Cardiogenic shock

dr M. Arman Nasution SpPD

Introduction
Cardiogenic shock (CS) occurs in 5% to 8% of patients
hospitalized with ST-elevation myocardial infarction
(STEMI).
Recent research has suggested that the peripheral vasculature
and neurohormonal and cytokine systems play a role in the
pathogenesis and persistence of CS.
Early revascularization for CS improves survival substantially.
New mechanical approaches to treatment are available, and
clinical trials are feasible even in this high-risk population.
Most importantly, hospital survivors have an excellent
chance for long-term survival with good quality of life.

J Am Coll Cardiol. 1994;23:1630 1637.

This review will outline
Definition of cardiogenic shock
The causes of cardiogenic shock
Pathophysiology of cardiogenic shock
Diagnosis of cardiogenic shock
Treatment of CS with a focus on CS complicating myocardial
infarction (MI.)
Basic

Identify the 4 main catigories of shock

Discuss the goals of resuscitation in shock
Summarize the general principles of shock management
Describe the physiologic effects of vasopressors and inotropic
agents
 Shock is a syndrome of impaired tissue oxygenation and
perfusion due to a variety of etiologies
If left untreated
Irreversible injury ,Organ dysfunction And finally death
Clinical ulterations in shock
The presentation of patients with shock may be Subtle(mild
confusion,tachycardia)
Or easily identifiable(profound hypotesion.anuria)
 The clinical manifestation of shock result from
1- inadequate tissue perfusion and oxygenation
2- Compansatory respnses
3- The specific etiology
Clasification of shock
1-hypovolemic
a-Hemorrhagic
b-nonhemorrhagic
2-Cardiogenic
Ischemic
Myopathic
Mechanical
Arrhythmia
 3- Distributive
Septic
Adrenal crises
Neurogenic (spinal shock)
Anaphylactic
 4- Obstructive
Massive Pulmonary embolism
Tension pneumothorax
Cardiac tamponade
Constrictive pericarditis
HYPOVOLEMIC SHOCK
It occure when the intra vascular volume is depleted relative
to the vascular capacity as a result of
1- Hge.
2- G.I.T loss
3-urinary loss
4-dehydration
HYPOVOLEMIC SHOCK
Management
The goal is to restore the fluid lost
Vasopressors are used only as a temporary method to restore
B.P untill fluid resuscitation take place
Distributive shock
It is characterized by loss of vascular tone
The most comon form of ditribusive shock is septic shock
The hemodynamic profile of septic shock include
 Cardiac output normal or increased
Ventricular filing pressure normal or low
SVR low
Diastolic pressure low
Pulse pressure wide
Management of septic shock
The initial approach to the patient with septic shock is the
restoration and maintenance of adequate intravascular
volume
Prompt institution of appropriate antibiotic
CARDIOGENIC SHOCK
Forward flow of blood is inadequate bec. Of pump failure
due to loss of functional myocardium
It is the most severe form of heart failure and it is
distinguished from chronic heart failure by the presence of
hypotension,hypoperfusion and the need for different
therapuetic inteventions
 Hemodynamic chracteristics
Cardiac output low
Ventricular filing pressure high
SVR High
Mixed venous o2 sat low
MANAGEMENT OF CARDIOGENIC SHOCK
The main goal is to improve myocardial function
Arrhythmia should be treated
Reperfusion PCI is the treatment of choice in ACS
Inotropes and vasopresor
Obstructive shock
Obstruction to the outflow due to impaired cardiac filling
and excessive afterload
Cardiac tamponade and constrictive pericarditis impair
diastolic filling of the Rt.ventricle
Tension pneumothorax limit Rt.ventricular filing by
obstruction of venous return
Massive pulmonary embolism increase Rt.ventricular
afterload
 Hemodynamic profile in obst. Shock
Cardiac output low
Afterload high
Lt.Vent.filling pressure variable
Pulsus paradoxicus in Tamponade
Distended Jugular viens
Management Of Obstructive Shock

