Shock & Critical Care PDF

Shock & Critical Care Christine Ciszek, PA-C WakeMed General Surgery & Trauma 2024 Objectives 1. 2. 3. 4. 5. 6. Define shock. Compare and contrast the pathophysiology, etiology, clinical presentation and basic management of the following types of shock: a. Hypovolemic shock b. Cardiogenic shock c. O...

Shock & Critical Care Christine Ciszek, PA-C WakeMed General Surgery & Trauma 2024 Objectives 1. 2. 3. 4. 5. 6. Define shock. Compare and contrast the pathophysiology, etiology, clinical presentation and basic management of the following types of shock: a. Hypovolemic shock b. Cardiogenic shock c. Obstructive shock d. Neurogenic shock e. Distributive shock (septic and anaphylactic) Explain the multidisciplinary needs of the critically ill surgical patient and the coordination of care required of the critical care team practicing in the surgical intensive care unit (SICU). Explain indications and the use of mechanical ventilation in the seriously ill patient. Describe the benefits, and limitations of the following systems’ monitoring in the SICU: a. Hemodynamic monitoring b. Respiratory monitoring c. Renal monitoring d. Intracranial Pressure monitoring Discuss the prevention, pathophysiology, presentation, evaluation, treatment, and complications of the following disease entities that are frequently seen in the SICU: a. Respiratory Failure b. Cardiac Disease c. Infectious Diseases d. Delirium Shock The first step to managing shock is to recognize its presence! The second step in managing shock is to identify the probable cause of shock and adjust treatment accordingly Shock = abnormality of the circulatory system that results in inadequate organ perfusion and tissue oxygenation Initial Approach to the Critically Ill Patient “Tell me your name,” squeeze or shake my hand Not only can be comforting to the patient, but will give a good impression to level of consciousness, peripheral perfusion “Sick or not sick?” Review of vital sign trends including UOP Obtain a brief history Medications administered Recent lab values and imaging Clinical Observations Patient Category Appearance Neurological Respiratory Cardiovascular Not Critically Ill Normal Alert Cooperative Normal pattern RR>8 90 UO >0.5ml/kg/hr Potential Critical Illness Sweaty Pale Anxious Agitation Confusion Eyes open to voice only Accessory muscle use RR100 SBP 2) MODS (multiple organ dysfunction syndrome) – progressive organ dysfunction in acutely ill patient, at severe end of severity of illness spectrum of both infectious (septic) shock and non-infectious conditions (i.e. pancreatitis) SIRS = systemic inflammatory response syndrome Induced by infectious or non-infectious insult (pancreatitis, burns, trauma, embolism, postcardiac arrest syndrome) 2 or more abnormalities in temperature, HR, respiration, or WBC count Leading infective sources remain gram positive cocci from respiratory sources followed by gram negative bacterial pathogens Fungal sources have increased over past decade but remains lower than bacterial sepsis In approximately ½ of cases, organism not identified Viruses: influenza A and B, RSV, coronavirus, parainfluenza virus, adenovirus, enterovirus, rhinovirus Distributive Shock Septic Shock Early sepsis leads to hyperdynamic state of cardiac function with tachycardia and pro-inflammatory arrhythmias such as atrial fibrillation Later, myocardial depression may manifest Microcirculatory dysfunction leads to poor O2 utilization and resultant high mixed venous oxygen saturations Hypotension and dilated shock process ensue Respiratory dysfunction with ALI and potential ARDS often requires ventilator support Acute renal failure common secondary to inflammatory mediators and hypoperfusion GI system often manifests with paralytic ileus; hypoperfusion can lead to intestinal ischemia, acalculous cholecystitis, pancreatitis, gastritis, ulcer formation Dysregulation of coagulation system, immunologic response, and endocrine system common Distributive Shock Septic Shock Diagnosis Can be difficult to distinguish from hypovolemic shock – both have