Shock - Lecture Notes PDF

1/1/25 Introduction to shock Benjamin Brainard VMD VETM2951 Objectives Understand the oxygen delivery equation Understand how disruptions of various parts of the oxygen delivery equation...

1/1/25 Introduction to shock Benjamin Brainard VMD VETM2951 Objectives Understand the oxygen delivery equation Understand how disruptions of various parts of the oxygen delivery equation can result in shock Understand the physiologic response to shock Understand the concept of compensatory and decompensatory shock Understand the role of blood lactate as an indicator of oxygen delivery 1  1/1/25 Shock Decreased oxygen delivery to tissues Decreased ability of tissues to utilize delivered oxygen Oxygen delivery (DO2) Cardiac Output - DO2 = @ xCaO ·gen content (permc of blood a= artery 2  1/1/25 O2 carried in blood by : RBCs hemaglobin - Oxygen content (CaO2) - dissolved in blood 23 per mu Xhemaglobin of blood dissolved O2 XPaOz Ca0z mmHg in = 1 34. x [Hb] x SaOz + 0 003. xPaOz O2 bound to Hb Saturation of each 1402 per Hb) Hb molecule (Normal Saturation 95 - 100 % ) Oxygen content Amount of hemoglobin [Hb] normal is 15 g/dL Reflected as packed cell volume (PCV) in veterinary medicine PCV = Hct ⩰ 1/3 [Hb] Oxygen bound to hemoglobin 1.34 [Hb] SaO2 Oxygen dissolved in blood 0.003 PaO2 3  1/1/25 Oxygen binding curve SaO2 and PaO2 are related Sao Pa02 · Cardiac output = HRXSV Heart Rate Stroke volume Nervous input Cardiac contractility Medications Blood volume T Hormones Vascular tone R T Beat/min Iinthes mL/beat As in these Su affect 4  1/1/25 Decreased oxygen delivery Oxygen delivery factors Not enough oxygen in the blood - Lung Dz. Low oxygen content Inadequate tools to deliver oxygen - Cardiac Hypovolemia Output problem Cardiac disease Tissue usage factors Increased metabolic rate Fever - Shivering Exercise X tissue demand for Oz is very high a HRto a compensate Inability to use oxygen (relatively RARE) Cyanide Oxygen delivery to the cells Heart à aorta Arteries à arterioles Increase in area Decrease in flow velocity Arteriolesà Greatest resistance Smooth muscle Capillaries Site of gas exchange * low velocity * important in in capillaries diffusion of 02 but HUGE surface area from blood - > tissues 5  1/1/25 Cellular respiration Anaerobic and aerobic components - importantmechanismena ery Anaerobic XFAST Glycolysis Krebsin Less efficient Does not need oxygen * effective + efficient Aerobic way to ATP make Mitochondria Normal scenario When oxygen is available What happens with low tissue oxygenation anyway? Glycolysis Inefficient Metabolic Byproducts Acidosis Pyruvate à lactate Lactate and H+ Fast * ACID > has - effectee Energy in tissues with limited oxygen supply Decreased perfusion Decreased oxygen content 6  1/1/25 Lactate Produced by tissues utilizing anaerobic metabolism Lactic acidosis Decreased pH of blood Severe acidosis à dysfunction Can be measured in the blood Venipuncture artifact How can we estimate the oxygen demand (VO2) of the tissue? O2 Oxygen extraction ratio Diffusion varterial venous CaO2- CvO2 CaO2 CvO2 CaO2 20.1 mL/dL 15.2 mL/dL Normally 20-30% of O2 from blood tissues > - Diffusion Can increase up to 60-70% O2 If blood bypasses the tissues, artificially high 7  1/1/25 Aerobic respiration is important: compensation If DO2 is decreasing to near or below VO2, Increased heart rate Cardiac Output Increased stroke volume Increased OER extraction ratio ↳ oxygen Hard to change PaO2 quickly without assistance Y dissolved O2 Increased FiO2 Hard to change [Hb] quickly without assistance Blood transfusion DOCriter Apotietamol See consumption not changing but delivery add a tissueor Intros st fort decomperrock Vincent JL, De Backer D. Int Care Med. 2004;30(11):1990. 8  1/1/25 Decompensatory shock As DO2 dips below VO2 Some tissues must switch to anaerobic metabolism for lack of O2 Results in production of lactate from these tissues Prolonged decreased DO2 may lead to organ dysfunction Decreased ATP production à Cannot maintain cellular gradients à Decreased nervous transmission Heart, GI tract, Brain Increased intracellular Na+ Cellular edema (e.g. renal tubular epithelial cells, GI) Necrosis may follow (mmol/L) Vincent JL, De Backer D. Int Care Med. 2004;30(11):1990. 9  1/1/25 Shock: general physical examination Compensatory Tachycardia (usually) Tachypnea Pink/red mucous membranes Normal or elevated blood pressure Decompensatory Bradycardia may develop (late Stage) Tachypnea Grey/purple mucous membranes (no blood flow / perfusion to MM) Hypotension [email protected] 10