1 P a g e C H A P T E R 6 7 S h o c k S I R S a n d M O D S CLASSIFICATIONS OF SHOCK 1717 1724 Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism Result of an imbalance between the supply and demand for oxygen and nutrients Occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in CARDIOGENIC SHOCK reduced cardiac output CO Causes o Dysrhythmias o Structural factors Hemodynamic changes o Usually affects left ventricle decrease systemic circulation if right side pulmonary o Systolic dysfunction inability of the heart to pump blood forward Acute MI most common cardiomyopathy blunt cardiac injury severe systemic or pulmonary HTN myocardial depression from metabolic problems o Diastolic dysfunction inability of the heart to fill during diastole Pericardial tamponade ventricular hypertrophy cardiomyopathy Bradydysrhythmias and tachydysrhythmias Valvular stenosis regurgitation ventricular septal rupture tension pneumothorax o Increased HR SVR PVR CVP PAP PAWP o Decreased BP pulse pressure CO SvO2 ScvO2 o Impaired tissue perfusion and impaired cellular metabolism EARLY clinical manifestations o Similar to acute decompensated heart failure o Tachycardia o Hypotension o Narrow pulse pressure o SVR workload of the heart myocardial O2 consumption CO 4 L min and CI 2 5 L min m2 Later manifestations o Tachypnea o Pulmonary congestion crackles o PAWP and PVR o Peripheral hypoperfusion Cyanosis pallor diaphoresis weak peripheral pulses cool clammy skin and slow cap refill o renal blood flow Na water retention urine output o Decrease cerebral perfusion anxiety confusion agitation CLINICAL PRESENTATION BY SYSTEM Cardiovascula r Tachycardia BP cap refill Pulmonary Renal Skin Neurologic GI Diagnostic Tachypnea Crackles Cyanosis Na retention Water retention renal blood Pallor Cool Clammy Cerebral perfusion Anxiety Bowel sounds N V cardiac markers BNP Blood glucose 2 P a g e C H A P T E R 6 7 S h o c k S I R S a n d M O D S MVO Possible chest pain Rhonchi flow urine output Confusion Agitation BUN ECG dysrhythmias ECHO left vent dysfunction Chest x ray pulmonary infiltrates Specific collaborative care measures o Overall goal is to restore myocardium blood flow by restoring oxygen supply and demand balance o Hemodynamic management Thrombolytic therapy angioplasty with tenting emergency revascularization and valve replacement Cardiac catheterization is done as soon as possible after initial insult Reduce workload drug or mechanical interventions Medications nitrates dilation diuretics preload vasodilators afterload B adrenergic blockers HR and contractility Mechanical intraaortic balloon pump ventricular assisted devices VAD o Select group of patients may need heart transplant o SVR and workload HYPOVOLEMIC SHOCK Occurs when there is a loss of intravascular fluid volume o Volume is inadequate to fill the vascular space o Size of the vascular compartment is unchanged but the volume decreases reduction in intravascular volume decreased return to the heart decrease stroke volume preload and CO decreased tissue perfusion and impaired cellular metabolism Increase in HR SVR PVR Decrease in pulse pressure BP CVP PAP PAWP CO SvO2 ScvO2 Absolute o Fluid is lost through hemorrhage GI loss V D fistula drainage DI or diuresis Can compensate for 750 ml 15 loss SNS mediated response 15 30 HR CO RR depth stroke volume CVP and PAWP Reversible at this time with crystalloid fluids 30 compensatory mechanisms begin to fail May be reversible with blood products and albumin 40 irreversible death o Fluid volume moves out of the vascular space into the extravascular space Interstitial or intracavitary third spacing Relative Causes o Absolute External loss of whole blood hemorrhage from trauma surgery GI bleeding 3 P a g e C H A P T E R 6 7 S h o c k S I R S a n d M O D S Loss of other body fluids vomiting diarrhea excessive diuresis diabetes insipidus and diabetes mellitus o Relative Pooling of blood and fluids Bowel obstruction Fluid shifts Burn injuries and ascites Internal bleeding Massive vasodilation Sepsis Fracture of long bone spleen rupture hemothorax severe pancreatitis CLINICAL PRESENTATIONS BY SYSTEM Cardiovascula r Preload Stroke Volume Cap refill Early Tachypnea Late Bradypnea Pulmonary Renal Skin Neurologic GI Diagnostic Urine output Pallor Cool Clammy Cerebral perfusion Anxiety Confusion Agitation Absent bowel sounds H H Lactate Urine specific gravity Changes in electrolytes Specific collaborative care measures o Focus on stopping the loss of fluid and restoring circulating volume o 3 1 rule 3 ml isotonic crystalloid for every 1 ml estimated blood loss o More specific fluid resuscitation info in the shock care outline DISTRIBUTIVE SHOCK Neurogenic shock weeks Hemodynamic phenomenon that can occur within 30 minutes of a SCI at T5 and last up to 6 Occurs after the SCI that results in massive vasodilation leading to pooling of blood in blood vessels hypoperfusion and impaired cellular metabolism Injury massive vasodilation without compensation due to SNS vasoconstrictor tone loss pooling of blood in vessel decrease in circulating blood tissue hypoperfusion impaired cellular metabolism Emergency and treatment focuses on restoring the circulatory blood volume Causes o Hemodynamic consequence of spinal cord injury at or above T5 o Spinal anesthesia o Vasomotor center depression Severe pain drugs hypoglycemia and injury Decrease in all hemodynamic parameters o HR BP pulse pressure SVR CVP PAP PAWP CP SvO2 ScvO2 Most clinical manifestations o Hypotension from massive vasodilation o Bradycardia unopposed parasympathetic stimulation 4 P a g e C H A P T E R 6 7 S h o c k S I R S a n d M O D S o Unable to regulate temperature poikilothermia taking the temperature of the environment Spinal shock may also occur o Transient condition that is present after acute SCI o Absence of all voluntary and reflex neurologic activity below injury site o Often lasts less than 48 hours but can last for several weeks o Rehabilitation cannot begin until this has resolved o Assessment flaccid paralysis loss of activity below the level of injury bradycardia paralytic ileus and hypotension Autonomic dysreflexia o Known as autonomic hyperreflexia o Generally occurs after period of spinal shock is resolved and with lesions or injuries above T6 and in cervical lesions o Commonly caused by visceral distention from a distended bladder or impacted rectum o Is a