shock julye n. carew, m.d. december 9, 2005. shock definition clinical evaluation cardiogenic...
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Sepsis mortality Dellinger, Crit Care Med, 2003TRANSCRIPT
Shock
Julye N. Carew, M.D.December 9, 2005
Shock
Definition Clinical Evaluation Cardiogenic Shock Hypovolemia Sepsis Management of septic shock
Sepsis mortality
Dellinger, Crit Care Med, 2003
Definition
Often misdefined as “hypotension” Multisystem end-organ hypoperfusion and
hypoxia with lactic acidosis commonly seen Hypotension Tachycardia Tachypnea Cool skin and extremities Altered mental status Oliguria/Anuria
Clinical Evaluation
Patients are commonly hypotensive Initial evaluation should begin with identification
of adequate cardiac output (CO) DIMINISHED—narrow pulse pressure, cool
extremities and delayed capillary refill INCREASED– widened pulse pressure, warm
extremities, bounding pulses and rapid capillary refill
Pulse pressure is a surrogate for SV
Clinical Evaluation
MAP= CO X SVR CO= SV X HR
Pulse pressure is a surrogate for stroke volume: Increased in high output states, Reduced in hypovolemia and cardiogenic shock
Clinical Evaluation
Jugular venous pulse Cardiac gallop Edema Rales CXR—cardiomegaly, Kerley B lines,
pulmonary edema
CHF
Murray and Nadel, Textbook of Resp. Medicine, 4th ed
Clinical Evaluation
Fever Leukocytosis/leukopenia Pancreatitis, hepatic failure, burns,
anaphylaxis, thyrotoxicosis
Evidence of GI blood loss, diarrhea, vomiting, polyuria
Resuscitation
Few minutes to complete history and physical examination
Begin aggressive, early resuscitation to establish perfusion and minimize end-organ damage
ABCs Ventilatory failure due to increased load on respiratory system– LA, pulmonary edema, inadequate perfusion to RR muscles
Resuscitation
Aggressive IVFs in patients with decreased volume status, sepsis
Crystalloid is preferred, may be increased mortality with colloid
Early administration of vasoactive drugs in hypovolemic patient is not recommended
Transfusion of PRBCs to hemoglobin of 7 g/dL GOAL IS OXYGEN DELIVERY AND END
ORGAN FUNCTION, not BP– mental status, UOP
Resuscitation
If evidence of hypoperfusion persists, then consider vasoactive drugs and invasive monitoring (PA catheter), echocardiography, etc.
Cardiogenic Shock
Cardiac output is low despite adequate venous return (RAP) 50-80% mortality
Systolic dysfunction Diastolic dysfunction Valvular disease Right heart failure “Other”
Systolic dysfunction
Most common cause is acute coronary ischemia
Starling mechanism of compensation—and by fluid retention and increase in sympathetic tone
Cardiogenic shock reported to complicate 10% of all acute MI
Inotropes, intra-aortic balloon pump No data to suggest that lytics improve mortality
(Col, et al, 1994)
Cardiogenic Shock
Improved mortality with early revascularization—PTCA and CABG
Hochman, et al. 1999 randomized 152 patients to revascularization (PTCA or CABG) vs. medical therapy alone
Six-month mortality was 50.3 vs. 63.1% (P=0.027). Treatment benefit was only achieved in those younger than 75 years
Diastolic dysfunction
VERY common phenomenon, less likely to cause frank shock
LV chamber stiffness with impaired LV filling
May be difficult to treat Inotropes may be ineffective Aggressive management of tachycardia
with volume administration and negative chonotropic agents. NSR very important
Valvular Disease
AS– decrease HR, NSR, NO afterload reduction
AI– use of chronotropic agents to decrease regurgitant filling time and afterload reduction
MR– NSR, afterload reduction MS—negative chronotropic agents to
maximize diastolic filling time ARRYTHMIAS
Right heart failure
Murray and Nadel, Textbook of Resp. Medicine
Right Ventricular Failure
Most common cause is concominant LV failure
Elevated JVP with clear lungs, LE edema
PE, ARDS, RV infarction Volume administration, Dobutamine and
NE Treat underlying condition—eg., Lytic
therapy
“Others”
Cardiac tamponade (Kussmaul’s sign=increased JVP with inspiration, pulsus and RAP=RVP=PCWP
Pericardial effusion, tension pneumothorax, ascites, pneumopericardium, large pleural effusions
Hypovolemia
GI blood loss, trauma, coagulopathy Aggressive volume resuscitation with large
volumes of crystalloid and blood products “Wigger’s preparation” 1. several hours of severe hypotension
produced “irreversible shock” 2. ECF deficit could be corrected with
administration of crystalloid in volumes 2-3X blood loss “3:1 rule”
Wiggers, NY Commonwealth Fund, 1950.