tachycardia, cutaneous vasoconstriction, dec UOP, low SBP, narrow pulse pressure Initially warm and dilated extremity perfusion; skin mottling can proceed once tissue hypoperfusion and microcirculatory dysfunction have set in qSOFA (quick Sequential Organ Failure Assessment) Alteration in mental status SBP < 100 RR > 22 CBC (leukocytosis, leukopenia, bandemia, thrombocytopenia) BMP (electrolyte assessment, acid/base, anion gap/base excess, renal function) LFTs (may guide source diagnosis, end organ dysfunction of liver) Coags, lactate, ABG, Procalcitonin Cultures – blood, urine, respiratory Imaging studies – to guide diagnosis and source control SOFA Score – Mortality Prediction Distributive Shock Septic Shock Treatment Infection identification and control Broad spectrum antibiotics initiated within 1 hour Cultures, preferably prior to antibiotic administration Source control – may necessitate prompt surgical and procedural intervention Resuscitation and life support in critically ill patients Fluid management 30 cc/kg crystalloid fluid bolus Assess response to volume and end points to resuscitation Passive leg raise, urine output > 0.5 cc/kg CVP (central venous pressure), MAP, SvO2, lactate clearance Vasopressors Norepinephrine (Levophed) first line – vasoconstrictive properities, inotropic support Epinephrine seconed line – sympathomimetic increasing HR and tone Vasopressin – potent vasoconstrictor, raises systemic vascular resistance and enhances water reabsorption from kidney Typically, after 3 pressors/refractory shock consider corticosteroids to empirically treat Critical Illness-Related Corticosteroid Insufficiency Mechanical Ventilation Tidal volume of 6 mL/kg of predicted body weight Plateau pressures 85 to maintain spinal cord perfusion Pressors: Norepinephrine, dopamine, phenylephrine For how long? Distributive Shock Anaphylactic Shock Anaphylactic shock Massive systemic vasodilation leading to cardiovascular collapse, facial and tongue swelling leading to airway compromise, bronchospasm Largely clinical diagnosis Halt exposure to trigger while assessing airway and hemodynamic stability Secure airway (intubation for impending airway compromise), supplemental O2 and continuous monitoring Epinephrine (0.3 – 0.5 mg IM, repeat q5-15 min), epi drip for refractory response IV access, crystalloid administration H1 and H2 antihistamines Consider steroid (125 mg of IV methyprednisolone) Epinephrine vasopressor of choice to maintain MAP >65 Drug and toxin-induced shock (i.e. drug overdose, snake and insect bites, poisoning, TSS, cyanide and carbon monoxide) Distributive Shock Adrenal insufficiency Insufficient adrenal production (primary adrenal insufficiency from Addison’s disease or adrenal infarct or surgical removal) Insufficient pituitary stimulation (secondary adrenal insufficiency) Insufficient exogenous pharmacologic support (tertiary adrenal crisis) Fatigue, lethargy, abdominal complaints, fever, psychiatric manifestations often accompany hypotension in adrenal crisis Often precipitated by another pathology such as infection; history of steroid use may suggest adrenal insufficiency Short corticotropin test is “gold standard” diagnostic tool Treatment: volume repletion and hormonal replacement IV crystalloid (0.9% NS + D5) Dexamethasone 4 mg q 12 hours for those who require diagnostic workup for confirmation of adrenal insufficiency (will not interfere with serum cortisol levels) Hydrocortisone 100 mg IV bolus followed by 50 mg q6 hours in those with known primary adrenal insufficiency Treatment of infection or other trigger Hypovolemic Shock Loss of intravascular circulating volume Bleeding (trauma or atraumatic bleeding such as AAA rupture or GI bleed) Fluid losses - excessive vomiting or diarrhea, malabsorption, or hormone imbalances such as DI can result in excessive volume loss H&P to direct diagnosis – hx of trauma, recent surgery or evidence of bleeding; vomiting, diarrhea or GI illness Cold shock picture with pallor CBC: Hgb / Hct – may be decreased in acute blood loss, however not reliable indicate of the amount of blood loss in early exsanguinating hemorrhage Hgb may remain preserved in early blood loss while the circulating volume may be significantly reduced Trends in Hgb and Hct better than single value With severe fluid loss, may see hemoconcentration BMP – electrolyte assessment (GI loss may lead to hypokalemia, massive transfusion may lead to low ionized calcium); Acid-Base status Coagulation studies (PT/INR, PTT, fibrinogen, TEG) CXR, Pelvis XR, FAST, CT scan, Angiography Hypovolemic Shock Hemorrhagic Shock Hemorrhage is the most common cause of shock in trauma patients! 