Shock

1. Shock Ghassan Fraij UNC Internal Medicine Morning Report 12/6/2008

2. Final Diagnosis Subfulminant Hepatic Failure Distributive Shock Rapidly Progessive Non-Hodgkins Lymphoma (Diffuse Large B-cell) Metabolic Echephalopathy Disseminated Intravascular Coagulation Acute Renal Injury (ATN)

3. Shock Serious medical condition that results from a profound and widespread reduction in effective tissue perfusion leading to cellular dysfunction and organ failure. Classified according to etiology and cardiovascular physiology. SBP < 90 mm Hg or a reduction of > 40 mm Hg from baseline in the absence of other causes for hypotension

4. Hypovolemic Shock Results from blood and/or fluid loss and is due to a decreased circulating blood volume leading to reduced diastolic filling pressures and volumes The result is inadequate cardiac output, hypotension, and shock.

5. Cardiogenic Shock Tissue hypoperfusion as a result of acute myocardial infarction or end-stage heart failure from any cause. Hallmarks include: hypotension, and elevated left ventricular filling pressure greater than 15 mm Hg and a reduction in the cardiac index to less than 2.2 L/minute/m2

6. Extracardiac Obstructive Shock Results from obstruction to flow in the cardiovascular circuit, leading to inadequate diastolic filling or decreased systolic function due to increased afterload Results in inadequate cardiac output and hypotension

7. Distributive Shock Defined by vasodilatation: the venodilatation leads to decreased preload, the arterial vasodilatation leads to hypotension with a normal or elevated cardiac output. Myocardial depression often present Hallmark is decreased vascular resistance, normal or elevated cardiac output, and hypotension.

8. Etiology of Hypovolemic Shock Hemorrhagic: trauma, GI, retroperitoneal External Fluid loss: Dehydration, vomiting, diarrhea, polyuria Interstitial Fluid Redistribution: thermal injury, trauma, anaphylaxis Increased Vascular Capacitance (vendilatation): sepsis, anaphylaxis, toxins/drugs

9. Etiologies of Cardiogenic Shock Myopathic: myocardial infarction (left or right), contusion, myocarditis, postischemic myocardial stunning, septic myocardial depression Pharmacologic: anthracycline cardiotoxicity, calcium channel blockers Mechanical: valvular failure (stenotic or regurgitant), hypertrophic cardiomyopathy, VSD Arrhythmic: bradycardia, tachycardia Peripartum Cardiomyopathy Pericardial Disease with effusion

10. Etiologies of Extracardiac Obstructive Shock Impaired Diastolic Filling: direct venous obstruction (vena cava), intrathoracic obstructive tumors Increased Intrathoracic-Pressure: tension pneumothorax, mechanical ventilation (with excessive pressure or volume depletion), asthma

11. Etiologies of Extracardiac Obstructive Shock Continued Decreased Cardiac Compliance: constrictive pericarditis, cardiac tamponade Impaired Systolic Contraction (increased ventricular afterload): Right Ventricle: pulmonary embolus, acute pulmonary hypertension Left Ventricle: aortic dissection

12. Etiologies of Distributive Shock Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic Neurogenic (spinal shock) Acute/Subfulminant Liver Failure Toxic (e.g., nitroprusside, bretylium) Endocrinologic: adrenal crisis, thyroid storm

13. CNS Dysfunction in Shock Autoregulation protects the ischemia-sensitive neurons by maintaining adequate blood flow down to an MAP of approximately 50 to 60 mm Hg Below this level, cortical necrosis ensues, marked by alterations in the level of consciousness ranging from confusion to coma

14. Cardiac Dysfunction in Shock Marked by sympathoadrenal stimulation, with tachycardia being the most sensitive indicator that shock is present. Autoregulation ensures good coronary perfusion down to an MAP of approximately 50 mm Hg, below which myocardial ischemia ensues Septic myocardial dysfunction has been linked to cytokine-induced (TNF and IL-1) depression of myocardial contraction There is evidence of decreased B-receptor function.

