Subject: Surgery Topic: Non-Cardiogenic Shock Lecturer: Raymundo Resureccion,MD Date of Lecture: August 10, 2011 Transcriptionist: JAK

stat Editor: huwaistein virus *_* Pages: 8

Case Scenario  27 year-old male was rushed to the Quirino Memorial Medical Center ER for injuries sustained in a vehicular crash History  1 hour earlier, the patient was driving a taxi that crashed into an electrical pole. The patient was pinned by the steering wheel and took 30 minutes to be extricated by which time he was noted to be lapsing in and out of consciousness. Physical Examination  BP 80/60 HR 112 RR 30 T 35 C  Disoriented, in mild respiratory distress  Cold clammy skin, weak pulse  Anicteric, circumoral pallor  Symmetric chest expansion, clear breath sounds, tachypneic  Adynamic, tachycardic, irregular rhythm  Globular, hypoactive BS, dull, tense Course in the Wards  Large-bore peripheral lines inserted and crystalloids infused  UTZ of the abdomen: (+) free fluid  On abdominal exploration:  4.5 liters of hemoperitoneum  Lacerated liver  Evacuation of hemoperitoneum and perihepatic packing  Intraop blood transfusion of 8 u FWB  Transferred to SICU on mechanical ventilation, ongoing transfusion, crystalloids and inotrope infusion  Patient hypotensive, pale and anuric  On the 10th hour post-op, patient went into CP arrest and could not be revived  C.O.D.: Hypovolemic shock secondary to liver injury What is shock?  Shock is not a disease but the end result of many differing processes.

 It is a condition in which systemic blood pressure is inadequate to provide perfusion to the vital organs. Diagnosis of Shock  Two requirements:  A reduction in mean systemic blood pressure, usually below 70 mmHg  Evidence of hypoperfusion of vital organs  Most importantly, altered mentation and low urine volume  Increased levels of lactic acid are also suggestive of global ischemia resulting in shock Determinants of Cardiac Output  Pump (heart)  Fluid volume (blood)  Container (blood vessels)  Any derangement of any of these components can affect perfusion  Blood flow through a vascular bed is directly related to perfusion pressure (the difference between arterial and venous pressures) Determinants of Cardiac Output  BP = CO x TPR  CO = HR X SV  BP = blood pressure  CO = cardiac output (volume of blood flow in L/min)  TPR = peripheral resistance  HR = heart rate  SV = stroke volume (volume of blood with each ventricular contraction) Heart Rate Alterations are called chronotropy Because CO is a function of SV x HR, it is easy to see how HR can increase CO Intrinsic control Extremely rapid HR or prolonged tachycardia can reduce the diastolic filling time and therefore reduce volume

SY 2011-2012

Types of Shock  Hypovolemic: inadequate blood volume  Cardiogenic: failure of the heart as a pump  Distributive:  Neurogenic: neural alterations of vascular smooth muscle tone  Anaphylactic: immunologic processes or allergic reactions  Septic: systemic inflammatory response to microorganisms and/or damaged tissue Major Types of Shock  Cardiogenic  Myocardial infarction, Ventricular rupture, Arrhythmia, Cardiac tamponade, Pulmonary embolism  Hypovolemic  Hemorrhage  Fluid loss  Plasma (burns)  Interstitial fluid (diaphoresis, DM/hyperglycemia, DI, emesis or diuresis)  Septic  Endotoxic shock, overwhelming infection, fungal sepsis, Gram positive septicemia  Neurogenic  Spinal cord injury, high spinal anesthesia  Anaphylactic Different Forms of Shock

 Internal hemorrhage  Hemothorax  Hemoperitoneum  Pelvic fractures Determinants of Cardiac Output  Decrease in volume leads to decreased preload  CVP  LVEDV  Decrease in stroke volume leads to decreased CO and MAP Compensatory Mechanisms  Baroreceptor and chemoreceptor reflexes  Circulating vasoconstrictors  Reabsorption of interstitial fluid  Renal reabsorption of sodium and water  Activation of thirst mechanism  Shift to the right in O2 dissociation curve Arterial Baroreceptors

Hypovolemic Shock  A clinical syndrome resulting from decreased blood and oxygen perfusion of vital organs resulting from a loss of circulating blood volume. Shock in Trauma  Exsanguination  Gunshot wound to the neck, head  Open extremity fractures

