Shock GR PDF

Shock Garrett Rogers, MSPA, PA-C  Shock Overview Life-threatening circulatory failure Decreased oxygen delivery, increased oxygen consumption, or impaired oxygen utilization that results in cellular and tissue hypoxia Inadequate end-organ perf...

Shock Garrett Rogers, MSPA, PA-C  Shock Overview Life-threatening circulatory failure Decreased oxygen delivery, increased oxygen consumption, or impaired oxygen utilization that results in cellular and tissue hypoxia Inadequate end-organ perfusion *Cellular death and dysfunction of vital organs*  Distributive Shock Cardiogenic Classifications Obstructive Hypovolemic  Types of shock Shock Type Skin Wedge Pressure (preload) Systemic Vascular Cardiac Output Resistance (Afterload) Hypovolemic ↓↓ ↑ ↓ (Traumatic) Cardiogenic Cold and ↑ ↑ ↓ (Pump Failure) clammy skin Obstructive ↓ or ↑ ↑ ↔ or ↓ Distributive Warm and dry ↔ or ↓ ↓↓ ↓ or ↑ (Vasodilation)  Inadequately perfused / oxygenated cells Deprived of essential substrates for aerobic metabolism Compensation: cells shift from aerobic to anaerobic metabolism Inefficient / inadequate ATP production (36 ATP vs 2 ATP) Formation lactic acid = lactic acidosis Increase metabolic acidosis Shock: Prolonged shock Cell membrane loses ability to maintain integrity Cellular Level Loss of normal electrical gradient Release of proinflammatory mediators Nitric oxide synthase Tumor necrosis factor (TNF) Sets stage for end-organ damage / Multiple Organ Failure Other cytokines Eventual death if not treated aggressively Stages of Shock Pre-shock (compensated shock) Compensatory mechanism to counter decreased tissue perfusion – tachycardia, peripheral vasoconstriction and normal or increased blood pressure Shock Classic: hypotension, tachycardia, tachypnea, obtunded, AMS, cold/clammy/mottled skin, oliguria, metabolic acidosis Early organ dysfunction End-organ dysfunction Irreversible damage, multiorgan failure, and death Shock Treatment Always start with the ABC’s Airway / Breathing / Circulation Restore end-organ perfusion Identify / treat the source of shock Trauma: Stop the bleeding Distributive: Early antibiotics / Fluid resuscitation / Source control Cardiac: Optimize cardiac defect Obstructive: Alleviate the obstruction via chest tube / pericardiocentesis /heparin Definitions  Pulmonary Capillary Wedge Pressure Used to assess left ventricular filling, represent left atrial pressure, and assess mitral valve function. Measured by inserting a balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a central vein and advancing the catheter into a branch of the pulmonary artery. The balloon is then inflated, which occludes the branch of the pulmonary artery and then provides a pressure reading that is equivalent to the pressure of the left atrium. Definitions Indications Differentiate between cardiogenic pulmonary edema and noncardiogenic pulmonary edema Confirm the diagnosis of pulmonary artery hypertension Assess the severity of mitral stenosis Differentiate between different forms of shock Measure key hemodynamic parameters and assess response to therapy Swan-Ganz catheter  Systemic Vascular Resistance AKA Total Peripheral Resistance (TPR) The amount of force exerted on circulating blood by the vasculature of the body MAP = CO x TPR Cardiac Output Definitions Cardiac output (CO) is the amount of blood pumped by the heart minute Mechanism whereby blood flows around the body, especially providing blood flow to the brain and other vital organs CO = SV x HR  Types of shock Shock Type Skin Wedge Pressure (preload) Systemic Vascular Cardiac Output Resistance (Afterload) Hypovolemic ↓↓ ↑ ↓ (Traumatic) Cardiogenic Cold and ↑ ↑ ↓ (Pump Failure) clammy skin Obstructive ↓ or ↑ ↑ ↔ or ↓ Distributive Warm and dry ↔ or ↓ ↓↓ ↓ or ↑ (Vasodilation) Distributive Shock Distributive Shock Shock secondary to severe peripheral vasodilation Neurogenic shock (Loss sympathetic tone /spinal cord injury > T6) Anaphylactic shock (Histamine release) Adrenal insufficiency SIRS and SEPSIS (More on this in next lecture) Pathogenesis An underlying event (such as infection or anaphylaxis) causes severe peripheral vasodilation → ↓↓ systemic vascular resistance (SVR) → hypotension Interruption of autonomic pathways (traumatic brain injury) → decreased SVR ↓ SVR → compensatory ↑ cardiac output (CO) initially in