SHOCK Aayed Al-Qahtani, FRCSC, FACS Ass. Prof. & Consultant Department of Surgery Division of Pediatric Surgery College of medicine KSU

To understand Physiology of sustaining blood pressure To understand Physiology of sustaining blood pressure To learn about the classifications of shock To learn about the classifications of shock To understand the consequences of the natural history of shock To understand the consequences of the natural history of shock To be able to diagnose and plan appropriate treatments for different types of shock To be able to diagnose and plan appropriate treatments for different types of shock OBJECTIVES

HEMODYNAMIC RESPONSE TO SHOCK Venoconstriction Reduced venous capacitance Arteriolar constriction Decreased capillary P Fluid shift from interstitium into vascular compartment Increased distal tubular reabsorption Increased proximal tubular reabsorption Increased myocardial contractility Restoration of blood volume Increased ventricular filling P Increased ventricular ejection fraction Increased stroke volume IncreasedCO IncreasedBP Increased heart rate Increased SVR due to arteriolar construction

Intravascular volume Intravascular volume Heart Heart Arteriolar bed Arteriolar bed Capillary exchange network Capillary exchange network Venules Venules Venous capacitance circuit Venous capacitance circuit Large vessel patency Large vessel patency CHANGES IN MANY ELEMENTS REGULATE BP AND PERFUSION

Decreased peripheral resistance Decreased arterial blood pressure (MAP = CO X PR) Increased peripheral resistance Decreased venous return Decreased EDV Decreased SV Decreased CO (CO = HR X SV) Decreased arterial blood pressure (MAP=CO X PR)

Heart Rate X Stroke Volume = Cardiac Output Cardiac Output X Peripheral Resistance = Arterial Pressure CARDIAC OUTPUT ARTERIAL PRESSURE

Alters mean blood pressure Alters mean blood pressure Decrease in intravascular volume=decreased BP Alters venous return to the heart Alters venous return to the heart Decrease in intravascular volume= Decreased venous return= Decreased end diastolic volume CO = HR x SV CO X SVR CO X SVR  MAP How can intravascular volume be lost? How can intravascular volume be lost? Examples: Bleeding Failure to rehydrate Loss of third space fluids (sweating) HOW DOES INTRAVASCULAR VOLUME AFFECT BP AND PERFUSION?

CARDIAC OUTPUT = HR X SV HEART RATE STROKE VOLUME Decreased intravascular volume= decreased EDV Cardiac Output X Peripheral Resistance  Arterial Pressure

Cardiac output is the result of: Cardiac output is the result of: Heart rate Contractility Loading conditions Examples of changes that can alter cardiac output Examples of changes that can alter cardiac output Heart rate (bradycardia or tachycardia) Contractility (MI or cardiomyopathy) Load (histamine release: vasodilation) HOW DOES CARDIAC FUNCTION ALTER BP AND PERFUSION?

CARDIAC OUTPUT = HR X SV Bradycardia Vasodilatation: decreased EDV MI (pump failure)

Decreases in arteriolar tone produce: Decreases in arteriolar tone produce:Hypotension Decreased perfusion to vital organs Increases in tone will prevent optimal cardiac performance (increased afterload=decreased contractility) Increases in tone will prevent optimal cardiac performance (increased afterload=decreased contractility) HOW DOES THE RESISTANCE CIRCUIT: ARTERIOLAR BED AFFECT BP AND PERFUSION?

Heart Rate X Stroke Volume = Cardiac Output Cardiac Output X Peripheral Resistance = Arterial Pressure CARDIAC OUTPUT ARTERIAL PRESSURE

Largest area of the vascular tree Largest area of the vascular tree Site of exchange of nutrients, electrolytes and fluids Site of exchange of nutrients, electrolytes and fluids Alterations in microvascular integrity (e.g., capillary leak syndrome) result in loss of intravascular volume Alterations in microvascular integrity (e.g., capillary leak syndrome) result in loss of intravascular volume Blockage of or shunting away from small vessels leads to decreased tissue perfusion Blockage of or shunting away from small vessels leads to decreased tissue perfusion HOW DOES THE CAPILLARY EXCHANGE NETWORK AFFECT BP AND PERFUSION?

