JASHANPREET SINGH BALLAGAN ROLL NO- 1437 MD-4 SHOCK JASHANPREET SINGH BALLAGAN ROLL NO- 1437 MD-4

Shock Is generalized reduced perfusion ( hypoperfusion) of tissues with blood - which results in impaired oxygenation of tissues. Occurs due to: Reduced cardiac output Reduced blood volume Reduced vascular tone Resulting in: hypotension  impaired tissue perfusion  cellular hypoxia  multiple organ failure.

Shock Is final common pathway for many lethal conditions: Example: Severe hemorrhage Large myocardial infarction Pulmonary embolism Sepsis (e.g.bacterial infection)

Types of shock Hypovolemic Cardiogenic Septic (endotoxic) shock Neurogenic Anaphylactic shock

Hypovolemic shock Due to excessive blood or fluid loss. Hemorrhage: MCC of hopovolemic shock Loss of >20% of the blood volume (~1000 ml) results in shock. Excessive fluid loss is seen in: Excessive sweating, diarrhea, severe burns and excessive vomiting. Most common cause : Hemorrhage Could be due to arterial trauma or rupture of an aneurysm.

Pathogenesis Decreased Cardiac output (CO): Due to decreased volume of blood. Increased total peripheral resistance (TPR): due to vasoconstriction of arterioles from catecholamines and angiotensin II which are released in response to decreased CO. Decreased left ventricular end diastolic volume (LVEDV). Angiotensin II  causes vasoconstriction and increased release of aldosterone from adrenal glands

4.Decreased Mixed venous oxygen content: Best indicator of tissue hypoxia Indicates the degree of extraction of O2 from the blood delivered to tissue In hypovolemic shock decreased blood flow through microcirculation leads to increased extraction of O2 from the blood and a decreased MVO2 Decreased Mixed venous oxygen content (MVO2): Best indicator of tissue hypoxia Measured in the right side of the heart with a Swan-Ganz catheter Indicates the degree of extraction of O2 from the blood delivered to tissue In hypovolemic shock decreased blood flow through microcirculation leads to increased extraaction of O2 from the blood and a decreased MVO2

Clinical findings: Treatment: Cold clammy skin from vasoconstriction of skin vessels Hypotension (decreased CO) Rapid, weak pulse (compensatory response to decreased CO). Treatment: IV fluids and whole blood. Kidney in hypovolemic shock: renal medulla is most adversely affected ischemic tubular necrosis common

Cardiogenic shock Due to myocardial pump failure, due either to: 1.damage to cardiac muscle 2.extrinsic pressure 3.obstruction to outflow. Clinical examples Myocardial infarction Arrhythmia Cardiac tamponade Pulmonary embolism

THROMBUS Coronary artery Area of INFARCTION Heart: Gross changes THROMBUS Coronary artery Area of INFARCTION Gross or naked eye examination of heart of the patient reveals: a thrombus (blood clot) in the coronary artery and an area of dead myocardial tissue (necrosis) Death of tissue due to blockage in blood supply is known as INFARCTION

Cardiogenic shock Most commonly after acute myocardial infarction. Findings: Decreased CO : due to decreased force of contraction in LV. Increased LVEDV**: blood accumulates in the left ventricle. Increased PVR: same mechanism as in hypovolemic shock. Decreased MVO2: Same mechanism as in hypovolemic shock Clinical findings: similar to those in hypovolemic shock.

Neurogenic Shock Due to sudden widespread loss of vasomotor tone in venules and small veins (vasodilation) vessel volume increases  pooling of blood  decreased venous return to heart  decreased CO Examples: Fainting Spinal cord injury

Anaphylactic shock IgE mediated type 1 hypersensitivity response Characterized by vasodilation & increased vascular permeability due to release of histamine from mast cells. Could be seen following a bee sting, hornet sting or intravenous administration of certain drugs. SYMPTOMS- Difficulty breathing, Difficulty swallowing, anxiety, Nasal congestion, Nausea,itchiness, Swelling of the face, eyes, or tongue. Treatment is subcutaneous injection of epinephrine.

Due to overwhelming microbial infection Gram negative septicemia Septic shock Most common type of shock with highest mortality. Due to overwhelming microbial infection Gram negative septicemia Gram positive septicemia Fungal sepsis Most cases caused by endotoxin producing gram-negative bacteria (usually E.coli) therefore, also k/a Endotoxic shock*

Septic shock Common Causes of septic shock: E.coli sepsis from indwelling urinary catheter most common cause of septic shock. Urinary retention secondary to prostate hyperplasia also common cause. Spread of localized infection to blood stream: E.g. an abscess, pneumonia

Septic shock Pathogenesis Endotoxins are component of cell wall of gram negative bacteria Are lipopolysacchrides (LPS) Released when bacterial cell wall is degraded. Endotoxins bind to CD14 receptor on WBC and endothelial cells causing toxic shock syndrome.