Directed Mainly to Management of the cause

GENERAL Principles of shock management
The overall goal of shock management is to improve oxygen
delivery or utilization in order to prevent cellular and organ
injury
Effective therapy requires treatment of the underlying
etiology
 Restoration of adequate perfusion,monitoring and
comperhensive supportive care
Interventions to restore perfusion center on achieving an
adequate B.P, increasing cardiac output and optimizing
oxygen content of the blood
 Oxygen demand should also be reduced
In Summery
Management of shock
1- Monitoring
2- Fluid Therapy
3- Vasoactive agents
Definition
CS is a state of end-organ hypoperfusion due to cardiac failure.
The definition of CS includes hemodynamic parameters:
Persistent hypotension (systolic blood pressure < 80 to 90 mm Hg
or mean arterial pressure 30 mm Hg lower than baseline) with
Severe reduction in cardiac index ( <1.8 L min1 m2 without
support or <2.0 to 2.2 L min1 m2 with support) and
Adequate or elevated filling pressure (eg, left ventricular [LV] end-
diastolic pressure >18 mm Hg or right ventricular [RV] end-
diastolic pressure >10 to 15 mm Hg).

J Am Coll Cardiol. 1994;23:1630 1637.

Causes of cardiogenic shock - LV failure
Systolic dysfunction
- CAD : acute MI or ischemia(most
common cause)
- other conditions : severe myocarditis, end stage
cardiomyopathy (including valvular cause), myocardial
contusion
Prolonged cardiopulmonary bypass, global hypoxemia,
myocardial depression( betablocker, calcium blocker,
antiarrhythmic drug), respiratory acidosis,
Metabolic derangement eg.acidosis, hypoPO4,
hypo Ca
Tachycardia related cardiomyopathy

Heart. 2007;93:177182
Causes of cardiogenic shock -LV failure
Diastolic dysfunction
- CAD
- ventricular hypertrophy,
Restrictive cardiomyopathy
Consequent of prolonged hypovolemia or septic shock
External compression by pericardial tamponade

Heart. 2007;93:177182
Causes of cardiogenic shock -LV failure
Greatly increased afterload
AS
HOCM: dynamic ventricular outflow obstruction
Coarctation of aorta
Malignant HT

Heart. 2007;93:177182
Causes of cardiogenic shock -LV failure
Valvular or structural abnormality
- MS
- endocarditis
- MR, AR
- obstruction due to atrial myxoma or thrombus
- MI complication : papillary muscle dysfunction or
ruptured with severe MR(1%),
: ruptured LV free wall
(0.8-6.2%)
: ventricular septal rupture(1-3%)

Heart. 2007;93:177182
Causes of cardiogenic shock -LV failure
Arrhythmia
-VT/VF, bradycardia can cause shock
- sinus tachycardia or atrial tachycardia can aggravate shock

Heart. 2007;93:177182
Causes of cardiogenic shock -RV failure
Greatly increased after load
- pulmonary emboli
- pulmonary vascular disease eg.
PAH, venoocclusive disease
- hypoxic pulmonary vasoconstriction
- PEEP
- high alveolar pressure
- ARDS
- pulmonary fibrosis
- sleep disorder breathing
- COPD
. RV infarction : 50% of inferior MI( 10-15% with hemodynamic
problem)

Heart. 2007;93:177182
 Causes of Cardiogenic Shock
Tamponade/rupture
Other
1.7%
Isolated RV Shock 7.5%
3.4%

VSD
4.6%

Acute Severe MR
8.3%

Shock Registry
JACC 2000 35:1063
Predominant LV Failure
74.5%
INCIDENCE
After decades of remarkable stability in the incidence of CS,
it appears that the incidence is on the decline in parallel with
increasing rates of use of primary PCI for acute MI.
CS continues to complicate approximately 5% to 8% of
STEMI and 2.5% of non-STEMI cases.
The routine use of troponin to define non-STEMI will result
in a drop in this percentage as more MIs are detected but will
not alter the total number of cases of CS.