Hypovolemia
More recent studies suggest that more moderate volume repletion with crystalloid is preferable (Kaweski,1990. Bickell, 1994)
Mechanism? Interference of effective thrombus and continued secondary hemorrhage
Bottom line: Volume resuscitate, correct coagulopathy, fix the underlying problem
Septic shock
Infection with state of hypoperfusion and end-organ damage
SIRS, sepsis, severe sepsis, septic shock High cardiac output state Widened pulse pressure, warm extremities,
brisk capillary refill Subgroup of patients with depressed cardiac
function (myocardial depressant factors)-- ?NE and dobutamine
Septic shock
Sepsis is the leading cause of death in non-CCUs, 750,000 cases/year
Unregulated inflammation and a hypercoagulable state favoring microvascular coagulation
ARF carries a poorer prognosis >80% of patients will require mechanical
ventilation
Delli
Dellinger, Crit Care Med 2004.
Septic Shock Society of CC Medicine wrote consensus opinion on
recommendations treatment of septic shock, 2004 Graded recommendations based upon available data Grade A- at least two level I studies (large, randomized
with clear results) Grade B- one level I study Grade C- level II investigations (small, randomized with
uncertain results) Grade D- at least one level III (nonrandomized) Grade E- level IV and V support (historical controls,
expert opinion; case series)
Dellinger,Crit Care Med, 2004
Reommendations for treatment of septic shock Resuscitation (B): CVP 8-
12 mmHg MAP>65 mm Hg UOP > 0.5 ml/kg/hr Mixed venous> 70%
Diagnosis (D): Appropriate cultures prior to ABX therapy
Antibiotics (E and D): Begun within 1 hour and cover appropriate organisms (eg. Neutropenia)
Source Control (E): drain abscesses and removed infected devices
Fluids (C and E): crystalloid or colloid, 1 L over 30 minutes and repeat if necessary
Dellinger, Crit Care Med, 2004
Treatment of septic shock Vasopressors: 1. DA or NE (D) 2. NO low-dose DA for “renal
protection”(B) 3. Vasopressin in refractory patients(E)
Dellinger, Crit Care Med, 2004
Recommendations for treatment of septic shock Inotropes (E and A): patients with low
CO—try dobutamine, a pre-defined CI is not recommended
Dellinger, Crit Care Med, 2004
Treatment of septic shock
Steroids: 1. Stress-dose hydrocortisone in
refractory shock for 7 days 2. ACTH stimulation test (E) 3. DO NOT use doses >300 mg/day (A) 4. In the absence of shock steroids
should not be used, except for usual dose or if adrenal insufficiency is suspected (E)
Dellinger, Crit Care Med, 2004
Treatment of septic shock
rhAPC: for those at high risk of death (APACHE>25, MOFS, shock) without contraindication (B)
Blood products: 1.Transfuse PRBCs only when Hgb<7 (B)
2. No routine EPO (B) 3. No FFP (E) or AT3 (B) 4. PLT for PLT<5000 (E)
Mechanical ventilation: 1. Low tidal volume (6 cc/kg), plateau pressures<30 (B)
2. Hypercarbia is acceptable to reduce plateau pressure (C)
3. PEEP to lower FiO2(E)
4. Keep patients at 45 degrees to prevent VAP (C)
5. Weaning protocol and spontaneous breathing trials (A)
Dellinger, Crit Care Med, 2004
Treatment of septic shock
Sedation: 1. Sedation protocols and
scales should be used (B)
2. Bolus vs. continuous with daily interruptions (B)
3. NM blockers should be avoided, but if necessary train of four should be followed (E)
Modified Ramsey Sedation Scale.
1. Anxious, Agitated, Restless
2. Cooperative, Oriented, TranquilAccepts mechanical ventilation.
3. Responds to commands only
4. Brisk response to light glabellar tap or loud noise.
5. Sluggish response to light glabellar tap or loud noise.
6. No Response.
Dellinger, Crit Care Med, 2004
Treatment of Septic Shock
Glucose Control: Maintain CBG<150 (D), enteral feeding preferable (E)
Renal Replacement: CVVH and intermittent HD are equivalent in hemodynamically stable patients (B)
Bicarbonate: NOT recommended for pH>7.15 (C)
DVT prophylaxis:YES!!! (A)
Ulcer prophylaxis: YES!!! (A)`
Hydrocortisone
Oppert, et al. (German) looked at 41 patients with septic shock
18 received hydrocortisone 50 mg bolus followed by 0.18 mg/kg/hr (70 kg would receive 350 mg/24 hours), 23 placebo
Primary endpoints: duration of shock, reduction in pro-inflammatory cytokines
Hydrocortisone
Oppert, Crit Care Med, 2005
Hydrocortisone
Oppert, Crit Care Med, 2005
Hydrocortisone
Oppert, Crit Care Med, 2005
Hydrocortisone
Not adequate power to determine mortality benefit
Showed a trend toward better outcome with ACTH responders
The jury is still out
Vasopressors
Sharshar, et al. Looked at circulating vasopressin levels in septic shock
Found that plasma vasopressin levels were almost always increased at the initial phase of septic shock and decrease afterward. Vasopressin deficiency was seen in 1/3 of late septic shock patients
I use vasopressin for patients who do not initially respond to NE (dose .04 units/min)
The End!!