A. Basic Equations
1. Arterial Pressure = cardiac output x total vascular resistance
2. Mean arterial pressure = [(diastolic pressure x 2) + systolic pressure]/3
3. Cardiac output = heart rate x stroke volume
a) Determinants of stroke volume = preload, afterload, intropy
b) Cardiac output normally estimated using thermodiluation using a Swan-Ganz catheter
c) Cardiac index = cardiac output/body surface area (normal = 2.5 - 4.0 L/min/m2)
4. Systemic vascular resistance = 79.92 x (MAP - CVP)/CO (normal = 900 - 1,400)
B. Identify the Etiology of Shock
1. Cardiogenic shock
a) acute myocardial infaraction (implies > 40% LV muscle loss)
(1) shock accompanies 6-20% of all acute MIs
(2) more common in patient with anterior MI
b) dilated cardiomyopathy
c) acute myocarditis
d) mechanical (mitral regurgitation, ventricular septal defect, left ventricular aneurysm, left ventricular outflow obstruction
e) metabolic and pharmacologic myocardial depression
f) arrhythmias
2. Extracardiac obstructive shock
a) massive pulmonary embolism
b) severe pulmonary hypertension
c) pericardial tamonade
d) tension pneumothorax
3. Oligemic shock
a) hemorrhagic
b) volume depletion
c) adrenal insufficiency
4. Distributive shock
a) septic
b) toxic agents (including adverse reaction to medications and certain drug overdoses)
c) anaphylaxis
d) neurogenic
5. Bedside clues to distinguish sepsis and cardiogenic shock:
Physical Finding Cardiogenic Septic Pulse Pressure decreased increased Diastolic Pressure mildly reduced severely reduced Extremities cool & pale warm & pink Nailbed Return slow brisk
C. Initial approach to the patient in shock: ABC:
1. Airway
a) indications for intubation in patients with shock:
(1) severe hypoxemia
(2) inappropriately high pCO2
(3) obtundation (insure airway protection)
(4) vital organ hypoperfusion (resting ventilatory muscles will permit diversion of cardiac output to other organs)
2. Breathing
3. Circulation
a) immediate determination of relative intravascular volume status is required
(1) unless there are signs of intravascular volume overload, initial resuscitation with IV fluids is generally indicated
(2) early, goal-directed therapy dictates early placement of a central venous catheter and determination of the central venous pressure (see below)
b) vasopressor medications should be selected based on the cause of shock (see table)
D. Correction of the inciting cause of shock
E. Maintain and support vital organ function
F. Correct the secondary consequences of the shock state:
1. disseminated intravascular coagulation
2. acute respiratory distress syndrome
3. acute renal failure
A. Cardiac rhythm monitoring
B. Arterial blood pressure monitoring: target a mean arterial pressure of > 65 mm Hg
C. Central venous pressure monitoring
D. Pulmonary artery (Swan-Ganz) catheterization - primarily useful in cardiogenic shock
E. Urinary catheterization: target a urine output > 0.5 ml/kg/hr
A. Definitions:
1) clinical: tachycardia, oliguria, cyanosis, altered mentation, cool extremities
2) hemodynamic:
(a) hypotension (systolic blood pressure < 90 mm Hg)
(b) low cardiac index (< 2.2)
(c) elevated pulmonary capillary wedge pressure (> 18 mm Hg)
(d) the LV ejection fraction can be misleading and in one study of patients with cardiogenic shock, the average LV EF% was 31% (Circulation 2003; 107:279-84)
B. Prognosis: In the GUSTO-I study, few patients presented to the emergency department with cardiogenic shock (11%); the majority of patients developed shock while in the hospital (89%). Overall, shock occurred in 7.2% of all patients with acute MI. The mortality rate was 55% in those developing shock vs. 3% in those not developing shock (J Am Coll Cardiol, 1995; 26:668-74)
C. Management:
1) Establish airway and insure ventilation if necessary
2) Assesment:
(a) identify and correct rhythm disturbances
(b) exclude other mimics of cardiogenic shock (pulmonary embolus, pericardial tamponade, aortic dissection, sepsis, etc.)
