Shock Recognition & Treatment PDF

# Shock Recognition & Treatment ## Learning Objectives At the end of the lecture, you should be able to list and describe: - Definition of shock - Categories for causes of shock - Common examples of each category for each species - Parts of a triage exam - Stages of shock & signs associated w...

# Shock Recognition & Treatment ## Learning Objectives At the end of the lecture, you should be able to list and describe: - Definition of shock - Categories for causes of shock - Common examples of each category for each species - Parts of a triage exam - Stages of shock & signs associated with each - Basic treatments for shock and their mechanism of action - End points of shock resuscitation ## What is Shock? - Inability to meet energy requirements. - Cellular needs exceed delivery of oxygen/ nutrients - ↓ oxygen delivery (DO₂) - ↑ cellular demand ### Oxygen Delivery (DO₂) - DO₂ = CO x C_aO₂ > Where: > - **CO** = Cardiac Output > - CO = HR x SV > - CO = Preload x Afterload x Contractility > - **C_aO₂** = Arterial Oxygen Content > - C_aO₂ = (1.36 x SpO₂ x Hb) + 0.003(P_aO₂) > **Note**: > - Increase in metabolic rate will increase DO₂ > - Decrease in oxygen utilization will increase DO₂ ## Categories of Shock - Hypovolemic - Distributive - Septic - Cardiogenic - Obstructive - Metabolic ## Hypovolemic Shock - Low circulating blood volume - Reduced preload - Fluid losses exceeding intake - Gastrointestinal, Renal - Third spacing (effusions, edema) - Evaporative - burns - Severe dehydration - Hemorrhagic shock ## Distributive Shock - Also called vasodilatory shock - Relative state of hypovolemia - Inflammatory mediators cause vasodilation ### Distributive Shock Mechanism - DO₂ = CO x C_aO₂ > Where: > - **CO** = Cardiac Output > - CO = HR x SV > - CO = Preload x Afterload x Contractility > - **C_aO₂** = Arterial Oxygen Content > - C_aO₂ = (1.36 x SpO₂ x Hb) + 0.003(P_aO₂) > **Note**: > - Increase in metabolic rate will increase DO₂ > - Decrease in oxygen utilization will increase DO₂ ### Specific Causes of Distributive Shock - Sepsis - Anaphylaxis, mast cell tumor degranulation - Trauma - Especially brain injury - Neurologic causes - Hypoadrenocorticism - Vasodilatory drugs (eg: amlodipine, nitroprusside) ## Cardiogenic Shock - Failure of the heart to pump blood to the periphery - **Note**: Not the same as congestive heart failure ### Cardiogenic Shock Mechanisms - DO₂ = CO x C_aO₂ > Where: > - **CO** = Cardiac Output > - CO = HR x SV > - CO = Preload x Afterload x Contractility > - **C_aO₂** = Arterial Oxygen Content > - C_aO₂ = (1.36 x SpO₂ x Hb) + 0.003(P_aO₂) > **Note**: > - Increase in metabolic rate will increase DO₂ > - Decrease in oxygen utilization will increase DO₂ ### Cardiogenic Shock: ↓ contractility - Dilated cardiomyopathy - End stage valvular disease (leaky valves) - Sepsis - Myocardial depressant factor - Reversible - Cardiac damage - Thrombosis, trauma - Anesthetic drugs ### Cardiogenic Shock with ↓ preload - Hypertrophic cardiomyopathy - Later decreased contractility ### Cardiogenic Shock: ↓ preload - Hypertrophic cardiomyopathy - Tachyarrhythmias, sustained ### Cardiogenic Shock: ↓ HR - Bradyarrhythmias, sustained ### Multiple Cardiac Effects: Cardiotoxins - Monensin in horses - Avocados (persin) in birds - Gossypol and selenium in pigs - Plants containing cardiac glycosides - Lily of the valley (Convalaria) - Oleander - Foxglove (Digitalis) - Rhododendron/azaleas (grayanotoxins) - Doxorubicin (chemotherapy) ## Obstructive Shock - Blood flow is impeded by physical obstruction - Affecting CENTRAL circulation ### Obstructive Shock Mechanisms - DO₂ = CO x C_aO₂ > Where: > - **CO** = Cardiac Output > - CO = HR x SV > - CO = Preload x Afterload x Contractility > - **C_aO₂** = Arterial Oxygen Content > - C_aO₂ = (1.36 x SpO₂ x Hb) + 0.003(P_aO₂) > **Note**: > - Increase in metabolic rate will increase DO₂ > - Decrease in oxygen utilization will increase DO₂ ### Specific Causes of Obstructive Shock - Pericardial effusion - Traumatic reticulopericarditis - Neoplasia - Blood clots - Compressed vessels - Gastric dilatation and volvulus (GDV) - Colonic torsion - Tumors/mass ## Metabolic Shock - Inadequate delivery of substrates needed to meet energy requirements ### Metabolic Shock Mechanisms - DO₂ = CO x C_aO₂ > Where: > - **CO** = Cardiac Output > - CO = HR x SV > - CO = Preload x Afterload x Contractility > - **C_aO₂** = Arterial Oxygen Content > - C_aO₂ = (1.36 x SpO₂ x Hb) + 0.003(P_aO₂) > **Note**: > - Increase in metabolic rate will increase DO₂ > - Decrease in oxygen utilization will increase DO₂ ### Specific Causes of Metabolic Shock - Decreased O₂ carrying capacity - Anemia, Severe - Hemoglobinopathy - MetHb - Tylenol toxicity (dogs, cats) - Nitrate toxicity (ruminants) - Red maple toxicity (horses) - CarboxyHb – CO poisoning - Hypoxemia - Decreased FiO₂ - V/Q mismatch - pulmonary disease - Diffusion impairment – COPD - Hypoventilation - Right to left shunt – PDA - Altered oxygen utilization - Decreased capacity to use O₂ - Hypoglycemia - Cyanide poisoning - Sepsis - Increased O₂ demand - Sepsis - Heat stroke ## Multiple Shock States - Multiple shock states can occur at the same time. - **GDV** and **colonic torsion** - Hypovolemic, obstructive - Possibly distributive - **Sepsis** - Distributive, hypovolemic, metabolic ## Clinical Presentation of Shock - **Triage Examination** - **Neurologic System** - Mentation - **Respiratory System** - Rate and effort, pattern - **Cardiovascular System** - Color of mucous membranes, capillary refill time, pulse quality - Relative rate, rhythm - **Urinary** - Can it urinate? ## Stages of Shock - **Compensatory** - **Early Decompensatory Shock** - **Late Decompensatory Shock** (aka Terminal shock) ## Shock is a Continuum... The progression from normal to death can be visualized as a sliding scale including: 1. Normal 2. Compensatory 3. Early Decompensatory 4. Late Decompensatory 5. Death ## Shock: Compensatory - **Neurologic System** - Normal mentation - **Respiratory System** - Increased respiratory rate - **Cardiovascular System** - Tachycardia - Normal mucous membrane color and capillary refill time - Normal pulse quality (sometimes bounding) - Normal blood pressure ## Shock: Early Decompensatory - **Unable to meet metabolic demands** - **Ongoing catecholamine influence** - Vasoconstriction, increase cardiac output - **Redistribution of blood flow to vital organs** - **Poorly perfused organs begin anaerobic metabolism** - Lactic acidosis ensues ### Early Decompensatory Shock - Oxygen Consumption vs. Delivery - The graph shows the relationship between oxygen consumption and oxygen delivery during shock. - Oxygen consumption remains at a constant level even when oxygen delivery is sharply decreased. - This is because the body increases its use of anaerobic respiration to compensate when it does not have enough oxygen. - However, anaerobic respiration only produces a small amount of ATP, and it also produces lactic acid - which accumulates and causes lactic acidosis and leads to organ dysfunction. ## Shock: Stages of Shock - Clinical Presentation - **Neurologic System** - Depressed mentation - **Respiratory System** - Increased respiratory rate - **Cardiovascular System** - Tachycardia (most) - Bradycardia (cats) - Pallor, prolonged capillary refill time - Weak pulse quality - Hypotension – in some - Hypothermia – smaller animals ## Mucous Membranes Differ for Distributive/Vasodilatory Shock - **Red** or **inappropriately pink** mucous membranes distinguish distributive/vasodilatory shock from all other types. > **Note**: This is the first differential diagnosis to consider when assessing a patient in shock. - **Horses with sepsis develop a “toxic line” from endotoxin** ## Shock: Late Decompensatory - Normal compensatory mechanisms fail, due to ongoing oxygen and nutrient deprivation - **Death is imminent** ## Shock: Late Decompensatory - Clinical Presentation - **Neurologic System** - Stupor or coma - **Respiratory System** - Increased respiratory rate - **Cardiovascular System** - Bradycardia, decreased cardiac sounds - Marked pallor to cyanotic mucous membranes - Very prolonged to absent capillary refill time - Very poor to absent pulses - Hypotension - Hypothermia - Decreased urine output ## Shock Related Activity - On ELC - Read case summary - Decide most likely stage of shock and predominant category of shock ## Signs Secondary to Shock - Related to multiorgan dysfunction - Vomiting (species dependent), diarrhea - Hematochezia, melena - Leaky vasculature (SIRS) - Pulmonary edema (ARDS), pleural effusion - Coma, possibly seizures - Renal failure - Arrhythmias ## Treatment for Shock - **Goal**: Increase oxygen delivery - **DO₂ = C_aO₂ x CO** > Where: > - **CO** = Cardiac Output > - CO = HR x SV > - CO = Preload x Afterload x Contractility > - **C_aO₂** = Arterial Oxygen Content > - C_aO₂ = (1.36 x SpO₂ x Hb) + 0.003(P_aO₂) ### Increasing Oxygen Delivery - **Oxygen** - **Improve effective circulating volume** - Fluids - **Treat the underlying cause** - **Inotropes/chronotropes**: Increase contractility & HR - Beta agonists: Dobutamine, mil-dose dopamine - **Pressors**: cause vasoconstriction - Alpha agonists: Norepinephrine, epinephrine, high dose dopamine, phenylephrine - Vasopressin (V1) agonist ### Address O₂ Carrying Capacity PRN - Increase hemoglobin concentration - Red blood cell transfusion - Decrease metHb or carboxyHb conc ### Treating Altered O₂ Utilization - **Treating decreased capacity to use O₂** - Hypoglycemia -> give Dextrose - Sepsis – antimicrobials and supportive care - Cyanide poisoning -> oxygen and antidote - **Treating increased O₂ demand** - Heat stroke -> decrease body temperature - Sepsis -> treat underlying cause ## Other Treatments for Shock - **Rewarming** - Especially cats, exotics - **Antibiotics** - Sepsis, infection - Breached defenses - **Steroids** – usually not indicated - Anaphylaxis - Adrenal insufficiency - **Treat underlying cause** ## Endpoints of Shock Resuscitation - **Minimum treatment necessary to restore effective circulating volume** - Pink mucous membranes, normal capillary refill time - Normal heart rate, pulse quality and blood pressure - Normal body temperature - Improved mentation - Adequate urine production ## Monitoring - Even after stable - Signs of adequate perfusion - Signs of cell/organ dysfunction - May not appear for several days