SHOCK Sevgi Bilgen 2014 2015 Students should learn

SHOCK Sevgi Bilgen 2014 -2015

Students should learn; The definition of shock Types of shock Shock treatment

Introduction In order to treat shock appropriately, it must first be recognized, then identify the cause In order to recognize it, it is important to understand some of the physiology of the disease process

The definition of shock Shock is a physiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery Hypotension is not a requirement Shock can occur with a normal blood pressure and hypotension can occur without shock Results in multiple organ failure and death

Inadequate oxygen delivery leading to shock can occur despite the patient being hypertensive or normotensive Clinicians should not wait for the presence of hypotension before aggressively attempting to reverse shock and restore adequate tissue perfusion.

Basic Physiology Tissue perfusion is dependent on SVR and CO Imbalance between oxygen delivery and oxygen consumption which leads to cell death, end organ damage, multi-system organ failure, and death.

Basic Physiology Oxygen Delivery = CO x arterial content of O 2 Cardiac Output = HR x Stroke Volume Ca. O 2 = (1. 34 x Hgb x Sa. O 2) + (Pa. O 2 x 0. 0031) Stroke Volume is a function Preload Afterload Myocardial Contractility

Basic Physiology

Understanding Shock Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery • Sympathetic nervous system • NE, epinephrine, dopamine, and cortisol release • • Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) Renin-angiotensin axis • Water and sodium conservation and vasoconstriction • Increase in blood volume and blood pressure Goal is to maintain cerebral and cardiac perfusion

Understanding Shock Prolonged oxygen deprivation leads to cellular hypoxia, derangement of critical biochemical processes at the cellular level, which can progress to the systemic level

Understanding Shock Cellular effects include cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents into the extracellular space, inadequate regulation of intracellular p. H

Understanding Shock Systemic effects include alterations in the serum p. H, endothelial dysfunction, redox state, further stimulation of inflammatory and anti-inflammatory cascades.

Understanding Shock The effects of oxygen deprivation are initially reversible, but rapidly become irreversible. The result is sequential cell death, end-organ dysfunction. Progressive end-organ dysfunction leads to irreversible organ damage and patient death.

Clinical Endpoints of Shock DECREASED BLOOD FLOW TO BRAIN AND HEART Restless, agitated, confused, lethargy Hypotension Tachycardia Tachypnea END-STAGE SHOCK Bradycardia Arrhythmia Death

Initial Patient Assessment Recognition of Shock Clinical signs and symptoms depends on the severity of the shock Early manifestations include tachycardia and cutaneous vasoconstriction

Cardinal features of shock include; hypotension, oliguria, abnormal mental status, metabolic acidosis, and, in some patients, cool and clammy skin.

Types of shock and differential diagnosis 1. Hypovolemic shock 2. Cardiogenic shock 3. Obstructive shock 4. Distributive shock

Common Causes 1. Hypovolemic shock Due to decreased circulating blood volume in relation to the total vascular capacity Characterized by a reduction of diastolic filling pressures.

Hypovolemic shock Loss of blood (hemorrhagic shock) Loss of plasma Loos of fluid and electrolytes

Loss of blood (hemorrhagic shock) External hemorrhage Trauma Gastrointestinal tract bleeding Internal hemorrhage Hematoma Hemothorax or hemoperitoneum

Loss of plasma Burns Exfoliative dermatitis

Loos of fluid and electrolytes External Internal (third-spacing) Vomiting Pancreatitis Diarrhea Ascites Excessive sweating Bowel obstruction Hyperosmolar states (diabetic ketoacidosis, hyperosmolar nonketotic coma)

Hypovolemic shock Depending upon the cause of the hypovolemic shock, patients may report; hematemesis, hematochezia, melena, vomiting, diarrhea, abdominal pain. There may be evidence of blunt or penetrating trauma, or the patient may be postoperative.

Hypovolemic shock Physical manifestations may include; decreased skin turgor (in younger patients), dry skin, dry axillae, dry tongue, dry oral mucosa.