3) Assess volume status
(a) an adequate pre-load is prerequisite to successful resuscitation
(b) clinical assessment is frequently inaccurate
(c) insertion of a Swan-Ganz catheter is indicated in patients with hypotension unresponsive to fluid administration or if fluids are contraindicated (Circulation 2004; 110: 588 and J Am Coll Cardiol, 2008; 51:210-247)
4) Replace volume: in the absence of clinical evidence of pulmonary edema, an immediate fluid challenge is indicated; often a small volume of fluid (eg, 250 ml) can make the difference between adequate and inadequate volume repletion
5) Vasopressors
a) dobutamine (2.5 - 20 mcg/kg/min): first line drug if shock is mild with a relatively preserved blood pressure; beware of patients in cardiogenic shock who have compensated by increasing their systemic vascular resistance to maintain an adequate blood pressure - the vasodilating properties of dobutamine can result in acute deterioration in this setting.
b) dopamine (2.5 - 20 mcg/kg/min): in moderate to severe cardiogenic shock, dopamine is the drug of 1st choice
c) levarterenol (0.05 - 1.0 mcg/kg/min): use is usually reserved for patients failing to respond to dopamine
d) phenylephrine (0.5 - 10 mcg/kg/min): use is primarily reserved for patients with septic shock with high cardiac outputs refractory to levophed & dopamine
e) digoxin: not indicated in shock (risks outweigh benefits)
6) Vasodilators - rarely useful in acute cardiogenic shock
7) Intra-Aortic balloon Counterpulsation (IABP) can enhance diastolic coronary artery blood flow thus reducing ischemia to "stunned" myocardium and should be used in the following settings accompanying cardiogenic shock:
a) if shock does not quickly reverse with pharmacologic therapy
b) persistent low urinary output
c) recurrent ischemic chest pain and hemodynamic instabililty, poor left ventricular function, or large amount of at-risk myocardium
d) refractory ventricular tachycardia
9) Percutaneous coronary intervention (PCI): results of the SHOCK study (SHould we emergently revascularize Occluded Coronary for cardiogenic shocK) indicated that patients who underwent emergent coronary revascularization with either PTCA or CABG had improved 1-year survival compared to patients who unwent thrombolysis and/or intra-aortic balloon counterpulsation (46.7% survival versus 33.6% survival) (JAMA 2001; 285:190-2)
10) Thrombolytics: primarily used if patients will not or cannot undergo PCI; in general, PCI is preferrred for managing shock accompanying acute myocardial infarction
11) Identify surgically correctable causes of cardiogenic shock: acute mitral regurgitation, ventricular aneurysm, acute VSD, ruptured ventricle, papillary muscle rupture, significant left main coronary artery disease (CABG preferred over PCI in this setting)
D. The special case of the right ventricular infarction accompanied by shock
1) pathogenesis: usually right coronary artery occlusion and more frequent in inferior myocardial infarctions
2) physical examination: hypotension, clear lungs, elevated jugular venous pressure, Kussmaul's sign (jugular venous distension with inspiration)
3) hemodynamics: right atrial pressure > 10 mm and within 5 mm of the PCWP
4) frequent EKG findings: RBBB, complete heart block, 1 mm ST elevation in lead V4R
5) treatment:
a) IV volume loading with saline
b) avoid preload reducers (nitrates, morphine, diuretics)
c) correct arrhthmias
d) dobutamine if shock persists; consider IABP
e) pacemaker if relatively bradycardic
f) consider PCI
A. Pulmonary embolus: thrombolytics
B. Pericardial tamponade: IV fluids and pericardiocentesis
C. Pneumothorax: chest tube
D. Pulmonary hypertension: pulmonary vasodilators
A. Protect/ensure patent airway and provide ventilation if necessary
B. Establish adequate venous access
(1) flow dependent on cathether diameter plus catheter length
(2) flow through a short (2 inch), wide bore (16 gauge) peripheral IV is far better than through a central line port
(3) optimally, place 2 wide bore peripheral IVs
C. Volume replacement
(1) isotonic crystalloid (saline or lactated Ringer's solution) is preferred over colloid solutions (such as albumin) for immediate phase of volume replacement
(2) volume expansion equivilents: 6 liters D5W = 2 liters saline/Ringer's = 1 liter albumin = 1 unit PRBCs
(3) send type and cross for PRBCs immediately
D. Determine the site of blood loss:
(1) emergency department: usually trauma or gastrointestinal
(2) hospitalized patients: usually gastrointestinal, pleural, peritoneal, or retroperitoneal
E. Correct coagulopathy (PTT, INR, platelets)
A. Pathogenesis of sepsis
(1) Invasive factors: endotoxins (lipopolysaccharide), exotoxins, other microbial antigens
(2) Host factors: tumor necrosis factor, interleukin-1, interleukin-8, complement, platelet activating factor, nitric oxide, etc.