Stretch receptors in heart and baroreceptors in aorta and carotid arteries sense a decrease in blood volume, the HPA and neuroendocrine axes are triggered resulting in the fight or flight response Arterial Baroreceptors  Arterial baroreceptor firing inhibits sympathetic outflow and stimulates parasympathetic outflow  Therefore, reduced firing, which occurs during hemorrhage, leads to sympathetic activation and parasympathetic inhibition *see picture @ next page

Central Venous Pressure During Hemorrhage  Hemorrhage decreases blood volume and decreases CVP (A B)  Peripheral venous constriction decreases venous compliance (B C), which increases CVP and shifts blood volume toward heart  Increased CVP increases ventricular preload and force of contraction (Frank-Starling mechanism)

* Aortic pressure after blood loss and baroreceptor denervation Chemoreceptor Reflexes  Peripheral chemoreceptors  Carotid bodies  Aortic bodies  Central chemoreceptors  Medulla (associated with cardiovascular control centers )  Acidosis stimulates central and peripheral chemoreceptors p sympathetic activation  Hypoxia in carotid bodies enhances peripheral vasoconstriction Baroreceptor Reflex  Location: Venoatrial Junction  Tonic receptor firing decreases ADH release leading to diuresis and vasodilation  Hemorrhage decreased receptor firing increase ADH (reduced urine formation and increased vasoconstriction) Humoral Compensatory Mechanisms

 Angiotensin II, vasopressin & catecholamines reinforce sympathetic mediated vasoconstriction  oSVR p maintain MAP  q venous compliance p oCVP & SV  Angiotensin II, aldosterone, vasopressin act on kidneys to retain fluid p o blood volume

*Compensatory Mechanisms  Redistribution of cardiac output  Vasoconstriction in skin, skeletal muscle, renal and splanchnic circulations increases SVR  Coronary and cerebral circulation spared  HR and force of contraction increase Reabsorption of Tissue Fluids  Capillary pressure falls  Reduced arterial and venous pressures  Increased precapillary resistance  Transcapillary fluid reabsorption (up to 1 liter/hr autoinfused)  Capillary plasma oncotic pressure can fall from 25 to 15 mmHg due to autoinfusion thereby limiting capillary fluid reabsorption  Hemodilution causes hematocrit to fall which decreases blood viscosity Changes in Starling Forces Following Hemorrhage

 Increased respiratory function, bronchodilation  Initially HR and SVR increase as a result of release of catecholamines by the adrenals (SNS) to maintain CO & tissue perfusion  capillary hydrostatic pressure interstitial fluid moves into vascular space  Spleen disgorges its blood (200-300cc max)  Renin causes vasoconstriction and stimulates release of aldosterone and ADH to increase water and Na retention

 Starling Equation for Fluid Balance FM = K x A [(PC -PT) (TC - TT)] *Compensatory Mechanisms  Cerebral ischemia  Autoregulatory mechanisms maintain cerebral perfusion until MAP below 60mmHg  Cerebral ischemia produces intense sympathetic discharge several times greater than maximal sympathetic activation from baroreceptor reflex Stages of Shock Compensated Shock  Body defense mechanisms attempt to preserve major organs  Precapillary sphincters close, blood is shunted  Increased heart rate and strength of contractions

 Will continue until problem solved or shock progresses to next stage  Can be difficult to detect with subtle indicators  Tachycardia  Decreased skin perfusion  Alterations in mental status  Some medications such as propranolol can hide signs and symptoms Classes of Hemorrhage
Class I Blood Loss (ml) Blood Loss (% blood volume) Pulse Rate BP Pulse Pressure RR (cpm)
Urine output

Class II 750-1500 15-30%

Class III 15002000 30-40%

Class IV >2000 >40%

Up to 750 Up to 15%

<100 normal normal or decreased 14-20 >30 Slightly anxious

>100 normal decreased 20-30 20-30 Mildly anxious

>120 decreased decreased 30-40 5-15 Anxious, confused

>140 decreased decreased >35 negligible Confused, lethargic

(mL/hr) CNS/mental status

Stages of Hypovolemia  Progressive:  Loss of 30-40% of total blood volume  Risk of major dysfunction of organs leading to multiple organ dysfunction  Drop in BP and narrowing pulse pressure  Symptoms will be specific to the organs effected: brain, heart, kidney, liver, lungs, coagulation  Refractory:  Loss of >40% of TBV (>2000mL)  Compensation is non-functioning  Stage is almost always irreversible  Leads to cellular necrosis and multiple organ failure