Portion of the circulatory system contains 80% of the intravascular volume Portion of the circulatory system contains 80% of the intravascular volume Decrease in effective circulating blood volume and MAP caused by: Decrease in effective circulating blood volume and MAP caused by: Decreases in venous tone Increases in venous vascular capacitance HOW DOES THE VENOUS CAPACITANCE CIRCUIT AFFECT BP AND PERFUSION?

NORMAL INCREASED VENOUS CAPACITANCE Decreased effective blood volume Decreased MAP

Obstruction of the systemic or pulmonic circuit will decrease ventricular ejection and systemic perfusion Obstruction of the systemic or pulmonic circuit will decrease ventricular ejection and systemic perfusion Venous obstruction will decrease venous return Venous obstruction will decrease venous return Examples of obstructive shock: Examples of obstructive shock: Massive pulmonary embolism Venous occlusion HOW DOES LARGE VESSEL PATENCY AFFECT BP AND PERFUSION?

VENOUS OBSTRUCTION Decreased effective blood volume Decreased MAP

DEFINITION OF SHOCK State of altered tissue perfusion severe enough to induce derangements in normal cellular metabolic function

TYPES OF SHOCK* Type of Shock Clinical causes Primary mechanism Hypovolemic Volume loss Exogenous blood, plasma, fluid or electrolyte loss CardiogenicPump failureMyocardial infarction, cardiac arrhythmias, heart failure DistributiveIncreased venous capacitance or arteriovenous shunting Septic shock, spinal shock, autonomic blockade, drug overdose ObstructiveExtra-cardiac obstruction of blood flow Vena caval obstruction, cardiac tamponade, pulmonary embolism, aortic compression or dissection *MORE THAN ONE TYPE MAY BE PRESENT

The clinical signs and symptoms of shock relate to decreased organ perfusion Mental status changes: decreased cerebral perfusion Mental status changes: decreased cerebral perfusion Decreased urine output: decreased renal perfusion Decreased urine output: decreased renal perfusion Cold clammy extremities: Cold clammy extremities: Decreased perfusion to the skin due to diverted blood flow EKG changes: EKG changes: 1. May indicate myocardial ischemia 2. May be primary event (cardiogenic shock) or due to decreased myocardial perfusion due to shock from other causes 2. May be primary event (cardiogenic shock) or due to decreased myocardial perfusion due to shock from other causes

Heart rate Heart rate Initial tachycardia (attempt to increase CO) Rhythm Rhythm Regular and tachycardic Blood pressure Blood pressureLow Cardiac output Cardiac output Usually low HEMODYNAMIC PARAMETERS THAT MAY INDICATE SHOCK

EFFECTS OF SHOCK AT THE ORGAN LEVEL Kidney Kidney Oliguric renal failure Liver Liver Liver failure GI tract GI tract Failure of intestinal barrier (sepsis, bleeding) Failure of intestinal barrier (sepsis, bleeding) Lung Lung Capillary leak associated with or caused by sepsis and infection (ARDS = adult respiratory distress syndrome)

HEMODYNAMIC RESPONSE TO SHOCK Mechanisms for restoring cardiovascular homeostasis Redistribution of blood flow Redistribution of blood flow Attempt to preserve perfusion to vital organs Augmentation of cardiac output Augmentation of cardiac output Increased heart rate Increased peripheral resistance Restoration of intravascular volume Restoration of intravascular volume

NEUROENDOCRINE STIMULATION HYPOTENSION BLOOD FLOW PROTECTED HeartBrain Adrenal/pituitary gland BLOOD FLOW DECREASED SkinMuscle Splanchnic circulation HEMODYNAMIC RESPONSE TO SHOCK REDISTRIBUTION OF BLOOD FLOW

HEMODYNAMIC RESPONSE TO SHOCK Venoconstriction Reduced venous capacitance Arteriolar constriction Decreased capillary P Fluid shift from interstitium into vascular compartment Increased distal tubular reabsorption Increased proximal tubular reabsorption Increased myocardial contractility Restoration of blood volume Increased ventricular filling P Increased ventricular ejection fraction Increased stroke volume IncreasedCO IncreasedBP Increased heart rate Increased SVR due to arteriolar construction

