration of symptoms

Nursing Assessment
Details of care received before hospitalization Allergies

Vaccinations

Nursing Diagnoses
Decreased cardiac output

Fear and anxiety

Potential complication: Organ ischemia/dysfunction

Planning
Goals for patient Adequate tissue perfusion Restoration of normal BP Return/recovery of organ function No complications

Implementation
Identify those at risk Elderly Immunocompromised Surgical/accidental trauma

Implementation
Limit infarct size Limit O2 demand Medic Alert bracelets for severe allergies and EpiPens Monitor F&E balance

Implementation
Monitor for progression of infection Monitor neurologic status Monitor BP, HR, CVP, PA pressures q 15 min

Implementation
Monitor PAWP q 1-2 hr Constantly monitor ECG for arrhythmias Assess heart sounds for S3, S4 Administer prescribed therapies

Implementation
Monitor rate, depth, and rhythm of respirations q 15-30 min Auscultate q 4 hr for sounds indicating fluid overload or accumulation of secretions Continuously monitor oxygen

Implementation
Monitor ABGs

Urine output measurements each hour BUN and creatinine levels

Implementation
Assess temperature each hour

Monitor skin for pallor, flushing, cyanosis, diaphoresis, piloerection

Implementation
Auscultate bowel sounds q 4 hr Test NG drainage, stools for occult blood Bathing/oral care according to O2 demands Passive ROM q 6-8 hr

Implementation
Assess level of anxiety and fear Medication prn Talk to patient Visit from clergy

Implementation
Comfort measures

Privacy
Call light within reach

Evaluation
Normal baseline BP, HR, CVP, and PAWP Warm, dry skin Urinary output > 0.5 ml/hr Normal RR and SaO2 > 90% Verbalization of fears, anxiety

Evaluation
Monitor S/S of ischemia Report deviations from acceptable parameters Carry out nursing interventions