Disturbance of Circulation Series -Shock Jianzhong Sheng, MD PhD 650000 new cases 2% hospital pts 75% ICU pts Mortality 20-50% Sirs 7 Sepsis 16 Severe sepsis 20 Septiv shock 46

Outline Definition Epidemiology Pathophysiology Classes of Shock Clinical Presentation Management Controversies

Definition A pathophysiologic state characterized by Inadequate tissue perfusion Clinically manifested by Hemodynamic disturbances Organ dysfunction

Microcirculation

What is shock ? Shock refers to a dangerous systemic pathological process under the effect of various drastic etiological factors, characterized by acute circulatory failure including decreased effective circulatory volume, inadequate tissue perfusion, cellular metabolism impediment and multiple organ dysfunction.

Etiology and classification 1. Classification according to cause ① Loss of blood or fluid: Blood loss: hemorrhagic shock; Fluid loss: dehydration shock (collapse); Burn: burn shock. (失血性休克) ② Trauma: traumatic shock. (创伤性休克) ③ Infection: infectious shock; endotoxic shock; septic shock (感染性休克) ④ Anaphylaxis: anaphylactic shock (过敏性休克) ⑤ Heart failure: cardiogenic shock ⑥ Strong stimulation on nerve system: neurogenic shock (神经性休克)

Etiology and classification 2. Classification according to the initial changes ① Hypovolemic shock ② Vasogenic shock (Distributive) ③ Cardiogenic shock

Etiology and classification 3. Classification by hemodynamic characteristics ① Hyperdynamic shock: warm shock high cardiac output, low vascular resistance, warm skin ② Hypodynamic shock: cold shock low cardiac output, high vascular resistance, cold skin

Epidemiology Mortality Septic shock – 35-40% (1 month mortality) Cardiogenic shock – 60-90% Hypovolemic shock – variable/mechanism

Pathophysiology Imbalance in oxygen supply and demand Conversion from aerobic to anaerobic metabolism Appropriate and inappropriate metabolic and physiologic responses

Pathophysiology Cellular pathophysiology Cell membrane ion pump dysfunction Leakage of intracellular contents into the extracellular space Intracellular pH dysregulation Resultant systemic pathophysiology Cell death and end organ dysfunction MSOF and death

Pathophysiology Characterized by three stages Preshock (warm shock, compensated shock) Shock End organ dysfunction

Pathophysiology Compensated shock Low preload shock – tachycardia, vasoconstriction, mildly decreased BP Low afterload (distributive) shock – peripheral vasodilation, hyperdynamic state

Pathophysiology Shock Initial signs of end organ dysfunction Tachycardia Tachypnea Metabolic acidosis Oliguria Cool and clammy skin

Pathophysiology End Organ Dysfunction Progressive irreversible dysfunction Oliguria or anuria Progressive acidosis and decreased CO Agitation, obtundation, and coma Patient death

 Microcirculatory mechanisms Pathogenesis of shock  Microcirculatory mechanisms Ischemic hypoxia stage Stagnant hypoxia stage Refractory stage  Cellular and molecular mechanisms

Microcirculatory mechanisms Ischemic hypoxia stage (compensatory stage) Stagnant hypoxia stage (reversible decompensated stage) Refractory stage (microcirculatory failure stage)

Microcirculation

Microcirculatory mechanisms 1. Ischemic hypoxia stage (compensatory stage) Microcirculatory changes  Mechanism of microcirculatory changes  Compensatory significances  Clinical manifestations 

Microcirculatory changes Normal Ischemic hypoxia stage

Microcirculatory changes Small blood vessel constriction. Precapillary resistance↑↑ > postcapillary resistance↑ Closed capillary↑. Blood inflows vein by straightforward pathway and A-V shunt. Characteristics of inflow and outflow: inflow and outflow↓↓; inflow < outflow.