B. Clinical findings:
(1) temperature (too low or too high)
(2) hemodynamic changes:
a. early: normal BP, low SVR, increased CO
b. intermediate: low BP, very low SVR, increased CO
c. late: very low BP, normal SVR, low CO
(3) ABG changes
a. early: respiratory alkalosis
b. intermediate: respiratory alkalosis + metabolic acidosis
c. late: metabolic acidosis
(4) acute respiratory distress syndrome (ARDS): exudative pulmonary edema ("vascular leak"), alveolar neutrophil accumulation, microatelectasis, shunt physiology
(5) acute tubular necrosis with renal insufficiency/failure
(6) hemotologic manifestations: WBC vacuolization, eosinopenia, thrombocytopenia, DIC
(7) neurologic manifestations: stupor, coma
(8) gastroenterologic: cholestatic jaundice (bilirubin generally remains below 10 and is mostly direct bilirubin), gastric stress ulcers/erosions
(9) cutaneous manifestations: cyanosis, extremity ischemia, purpura, petichiae
(10) metabolic manifestations: hypocalcemia, lactic acidosis, hyperglycemia or hypoglycemia
C. Assessment:
(1) airway
(2) breathing
(3) circuation
(4) microbiologic assessment: identify source of infection, cultures, legionella & pneumococcal urine antigens (when pneumonia is suspected)
D. General Therapy:
(1) ICU setting
(2) hemodynamic monitoring:
a. all patients: foley catheter, rhythm monitoring, central venous catheter
1. early goal-directed therapy dictates early placement of a central venous catheter (N Engl J Med 2001 Nov 8;345(19):1368-77)
2. target to achieve CVP of 8-12 mm Hg
3. measurement of mixed venous blood gas can also indicate the adequacy of tissue oxygen delivery: target an SvO2 > 70%
b. most patients: arterial line
c. rare patients: Swan-Ganz catheter
1. not required for most patients
2. useful when the intravascular, left ventricular filling pressure cannot be accurately estimated using other means (eg, septic shock in the setting of underlying pulmonary hypertension when the CVP may be misleadingly elevated)
(3) remove potentially infected appliances
(4) drain pus
(5) maintaining a pH > 7.20 is theoretically advisable (usually by adjusting ventilator settings to achieve a respiratory alkalosis)
(6) keep hemoglobin > 7.5
(7) keep glucose between 80-110:
a. a prospective, randomized controlled trial of critically ill patients showed that maintaining a blood glucose between 80-110 compared to between 180-200 resulted in 34% reduction in mortality, 46% reduction in bloodstream infections, 41% reduction in renal failure, 50% reduction in need for blood transfusions, and a 44% reduction in critical care polyneuropathy (N Engl J Med 2001; 345:1359-67)
b. a more recent study of intensive insulin therapy in septic shock indicated that it can be associated with severe hypoglycemia, however (N Engl J Med 2008; 358: 125-39); this suggests that intensive insulin therapy should be used only in settings where inadvertant hypoglycemia can be avoided
(8) treat extreme hypocalcemia to keep calcium in the low-normal range
(9) empiric antibiotics
E. Hemodynamic Therapy
(1) volume replacement: saline or lactated Ringer's solution preferred; patients may require many liters of IV fluids for adequate resucitation
(2) adrenal insufficiency should be considered:
a. adrenal insufficiency is common in patients with septic shock and was present by ACTH stimulation testing in 24% of 21 patients in one study (Am J Med, 1995; 98:266-71) and in 52% of 33 children with septic shock in another study (Arch Dis Child 1999;80:51-5)
b. in a study of 129 patients failing an ACTH stim test, those that received 50 mg of hydrocortisone every 6 hours plus 50 mg fludrocortisone QD had a better survival than those who did not receive steroids (53% vs. 63%, p = 0.023; JAMA 2002;288:862-71)
c. in a study of 499 patients with septic shock, 47% failed to respond to an ACTH stimulation test, however, there was no difference in 28-day mortality in patients receiving either hydrocortisone (50 mg every 6 hours) or placebo (N Engl J Med 2008; 358:110-24)
d. at present, the role of treating adrenal insufficiency in septic shock is controversial with the most recent and largest study favoring not treating patients; if steroids are used, they should be in relatively low doses (eg, 50 mg hydrocortisone every 12 hours) and used with the consideration for discontinuing them in patients without a demonstrable benefit