Hasdai et al. JACC 2000;36:687

 Mortality of such patients approximately 80% or higher
Very few patients develop shock immediately after AMI
About half of the patients develop shock within 24h
Hasdai et al. JACC 2000;36:687
Factors that increase risk for cardiogenic
shock in STEMI
Age > 70 years
SBP < 120 mmHg
Sinus tachycardia rate > 110/min.
Bradycardia rate < 60/min.
Increased time from onset of STEMI
Anterior MI
H/O Hypertension, diabetes mellitus
Multi vessel coronary artery disease
Prior MI or angina
Prior diagnosis of heart failure, STEMI
Left bundle branch block.

JAMA. 2005;294:448454.
Pathophysiology of Shock
 Schematic
LVEDP elevation
Hypotension
Decreased coronary
perfusion
Ischemia
Further myocardial
dysfunction
Neurohormonal activation
Vasoconstriction
End organ hypoperfusion
 Pathophysiology of Shock

Effect of Hypotension
Flow in normal coronary:
Regulated by microvascular resistance
Coronary flow may be preserved at AO pressures as
low as 50 mm Hg
In coronary vessel with critical stenosis:
Vasodilator reserve of microvascular bed is exhausted
Decrease in AO pressure => Coronary hypoperfusion

J Am Coll Cardiol. 2006;47(suppl

A):111A.
 Pathophysiology of Shock

Effect of Hypotension (continued)

Normal heart extracts 65% of the O2 present in the blood

Little room for augmentation of O2 extraction
 Pathophysiology of Shock

Hypotension + LVEDP and critical stenosis

Myocardial Hypoperfusion LV dysfunction
Systemic lactic acidosis Impairment of non-ischemic
myocardium worsening hypotension.
Right Ventricle
RV dysfunction may cause or contribute to CS.
Predominant RV shock represents only 5% of cases of CS
complicating MI.
RV failure may limit LV filling via a decrease in CO,
ventricular interdependence, or both.
Treatment of patients with RV dysfunction and shock has
traditionally focused on ensuring adequate right-sided filling
pressures to maintain CO and adequate LV preload; however,
patients with CS due to RV dysfunction have very high RV
end-diastolic pressure, often >20 mm Hg.

J Am Coll Cardiol. 2003;41:12731279

Peripheral Vasculature, Neurohormones, and
Inflammation
Hypoperfusion of the extremities and vital organs is a
hallmark of CS.
The decrease in CO caused by MI and sustained by ongoing
ischemia triggers release of catecholamines, which constrict
peripheral arterioles to maintain perfusion of vital organs.
Vasopressin and angiotensin II levels increase in the setting of
MI and shock, which may further impair myocardial
function.
Activation of the neurohormonal cascade promotes salt and
water retention; this may improve perfusion but exacerbates
pulmonary edema

Arch Intern Med.

2005;165:16431650.
CS May Be an Iatrogenic Illness
Approximately three fourths of patients with CS
complicating MI develop shock after hospital presentation.
In some, medication use contributes to the development of
shock.
Several different classes of medications used to treat MI have
been associated with shock, including Beta-blockers,
angiotensin- converting enzyme inhibitors, and morphine.
Although early use of each of these medications is associated
with only a small excess risk of CS, the large number of
patients treated with these therapies translates into a
substantial potential number of events.

Circulation. 2003;107:2998 3002

 When high-dose diuretics are administered, plasma volume
declines further.
A trial of a low diuretic dose coupled with low-dose nitrates
and positional measures to decrease preload (eg, seated
position with legs down) should be attempted in patients
with MI and pulmonary edema to avoid precipitating shock.
Excess volume loading in patients with RV infarction may
also cause or contribute to shock.