Decompensated Shock  Cardiogenic shock  Impaired coronary perfusion causing myocardial hypoxia, systolic and diastolic dysfunction, arrhythmias  Sympathetic escape  Loss of vascular tone causing progressive hypotension and organ hypoperfusion  Increased capillary pressure causing fluid filtration and further hypovolemia  Metabolic acidosis  Cerebral ischemia  Loss of autonomic outflow due to severe cerebral hypoxia  Rheological  Increased microvascular viscosity  Microvascular plugging by leukocytes and platelets  Intravascular coagulation  Systemic Inflammatory Response  Increased capillary permeability  Multiple organ failure

*Effects Blood Volume Loss on Mean Arterial Pressure

Irreversible Shock  Compensatory mechanisms fail, cell death begins, vital organs falter  Patient may be resusitated but will die later of (ARDS, renal and liver failure, sepsis)  Poor survival rate even if hemodynamic defects are corrected *Time-Dependent Changes in Cardiac Function  Dogs hemorrhaged and arterial pressure held at 30 mmHg  Precipitous fall in cardiac function occurred after 4 hours of severe hypotension Initial Management  Recognize shock  Stop the bleeding!  Replace effective circulating volume  Restore tissue perfusion Recognition of Shock  Narrowed pulse pressure  Cutaneous vasoconstriction  Tachycardia  Hypotension Pitfalls of Shock Recognition  Extremes of age 5

 Athletes  Pregnancy  Medications  beta blockers  pacemakers  Hypothermia Treatment of Hypovolemia  Early detection and minimizing further blood loss are key  Restoration of fluids and plasma volume  Dictated by the severity of loss and hemodynamic status  Replacement chosen based on volume lost History  History taking should address the following:  Specific details of the mechanism of trauma or other cause of hemorrhage are essential.  Inquire about a history of bleeding disorders and surgery.  Prehospital interventions, especially the administration of fluids administered, and changes in vital signs should be determined. Detecting Site of Blood Loss  In hypovolemic shock consider 5 sources of ongoing hemorrhage as follows: 1. Chest/Pleural space 2. Abdomen/Peritoneal cavity 3. Pelvis and/or retroperitoneum 4. Long bone fracture 5. External Hypovolemic Shock: Treatment  Control of ongoing losses  Direct pressure and dressing for external and minor sources  Penetrating injuries commonly require operative intervention  Must have high index of suspicion for intracavitary losses  Investigation of source of bleeding  Rapid reexpansion of the circulating blood volume  Rapid infusion of isotonic saline or Lactated Ringer s at 2 L over 20-30min to restore hemodynamic parameters to normal  Continued blood loss and decreasing Hgb concentration (<70g/L) warrants blood transfusion

 Prolonged hypovolemia may require adminstration of inotropic agents Volume Replacement in Hypovolemic Shock  Crystalloids  Expands intravascular and interstitial  0.9% PNSS at 20-40ml/kg in 20 mins  2-3x volume loss  Colloids  Raises capillary oncotic pressure  Remain in vascular space longer Blood Replacement in Hypovolemic Shock  Blood:  500 ml whole blood increases hematocrit 2-3%,  250ml pRBC s increases Hct 3-4%  Increases oxygen carrying capacity  Used with acute hemorrhage Resuscitation End Points  Normalization of vital signs  Restoration of circulating volume  Restoration of aerobic metabolism Septic Shock  A complex hormonal and chemical release of substances is produced through the body s immune system in response to adverse effects of endotoxins.  Invading micoorganisms increase vasoactive toxins (histamine and kinins) resulting in vasodilation  The pathogens also create a high flow, low resistance state (increased CO, decreased SVR)  Decreased ability to extract O2 from blood causing tissue hypoxia and lead to a oxyhemoglobin curve shift to the left  Any type of microorganism can cause sepsis but gram-negative bacteria is most common  Escherichia coli  Klebsiella  Enterobacter  Serratia  Pseudomonas aeruginosa  Bacteroides  Proteus  Late stages lead to irreversible state similar to cardiogenic or hypovolemic:  Hypotension  Vasoconstriction (extreme SVR)  Decreased CO/CI  Hypoxia (even with 100% O2)  Profound acidosis  Mortality rates for septic shock are 60- 80% 6