CLINICAL FINDINGS Hypotension Tachycardia Tachypnea Oliguria DECREASED CARDIAC FUNCTION Decreased ventricular function Myocardial infarction Pericaridal tamponade Tension pneumothorax Ineffective cardiac contraction Primary arrhythmias CARDIOGENIC SHOCK

Caused by the progressive loss of myocardium Caused by the progressive loss of myocardium · Usually due to an acute myocardial infarction When the total amount of myocardium affected reaches a critical point, When the total amount of myocardium affected reaches a critical point, myocardial function begins to deteriorate myocardial function begins to deteriorate While stroke volume decreases, the heart rate increases in an effort to While stroke volume decreases, the heart rate increases in an effort to maintain cardiac output (CO = SV x HR) maintain cardiac output (CO = SV x HR) · But increased HR is limited and CO falls to levels that are inadequate to support end-organ function support end-organ function Coronary perfusion decreases and this in turn causes progressive myocardial Coronary perfusion decreases and this in turn causes progressive myocardial ischemia with progression of myocardial injury ischemia with progression of myocardial injury CARDIOGENIC SHOCK

1. Decreased myocardial blood flow 2. Decreased contractility=decreased stroke volume 3. Heart rate increases to maintain CO (CO=HR X SV) 5. Decreased myocardial perfusion leads to further decrease in contractility 4. If HR cannot maintain CO, then compromised end- organ perfusion

EVENTS IN CARDIOGENIC SHOCK

HYPOVOLEMIC SHOCK DECREASE IN INTRAVASCULAR BLOOD VOLUME DECREASE IN CARDIAC OUTPUT AND TISSUE PERFUSION Hemorrhage Vomiting Diarrhea Fluid sequestration Intraluminal – bowel obstruction Intraperitoneal – pancreatitis Interstitial - burns

HYPOVOLEMIC SHOCK DECREASE IN INTRAVASCULAR BLOOD VOLUME BLOOD DIVERTED FROM SKIN TO MAINTAIN ORGAN PERFUSION Pale and cool skin Postural hypotension and tachycardia BLOOD DIVERTED PREFERENTIALLY TO HEART AND BRAIN Oliguria Tachycardia Hypotension

END-STAGE SHOCK Bradycardia Arrythmias Death DECREASED BLOOD FLOW TO BRAIN AND HEART Restless, agitated, confused Hypotension Tachycardia Tachypnea HYPOVOLEMIC SHOCK

SEPTIC SHOCK SEVERE INFECTION W RELEASE OF MICROBIAL PRODUCTS Release of vasoactive mediators HYPERDYNAMIC STATE Peripheral vasodilation Increased cardiac output Fever, tachycardia, tachypnea, warm skin MAINTENANCE OF INTRAVASCULAR VOLUME Hyperdynamic shock FAILURE TO MAINTAIN INTRAVASCULAR VOLUME Hypodynamic shock Cool skin, tachycardia, hypotension, oliguria

DIAGNOSING SHOCK STATE BASED ON HEMODYNAMIC PARAMETERS TYPE Hypovolemic Cardiogenic Septic Traumatic Neurogenic Hypoadrenal Central Venous Pressure Decreased Increased Decreased or increased Decreased Decreased or increased Cardiac Output Decreased Increased Decreased or increased Decreased Decreased or increased SVR Increased Normal or Increased Decreased Decreased or increased Decreased Decreased or increased

Systemic Inflammatory Response Syndrome (SIRS) lThe patients demonstrate a similar response as sepsis but without infective agents. lThe criteria are : (two or more to call it SIRS) uTemperature >38 or < 36 uHeart rate >90 uRR > 20 or a pco2 < 34 mmHg (4.3 kpa) uWBC > 12,000 0r < 4,000 with more than 10% bands

Neurogenic Shock lIt is a shock that result from a high spinal cord injury ( e.g Cervical spine injury) lThis will result in loss of sympathetic tone lLoss of sympathetic tone will result in: uArterial and venous dilatation causing hypotension. uBradycardia as a result of unopposed vagal tone. lThe typical feature is hypotension with bradycardia

Management of neurogenic shock lAssessment of airway lStabilization of the entire spine lVolume resuscitation lR/O other causes of shock lHigh dose corticosteroids.