Mechanism of microcirculatory changes Blood lose, Trauma etc. Activation of sympathetic-adrenal system Vasoconstrictive substance ↑ ↑ (catecholamine, angiotension Ⅱ, vasopressin, TAX2, endothelin) Activation of α-receptors Activation of β-receptors Constriction of micrangium Opening of A-V shunts

Compensatory significances 1. Maintain normal arterial pressure (1) returned blood volume↑ (2) cardiac output ↑ (3) peripheral resistances↑ Auto blood transfusion Auto fluid transfusion Aldosterone and antidiuretic hormone (ADH) heart rate↑ contractility ↑ returned blood volume ↑

Compensatory significances 2. Maintain blood supplying to heart and brain (1) blood vessel of brain (2) coronary artery (3) normal arterial pressure

Hypovolemic Shock Results from decreased preload Etiologic classes Hemorrhage - e.g. trauma, GI bleed, ruptured aneurysm（血管瘤） Fluid loss - e.g. diarrhea, vomiting, burns, third spacing, iatrogenic（医源性）

Hypovolemic Shock Hemorrhagic Shock Parameter I II III IV Blood loss (ml) <750 750–1500 1500–2000 >2000 Blood loss (%) <15% 15–30% 30–40% >40% Pulse rate (beats/min) <100 >100 >120 >140 Blood pressure Normal Decreased Respiratory rate (bpm) 14–20 20–30 30–40 >35 Urine output (ml/hour) >30 5–15 Negligible CNS symptoms Anxious Confused Lethargic Crit Care. 2004; 8(5): 373–381.

Cardiogenic Shock Results from pump failure Etiologic categories Decreased systolic function Resultant decreased cardiac output Etiologic categories Myopathic Arrhythmic Mechanical Extracardiac (obstructive)

Distributive Shock Results from a severe decrease in SVR Vasodilation reduces afterload May be associated with increased CO Etiologic categories Sepsis Neurogenic / spinal Other (next page) SVR: Systemic vascular resistance

Distributive Shock Other causes Systemic inflammation – pancreatitis, burns Toxic shock syndrome Anaphylaxis and anaphylactoid reactions Toxin reactions – drugs, transfusions Addisonian crisis Myxedema coma

Distributive Shock Septic Shock SIRS: systemic inflammatory response syndrome

Clinical Presentation Clinical presentation varies with type and cause, but there are features in common Hypotension (SBP<90 or Delta>40) Cool, clammy skin (exceptions – early distributive, terminal shock) Oliguria Change in mental status Metabolic acidosis

Clinical manifestations Sympathetico-adrenal-medullay system exitation Catecholamines ↑ Heart rate↑ Contractility↑ Small blood vessel constriction Sweat gland secretion ↑ Excitation of CNS Peripheral resistances↑ Renal ischemia Skin ischemia BP(-) Thread pulse Narrowing pulse pressure Urine↓ Pallor Cool limbs Sweating Clammines Agitate Restless

Microcirculatory mechanisms 2. Stagnant hypoxia stage (reversible decompensated stage) Microcirculatory changes  Mechanism of microcirculatory stasis  Effect of microcirculatory stasis  Clinical manifestations 

Microcirculatory changes Stagnant hypoxia stage Normal

Microcirculatory changes Precapillary resistance↓↓ > postcapillary resistance(-) or ↓. Opened capillary↑. Characteristics of inflow and outflow: inflow↑ and outflow↓; inflow > outflow.

Mechanism of microcirculatory stasis Acidosis Local accumulation of metabolic products Alteration of hemorheology Endotoxin Effects of humoral factors

Effect of microcirculatory stasis Effective circulating blood volume ↓ ↓ Blood flow resistance ↑ ↑ Blood pressure ↓ ↓ Blood supply for vitals ↓ ↓ and dysfunctional

Clinical manifestations Microcirculation stasis Returned blood volume ↓ Blood pressure ↓ Cardiac output ↓ Brain ischemia Renal blood flow ↓ Stasis in kidney Stasis in skin Dull or coma Oliguria or anuria Cyanosis or maculation