Hypovolemic shock Patients may have postural hypotension, decreased jugular venous pressure, diminished central venous pressure. There may be anemia, or the amylase and lipase may be elevated

2. Cardiogenic shock Due to cardiac pump failure related to loss of myocardial contractility or structural/mechanical failure of the cardiac anatomy characterized by elevations of diastolic filling pressures and volumes

Cardiogenic shock Pump failure (secondary to myocardial infarction or other cardiomyopathy) Acute myocardial ischemia is most common cause Arrhythmia Tachyarrhythmia Bradyarrhythmia Acute valvular dysfunction Rupture of ventricular septum or free ventricular wall

Cardiogenic shock Depending upon the cause of the cardiogenic shock, patients may report; dyspnea, chest pain, palpitations. Many patients have a history of cardiovascular disease.

Cardiogenic shock Lung examination may reveal diffuse crackles cardiac examination may reveal a new murmur, gallops, or soft heart sounds. The jugular venous pressure and central venous pressure may be increased, the distal arterial pulses may be diminished.

Cardiogenic shock There may be evidence of pulmonary congestion or pulmonary edema on a chest radiograph, recent or current ischemia on an electrocardiogram. Cardiac enzymes may be elevated. An echocardiogram may demonstrate the etiology.

3. Obstructive shock Due to obstruction to flow in the cardiovascular circuit Characterized by either impairment of diastolic filling or excessive afterload

Obstructive shock Tension pneumothorax Pericardial disease (tamponade) Disease of pulmonary vasculature (massive pulmonary emboli, pulmonary hypertension) Cardiac tumor (atrial myxoma) Left atrial mural thrombus Obstructive valvular disease (aortic or mitral stenosis)

Tension pneumothorax/exam absent unilateral breath sounds on the affected side; trachea deviated to the opposite side; hyper-resonance to percussion on affected side

Cardiac tamponade/exam muffled hearts sounds low BP jugular venous distention pulsus paradoxus

Pulmonary emboli/exam possible cyanosis respiratory distress with use of accessory muscles lung auscultation normal jugular venous distention if large embolism calf tenderness tachycardia low oxygen saturations

4. Distributive shock Caused by loss of vasomotor control resulting in arteriolar/venular dilatation characterized (after fluid resuscitation) by increased cardiac output and decreased SVR

Distributive shock Septic shock Anaphylactic shock Neurogenic shock Vasodilator drugs Acute adrenal insufficiency

Depending upon the cause of the distributive shock; patients may report dyspnea fatigue productive cough malaise dysuria, hematuria headache chills photophobia myalgias pain rashes recent ingestion

Distributive shock There may be fever tachypnea tachycardia leukocytosis abnormal mental status flushing

Clinical classification of hemorrhagic shock Mild (<20% of blood volume lost) Moderate (20 -40% of blood volume lost) Severe (>40% of blood volume lost)

Mild (<20% of blood volume lost) Pathophysiology Decreased peripheral perfusion only of organs able to withstand prolonged ischemia (skin, fat, muscle, and bone). Arterial p. H normal Clinical Manifestations Patient complains of feeling cold. Postural hypotension and tachycardia. Cool, pale, moist skin; collapsed neck veins; concentrated urine.

Moderate (20 -40% of blood volume lost) Pathophysiology Decreased central perfusion of organs able to tolerate only brief ischemia (liver, gut, kidneys). Metabolic acidosis present Clinical Manifestations Thirst Supine hypotension and tachycardia (variable) Oliguria and anuria.

Severe (>40% of blood volume lost) Pathophysiology Decreased perfusion of heart and brain. Severe metabolic acidosis. Respiratory acidosis possibly present. Clinical Manifestations Agitation, confusion or obtundation. Supine hypotension and tachycardia invariably present. Rapid, deep respiration.

DIAGNOSTIC APPROACH When a patient is suspected of having shock, diagnostic evaluation should occur at the same time as resuscitation. Resuscitative efforts should NOT be delayed for history, physical examination, laboratory testing, or imaging.

