SHOCK Assoc Prof Dr SEVG BLGEN DEPARTMENT OF

SHOCK Assoc. Prof. Dr. SEVGİ BİLGEN DEPARTMENT OF ANESTHESIOLOGY AND REANIMATION YEDITEPE UNIVERSITY SCHOOL OF MEDICINE 2017 -2018

The definition of shock Mechanism of shock Basic Physiology Patient assessment Types of shock Shock treatment

The definition of shock Shock represents an imbalance between oxygen demand delivery

The definition of shock Shock is a life-threatening condition that occurs when the body is not getting enough blood flow. Lack of blood flow means that the cells and organs do not get enough oxygen and nutrients to function properly. Imbalance between oxygen delivery and oxygen consumption which leads to cell death, end organ damage, multi-system organ failure, and death.

The definition of shock The effect of shock are initially reversible, but rapidly become irreversible, resulting in multiorgan failure (MOF) and death. Shock must be recognized and treated immediately to prevent progression to irreversible organ dysfunction.

The definition of shock Undifferentiated shock refers to the situation where shock is recognized but the cause is unclear. When a patient presents with undifferentiated shock; it is important that the clinician immediately initiate therapy while rapidly identifying the etiology so that definitive therapy can be administered to reverse shock and prevent MOF and death.

The definition of shock Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or inadequate oxygen utilization This most commonly occurs when there is circulatory failure manifested as hypotension (reduced tissue perfusion) But, hypotension is not a requirement Shock can occur with a normal blood pressure and hypotension can occur without shock

The definition of shock 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.

Mechanism of shock Cellular hypoxia occurs as a result of reduced tissue perfusion/oxygen delivery and/or increased oxygen consumption or from inadequate oxygen utilization. Cellular hypoxia, in turn, causes cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular contents into the extracellular space, inadequate regulation of intracellular p. H.

Mechanism of shock These biochemical processes, when unchecked, progress to the systemic level, resulting in acidosis, and endothelial dysfunction, as well as further stimulation of inflammatory and anti-inflammatory cascades.

Mechanism of shock Serum lactate levels, when elevetated, have traditionally been used as surrogates for hypoperfusion and tissue hypoxia. Elevations in serum lactate level are useful riskstratification tools in undifferentiated shock.

Basic Physiology 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

Basic Physiology The major physiologic determinants of tissue perfusion (and systemic blood pressure [BP]) are cardiac output (CO) and systemic vascular resistance (SVR). BP= CO X SVR CO is the product of heart rate (HR) and stroke volume (SV). CO= HR X SV

Basic Physiology The stroke volume is a determined by Preload Afterload Myocardial Contractility SVR is governed by o o o Vessel length Blood viscosity Vessel diameter (ie, vessel tone)

Basic Physiology Biologic processes that change any one of these physiologic parameters can result in hypotension and shock. Common to most from of shock is diminished CO and/or SVR.

Basic Physiology In general, severe hypovolemia, cardiogenic shock, and late stage obstructive shock are characterized by a low CO and compensatory increase in the SVR to maintain perfusion to vital organs. Distributive shock is classically associated with reduced SVR and compensatory increase in the CO. However, the CO may be normal in the early phases of hypovolemic and obstructive shock.

Basic Physiology Some form of shock have normal CO and SVR. Patients with profound mitochondrial dysfunction (inheritable mitochondrial disease, carbon monoxide, and cyanide poisoning) are shock state that occur despite normal CO, SVR, and tissue perfusion. Because they are due to inadequate oxygen utilization.

Patient Assessment 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.

Patient Assessment Clinical signs and symptoms depends on the severity of the shock

Patient Assessment In hypovolemic shock, clinical signs and symptoms are associated with a 20 to 25 percent reduction in arterial blood volume, In cardiogenic shock, a fall in the cardiac index to less than 2. 5 L/min/m 2 is required before signs and symptoms appear.

Patient Assessment Obvious and immediately detectable manifestations of the shock state include: tachycardia, hypotension, cool extremities, weak peripheral pulses, prolonged capillary refill (>2 seconds), narrowing of the pulse pressure (<25 mm. Hg), and altered mental status.

Patient Assessment Tachycardia, a modest change in systemic blood pressure (increase or decrease), or mild to moderate hyperlactatemia, may be the only clinical signs of early shock. During shock, the compensatory mechanisms become overwhelmed, Signs and symptoms of organ dysfunction appear including symptomatic tachycardia, dyspnea, restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, and cool, clammy skin.