1) Definitive control of hemorrhage 2) Restoration of adequate circulating volume Vasopressors are contraindicated as first-line treatment because they worsen tissue perfusion Many hemorrhagic shock patients require surgical intervention or angioembolization to reverse the shock state Blood Loss Pathophysiology Early circulatory response to blood loss is compensatory – vasoconstriction to preserve blood flow to kidneys, heart and rate Increase in HR to preserve cardiac output Release of catecholamines to increase peripheral vascular resistance, inc diastolic BP and reduce pulse pressure (does little to increase organ perfusion/oxygenation) Venous return preserve to some degree of contraction of volume of blood in venous system (limited) The most effective method of restoring CO, end-organ perfusion, and tissue oxygenation is to restore venous bleeding to normal by locating and stopping the source of bleeding Volume repletion only useful when the bleeding has stopped! Hemorrhage Normal blood volume ~7% of body weight (70 kg male has blood volume approx 5L) Blood volume of obese patients based on their ideal body weight Blood volume for child is calculated as 8-9% of body weight Clinical Signs: Stage 1 Up to 15% blood volume loss (750 mL) Compensated by constriction of vascular bed Blood pressure maintained, narrower pulse pressure Normal respiratory rate Pallor of the skin Normal mental status to slight anxiety Normal capillary refill Normal urine output Base deficit: 0 to -2 mEq/L Exemplified by the condition of an individual who has donated 1 unit of blood Clinical Signs: Stage 2 15–30% blood volume loss (750–1500 mL) Cardiac output cannot be maintained by arterial constriction Normal to tachycardic >100bpm Normal to increased respiratory rate Blood pressure maintained Increased diastolic pressure Narrow pulse pressure Sweating from sympathetic stimulation Mildly anxious/Restless but normal GCS Urine output normal/slightly dec 20-30 milliliters/hour BE -2 to -6 Uncomplicated hemorrhage for which crystalloid fluid resuscitation is required Clinical Signs: Stage 3 30–40% blood volume loss (1500–2000 mL) Normal to dropping BP (100mmHg or less) Classic signs of hypovolemic shock Marked tachycardia >120 bpm Normal to increased tachypnea >30 bpm Alteration in mental status (confusion, anxiety, agitation) Sweating with cool, pale skin Delayed capillary refill Urine output of approximately 20 milliliters/hour BE -6 to -10 Need at least crystalloid but likely blood products Clinical Signs: Stage 4 Loss greater than 40% (>2000 mL) Extreme tachycardia (>140) with weak pulse Pronounced tachypnea Significantly decreased systolic blood pressure Decreased level of consciousness, lethargy, coma Skin is sweaty, cool, and extremely pale Absent capillary refill Negligible urine output BE at least -10 Preterminal event, patient will die Needs massive transfusion protocol Confounding Factors Patient Age Children and pregnant patients will often compensate until the point of circulatory collapse Elderly may not be able to mount tachycardic response to hemorrhage due to beta blockade, medications, pacer dependence; baseline hypertension Severity of injury (type and anatomic location) Time lapse between injury and treatment Prehospital fluid therapy Medications used for chronic conditions Don’t wait until a trauma patient fits a precise physiologic classification of shock before initiating appropriate volume resuscitation! Sources of Bleeding “Blood on the floor and 4 more” Life-threatening amount of blood loss can