[No title]


Published on

  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

[No title]

  1. 1. Shock Jon Rumohr (jrumohr@) and Prabhu Rajappa (prajappa@) An expanded and revised version of Santosh Pandapati’s efforts We recognize the redundancy in the following notes…and figure it can’t hurt Good luck everybody • 5 kinds of shock: hypovolemic, septic, cardiogenic, neurogenic, anaphylactic Hypovolemic shock I. General • hypoperfusion secondary to hypovolemia which results in a marked reduction of oxygen delivery to tissues (intravascular volume) • Most common cause of shock in surgical patients • Symptoms are determined by amount of volume loss AND rate of volume loss • 3 Classes: • Mild: <20% volume loss. Decreased perfusion to non-vital tissues. Pale, cool, skin and anxiety may be seen • Moderate: 20%-40% loss: Decreased perfusion to more vital organs (liver, kidneys, intestine). Oliguria, decreased BP, and agitation seen. • Sever: >40% volume loss: Decreased perfusion to brain and heart. Manifested by mental status changes and hypotension, and of course, OLIGURIA (SURGEONS ARE OBSESSED WITH OLIGURIA…DO NOT FAIL TO MENTION THIS. NOTE THAT SIMPLY LOOKING AT THE FOLEY OUTPUT CAN BE ALL YOU NEED TO DX A HYPOVOLEMIC STATE) II. Etiologies • Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal • Fluid depletion (nonhemorrhagic) • External fluid loss • Dehydration • Vomiting • Diarrhea • Polyurea • Interstitial fluid redistribution • Thermal injury • Trauma • Anaphylaxis • Pancreatitis, peritonitis • Increased vascular capacitance (venodilatation) • Sepsis • Anaphylaxis • Toxins/drug III. Pathophysiology • Neurohumoral response • Hypovolemia results in decreased venous return which ultimately decreases cardiac output • The body responds with tachycardia (epi, NE, dopamine), vasoconstriction (NE, ADH, angiotensin), oliguria with sodium and water retention (ACTH, cortisol, aldosterone, ADH), and hyperglycemia. (epi, glucagon, cortisol, inhibition of insulin). • The goal is to preserve blood flow to vital organs (heart, lungs, brain) at the expense of other systems. • Cellular dysfunction and death
  2. 2. • Shock produces cellular dysfunction through three major mechanisms: cellular ischemia, inflammatory mediators, and free radical injury. In hypovolemic shock, the major mechanism of damage is cellular ischemia. • A lack of oxygen at the cellular level results in anaerobic metabolism which leads to elevated levels of lactic acid and impaired ATP production. • Cell membrane function is impaired by decreased intracellular ATP. Sodium (with water following) and calcium move into cells. Water becomes sequestered in the intracellular compartment, and electrolyte imbalances result in enzyme and organelle dysfunction ultimately leading to cell death. IV. Diagnosis • History--Patients suffering from hypovolemic shock will often have a history suggestive of fluid losses: • Trauma (hemorrhage) • Burns • Recent surgery • Vomiting, diarrhea, etc. • Physical Exam • Classic signs include hypotension, tachycardia, tachypnea, hyper- or hypothermia, cool extremeties, agitation/altered mental status, oliguria (Note: a patient can be NORMOtensive with up to a 30% loss of blood volume if loss gradual--ie there are always exceptions) • Laboratory abnormalities • Metabolic acidosis • Elevated BUN and creatinine • Elevated blood glucose • Decreased ionized calcium • Decreased CVP, PCWP and CO V. Treatment—must be simultaneous with diagnostic measures. The goal is to restore circulation and correct the underlying cause of hypovolemia. • Restore circulation (remember ABC’s!) • A hypotensive patient who is not in CHF is likely to have lost >30% of their intravascular volume. Replacement with cystalloid (Ringers, 0.9NS) requires a 3:1 ratio (due to redistribution to extracellular space). Start two large bore IV’s. • Packed RBC’s may be needed if hypovolemia is due to blood loss. Get a blood type and crossmatch. • Place a foley to monitor urine output. Order labs (ABG, basic, CBC, coags, lactic acid level). If possible, place Swan-Ganz catheter to monitor circulatory status. • If patient continues to be hypovolemic, pressors such as dopamine and/or NE may be used. • Determine cause of hypovolemia (we are in surgery—think HEMORRHAGE or THIRD SPACING) • Examine