Patient Assessment Progressive shock leads to irreversible organ damage, multiorgan failure (MOF), and death. During this stage, anuria and acute renal failure develop, acidemia further depresses CO, hypotension becomes severe and recalcitrant to therapy, hyperlactatemia often worsens, and restlessness evolves into obtundation and coma. Death is common in this phase of shock.

Patient Assessment 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

Patient Assessment Laboratory Hgb, WBC, platelets PT/PTT Electrolytes Arterial blood gases BUN, Cr Serum lactate Mixed venous oxygen saturation (SVO 2) ECG

Patient Assessment Invasive 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

Types of shock The main types of shock include: 1. Distributive shock 2. Cardiogenic shock 3. Hypovolemic shock 4. Obstructive shock

Types of shock Septic shock, a form of distributive shock, is the most common form of shock among patients admitted to the intensive care unit, followed by cardiogenic and hypovolemic shock, obstructive shock is rare.

1. Distributive Shock Distributive shock is characterized by severe peripheral vasodilatation (vasodilatory shock). Classically associated with reduced SVR and compensatory increase in the CO.

1. Distributive shock Septic shock Systemic inflamatuary response syndrome (SIRS) Neurogenic shock Anaphylactic shock Drug and toxin-induced shock Endocrin shock

1. Distributive shock/Septic shock Sepsis, defined as a dysregulated host response to infection resulting in life-threatening organ dysfunction. Sepsis is the most common cause of distributive shock. The type of pathogen causing sepsis varies with the population studied. Septic shock is a subset of sepsis associated with mortality in the 40 to 50 percent range, It can be identified by the use of vasopressor therapy and the presence of elevated lactate levels (>2 mmol/L) despite adequate fluid resuscitation.

1. Distributive shock/ Systemic inflammatory response syndrome (SIRS) SIRS is a clinical syndrome that is characterized by a robust inflammatory response, Usually induced by a major body insult that can be infectious and noninfectious.

1. Distributive shock/ Systemic inflammatory response syndrome (SIRS) Noninfectious conditions that can be complicated by SIRS: Pancreatitis Burns Hypoperfusion caused by trauma Significant blunt trauma and crush injury Amniotic fluid embolism Fat embolism Post successful return of spontaneous circulation after a cardiac arrest, myocardial infarction, or cardio-pulmonary bypass

1. Distributive shock/Neurogenic shock Hypotension and in some cases, shock are common in patients with severe traumatic brain injury and spinal cord injury. Interruption of autonomic pathways, causing decreased vascular resistance and altered vagal tone, is thought to be responsible for distributive shock in patients with spinal cord injury. Hypovolemia from blood loss and myocardial depression may also contribute to shock in this population.

1. Distributive shock/Anaphylactic shock Shock from anaphylaxis is most commonly encountered in patients with severe, immunoglobulin-E mediated, allergic reactions to insect stings, food, and drugs. Hemodynamic collapse, bronchospasm and increased airway resistance are features of anaphylaxis.

1. Distributive shock/ Drug and toxin-induced shock Drug overdoses Snake bites Insect bites including scorpion envenomation and spider bites Transfusion reactions Heavy metal poisoning including arsenic, iron, and thallium Infections associated with toxic shock syndrome

1. Distributive shock/Endocrine shock Addisonian crisis and myxedema can be associated with hypotension and state of shock. In state of mineralocorticoid deficiency, vasodilation can occur due to altered vascular tone and aldosterone-deficiency-mediated hypovolemia.

2. Cardiogenic shock is due to intracardiac causes of cardiac pump failure that result in reduced cardiac output (CO). Causes of cardiac pump failure are diverse, but can be divided into three categories; Cardiomypathic Arrhythmic Mechanical

2. Cardiogenic shock/Cardiomyopathic causes of shock include; myocardial infarction, acute exacerbation of heart failure in patients with severe underlying dilated cardiomyopathy, stunned myocardium following cardiac arrest, prolonged ischemia or cardiopulmonary bypass, myocardial depression due to advanced septic or neurogenic shock, and myocarditis.

2. Cardiogenic shock/Arrhythmic Both atrial and ventricular tachyarrhythmias and bradyarrhythmias may induce hypotension, often contributing to states of shock.