(3) vasopressors (Chest 2007; 132:1678-87): the primary problem in sepsis is inappropriate vasodilation with resultant distributive shock, therefore, the best agents for correcting the hypotension are those with predominately alpha adrenergic properties that result in vasoconstriction (see table)
a. levarterenol (Levophed; 0.05 - 1.0 mcg/kg/min) is an alpha adrenergic vasopressor with some limited beta adrenergic properties and is the first line drug for most patients
b. dopamine (2.5 - 20 mcg/kg/min) is a beta adrenergic vasopressor with some alpha adrenergic properties that is an alternative to levarterenol in some patients, particularly those who have accompanying myocardial dysfunction
c. phenylephrine (Neosynephrine; 0.5 - 10 mcg/kg/min) is a pure alpha adrenergic vasopressor with no beta adrenergic properties that is particularly useful when it is necessary to avoid tachycardia (eg, sepsis in the setting of atrial fibrillation)
d. dobutamine is a vasodilating inotroph that was for a time thought to be effective in septic shock by enhancing tissue oxygen delivery but subsequent studies controlled studies failed to demonstrate an improved outcome in patients receiving dobutamine to boost oxygen delivery by increasing cardiac output in critically ill patients (NEJM 1995; 333:1025-32)
e. epinephrine is a mixed adrenergic vasopressor that has been shown to be inferior to either dopamine or norepinephine in terms of splanchnic blood flow in treating patients with septic shock (Crit Care Med 2003; 31:1659-67)
f. vasopressin is a non-adrenergic hormone that appears to improve short-term hemodynamic parameters but does not affect long-term survival: in a retrospective study of 316 patients, vasopressin improved heart rate, cardiac output, and need for other vasopressors (Crit Care Med 2005; 33:2713-4); in a prospective, randomized, controlled clinical trial of vasopressin in vasodilatory shock involving 48 patients, the use of vasopressin was associated with improved gastrointestinal perfusion, reduced heart rate, and less need for concurrent norepinephrine than placebo (Circulation 2003; 107:2313-9)
1. usual dose is 0.04 units/min
2. a large randomized study of 778 patients compared vasopressin to escalating doses of norepinephrine found no 28-day mortality difference overall; however, there was a trend for lower mortality in patients with less severe shock who were recieving vasopressin (N Engl J Med 2008; 358:877-87)
(4) Activate protein C (drotregin alfa; Xigris), (N Engl J Med 2000; 344:699-709)
a. effects in septic shock: reduces intravascular coagulation, reduces adherence of monocytes and neutrophils to endothelium, reduces IL-1, TNF, and IL-6 production
b. in a randomized, double blinded study in 1690 patients, those who received activated protein C had a mortality rate of 24.7% whereas those receiving placebo had a mortality rate of 30.8%; only those patients with severe sepsis had an improvement in survival
1. serious bleeding was more common in the patients receiving activated protein C (3.5% vs. 2.0%), therefore
2. the population targeted should be those with the most severe forms of sepsis who are the sickest in order to avoid subjecting less severely ill patients to the risk of bleeding without the benefit of improved outcome
c. presently, activated protein C (Xigris) is indicated in patients with severe sepsis (eg, APACHE II score greater than 25) with no contraindicating conditions
(5) intravenous immunoglobulin: a meta-analysis indicated that IV IgG may be beneficial in patients with sepsis but no large clinical trials have been performed to date (Ann Intern Med 2007; 146:193-203)
A. Pathophysiology:
(1) syndrome caused by excess release of IL-1 & TNF in response to a number of bacterial toxins, most commonly TSST-1 (toxic shock syndrome toxin-1) produced by Staphylococcus aureus; TSST-1 is a "super antigen" that is capable of activating very large numbers of T-lymphocytes simultaneously, resulting in massive cytokine release
(2) TSS is usually caused by toxins released in conjunction with local infection and is uncommonly associated with bacteremia
(3) group A beta hemolytic streptococci, group C strep, and group G strep are also capable of a similar syndrome
(4) common sites of infection:
a. vagina (menstrual TSS - can be associated or unassociated with tampon use)
b. skin trauma (surgical wound, insect bite, etc.)