patient thoroughly (look for signs of hemorrhage, trauma) • Order imaging studies and other diagnostic tests if indicated (look for causes such as pancreatitis, perforated bowel, PUD etc) • Attempt appropriate therapeutic intervention • A note on hypovolemic shock in general from Dr. Ramsburgh: If a surgeon is talking about hypovolemic shock with ya, he/she is likely to have third spacing on his/her mind. “It’s a surgeon…do you think he’s going to suspect post-op bleeding? He would never make that kind of mistake…no, it’s going to be third spacing of course. Also, think about the differences in ‘crit between a hemorrhagic and non-hemorrhagic hypovolemic picture…” Anyone who’s seen bowel surgery has seen how swollen and edematous the bowels can get over the course of their manipulation. That fluid came from the intravascular compartment. Just remember this as an important surgical etiology for hypovolemia, and one that we 3rd years often forget about. This is not to say that we should forget about hemorrhage, etc. Septic Shock 1) General a) Septic shock is defined as sepsis-induced hypotension that persists despite adequate fluid resuscitation and is associated with hypoperfusion abnormalities or organ dysfunction. b) Is uncommon in patients <40 y.o. except in septic abortions and neonates c) Second to hypovolemic for shock in surgical patients d) 100,000 deaths/year, 400,000 cases
  3. 3. 2) Etiologies: a) Suspect particularly in the setting of… i) UTIs, especially after instrumentation. For example, TURBTs, Foleys, etc. ii) Pyelonephritis iii) Pneumonia iv) Peritonitis v) Intraabdominal abscess vi) Meningitis vii) IV catheter infection viii)Wound infection ix) HIV/AIDS, immunosuppression, or chemotherapy x) Trauma, especially “dirty” variety xi) Corticosteroid use xii) Diabetes b) Bugs…most common these days are: i) Gram negatives like pseudomonas ii) Gram positives like staph and enterococci. 3) Pathophysiology, general a) Unknown precisely, but is probable due to inadequate oxygen delivery due to either i) Supernormal oxygen demand by the increased metabolic rate of septic cells or… ii) Metabolic derangement of cellular metabolism such that cells cannot utilize oxygen even though plenty of it is around. iii) In other words, either oxygen is not making it to cells or the cells aren’t utilizing it. b) Big picture i) Endotoxins and exotoxins are released by invading bacteria…such as teichoic acid. (1) Leads to massive release of endogenous cytokines—TNF and IL-1 in particular. Complement system activated as well. (a) Vascular permeability increasesThird spacing, and massive vasodilatation combine to cause a relative hypovolemia. (2) PMN’s migrate to endothelium and damage it. This sets up patients for DIC 4) Pathophysiology, specific a) Early shock (warm shock) i) Patient is vasodilated w/ low systemic resistance (1) skin warm and dry d/t peripheral vasodilation. (2) low bpdecreased carotid sinus firingtachycardia ii) Relative hyovolemia iii) Pulse pressure and stroke volume are normal iv) Increased metabolism in face of oxygen debtanaerobic metabolismsome metabolic acidosis (get a BASIC and look for mildly elevated bicarb)tachypneamay lead to moderate respiratory alkalosis (get an ABG and look for low PaCO2) v) Left and right atrial filling pressures can be normal vi) Pulmonary artery pressure and vascular resistance can be normal vii) Oxygen consumption may be low (1) Due to impaired oxygen extraction secondary to systemic toxins b) Late shock (cold shock) i) Multiple organs start to malfunction…MOSF ii) Capillary permeability continues to increase iii) Increased cell membrane dysfunction Sodium, calcium and water enter cellsextracellular volume decreases, compounding relative hypovolemia iv) Oncotic pressures between intravascular and extravascular spaces have normalized v) Cardiac index falls…is caused by high levels of cytokines which somehow affect cardiac function… vi) Lactic acidosis worsensbicarb levels quite low (1) Tachypnea continues, minute ventilation high and PaCO2 low vii) Peripheral vasoconstriction (1) cold, clammy, mottled, cyanotic skin (2) organ perfusion and function compromised viii)Mental status changes include lethargy and confusion ix) DIC (1) Low levels of coag factors, complement, antithrombin etc.