2. Cardiogenic shock/Mechanical causes of cardiogenic shock include; ü severe aortic or mitral valve insufficiency, ü retrograde dissection of the ascending aorta, ü an abscess of the aortic ring. Additional causes include; ü severe ventricular septal defects; ü acute rupture of the intraventricular septum, ü atrial myxomas, ü a ruptured ventricular free wall aneurysm.

3. Hypovolemic shock is due to reduced intravascular volume (ie, reduced preload), which, in turn, reduces CO. In response to baroreceptor stimulation, the heart rate increases to maintain cardiac output.

3. Hypovolemic shock can be divided into two categories Hemorrhagic Nonhemorrahagic The most common cause of hypovolemic shock is major blood loss, such as occurs with trauma, surgery, or massive gastrointestinal hemorrhage.

3. Hypovolemic shock/ Hemorrhagic shock Reduced intravascular volume from blood loss can result in shock. There are multiple causes of hemorrhagic shock. Blunt or penetrating trauma (includes multiple fractures without vessel injury) Upper or lower gastrointestinal bleeding

3. Hypovolemic shock/ Hemorrhagic shock Less common causes: Intraoperative or postoperative bleeding Ruptured abdominal aortic or left ventricle aneurysm Hemorrhagic pancreatitis Iatrogenic (inadvertent biopsy of arteriovenous malformation) Postpartum hemorrhage Uterine or vaginal hemorrhage from other causes (infection, tumors) Ruptured hematoma

3. Hypovolemic shock/ Nonhemorrhagic shock Reduced intravascular volume from fluid loss other than blood can cause shock. Volume depletion from loss of sodium and water occur from a number of anatomic sites.

3. Hypovolemic shock/ Nonhemorrhagic shock Gastrointestinal losses (diarrhea, vomiting, external drainage) Skin losses (heat stroke, burns, severe dermatologic conditions including Stevens. Johnson syndrome) Renal losses (excessive drug-induced or osmotic diuresis, hypoaldesteronism) Third space losses into the extravascular space or body cavities (postoperative and trauma, intestinal obstruction, crush injury, pancreatitis, cirrhosis)

4. Obstructive shock is mostly due to extracardiac causes of cardiac pump failure. Often associated with poor right ventricle output. The causes of obstructive shock can be divided into the following two categories: ü Pulnonary vascular ü Mechanical

4. Obstructive shock/ Pulmonary vascular Most cases of obstructive shock are due to right ventricular failure from, ü hemodynamically significant pulmonary embolism, ü severe pulmonary hypertension. ü Patients with severe stenosis or with acute obstruction of the pulmonary or tricuspid valve may also fall into this category

4. Obstructive shock/Mechanical Patients in this category present clinically as hypovolemic shock because their primary physiologic disturbance is decreased preload, rather than pump failure (eg, reduced venous return to the right atrium or inadequate right ventricle filling). Mechanical causes of obstructive shock include the following: ü Tension pneumothorax ü Pericardial tamponade ü Constrictive pericarditis ü Restrictive cardiomyopathy

Treatment Identify & reverse the cause Restore tissue perfusion Restore 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 • 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

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 • • • MAP: above 65 mm. Hg or Systolic blood pressure: above 90 mm. Hg Heart rate: between 60 -100/min Urine output: > 0. 5 m. L/kg/hr CVP: 8 -12 mm. Hg Central venous oxygen concentration: > 70%

Hypovolemic shock /Treatment of hypovolemic shock involves restoration of circulation blood volume and treatment of the underlying cause of the hypovolemia. Treatment of the underlying cause of the hypovolemic shock can be undertaken only when adequate intravenous access and aggressive fluid therapy are achieved. Vasopressor therapy may be used to increase systemic blood pressor, But it will probably be unsuccessful until intravascular volume is restored.

Cardiogenic shock/Treatment The goals in treatment of cardiogenic shock are to improve cardiac output and decrease afterload. These interventions allow; ü the ventricle to eject more efficiently, ü decrease myocardial work, ü lower myocardial oxygen consumption, and ü reverse the dangerous spiral of cardiac failure.

Cardiogenic shock/Treatment Depending on the type of cardiac failure and ventricular filling conditions, diuretics are generally indicated, But must be used judiciously to avoid worsening the hypotension. Afterload and preload can be reduce with vasodilatators and venodilatators such as; nicardipin, nitroglycerin, or nitropurisside. Dobutamine improves cardiac output and reduces afterload with a minimal increase in myocardial oxygen demand.