 Diagnosis of sepsis usually requires isolation of etiologic agent in blood, sputum, urine or tissue cultures

 Maintain oxygen delivery (DO2) at 450-600ml/min/m2 Distributive Shock Neurogenic Shock  Diminished tissue perfusion as a result of loss of vasomotor tone  Results in increased venous capacitance, decreased venous return and ultimately cardiac output  Sympathetic input to the heart, which normally increases heart rate and cardiac contractility, and input to the adrenal medulla, which increases catecholamine release, may also be disrupted, preventing the typical reflex tachycardia that occurs with hypovolemia  Spinal cord injuries from vertebral body fractures of the cervical or high thoracic region that disrupt sympathetic regulation of peripheral vascular tone  Dominance of PSNS control produces massive vasodilatation and a pooling of blood in the periphery  Spinal anesthesia or altered function of the vasomotor center in response to low blood sugar or drugs, including sedatives, barbiturates and narcotics  Firing of brainstem vasomotor center vasomotor tone generalized systemic vasodilatation

Pathophysiology of Severe Sepsis  Severe sepsis is associated with 3 integrated responses:  Activation of inflammation  Activation of coagulation  Impairment of fibrinolysis  These responses are d/t a variety of proinflammatory mediators (cytokines), procoagulant factors (enzyme thrombin), and inhibitors of fibrinolysis (plasminogen activator inhibitor-1) Treatment of Septic Shock  Goal is to maintain adequate tissue perfusion while treating infection  Early detection  Source control  Appropriate antibiotics  Improve CO  Fluid replacements (utilize fluid challenges to optimize preload watch CVP)  Inotropic agents (dobutamine)  Provide hemodynamic support  Vasopressors to increase SVR/afterload (dopamine, norepinephrine)  Optimize oxygenation

 Classic description of neurogenic shock consists of:  Decreased blood pressure  Bradycardia  Warm extremities  Motor and sensory deficits indicative of a spinal cord injury  Radiographic evidence of a vertebral column fracture 7

Hallmark indicator is very low SVR . Blood volume has not changed, but the space containing the blood has increase. Any indicator of excessive PSNS activity *Esp. bradycardia in the early stages (absence of reflexive tachycardia due to disrupted sympathetic discharge) *Warm extremities (loss of peripheral vasoconstriction)  Airway and ventilatory support  Increase vascular tone and improve CO  Increase preload with fluids  CVP  PAWP  Increase vascular tone  Vasopressors  Maintain heart rate  Treat bradycardia if symptomatic Anaphylactic Shock  Result of a severe allergic or antigen-antibody reaction  Reaction causes a release of histamine, serotonin, and bradykinin causing vasodilation and increased capillary permeability  Slow reacting substances of anaphylaxis are also released causing bronchoconstriction Causes of Anaphylactic Shock  Substances that act as antigens:  Drugs (ex: PCN)  Contrast media  Transfused blood  Insect venoms  Foods (ex: shellfish)  Pollens  Latex allergies  Once in the body, the antigen causes an extensive immune and inflammatory response causing vasodilation and increased vascular permeability Pathophysiology  Anaphylaxis causes both hypotension and hypovolemia  Exposure to allergen triggers wide-spread type I immune reaction (antigen-antibody reaction)  Release of vasoactive mediators  Massive vasodilation  Increased capillary permeability p edema of membranous tissues p respiratory obstruction Symptoms  Onset of symptoms is within seconds and progression can lead to death in minutes

 Capillary refill: delayed d/t decreased CO  Heart rate: extreme tachycardia  Allergic reaction sx:  Edema  Urticaria (hives)  Burning, itching skin  Difficulty breathing  Anxiety  Enlarged tongue

Treatment  Remove the antigen!!  Goal is to stop reaction, restore vascular tone and fluid volume  Epinephrine is used to cause vasoconstriction and reverse airway constriction  Antihistamines used to stop the inflammatory reactions  Bronchodilators &/or steroids to open airways  Fluid of choice is usually LR

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