SHOCK-1 presentation medicine ppt ug.pptx

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1. SHOCK Topic: Pathophysiology and Types of Shock 1

2. Introduction Systemic state of low tissue perfusion that is inade­quate for normal cellular respiration. Cells switch from aerobic to anaerobic metabolism If perfusion is not restored cell death occurs 2

3. Pathophysiology Cellular Cells deprived of oxygen Switches from aerobic to anaerobic metabolism. Accumulation of lactic acid Systemic metabolic acidosis Glucose within cells is exhausted Anaerobic respiration ceases Failure of sodium/potassium pumps in the cell membrane and intracellular organelles Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents, including potassium, are released into the bloodstream. 3

4. Microvascular Activation of the immune and coagulation systems due to hypoxia Activate complement and leuko­cytes Generation of oxygen free radicals and cytokine release Injury of the capillary endothelial cells causing leakage Tissue oedema ensues, exacer­bating cellular hypoxia Ischemic cell death releases potassium into the circula­tion, leading to systemic hyperkalemia and acidosis, as well as further damage to molecules that systemically activate the immune system. 4

5. Cardiovascular Preload and afterload decreases Compensatory baroreceptor response Increased sympathetic activity and release of catecholamines Tachycardia and systemic vasoconstriction 5

6. Respiratory Metabolic acidosis and increased sympathetic response Increased respiratory rate to increase the excretion of carbon dioxide and to produce a compensatory respiratory alkalosis 6

7. Renal Decreased perfusion pressure in the kidney Reduced filtration at the glomerulus and a decreased urine output. Stimulation of renin–angiotensin–aldosterone axis vasoconstriction and increased sodium and water reabsorption by the kidney. 7

8. Endocrine Vasopressin (antidiuretic hormone) is released Results in vasoconstriction and resorption of water in the renal collecting system Cortisol is also released from the adrenal cortex, contributing to the sodium and water resorption and sensitizing cells to catechol­amines. 8

9. Types of Shock Haemorrhagic/Hypovolaemic shock Cardiogenic shock
Obstructive shock
Distributive shock Endocrine shock 9

10. Haemorrhagic and Hypovolemic Shock Most Common form of shock Caused due to reduced circulatory volume due to Haemorrhagic or non haemorrhagic causes Non- ­haemorrhagic causes include poor fluid intake (dehydration), excessive fluid loss due to vomiting, diarrhea, urinary loss (e.g. diabetes) or in ‘third­ spacing’(seen in pancreatitis & Bowel obstruction) 10

11. Types of Hypovolemia Covert Compensated Hypovolemia: <15% loss, Normal Vitals Overt Compensated Hypovolemia: 15-40% loss, Cold periphery, tachypnoea, confusion, metabolic acidosis, tachycardia, systolic BP is maintained Decompensated Hypovolemia: >40% loss, leads to multiorgan dysfunction 11

12. Cardiogenic Shock Primary failure of the heart to pump blood to the tissues Causes include myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy. Occurs when 50% of LV is damaged Venous hypertension with pulmonary or systemic oedema may also occur 12

13. Distributive Shock Describes the pattern of cardiovascular responses characterizing a variety of conditions, including septic shock, anaphylaxis and spinal cord injury. In Anaphylaxis , vasodilatation is due to histamine release In High spinal cord injury there is failure of sympathetic outflow and adequate vascular tone (neurogenic shock). In Sepsis it is due to release of bac­terial products (endotoxin) and the activation of cellular and humoral components of the immune system. This further causes redistribution of fluids causing hypovolemia 13

14. Septic Shock Caused by gram + ve or gram – ve bacteria, fungi, viruses etc Involvement of Pro inflammatory Cytokines NO production and endothelial dysfunction Stages: Hyperdynamic (warm) stage: Pyrogenic response present Hypodynamic hypovolemic septic shock: decompensated stage, leading to multiorgan failure and eventually death 14

15. Endocrine Shock Causes include hypo­ and hyperthyroidism and adrenal insufficiency Hypothyroidism causes disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls as a result of low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high­ output cardiac failure Adrenal insufficiency leads to shock due to hypovole­mia and a poor response to circulating and exogenous catecholamines. 15

16. Obstructive Shock Reduction in preload owing to mechanical obstruction of cardiac filling Causes are cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus. Reduced filling of the left and/or right sides of the heart, leading to low cardiac output 16

17. Thank You 17