PRINCIPLES OF RESUSCITATION Maintain ventilation: ensure oxygen delivery Maintain ventilation: ensure oxygen delivery Enhance perfusion Enhance perfusion Treat underlying cause Treat underlying cause

TREATMENT OF SHOCK ENHANCING PERFUSION/OXYGEN DELIVERY Oxygen delivery = HR X SV X Hb X S0 2 X Hb X paO 2 Cardiac output Arterial O 2 content Fluids Transfuse Partially dependent on FIO 2 and pulmonary status Inotropes

SUMMARY Shock is an altered state of tissue perfusion severe enough to induce derangements in normal cellular function Shock is an altered state of tissue perfusion severe enough to induce derangements in normal cellular function Neuroendocrine, hemodynamic and metabolic changes work together to restore perfusion Neuroendocrine, hemodynamic and metabolic changes work together to restore perfusion Shock has many causes and often may be diagnosed using simple clinical indicators Shock has many causes and often may be diagnosed using simple clinical indicators Treatment of shock is primarily focused on restoring tissue perfusion and oxygen delivery while eliminating the cause Treatment of shock is primarily focused on restoring tissue perfusion and oxygen delivery while eliminating the cause

10 yo female 10 yo female Fell off bike riding down a hill. Initially well but 4 hrs later complained of abd pain and L shoulder pain Fell off bike riding down a hill. Initially well but 4 hrs later complained of abd pain and L shoulder pain VS: BP 90/60, P 120 (tachycardic), RR 30 (tachypneic), T 100.1, O 2 sat 95% (low) VS: BP 90/60, P 120 (tachycardic), RR 30 (tachypneic), T 100.1, O 2 sat 95% (low) GEN: pale, anxious GEN: pale, anxious LUNG: clear to auscultation LUNG: clear to auscultation COR: tachycardic with murmur best at base COR: tachycardic with murmur best at base ABD: diffuse tenderness w/o peritonitis or mass ABD: diffuse tenderness w/o peritonitis or mass Hb 7.5 (low) Hb 7.5 (low) CASE PRESENTATION CIRCULATORY SHOCK ABD CT: splenic laceration with free peritoneal fluid

Time % surviva l Fast rate Slow rate None Resuscitation RESUSCITATION NEED FOR SPEED

17 yo male 17 yo male Diving into water Diving into water VS: BP 90/60 (low), P 110 (high), RR 24 (high) VS: BP 90/60 (low), P 110 (high), RR 24 (high) PE: paralysis below C5 PE: paralysis below C5 Cervical X-ray: C5 fracture Cervical X-ray: C5 fracture Hemodynamics: Hemodynamics: Central venous pressureDecreased Cardiac outputDecreased Systemic vascular resistanceDecreased CASE PRESENTATION NEUROGENIC SHOCK

15 yo male 15 yo male 4 day history of abdominal pain, N/V and anorexia 4 day history of abdominal pain, N/V and anorexia VS: BP 70/60 (low), P 130 (high), RR 28 (high), T102.4, O 2 sat 99% VS: BP 70/60 (low), P 130 (high), RR 28 (high), T102.4, O 2 sat 99% GEN: moderate distress from abd pain GEN: moderate distress from abd pain COR: tachycardic COR: tachycardic ABD: diffuse tenderness w peritonitis ABD: diffuse tenderness w peritonitis WBC 19,600 (high), 90% segs, Hb 14.2 WBC 19,600 (high), 90% segs, Hb 14.2 Hemodynamics: Hemodynamics: Cardiac outputIncreased Systemic vascular resistanceDecreased CASE PRESENTATION SEPTIC SHOCK

Splenic laceration with hypovolemia (blood loss) Decreased CO Decreased oxygen delivery, increased oxygen requirement Metabolic acidosis, hypoxemia  tachypnea SBP 60, P 150, RR 32, O 2 sat 89% TREATMENT: Primary resuscitation Oxygen Mechanical ventilation if needed TREATMENT OF RESPIRATORY FAILURE