Microcirculatory mechanisms 3. Refractory stage (microcirculatory failure stage) Microcirculatory changes  Mechanism of microcirculatory failure  Effect of microcirculatory failure  Clinical manifestations 

Microcirculatory changes Normal DIC stage Characteristic: neither inflow or outflow; inflow = outflow

Cellular and molecular mechanisms  Alteration of cellular metabolism  Cell injury and apoptosis  Humoral factors Vasoactive amines Endothelium-derived vasoactive mediators Regulation peptides  Inflammatory mediator and inappropriate inflammatory response

Alterations of metabolism and function Disturbance of microcirculation Inappropriate inflammatory response Metabolic alteration Multiple organ dysfunction Negative Nitrogen balance Anaerobic glycolysis kidney GI brain lung liver heart Bleeding endotoxin translocation Dull coma Acute renal failure ATP↓ Metabolic acidosis ARDS Na+-K+-ATPase ↓ Respiratory acidosis Cell swelling vasodilation Jundice enzymes↑ Cardiac dysfunction

Pathophysiologic basis of prevention and treatment Improve microcirculation Volume replacement Acidosis correction Vasoactive drugs application Treatment of DIC Blockage of humoral factors Cell protection Organ protection

Case presentation A young man is brought to the emergency department by ambulance on the next day after a severe traffic accident. He is unconscious. his blood pressure is 78/48 mmHg, heart rate is 130 beats per minute. There is no evidence of head trauma. The pupils are 2 mm and reactive. He withdraws to pain. Cardiac examination reveals no murmurs, gallops, or rubs. The lungs are clear to auscultation. The abdomen is tense, with decreased bowel sounds. The patient shows cyanosis, with thready pulses. Question: What are the three major pathophysiologic causes of shock? Which was likely in this patient? Why? What are the three general stages of shock according to the different changes in microcirculation? Which was likely in this patient? Why? What pathogenetic mechanism accounts for this patient’s unresponsiveness and cyanosis? What therapeutic measures are essential for this patient?

Evaluation Done in parallel with treatment! Heart & Blood Pressure – helpful to distinguish type of shock Full laboratory evaluation including hemoglobin and hematocrit (H&H), cardiac enzymes, arterial blood gases (ABG) Basic studies – CxR, EKG, UA Basic monitoring –urine output (UOP), central venous pressure (CVP) Imaging if appropriate – FAST, CT Echo vs. PA catheterization

Treatment Manage the emergency Determine the underlying cause Definitive management or support

Manage the Emergency Your patient is in extremis – tachycardic, hypotensive, obtunded How long do you have to manage this? Suggests that many things must be done at once Draw in ancillary staff for support! What must be done?

Manage the Emergency One person runs the code! Control airway and breathing Maximize oxygen delivery Place lines, tubes, and monitors Get and run IVF on a pressure bag Get and run blood (if appropriate) Get and hang pressors Call your senior/fellow/attending

Determine the Cause Often obvious based on history Trauma most often hypovolemic (hemorrhagic) Postoperative most often hypovolemic (hemorrhagic or third spacing) Debilitated hospitalized pts most often septic Must evaluate all pts for risk factors for MI and consider cardiogenic Consider distributive (spinal) shock in trauma

Determine the Cause What if you’re wrong? 85 y/o M 4 hours postop S/P sigmoid resection for perforated diverticulitis is hypotensive on a monitored bed at 70/40 Likely causes Best actions for the first 5 minutes?

Definitive Management Hypovolemic – Fluid resuscitate (blood or crystalloid) and control ongoing loss Cardiogenic - Restore blood pressure (chemical and mechanical) and prevent ongoing cardiac death Distributive – Fluid resuscitate, pressors for maintenance, immediate abx/surgical control for infection, steroids for adrenocortical insufficiency

Controversies IVF Resuscitation Pressors Monitoring Limited resuscitation in penetrating trauma Use of hypertonic saline resuscitation in trauma Endpoints for prolonged resuscitation Pressors Best pressors for distributive shock Monitoring Most appropriate timing and use for PA catheterization or intermittent echocardiogram

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