  4. 4. (2) So, massive clotting with increased propensity to bleeding as platelets and factors are consumed. (3) Clinically manifested as purpura. x) Cardiac index continues to sufferejection fraction may be 33% or so xi) MOSFDeath 5) Organ system approach if you like that sort of thing… a) Neuro i) Confusion, delirium d/t poor perfusion and cellular metabolic derangements. b) Cardiac i) Depressed contractility. ii) Compensatory tachycardia to increase cardiac output in face of hypotension and low ejection fractions c) Vasculature i) Peripheral vasodilatation, hypotension, perfusion pressure bottoms out… d) Hematologic i) DIC, thrombocytopenia (1) Purpura e) Pulmonary: ARDS can develop… i) Leaky capillaries mean stiff lungs. Acute lung injury causes impaired gas exchange, decreased compliance, and shunting of blood through underventilated areas. The work of breathing is increased, and respiratory muscle fatigue and ventilatory failure ensue, often requiring mechanical ventilation. f) Renal i) HypoperfusionATNrenal insufficiency, oliguria. ii) Is a major source of shock mortality g) Liver i) Focal necrosis ii) Unconjugated bilirubinemia h) GI tract i) Poor perfusion can lead to necrosis…good chance of hemorrhaging… ii) Barrier function may be compromised leading to further bacterial translocation into bloodstream i) Endocrine i) REMEMBER: SEPSIS IS A CATABOLIC STATEGlucagon, cortisol and other stress hormone levels are high. This contributes to the high metabolic rate, a hyperglycemia, lactic acidosis, etc. This is of course particularly important for diabeticsDKA, HONK 6) Diagnosis a) Sx/sxms i) Symptoms related to primary focus of infection (1) UTI pain, wound infection signs, pneumonia, cellulitis, etc. ii) Signs of systemic inflammatory response (1) Fever/chills (a) Note that elderly patients may be normothermic iii) Signs of shock/organ failure. (1) Hypotension, tachycardia. (2) Toxic-looking, nausea…ask yourself how the patient looks (3) Confusion. (4) Gut pain. (5) Oliguria…look at the Foley output (6) Tachypnea b) Labs i) Early (1) ABG: respiratory alkalosis (low PaCO2 d/t tachypnea) (2) BASIC panel: hyperglycemia (remember, is a catabolic state) (3) CBC: hemoconcentration (I believe d/t the relative hypovolemia), leukopenia (perhaps d/t the leukocyte margination? Regardless, it helps me to think about it like that) (4) Urinalysis: Glycosuria ii) Late: (1) ABG: metabolic acidosis and respiratory alkalosis (2) BASIC: Elevated BUN and creatinine (3) CBC: Leukocytosis, low platelets if DIC picture (4) Coags: prolonged PT/PTT if DIC picture. Can check d-dimer if you get the notion… (5) Liver: indirect bilirubinemia b/c cells in the canaculi aren’t functioning too swiftly; alk phos may be elevated d/t dying liver cells
  5. 5. 7) Treatment, Rx: Has two components a) Control primary focus i) Incision and drainage of abscesses if necessary ii) Antimicrobials: Broad spectrum at first, then focus when bug identified. Vancomycin, gentamycin, and metronidazole is a reasonable primary approach. (1) Get blood cultures as you go so you can tailor therapy (3) (2) IV antibiotics at maximum doses. (3) Buzz: (a) IV catheter infxn is likely to be MRSA, so Vancomycin the ticket b) Resuscitate: The first step, really i) Initial emphasis should be placed on restoring mean blood pressure to greater than 65 mm Hg. It might be worthwhile to float a Swan-Ganz to monitor PCWP and CVP. Also, start one or two large bore peripheral lines, insert a Foley, and start constantly monitoring vitals. ii) REMEMBER, VOLUME FIRST! Then, move on… (1) Aggressive volume resuscitation using blood (if hemoglobin is less than 10 g/100 mL), colloid (if serum albumin is less than 2 