Evaluation Airway: includes brief evaluation of mental status Breathing: If patient is conversing with you, A & B are fine Circulation: Vitals (HR, BP). Includes placement of adequate IV access Disability: identification of gross neurologic injury Exposure: ensures complete exam

Evaluation Laboratory Hgb, WBC, platelets PT/PTT Electrolytes, arterial blood gases BUN, Cr Ca, Mg Serum lactate, mixed venous oxygen saturation (SVO 2) ECG

Evaluation Invazive monitoring Arterial pressure catheter CVP monitoring Pulmonary artery catheter Mixed or central venous oxygen saturation (Sv. O 2/Scv. O 2) Oxygen delivery(DO 2) and oxygen consumption(VO 2) As indicated o Chest x-ray o Pelvic x-ray o Abd/pelvis CT o Chest CT o GI endoscopy o Bronchoscopy o Vascular radiology

Treatment Identify & reverse the cause Restore tissue perfusion Restore organ function

Goals of Shock Resuscitation Restore blood pressure Normalize systemic perfusion Preserve organ function

Treatment of Shock General Management • ABCDE • Airway • control work of Breathing • optimize Circulation • assure adequate oxygen Delivery • achieve End points of resuscitation

Airway • Determine need for intubation but remember: intubation can worsen hypotension • • Sedatives can lower blood pressure Positive pressure ventilation decreases preload • May need volume resuscitation prior to intubation to avoid hemodynamic collapse

Control Work of Breathing • Respiratory muscles consume a significant amount of oxygen • Resting ventilatory muscles will permit diversion of cardiac output to other hypo perfused organs • Tachypnea can contribute to lactic acidosis • Mechanical ventilation and sedation decrease WOB and improves survival

Optimizing Circulation • Unless there are signs of intravascular volume overload initial resuscitation with IV fluids is generally indicated. • Isotonic crystalloids • Titrated to: • CVP 8 -12 mm Hg • Urine output 0. 5 ml/kg/hr. (30 ml/hr. ) • Improving heart rate • May require 4 -6 L of fluids • No outcome benefit from colloids • Vasopressor medications should be selected based on the cause of shock

Maintaining Oxygen Delivery • Decrease oxygen demands • Provide analgesia and anxiolytics to relax muscles and avoid shivering • Maintain arterial oxygen saturation/content • • Give supplemental oxygen Maintain Hemoglobin > 10 g/d. L • Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction

End Points of Resuscitation • Goal of resuscitation is to maximize survival and minimize morbidity • Use objective hemodynamic and physiologic values to guide therapy • Goal directed approach • • Urine output > 0. 5 m. L/kg/hr. CVP 8 -12 mm. Hg MAP 65 to 90 mm. Hg Central venous oxygen concentration > 70%

Persistent Hypotension • Inadequate volume resuscitation • Pneumothorax • Cardiac tamponade • Hidden bleeding • Adrenal insufficiency • Medication allergy

Resuscitation Fluids Blood Lactated Ringers Normal Saline Colloids Hypertonic Saline Blood Substitutes

Evaluation of Treatment Assess organ perfusion Urinary output Mental Status Skin exam Vitals

Which Pressor should I choose? Hypovolemic shock Fluids and Blood Cardiogenic shock Dobutamine - 1 agonist Increases squeeze and heart rate Neurogenic shock Fluids, phenylephrine, norepinephrine, look for another type of shock if it is persistent Anaphylactic shock Fluids and epinephrine Septic shock Norepinephrine – (alpha+beta agonists) Epinephrine+ vasopressin Increases SVR by arteriolar constriction Dopamine Low Dose - increases renal blood supply Medium Dose - beta effects (increases heart rate and squeeze) High Dose - alpha effects (arteriolar constriction)

Survival and outcomes improve with early perfusion, adequate oxygenation, and identification with appropriate treatment of the cause of shock.