Circulation. 2003;107:2998 3002

Multivariable Mortality Predictors
Increasing age and female gender
Lower left ventricular ejection fraction
1Webb et al JACC 2003;42:1380
Chronic renal insufficiency 2 Sutton Heart 2005;91:339
Initial and Final TIMI Flow grade 3 Tedesco AHJ 2003:146; 472
4 Zeymer et al EHJ 2004;25:322
Lower systolic blood pressure 5 Tedesco JV Mayo Clin Proc 2003;
Diabetes mellitus 78:561
6 Sanborn JACC 2003:42; 1373
Prior MI
7 Klein et al AJC 2005; 96:35
Increasing time from symptom onset to PCI
Total Occlusion of the LAD
Mitral regurgitation
Multivessel PCI
 Diagnosis of cardiogenic shock
History
Physical examination
ECG
Cardiac biomarker
CXR
Echocardiography
Pulmonary artery catheterization
: Swan-Ganz catheter
Diagnosis:physical examination

Sign of hypoperfusion
Cyanosis, cooled skin, mottle extremities
Elevated JVP and pulmonary crackles
usually(but not always) presented
Peripheral edema may be presented
Heart sound : usually distant
: S3, S4 may be presented
Pulse pressure may be low, usually tachycardia
Parasternal thrill : ventricular septal ruptured
MR murmur may be limited to early systole
HOCM : systolic murmur- louder upon valsalva and
promp standing
 Diagnosis :ECG
Acute coronary syndrome : STEMI, nonSTE ACS, RV
infarction
Cardiomyopathy
Arrhythmia
Diagnosis
CXR : pulmonary congestion, bilateral pleural
effusion, cardiomegaly
: pericardial effusion
: widened mediastinum
: pneumothorax, pneumomediastinum
Echocardiogram
: LV function
: complication of MI eg. Acute MR,
ventricular septal ruptured,free wall
ruptured, cardiac tamponade
RV infarct : RV dilation and asynergy, abnormal inter
ventricular and interatrial septal motion,
Rt to Lt shunting through a patent PFO
Swan-Ganz catheter
 Pulmonary arterial catheterization:
Swan-Ganz catheter
Exclude other cause of shock
Diagnosis of cardiogenic shock
1-PCWP > 15, CI < 2.2
2-Larged V wave on PCWP, very high PCWP = severe MR
3-Step up in oxygen sat.from RA to RV
large V- wave on RA pressure
= ventricular septal ruptured
4-High right sided filling pressure in the absense of elevated
PCWP(RA > 10 and > 80% of PCWP) ( accompanied with ECG
criteria) = RV infarct
5-Classic sign of cardiac tamponade (equalization of diastolic
pressure among the cardiac chambers) = free wall ruptured
(not always present)
Cardiogenic shock in Acute MI
Cardiogenic shock is the most common cause of death in
patients with acute myocardial infarction (AMI)
The incidence within the community over a 23-year period
(1975-1997) was found to be 7.1%
In the, Global Utilization of Streptokinase and Tissue
Plasminogen Activator for Occluded Arteries (GUSTO-1)
trial , the incidence of cardiogenic shock was likewise 7.2%,
and consistent with other studies .
In the GUSTO trial, 11% of patients had shock on
presentation while 89% of patients subsequently developed
shock The GUSTO-I Investigators. Global utilization of
streptokinase and tissue plasminogen activator for
occluded coronary arteries.
J Am Coll Cardiol 1995; 26: 668-74.
 Despite emerging innovative treatments, in-hospital
mortality in patients with cardiogenic shock continues to be
as high as 70-80%
Cardiogenic shock seems to occur with a greater frequency
amongst patients with ST-segment elevation myocardial
infarction (STEMI). It was observed that shock developed in
7.5% of patients with STEMI and in 2.5% of patients with
non-ST-segment elevation myocardial infarction (NSTEMI)

SHOCK trial registry. J Am Coll Cardiol 2000; 36:

1091-96.
Causes of shock in AMI
Acute Myocardial Infarction
Left ventricular dysfunction
Acute mitral regurgitation
Ventricular septal rupture
Right ventricular shock
Cardiac Tamponade
Cardiac Rupture
Predisposing Factors for Cardiogenic Shock
Age
Sysolic blood pressure
Heart rate
Killip class
Diabetes
Anterior infarction
Previous infarction
Peripheral vascular disease
Reduced ejection fraction
Large infarctions
Cardiac power
Ventricular Septal Rupture
Incidence 1-2%
Timing 2-5 d p MI IABP
Murmur 90% Inotropic Support
Thrill common Surgical Timing is
Echo shunt
controversial, but
usually < 48 h
PA cath O2 step up > 9%
Free wall rupture
Free Wall Rupture
Incidence: 1-6%
Occurs during first week after MI
Classic Patient: Elderly, Female,Hypertensive
Early thrombolysis reduces incidence but Late increases risk
Echo: pericardial effusion,
PA cath: equal diastolic pressure
Treat with pericardiocentesis and early surgical repair

J Am Coll Cardiol.
2000;36:10631070.
Acute Mitral Regurgitation
Management of Acute MR
Incidence: 1-2%
Echo for Differential Diagnosis:
Free-wall rupture
VSD
Infarct Extension
PA Catheter: large v wave
Afterload Reduction
IABP
Inotropic Therapy
Early Surgical Intervention

J Am Coll Cardiol.
2000;36:10631070.
Right Ventricular Infarction: Diagnosis
Clinical findings:
Shock with clear lungs,
Elevated JVP
Kussmaul sign
ECG:
ST elevation in R sided leads
Echo:
Depressed RV function
V4R

Modified fromWellens. N Engl J Med 1999;340:381.

Management of RV Infarction
Cardiogenic Shock secondary to RV Infarct has better
prognosis than LV Pump Failure
IV Fluid Administration
IABP
Dobutamine
Maintain A-V Synchrony
Mortality with Successful Reperfusion = 2%
Unsuccessful Reperfusion = 58%
Outcomes of Cardiogenic Shock

The SHOCK registry

Similar mortality in the two groups

62.5% in non-ST elevation
60.4% with ST elevation
SHOCK Registry JACC Sept. 2000, Supp. A
Spectrum of Clinical Presentations

Respiratory
Mortality Hypotension Hypoperfusion
Distress

21%
1.4%
22%
5.6%
70%
28%
60%

65%
Treatment
 Supportive treatment
Inotropic agent : dopamine, dobutamine, milrinone, amrinone
Vasopressors : norepinephrine ,epinephrine, dopamine
IABP
Oxygen therapy and mechanical ventilator
Arrhythmia treatment
Magnesium, potassium, acidosis
Volume replacement for RV infarct ( 0.5 1 L) or HOCM
Ventricular assist device (VAD)
Relief of pain and anxiety : morphine ( or fentanyl if SBP is compromised)
 Dopamine
Precursors of norepinephrine and
epinephrine
. < 5 mcg/kg/min.: vasodilation of renal, mesenteric and coronary
bed
. 5-10 mcg/kg/min.: beta-1: increase contractility and HR
.>= 10 mcg/kg/min.: alpha: arterial vasoconstriction and increase
BP
.BP increasing : primarily due to inotropic effect
.undesirable effect : tachycardia, increase ,pulmonary shunt,
decrease splanchnic perfusion, increase PCWP
 Norepinephrine
Potent alpha with minimal beta adrnergic agonist
. Can increase BP successfully in patients remain hypotensive
with dopamine
0.2-1.5 mcg/kg/min.
. As high as 3.3 mcg/kg/min. for sepsis
( because of alpha receptor down
regulation)
 Epinephrine
Increase MAP : increase CI, SV, SVR, HR
Increase oxygen delivery and oxygen consumption
. Decrease splanchnic blood flow
. Increase systemic and regional lactate concentration
. Recommend only in patient who are unresponsive to
traditional agent
. Undesirable effect : increase lactate conc., increase myocardial
ischemia and arrhythmia,decrease splanchnic flow
 Dobutamine
Sympathomimetic agent
Beta-1, some beta-2, minimal alpha receptor activity
. Significant positive inotropic with mild chronotropic effect
. Mild peripheral vasodilation( decrease afterload)
. Significant increase CO
. Could increase infarct size of MI( increase oxygen consumption)
. Should be avoided in moderate to severe hypotension(SBP < 80 mmHg)
because of peripheral vasodilation
Phosphodiesterase inhibitor (PDIs): currently amrinone
and milrinone
Inotropic agent with peripheral vasodilation properties(decrease
after load)
. Decrease PVR(decrease preload)
. Long half life
. May require concomittant vasopressors
. Unlike catecholamine inotrope: not dependent on adreno receptor
activity- less likely to develop tolerance
. Less likely than catecholamine to cause adverse effect associated
with adrenergic activity(eg.increase myocardial oxygen demand,
myocardial ischemia, tachycardia)
. Incidence of tachyarrhythmia: PDIs> dobutamine
Inotropes and Vasopressors