g/100 mL), or crystalloid (in all other patients, which is probably most…) should be instituted to raise the pulmonary artery mean wedge pressure to 15 to 18 mm Hg. (2) If hypotension persists, dopamine (low-dose and then, if necessary, higher doses up to 20 mug/kg/minute) should be administered. (3) In patients who are unresponsive to dopamine, norepinephrine should be infused to raise mean blood pressure to higher than 65 mm Hg. (4) Patients who require high doses of norepinephrine may benefit from concomitantly administered low-dose dopamine to enhance renal blood flow. iii) Once blood pressure is adequate, attention should be turned to cardiac output and oxygen delivery. Although the role of achieving very high levels of oxygen delivery and consumptionis controversial, most investigators favor inotropic support (with dobutamine, if necessary) to offset the myocardial depression of sepsis and to maintain a cardiac index in the high normal range (higher than 4.0 L/minute/m2 ). iv) May need to ventilate in order to get saturation up to 90% v) May have to give bicarb if pH falls to below 7.1. vi) Serial measures of lactate, urine output, and organ function can provide good measures of patient prognosis. Figure: Skeleton for algorithmic approach to Dx and Tx of septic shock. (Cecil’s Textbook of Medicine, 2000)
  6. 6. Neurogenic Shock 1) General a) Hypotension secondary to CNS dysfunction b) Often seen in trauma, therefore is often coincident with hypovolemic or cardiogenic shock 2) Pathophysiology a) Hypothalamic, brainstem, cervical or thoracic spine injury i) Loss of symphathetic tonevasodilatation, decreased PVRhypotension ii) Loss of sympathetic tonebradycardia iii) You can see that this combination will decrease venous return and cardiac output…bad combo for tissue/organ perfusion 3) Diagnosis a) Recognize the hypotension combine with paradoxical bradycardia, vasodilatation (warm extremeties) and little or no agitation…basically, signs of loss of sympathetic tone b) Neuro deficits that may enhance diagnosis i) Warm feet, but no volitional control thereof ii) Complete flaccid paralysis iii) Absent bulbocavernous reflex: Compress penis or clitoris, and anal sphincter does not contract as it normally would… check the “tone” iv) Absent voluntary control of anal sphincter…check the tone c) Lab tests i) Generally no major perturbations in purely neurogenic shock…if there are major lab findings, then you have to look for another cause of the shock picture… 4) Treatment a) IV access…volume expansion b) Pressors if volume expansion fails… i) Phenylephrine is the drug of choice since it is a pure vasoconstrictor (alpha-1 agonist) w/ little effect on the heart ii) Norepinephrine should be avoided d/t it’s disregard for renal perfusion c) If traumatic… i) Rigid backboard restraint until spine injury ruled out (1) Cervical, thoracic, lumbar, and sacral spine X-rays should be obtained ii) CT of intracranial contents (1) If head injuries present, then neurosurgery should be consulted to treat possible epidural or subdural hematomas…or to relieve epidural pressure on the spinal cord Anaphylactic Shock 1) General a) Is inadequate tissue perfusion due to increased vascular permeability and vasodilatation, accompanied by smooth muscle constriction. Arises after exposure to an allergen one has been previously been exposed to. 2) Pathophys a) Basically, IgE which is stuck on mast cells and basophils binds to the antigen and aggregates. i) The mast cell is activated and spills histamine, leukotrienes, etc. 3) Sx/Sxms: depend on the site of exposure a) Urticaria b) Asthma: wheezing, dyspnea, tight chest c) Shock: Due to massive systemic release of cytokines… i) Hypotension, dyspnea, vomiting, abdominal cramping, angioedema, urticaria. 4) Taking a history… a) Ask about bee stings, penicillin, blood transfusions, and food intake 5) Tx a) Establish AIRWAY. b) Give epinephrine c) Give diphenhydramine (Bendaryl) d) Maybe give steroids e) Maybe give aminophylline Cardiogenic Shock 1) GENERAL