17 yo male 17 yo male Training for track team Training for track team VS: BP 70/50 (low), P 140 (high), RR 35 (high), O 2 sat 88% VS: BP 70/50 (low), P 140 (high), RR 35 (high), O 2 sat 88% PE: absent breath sounds in L lung field, distended neck veins PE: absent breath sounds in L lung field, distended neck veins DX: tension pneumothorax DX: tension pneumothorax Hemodynamics: Hemodynamics: Central venous pressureIncreased Cardiac outputDecreased Systemic vascular resistanceNormal CASE PRESENTATION CARDIOGENIC SHOCK

15 yo male 15 yo male 4 day history of abdominal pain, N/V and anorexia 4 day history of abdominal pain, N/V and anorexia VS: BP 70/60 (low), P 130 (high), RR 28 (high), T102.4, O 2 sat 99% VS: BP 70/60 (low), P 130 (high), RR 28 (high), T102.4, O 2 sat 99% GEN: moderate distress from abd pain GEN: moderate distress from abd pain COR: tachycardic COR: tachycardic ABD: diffuse tenderness w peritonitis ABD: diffuse tenderness w peritonitis WBC 19,600 (high), 90% segs, Hb 14.2 WBC 19,600 (high), 90% segs, Hb 14.2 Hemodynamics: Hemodynamics: Cardiac outputIncreased Systemic vascular resistanceDecreased DX: perforated appendicitis CASE PRESENTATION SEPTIC SHOCK

3 yo male 3 yo male Clothes ignited from roaster at Thanksgiving Clothes ignited from roaster at Thanksgiving VS: BP 60/60 (low), P 170 (high), RR 35 (high), T102.4, O 2 sat 89% VS: BP 60/60 (low), P 170 (high), RR 35 (high), T102.4, O 2 sat 89% GEN: moderate distress GEN: moderate distress LUNG: tachypneic, clear to auscultation LUNG: tachypneic, clear to auscultation COR: tachycardic, regular COR: tachycardic, regular SKIN: 60% TBSA partial and full thickness burn SKIN: 60% TBSA partial and full thickness burn Hemodynamics: Hemodynamics: Cardiac outputDecreased SVRIncreased CASE PRESENTATION CAPILLARY LEAK DX: 60% TBSA burn HYPOVOLEMIC SHOCK (LOSS OF FLUID INTO INTERSTITIUM)

10 yo female 10 yo female Fell off bike riding down a hill. Initially well but 4 hrs later complained of abd pain and L shoulder pain Fell off bike riding down a hill. Initially well but 4 hrs later complained of abd pain and L shoulder pain VS: BP 90/60, P 120 (tachycardic), RR 30 (tachypneic), T 100.1, O 2 sat 95% (low) VS: BP 90/60, P 120 (tachycardic), RR 30 (tachypneic), T 100.1, O 2 sat 95% (low) GEN: pale, anxious GEN: pale, anxious COR: tachycardic with murmur best at base COR: tachycardic with murmur best at base ABD: diffuse tenderness w/o peritonitis or mass ABD: diffuse tenderness w/o peritonitis or mass Hb 7.5 (low) Hb 7.5 (low) Hemodynamics: Hemodynamics: Central venous pressureDecreased Cardiac outputDecreased Systemic vascular resistanceDecreased CASE PRESENTATION CIRCULATORY SHOCK

Circulatory shock Critical reduction in tissue perfusion Results in organ dysfunction and, if not treated, death Usually accompanied by signs and symptoms: Oliguria Mental status changes Weak thready pulse Cool clammy limbs Septic shock Hypotension Vasodilatation with warm limbs. OVERVIEW GENERIC CLASSIFICATIONS OF SHOCK

MAINTAIN VENTILATION Increased oxygen demand Hyperventilation Respiratory fatigue Respiratory failure Respiratory acidosis, lethargy-coma, hypoxia Especially in: SepsisHypovolemiaTrauma

Vasodilatation A-V shunting Maldistribution of flow Increased capillary permeability + interstitial edema Decreased oxygen extraction Primary defect of oxygen utilization at cellular level CAPILLARY LEAK SYNDROME