ACC/AHA Guidelines
SBP <70:-
Norepinephrine (0.5-30 g/min)
Switch to Dopamine (5-15 g/kg/min) once SBP 80
SBP 70-100
Dopamine (5-15 g/kg/min)
Add dobutamine (2-20 g/kg/min) once SBP 90
Levosimendon
Levosimendan, a myofilament Ca2+ sensitizer with inotropic effects,
increases myocardial performance without substantial changes in oxygen
consumption and with neutral effects on heart rhythm.
Levosimendan has vasodilatory effects that are achieved by stimulation of
adenosine triphosphate-dependent potassium channels.
This action may be of specific interest in the setting of myocardial
ischemia.
The use of levosimendan is contraindicated in patients with: moderate-
to-severe renal impairment, severe hepatic impairment,
severe ventricular filling or outflow obstruction,
severe hypotension and tachycardia, and/or history of torsades de
pointes
Dose 12ugm/kg f/b 0.2 ugm/kg/min

Anesthesiology. 2006 Mar;104(3):556-69

Treatment cont..
Antithrombotic therapy with aspirin and heparin should be given
as routinely recommended for MI.
Clopidogrel may be deferred until after emergency angiography,
because on the basis of angiographic findings, coronary artery
bypass grafting (CABG) may be performed immediately.
Clopidogrel is indicated in all patients who undergo PCI, and on
the basis of extrapolation of data from MI patients who were not
in shock, it should also be useful in patients with shock as well.
Negative inotropes and vasodilators (including nitroglycerin)
should be avoided.
Arterial oxygenation and near-normal pH should be maintained to
minimize ischemia.
Mechanical Support: IABP
Intra-aortic balloon counterpulsation has long been the
mainstay of mechanical therapy for CS.
Use of an IABP improves coronary and peripheral perfusion
via diastolic balloon inflation and augments LV performance
via systolic balloon deflation with an acute decrease in
afterload.
Accurate timing of inflation and deflation provides optimal
support.
Not every patient has a hemodynamic response to IABP;
response predicts better outcome.
INDICATIONS

A) . Cardiogenic shock-(ACC/AHA Class IB recommendation)

Bridge to revascularization-
early placement of IABP - mortality.
(Anderson, JACC 1997)

Bridge to tertiary centre-

1 yr.survival rate (67%v/s 32%)

Sec. to ischemic myocarditis

(Kovack JACC,1997)
Despite more adverse events in the early IABP group and more episodes of
moderate bleeding, this cohort showed a trend toward lower 30-day and 1-
year mortality rates.
J Am Coll Cardiol 1997;30:708 15
Reperfusion
The survival benefit of early revascularization in CS,
reported in several observational studies, was shown
convincingly in the randomized SHOCK trial, which found a
13% absolute increase in 1-year survival in patients assigned
to early revascularization.
This corresponds to a number needed to treat of 8 patients to
save 1 life.
The benefit was similar in the incomplete, randomized Swiss
Multicenter Study of Angioplasty for Shock.