  7. 7. a) Intrinsic Cardiogenic shock: results from failure of the heart as a pump (eg: MI) b) Extrinsic cardiogenic shock: results from extrinsic compression of the heart that impairs ventricular filling (eg: tension pneumothorax) 2) ETIOLOGY a) Intrinsic i) Acute Ischemia (eg: Ventricular wall, Papillary muscle, or Ventricular septal defect) ii) Acute valvular disease (eg: mitral, tricuspid, or aortic regurg) iii) Arrhythmias (venticular tachycardia, bradycardia, rapid SVT) b) Extrinsic i) Pericardial tamponade ii) Tension pneumothorax iii) Increased abdominal pressure (leads to increased intrathoracic pressure as well as an increase in resistance of abdominal veins, including IVC) (1) Ascites, bowel distension, intraabdominal hemorrhage 3) DIAGNOSIS a) Intrinsic i) History (1) Any history of cardiac disease ii) Physical Exam (1) Many of the same signs common to all forms of shock: hypotension, tachycardia, tachypnea, cold extremeties (2) Distended neck veins (3) Agitation/confusion (4) S3 gallop (5) Rales and/or peripheral edema iii) Labs/Diagnostic tests (1) EKG--look for evidence of preexisting disease or acute changes (2) Chest X-ray--look for pulmonary vascular congestion, pulmonary edema, pleural effusions, or cardiomegaly (3) Cardiac enzymes--may indicate acute myocardial injury (4) ABG--provides information about inadequate ventilation and acid/base status (5) Echocardiogram--shows ventricular dysfunction, valvular disease (6) Increased CVP, PCWP b) Extrinsic i) History (1) Chest trauma (2) Cardiac surgery (3) Abdominal surgery or trauma, liver disease ii) Physical Exam (1) Tension pneumo (a) ipsilateral decreased breath sounds (b) tracheal deviation (away from affected side) (c) JVD (2) Pericardial tamponade (a) Beck's triad: hypotension, neck vein distention, muffled heart sounds (b) Pulsus paradoxus (3) Increased Abdominal pressure (a) firm, distended abdomen iii) Labs/Diagnostic tests (1) Chest x-ray--mediastinal deviation, depression of diaphragm, enlarged heart silhouette. (2) Echocardiogram--shows fluid around heart (3) Increased CVP 4) TREATMENT/MANAGEMENT a) Intrinsic i) ABC's (1) Supplemental oxygen, mechanical ventilation as needed (2) Correct hypovolemia ii) Treatment of arrhythmias iii) Ionotropic support (dopamine, dobutamine, etc) iv) Reduce preload (nitro, calcium channel blockers, diuretics) DO NOT GIVE FLUIDS
  8. 8. v) Invasive hemodynamic monitoring (place Swan-Ganz catheter) (1) Characteristic findings include low CO, high SVR, and high PCWP. vi) Coronary Revascularization if acute MI is cause (thrombolytics, balloon dilation, surgery) (1) vii) IABP (intraaortic balloon pump) for those unresponsive to volume expansion and drug therapy viii)Ventricular assist device b) Extrinsic i) ABC's ii) Tension pneumothorax (1) Urgent chest decompression (a) Chest tube placement or placement of 14-guage needle over 3rd rib in mid-clavicular line iii) Pericardial tamponade (1) Pericardiocentesis to remove fluid (2) Vigorous fluid administration to improve venous return (despite elevated CVP) iv) Abdominal pressure (1) Fluids to increase venous filling pressures (2) Paracentesis (3) Surgical decompression, if needed Table comparing hypovolemic and cardiogenic shock Type of Shock CVP & PCWP Cardiac Output PVR Venous O2 sat Hypovolemic  So give volume    Cardiogenic  So, maybe give volume…maybe not   