Septic shock : Pathogenesis Activation of alternative complement pathway Result: release of C3a and C5a (vasodilation and neutrophil chemotaxis) Direct injury to endothelial cells: Result : release of chemical mediators NO (vasodilator) and PG I2 (vasodilator). Macrophage release of IL-1/TNF: Result: Fever, sleep, increased release of thromboplaastin and NO Increased neutrophil adhesion to Endothelial cells (e.g. increased neutrophils in pulmonary capillaries) Actions of TNF alpha: Upregulation of adhesion molecules (selectins, integrins, IgG superfamily) for neutrophil (PMN) “sticking” to endothelial cells Induce NOS (nitric oxide synthase) increased release of NO Release tissue thromboplastin (Activates coagulation cascade) Systemic: fever, anorexia, somnolence Nitric oxide: causes vasodilation of peripheral resistance arterioles C5a and C3a : cause release of Histamine from mast cells  vasodilation

Pathophysiology Vasodilation results in Initial increase in CO: Due to rapid flow through dilated arterioles causing increased return to heart. Increased MVO2: Tissue unable to remove oxygen because of increased blood flow through microcirculation  tissue hypoxia Decreased Peripheral vascular resistance (PVR): Due to vasodilation of peripheral arterioles

Septic shock Clinical features Warm skin: Bounding pulse from vasodilation of skin vessels. Bounding pulse due to Increased CO Acute respiratory distress syndrome : due to neutrophil emigration into alveoli. Disseminated intravascular coagulation: due to activation of intrinsic and extrinsic coagulation system.

Septic shock: Differences from other types In septic shock patient has Warm rather than cold skin Increased CO Increased mixed venous oxygen content (MVO2): tissue cannot extract oxygen from increased flow rate. Decreased PVR Mixed venous oxygen content: (MVOC) measured with Swan-Ganz catheter threaded into the right heart best indicator of tissue hypoxia indicates how much or how little oxygen was extracted from the blood delivered to tissues decreased in: hypovolemic shock : decreased cardiac output allows tissue to extract more oxygen than normal cardiogenic shock : decreased: same reason increased in: endotoxic shock: tissue cannot extract oxygen from increased flow rate.

Shock: results Multiple organs get damaged: Kidney: acute tubular necrosis due to hypoxia causing renal failure. Kidney in shock: renal medulla is most adversely affected ischemic tubular necrosis common

Pathogenesis of acute tubular necrosis Pathogenesis of acute tubular necrosis. Sloughing and necrosis of epithelial cells result in cast formation. The presence of casts leads to obstruction and increased intraluminal pressure, which reduces glomerular filtration. Afferent arteriolar vasoconstriction, caused in part by tubuloglomerular feedback, results in decreased glomerular capillary filtration pressure. Tubular injury and increased intraluminal pressure cause fluid backleakage from the lumen into the interstitium. Pathogenesis of acute tubular necrosis

Acute Tubular Necrosis: Coagulation necrosis of proximal renal tubular cells (arrows) is evident with some detachment from the basement membrane. This will form renal tubular cell casts.

Shock: results Brain: GIT: Ischemia results in development of focal areas of necrosis. GIT: Widespread mucosal ischemia results in multiple hemorrhagic erosions or Gastric stress ulcers

Sum 11 A Jalan Multiple stress ulcers of the stomach, highlighted by dark digested blood on their surfaces.

Shock: results Lungs: Show signs of diffuse alveolar damage (DAD) also k/a ARDS (Acute Respiratory Distress Syndrome) Due to neutrophil mediated injury Endotoxic (septic) shock MCC of ARDS.

Shock: results Others: lactic acidosis due to tissue hypoxia Metabolic acidosis: lactic acidosis due to tissue hypoxia Severe absolute neutropenia : increased synthesis of adhesion molecule stimulated by endotoxin (in septic shock) DIC: due to activation of coagulation cascade (in septic shock) Multiorgan dysfunction: Most common cause of death

Stages of shock Stage I: stage of compensation Perfusion to vital organs is maintained by reflex mechanisms Increased sympathetic tone Release of catecholamines Activation of renin angiotensin mechanism Stage II: stage of decompensation Progressive decrease in tissue perfusion Potentially reversible tissue injury occurs Development of metabolic acidosis, electrolyte imbalances and renal insufficiency Stage III: irreversible shock Irreversible tissue injury and organ failure Ultimately resulting in death )

Stage I: stage of compensation: Clinical findings include: tachycardia ( a heart rate of >100 beats /minute skin pallor due to vasoconstriction , reduced urine output Stage II: stage of decompensation: clinical findings include: hypotension , tachypnea and dyspnea oliguria (urine output less than 500ml/day), acidosis Stage III: irreversible shock: clinical findings include: marked hypotension extreme tachycardia respiratory distress not responding to oxygen therapy loss of consciousness progressing to coma gastrointestinal bleeding anuria with elevated blood urea nitrogen and creatinine in blood severe acidosis

prevention Learn ways to prevent heart deseases, falls, injuries,dehydration , and other causes of shock. If you have a known allergy (for example, to insect bites or stings), carry an epinephrine pen.

references Hollenberg S. Cardiogenic shock. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Saunders Elsevier; 2011:chap 107. Tarrant AM, Ryan MF, Hamilton PA, Bejaminov O. A pictorial review of hypovolaemic shock in adults. Br J Radiol. 2008;81:252-257. Jones AE, Kline JA. Shock. In: Marx JA, ,Hockberger RS, Walls RM, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, Pa: Mosby Elsevier; 2013:chap 6. Rivers EP. Approach to the patient in shock. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 106.