severe cases, ↓ CO Shock Type Skin Wedge Pressure SVR (Afterload) Cardiac Output (Preload) Distributive Warm and ↔ or ↓ ↓↓ ↓ or ↑ (Vasodilation) dry  Septic shock Non-septic shock Systemic inflammatory response syndrome (SIRS) Distributive Neurogenic shock Anaphylactic shock Shock Types Mediated by IgE Toxin-induced shock Endocrine shock Adrenal insufficiency  Neurogenic Shock Injuries involving cervical and upper thoracic spinal cord can produce hypotension due to Loss of sympathetic innervation (of heart) Loss of vasomotor tone (No ability for vasoconstriction) Most common seen with cervical cord injury (20% cases) Rarely upper thoracic spinal cord injury (7% cases) Neurogenic Shock Loss of sympathetic stimulation of the heart (No tachycardia) Vasodilatation of visceral / lower extremity vessels Hypotension + Bradycardia Treatment Moderate fluid resuscitation + early use of vasopressors Anaphylactic Shock Severe systemic reaction to an antigen Rapid onset < 2-10 min Prior exposure to antigen is necessary Host produces antibodies / IgE on Mast cells Exposure to antigen produces sudden release of Histamine (Vasodilatation) Heparin Serotonin Most common offending agents Foods Drugs (IV contrast, penicillin, local anesthesia) Blood products (If blood mismatch) Pollen Bee stings  Sx Rashes Upper airway obstruction - throat closing in / lump in throat, dyspnea, wheezing Cardiovascular collapse / shock Anaphylactic Shock Tx Epinephrine (IV route if severe) Steroids / Benadryl +/- intubation IV resuscitation  Adrenal Insufficiency Inadequate CORTISOL production; +/- impaired production of aldosterone Signs and Symptoms if patient able to communicate Severe abdominal pains Vomiting Profound muscle weakness Fatigue/ depression Hypotension Shock (adrenal crisis) Adrenal crisis Lack of cortisol decreases systemic peripheral resistance /results in hypotension Most commonly seen in prolonged (days) stress states / septic shock / elderly Tx IV fluids + IV Steroids (Cortisol) + pressors Cardiogenic Shock  Cardiogenic Shock Shock secondary to intracardiac causes results in a decreased cardiac output and systemic hypoperfusion (This is self-perpetuating) Hypotension will result in decreased perfusion to the coronary vessels Worsening ischemia Decreased stroke volume will increase the amount of blood in the left ventricle Increases LV size and consequently myocardial oxygen demand  Cardiogenic Shock Pathogenesis an underlying event (such as MI) results in ↓ cardiac output, which causes ↓ perfusion to tissue ↓ cardiac output and blood pressure causes ↑ catecholamines, which ↑ vasoconstriction and ↑ myocardial oxygen demand ↑ renin-angiotensin-aldosterone system, which ↑ vasoconstriction and retention of sodium and water ↑ shunting of blood to the brain and vital organs, which causes ↓ perfusion to peripheral organs Shock Type Skin Wedge Pressure (preload) SVR (Afterload) Cardiac Output Cardiogenic Cold and ↑ ↑ ↓ (Pump Failure) clammy skin  Cardiogenic Shock Cardiomyopathies Arrhythmias Mechanical myocardial infarction (MI) septal defect or ruptured valve cardiomyopathy blunt cardiac trauma myocarditis drug-induced  Cardiogenic Shock Patient presentation (depends on etiology): Cardiogenic Myocardial Infarction Chest pain,Shock dyspnea Arrhythmias Palpitations, syncope Pulmonary edema Diffuse lung crackles Distended jugular veins AMS Hypotension Cool extremities Decreased urine output Cardiogenic Shock Treatment Reverse underlying cause: CABG, valve replacement or repair Reduce preload: vasodilators, diuretics, fluid restriction Reduce afterload: vasodilators, diuretics Increase contractility: Inotropes Increase arterial O2 content: Oxygen, RBCs Cardiac support ** Excessive fluid administration can be detrimental** ->pulmonary edema Obstructive Shock Obstructive Shock Shock secondary to extracardiac causes of pump failure Cardiac tamponade Pulmonary embolism Tension pneumothorax  Patient presentation Typically present with features of the underlying cause (pleuritic chest pain in pulmonary embolism) Hypotension Tachycardia Obstructive JVD Shock Cold and clammy skin Shock Type Skin Wedge Pressure (preload) Systemic Vascular Cardiac Output Resistance (Afterload) Obstructive Cold and ↓ or ↑ ↑ ↔ or ↓ clammy skin  Pericardial Tamponade Due to acute (trauma / aortic dissection / myocardial