be found: Outside the body (“on the floor”) Thigh compartments of femur fractures Pelvis Abdomen Chest Soft Tissue Injury Blood is lost at site of injury, particularly in major fractures Fractured tibia or humerus can result in loss of up to 750 mL of blood Twice that (1500 mL) associated with femur fractures Several liters can accumulate in retroperitoneal hematomas associated with pelvic fractures Edema that occurs constitutes another source of fluid loss Elderly patients also at risk of more blood loss due to fragile skin, inelastic blood vessels and blood thinners Hypovolemic Shock Treatment Aggressive replacement of volume, definitive management of underlying etiology Trauma patients: Follow ATLS (temporary measures such as pressure, tourniquets, pelvic binders) Atraumatic bleeding: need identification of source Large bore IV access or central access Crystalloid resuscitation should be limited to 1-2 liters of crystalloid; then blood and plasma resuscitation in the exsanguinating patient Whole blood Component therapy – balanced resuscitation (PRBCs, FFP, Platelets) Massive transfusion Hypovolemic shock from fluid loss – aggressive repletion, address source of fluid loss Oral rehydration vs crystalloid Bolus 20-30 cc/kg, then assess response Judicious rehydration, avoid fluid overload Blood Replacement Cross-Matched, Type Specific & Type O blood Approx 1 hour to crossmatch Type O PRBCs in exsanguinating hemorrhage Rh-negative preferred for females of childbearing age Whole blood Prevent Hypothermia Autotransfusion Massive Transfusion >10 units PRBC within first 24 hrs, or >4 units in 1 hour Balance resuscitation 1:1:1 (PRBC, FFP, platelets) Coagulopathy – up to 30% of severely injured patients on admission PT/PTT/INR, TEG studies TXA administration (improved survival within 3 hours) Calcium Administration Usually only needed in massive transfusion, measure ionized calcium Measuring Patient Response Vital Signs Persistent acidosis (base deficit, lactate values) Trend Hgb/Hct Appropriate response to blood transfusion? 1u PRBC = increase 1 g/dL Hgb UOP is one of the prime indicators of resuscitation and patient response 0.5 mL/kg/hr in adults 1 mL/kg/hr in pediatrics Review: Hemodynamics of Shock Type of Shock Heart Rate Cardiac Output Blood Pressure Systemic Vascular Resistance SvO2 Cardiogenic Increased Decreased Decreased Increased Decreased Hypovolemic Increased Decreased Decreased Increased Decreased Distributive Increased Normal or Increased Decreased Decreased Normal or Increased Obstructive Increased Decreased Decreased Increased Decreased Shock Resuscitation ABCs Hypovolemic Shock Replace fluid and stop volume loss Cardiogenic Shock Ease afterload; assist cardiac contraction; treat cause Septic Shock Support circulation; support vasomotor tone and treat source of infection Obstructive Shock Recognition; relieve compression Neurogenic Shock Replace volume; vasoconstriction Multidisciplinary Care Critically ill patients require multidisciplinary needs and coordination of care Surgical Intensive Care Unit (SICU) Surgery/Trauma Providers – Attending trauma surgeon, APP (PA or NP), surgical residents Consulting specialists (orthopedics, neurosurgery, cardiology, nephrology, ENT, infectious disease, urology) Nursing – specially trained in critical care Respiratory therapist Pharmacist Physical Therapist/Occupational Therapist Wound care nurse Case Management/Social Work Monitoring in the SICU Hemodynamic Monitoring Respiratory Monitoring Renal Monitoring Intracranial Pressure Monitoring Hemodynamic Monitoring Goals: assure adequate perfusion, early detection of inadequate perfusion, titrate therapy to specific hemodynamic endpoints, differentiate amount various organ system dysfunctions EKG, telemetry monitoring Vitals (HR, blood pressure, temperature, pulse ox) Arterial Pressure Monitoring Continuous invasive blood pressure measurement Regular analysis of ABGs Central Venous Pressure (CVP) Needs central line Echo Non-invasive hemodynamic monitoring i.e. FloTrac Uses arterial pressure waveform analysis to calculate stroke volume and cardiac