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!!