rupture) or chronic fluid collections in the pericardial space Beck’s Triad Hypotension Muffled heart sounds Hypotension with elevated CVP Distended neck veins Pulsus paradoxus Fall in SBP > 15 mm with normal inspiration Dx: cardiac echo Treatment: pericardiocentesis vs surgical decompression Caution: Excessive resuscitation Pericardiocentesis  Pulmonary Embolism Thrombus within the pulmonary arterial system Most PEs develop from migration of iliofemoral deep vein thrombosis (DVT) Virchow’s Triad: Stasis of blood flow Endothelial injury Hypercoagulability Treatment Hemodynamic stabilization Urgent anticoagulation Unstable patients Thrombolytic therapy / catheter-based fragmentation/aspiration  Etiology Penetrating and blunt chest trauma Infection Tension Positive-pressure mechanical ventilation Pneumothorax Iatrogenic Placement of central venous line Epidural thoracic catheter placement  Patient presentation: Acute-onset, unilateral pleuritic chest pain Dyspnea/acute respiratory distress Syncope Tachypnea and tachycardia Tension Unilateral decreased or absent breath sounds Pneumothorax Hyperresonance Falling O2 sats Deviated trachea JVD Hypotension Subcutaneous emphysema Tension Pneumothorax Hypovolemic Shock  Hypovolemic Shock Shock secondary to reduced intravascular volume Reduced preload results in a decreased cardiac output Hemorrhagic Trauma Gastrointestinal bleeding (variceal bleed) Vascular (Ruptured aneurysm) Non-hemorrhagic Decreased intravascular volume not due to loss of blood Gastrointestinal losses (vomiting and diarrhea) Skin losses (heat stroke and burns) Third spacing (pancreatitis) Renal losses (diuresis)  Hypovolemic Shock Patient presentation Treatment Typically present with features of the Treat the underlying cause underlying cause Establish the ABCs - airway, Hypotension breathing, and circulation Intravenous fluids with large-bore Tachycardia IVs Reduced skin turgor Transfuse blood for hemorrhagic Nondistended jugular veins shock Dry mucous membranes Cold and clammy skin Hypovolemic Shock Critical Steps: Restore intravascular volume (Permissive hypotension) 1-2 liters crystalloid followed by RBCs + FFP / platelets Definitive Hemostasis Repair hole in the vessel External vs internal Angioembolization Pitfall Aggressive and continued volume resuscitation is NOT a substitute for definitive hemorrhage control. Lethal Triad of Death: Traumatic Shock Stop the Bleeding /Resuscitate the Patient  Blood Transfusion Goal of pRBC transfusion is to increase oxygen carrying capacity 1 unit of pRBC should increase Hb by 1 g/dL or Hct by 3-4% Indications Hb < 7 g/dL May increase based on presence of symptoms Goal Hb between 7 and 10 g/dL during active bleeding Higher Hb threshold (Hb < 10 g/dL) for patients with Uncontrolled bleeding Cardiovascular disease (coronary artery disease, diabetes) Pulmonary disease (COPD) Dilution of sickled Hb in sickle cell disease patients Clinical suspicion of blood loss - CBC will not demonstrate anemia in acute trauma Blood Transfusion "Type and Screen" (T&S) vs. "Type and Cross" (T&C) T&S determines blood group, Rh status, presence of major/minor autoantibodies T&C determines possible agglutination by mixing recipient and donor blood Whole blood vs Components FFP Platelets Cryoprecipitate Transfusion Reaction Signs and Symptoms  Transfusion Reaction Transfusion-associated Febrile Reactions Allergic Reaction Circulatory Overload (1:60) (1:250) (TACO) (1:100) Stop transfusion Mild – Urticaria Respiratory distress 2-4 and evaluate the hrs post transfusion and pruritis patient cardiogenic pulmonary APAP +/- edema Antihistamines diphenhydramine Severe – bronchospasm, Present 6-12 hours post wheezing, and anaphylaxis transfusion Bronchodilators, steroids, Diuretics before or between epinephrine transfusions  Transfusion Reaction Transfusion-related Sx develop 2-4 hours post transfusion –> acute hypoxemic Lung Injury respiratory distress Supportive care (TRALI)(1:12,000) ABO incompatibility Sx – fever and chills, low back pain, flushing dyspnea, tachycardia, Fatal Hemolysis and shock Stop transfusion -> leave IV in place and begin IV NS (1:972,000) Cardiorespiratory support Hemolytic workup  Transfusion Reaction Electrolyte Infections Abnormalities HIV – HEP C – Hypocalcemia Hyperkalemia Hypokalemia 1:1,467,000 1:1,149,000 Questions?