output Can assess fluid responsiveness Pulmonary arterial catheter i.e. Swan Ganz catheter Invasive Renal Monitoring Urine Output (at least 0.5 cc/kg/hr) Guide fluid resuscitation Monitor for oliguria/anuria BUN/Creatinine Electrolyte Levels and Acid-Base Balance Early recognition of AKI Most common etiologies: fluid volume deficit or kidney hypoperfusion and ATN due to shock, inflammatory state, or nephrotoxic drug Critically ill patients with acute renal failure may require CRRT (continuous renal replacement therapy) ICP Monitoring Intracranial Pressure Monitoring Normal ICP Range 5-15 mm Hg >20 usually threshold to treat elevated ICP HOB elevation, hyperventilation, antiseizure therapy, IV mannitol, hypertonic saline, sedation, barbiturates (pentobarbital), neuromuscular paralysis, decompressive craniectomy ICP monitors most commonly used in severe traumatic brain injury, also use for CSF circulatory disorders (can be either diagnostic or therapeutic by removing CSF to reduce pressures) Contraindications: coagulopathies or anticoagulation, scalp infections, brain abscess Complications: infection (meningitis, ventriculitis, wound infection), intracranial hemorrhage, device malfunction or difficulty with placement, ventricular collapse 2 basic ICP Monitor types: ICP data only (“bolts”) ICP data + CSF drainage (External ventricular drain or EVD) Respiratory Monitoring Vital Signs, Mental Status, Respiratory Effort Pulse Oximetry End-Tidal CO2 ABG Ventilator Monitoring CXR Respiratory Complications Many critically ill patients require respiratory support or mechanical ventilation Respiratory insufficiency or failure common in SICU Atelectasis, pneumonia, aspiration, ARDS, pulmonary embolism, fat embolism, narcotic overdose Management Supplemental O2 (NC or HFNC) Non-invasive ventilation BiPap or CPAP Intubation and mechanical ventilation Aspiration Gastric contents reflux beyond esophagus and enter the respiratory tract or when oropharyngeal secretions and food enter the respiratory tract from above Initially causes chemical pneumonitis but can progress to bacterial infection Can occur during induction of anesthesia or RSI, or inability to protect airway such as AMS, stroke, or heavy vomiting High risk for aspiration during induction: those who have not fasted, trauma patients, pregnant patients, bowel obstructions, GERD, paraesophageal hernia, delayed gastric emptying Usually affects R middle and lower lobes – why? Pulmonary Edema Caused by abnormal movement of fluid across alveolar capillary membrane leading to buildup of fluid in pulmonary interstitial and alveolar spaces leading to decreased diffusing capacity, hypoxemia and SOB Can be caused by heart failure (dec L ventricular cardiac output causes fluid to backup in pulmonary veins), and/or fluid overload Fluid overload can cause pulmonary edema even in those with normal EF, especially in patients with ESRD who are dependent on dialysis for removal of excess volume Indications for Mechanical Ventilation Airway compromise Airway protection in obtunded or airway compromise from trauma or infection Obstruction (proximal such as angioedema; or distal such as bronchospasm or COPD) Hypoventilation due to impaired drive, pump failure, inability to to exchange gases resulting in hypercapnic respiratory failure Impaired central drive such as drug overdose Respiratory muscle weakness such as muscular dystrophy Peripheral nervous system defects such as Guillain-Barre or myasthenia crisis Restrictive ventilatory defects such as chest wall trauma, PTX or effusion Hypoxemic respiratory failure due to inability to exchange oxygen or delivery to peripheral tissues Alveolar filling defects (pneumonia, ARDS, or pulmonary edema) Pulmonary vascular defects leading to VQ mismatch (massive PE or air emboli) Diffusion defects (advanced pulmonary fibrosis Increased ventilatory demand due to severe sepsis, shock or severe metabolic Indications for Mechanical Ventilation Bradypnea or apnea with respiratory arrest Acute lung injury and ARDS Tachypnea (>30) Vital capacity 10 L/min PaO2 < 55 PaCO2 > 500 with pH