Distributive shock/Treatment involves initial intravenous fluid therapy until adequate preload is established, typically at a central venous pressure of approximately 8 to 12 cm. H 2 O. Vasopressors (phenylephrine, dopamine, epinephrine, norepinephrine) are added if the patient remains hypotensive. The choice of drug depends on the specific clinical situation. The underlying cause of the disorder should be treated as soon as possible.

Inotropic drugs and vasopressors Dopamine Epinephrine Norepinephrine Phenylephrine Dobutamine Vasopressin

Dopamine Clinically, dopamine is regarded as a relatively weak vasopressor and is useful in mild hypotensive states. It is pharmacologic action varies with dose and within individuals as well. With small doses (0 to 5 µg/kg/min) dopamine causes dilatation of the renal arterioles and promotes diuresis (dopamine-1 receptor agonist activity). At moderate doses (5 to 10 µg/kg/min) dopamine causes an increase in myocardial contractility, heart rate, and cardiac output (ß 1 -adrenergic effect). At large doses (10 to 20 µg/kg/min) dopamine acts to increase vascular smooth muscle tone, which increases systemic vascular resistance (α 1 -agonist effect).

Epinephrine causes direct stimulation of α 1, ß 1, and ß 2 receptors. Main indications for epinephrine are; ü in the management of cardiac arrest, ü severe cardiogenic shock, ü anaphylactic and anaphylactoid reactions. When given as a continuous infusion, the usual range of epinephrine is between 1 and 20 µg/min. However, in patients with refractory, life-threatening shock, it may be necessary to administer epinephrine at even larger doses.

Epinephrine Increases in heart rate, myocardial activity, and cardiac output reflect ß 1 - receptor effects. The principal ß 2 - receptor effects are bronchial and vascular smooth muscle relaxation. With larger doses, the α 1 - receptor effects of epinephrine act to increase systemic vascular resistance and reduce splanchnic and renal blood flow while maintaining both cerebral and myocardial perfusion pressure.

Norepinephrine It is similar to epinephrine except that norepinephrine lack the ß 2 - receptor effect of epinephrine and has much stronger α 1 - receptor activity. Norepinephrine can be used for the treatment of septic shock. It is ß 1 activity may help offset the myocardial dysfunction associated with severe sepsis and septic shock. Norepinephrine must be given by continuous infusion, The typical dose range is between 1 and 20 µg/min.

Phenylephrine is a direct-acting, highly selective α 1 -receptor agonist which increases systemic vascular resistance and arterial blood pressure. Phenylephrine is frequently used for the treatment of septic and other forms of vasodilatory shock to increase systemic blood pressure. Phenylephrine is often administered to brain-injured patients to improve cerebral perfusion pressure. It does not cross the blood-brain barrier, It has no effect on the cerebral vasculature. The typical dosage range for phenylephrine is up to 200µg/min. Larger doses have little therapeutic effect, with only worsening of splanchnic ischemia.

Dobutamine is mixed ß 1 - and ß 2 - receptor agonist. The primary effect of dobutamine is to increase both heart rate and myocardial contractility. Dobutamine relaxes vascular smooth muscle via binding at ß 2 - receptors. Dobutamine is typically indicated for the treatment of patients in cardiogenic shock with high afterload and low cardiac output. Dobutamine is given by continuous infusion only, and the usual dosage range is between 1 and 20µg/kg/min.

Vasopressin is a potent vasoconstrictor that does not work via the adrenergic receptor system. Vasopressin binds to peripheral vasopressin receptors to induce potent vasoconstriction. Patients with severe sepsis and septic shock may have a relative deficiency of vasopressin. This group of patient is remarkably sensitive to the effects of vasopressin. For septic shock, the recommendation is to infuse vasopressin at 0. 04 U/min. Vasopressin has been successfully used for cardiogenic shock. In this patients, the dose of vasopressin (0. 1 U/min) is significantly larger than that used for septic shock.

Which Pressor should I choose? Hypovolemic shock Fluids and Blood Cardiogenic shock Dobutamine -β 1 agonist) Neurogenic shock Fluids, phenylephrine -α 1 agonist, norepinephrine -α 1 and β 1 agonists, look for another type of shock if it is persistent Septic shock Norepinephrine – α 1 and β 1 agonists Anaphylactic shock Fluids and epinephrine -α 1, ß 1, and ß 2 agonist

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