c. foreign body (sutures, orthopedic devices, vaginal diaphragm/sponge, etc.)
d. mucus membrane injury (viral/bacterial respiratory infection, mechanical trauma, etc.)
B. Clinical Findings:
(1) abrupt onset of fever, headache, nausea, myalgias, & diarrhea
(2) after 24 - 48 hours: edema, orthostatic hypotension, encephalopathy
(3) physical exam:
a. early: edema, conjunctival injection, generalized erythroderma
b. late: ulceration of mucus membranes, palmer desquamation (may be delayed 1-2 weeks)
c. evidence of multiple organ involvement (at least 3):
1. gastrointestinal: vomiting or diarrhea
2. muscular: severe myalgia or CK > 2-times normal
3. mucous membranes: vaginal, oropharyngeal, or conjunctival hyperemia
4. renal: BUN or creatinine > 2-times normal; or pyuria (> 5 WBC/hpf)
5. hepatic: bilirubin, AST, or ALT > 2-times normal
6. central nervous system: disorientation or altered consciousness
7. hematologic: platelets < 100,000
(4) laboratory: hypocalcemia, hypophosphatemia, hypoalbuminemia all common but not required for diagnosis
(5) microbiologic: blood cultures usually (but not always) negative
C. Treatment:
(1) overall, treatment is very similar to septic shock:
a. IV fluids (may require > 20 liters of fluid in first 24 hours)
b. dopamine
c. levophed if necessary
(2) remove foreign bodies (pelvic exam to exclude colonized tampons in women is mandatory); drain pus
(3) anti-staphylococcal antibiotics: because of its protein production inhibiting properties, clindamycin has theoretic advantages thus combination therapy with clindamycin + vancomycin is recommended
(4) many patients require mechanical ventilation for ARDS
(5) some patients require dialysis temporarily
(6) IV immunoglobulin G was shown to result in improved mortality and reduced organ failure in a small randomized, double blind, controlled trial (Clin Infect Dis 2003; 37:333-40); the typical dose is 1 g/kg
A. Diagnosis:
(1) generally a clinical diagnosis
(2) the offending agent can often be difficult to identify (eg. latex, metabisulfites, food allergy, etc.) and sometimes seemingly benign drugs can be responsible (diphenhydramine, steroid creams, oral steroids, lidocaine, etc.)
(3) serum tryptase may be useful in difficult diagnostic cases but is not immediately available in many laboratories - this may be primarily useful in autopsy cases and when serum can be saved for later determination of the cause of shock
B. Treatment:
(1) Maintain adequate ventilation: oxygen, establish an airway if needed
(2) Establish adequate venous access
(3) Stop absorption if possible
(4) Epinephrine is the initial pharmacologic drug of choice: 0.3 - 0.5 mg IV, SQ, or IM
(5) Anti-histamines: combine both an H1 and H2 agent (eg, diphenhydramine + ranitidine)
(6) Beta-agonists if accompanied by bronchospasm
(7) Corticosteroids: although these will not help in the immediate phase but will help prevent relapse several hours later; a typical dose is methylprednisolone 1 mg/kg/day
(8) Glucagon (1 mg IV) can be useful in patients which anaphylactic shock on beta-blockers as these patients may be resistent to epinephrine
(9) Patients should be observed for at least 24 hours because of the propensity to relapse
Heart Rate Contractility Vasoconstriction Dopamine
- 2 - 10 ug/kg/min
2+ 2+ 0
- > 10 ug/kg/min
2+ 2+ 3+ Dobutamine
1+ 4+ 1- Levarterenol
2+ 2+ 4+ Phenylephrine
1- 0 4+ Epinephrine
4+ 4+ 4+
Last updated 2/27/08
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