15. Respiratory Dysfunction in Shock Acute lung injury causes impaired gas exchange, decreased compliance, and shunting of blood with V/Q mismatch. Pathologic findings include: fibrin-neutrophil aggregates within the microvasculature, inflammatory damage to the interstitial and alveoli, and exudation of proteinaceous fluid into the alveoli Results in Acute Respiratory Distress Syndrome (ARDS).

16. Renal Dysfunction in Shock Acute renal injury is a major complication of shock and is associated with a high mortality rate. Initially, vasoconstriction may maintain the GFR, but when this compensation fails, acute tubular necrosis and renal insufficiency occur. Clinical challenge is to differentiate between acute tubular necrosis and hypovolemia since both will be marked by oliguria.

17. Gastrointestinal Dysfunction in Shock Typical clinical manifestations include: ileus, erosive gastritis, pancreatitis, acalculous cholecystitis, and submucosal hemorrhage. Studies suggest that gut barrier integrity may be compromised, leading to translocation of bacteria and their toxins into the blood stream.

18. Liver Dysfunction in Shock The most common manifestation of liver involvement in shock is mild increase in aminotransferases and LDH. With severe hypoperfusion, shock liver maybe manifested by massive aminotransferase elevations and extensive hepatocellular damage. With an acute insult that resolves, the transaminase elevations peak in 1 to 3 days and resolve by 10 days.

19. Liver Dysfunction in Shock Continued Decreased levels of clotting factors and albumin may occur and reflect decreased synthetic function. In septic shock, significant elevations of bilirubin may be seen with only modest elevations in aminotransferases because of dysfunction of bile canaliculi caused by inflammatory mediators or bacterial toxins.

20. Hematologic Dysfunction in Shock Activation of the coagulation cascade can lead to disseminated intravascular coagulation, which results in thrombocytopenia, decreased fibrinogen, elevated fibrin split products, and microangiopathic hemolytic anemia. Thrombocytopenia may also occur from dilution during volume repletion or from immunologic platelet destruction, which is especially common during septic shock.

21. Metabolic Dysfunction in Shock Early in shock, hyperglycemia usually occurs as a result of glycogenolysis and gluconeogenesis mediated by increases in adrenocorticotropic hormone, glucocorticoids, glucagon, and catecholamines as well as decreases in insulin. Later in shock, hypoglycemia may occur due to glycogen depletion or failure of glucose synthesis in the liver.

22. Immediate Goals In Shock Hemodynamic Support: MAP > 60 mmHg, PCWP of 15-18 mmHg, Cardiac index > 2.2 L/min/m2 (possibly > 4.0 L/min/m2 in septic and traumatic shock) Maintain Oxygen Delivery: Hgb > 10 g/dl, Arterial Sats > 92%, supplemental oxygen and mechanical ventilation Reversal of Organ Dysfunction: decreasing lactate (2.2 mM/L), maintain urine output, reverse encephalopathy, improving renal and liver function tests.

23. Triage of Hypovolemic Shock Rapid replacement of blood, colloid, or crystalloid Identify source of blood or fluid loss Endoscopy/colonoscopy Angiography CT/MRI scan

24. Triage of Cardiogenic Shock Left Ventricular Infarction Intraaortic balloon pump (IABP) Coronary Angiography with subsequent angioplasty or CABG Vasopressors, aspirin, heparin, and thrombolysis if revascularization not available. Right Ventricular Infarction Fluids and inotropes with pulmonary artery catheter monitoring.

25. Triage of Extracardiac Obstructive Shock Pericardial Tamponade Percardiocentesis Surgical Drainage (if needed) Pulmonary Embolism Heparin V/Q Lung Scan Pulmonary Angiography Consider: thrombolytic therapy, embolectomy surgery

26. Triage of Distributive Shock Identify site of infection and drain if possible Antimicrobial agents ICU monitoring and support with fluids, vasocompressors, and inotropic agents Goals: cardiac index > 4.0 L/m2, improving organ function, decreasing lactate levels

27. References Goldman et al., Cecil Textbook of Medicine, p. 608-620. 22nd Edition, 2004. Epstein et al., The Pathogenesis of Vasodilatory Shock, NEJM, Vol. 345, No. 8.