JAMA.
2006;295:25112515.
 Numerous registry studies have confirmed the survival
advantage of early revascularization, whether percutaneous
or surgical, in the young and the elderly.
Thrombolytic therapy is less effective but is indicated when
PCI is impossible or if a delay has occurred in transport for
PCI and when MI and CS onset were within 3 hours.
Timing of PCI

As in MI without shock, earlier revascularization is better in CS.

Presentation 0 to 6 hours after symptom onset was associated with
the lowest mortality among CS patients undergoing primary PCI
in the Arbeitsgemeinschaft Leitende Kardiologische
Krankenhausarzte (ALKK) registry, in which door-to-angiography
times were 90 minutes in approximately three fourths of patients.
In the SHOCK trial, there appeared to be increasing long-term
mortality as time to revascularization increased from 0 to 8 hours.
However, there is a survival benefit as long as 48 hours after MI
and 18 hours after shock onset

JAMA.
2006;295:25112515.
Stenting and Glycoprotein IIb/IIIa
Inhibition
Stenting and glycoprotein IIb/IIIa inhibitors were
independently associated with improved outcomes in patients
undergoing PCI for CS in multiple registries, including the
large ACC-National Cardiovascular Data Registry.
A trend toward benefit of abciximab was noted in a small
subset of STEMI patients with CS undergoing PCI in a
randomized trial.

JAMA.
2006;295:25112515.
Revascularization Approach: Surgery
or PCI
Revascularization in the SHOCK trial could be percutaneous
or surgical.
Thirty-seven percent of patients assigned to the early
revascularization strategy underwent CABG at a median of
2.7 hours after randomization.
Despite a higher prevalence of triple-vessel or left main
disease and diabetes mellitus in patients who underwent
CABG compared with PCI, survival and quality of life were
similar.
The rate of emergency CABG in CS is much lower in the
community (<10%).

JAMA.
2006;295:25112515.
 Survival in patients with CS who have CABG may improve
further with advancing surgical techniques.
In CS patients undergoing surgery, a trend toward better
survival with beating heart techniques was present despite
the use of slightly lower numbers of grafts.
This latter point could be of particular importance when one
considers the potential for long-term survival in CS patients

Eur Heart J. 1999;20:1030 1038

Circulation. 2004;110:588636
Thrombolytic therapy

The outcome of cardiogenic shock is closely

linked to the patency of the culprit coronary
arteries
Thrombolytic therapy has decreased the
occurrence of shock among patients with
persistent STEMI.
The GUSTO-I : t-PA is more efficacious than
streptokinase in preventing shock.
Thrombolysis in cardiogenic shock
Results have been disappointing
Cause : ? limited efficacy of lytics in the
setting of low perfusion pressure.

GISSI-I Study
Mortality of thrombolysis(streptokinase) group = 69.9%
Mortality of. control group = 70.1%

David Hasdai et al,Lancet 2000;356:753

Risk Stratification and Targeting the Population
for Revascularization
Mortality due to CS is not as high as many clinicians may
believe and is 50% in the modern era, far lower than historic
figures of 80% to 90%.
Mortality can range from10% to 80% depending on
demographic, clinical, and hemodynamic factors.
These factors include age, clinical signs of peripheral
hypoperfusion, anoxic brain damage, LVEF, and stroke work.
Female sex does not appear to be an independent predictor
of poor outcome.
Total Circulatory Support: LV Assist Devices and
Extracorporeal Life Support
Temporary mechanical circulatory support with LV assist
devices (LVADs) is theoretically appealing to interrupt the
vicious spiral of ischemia, hypotension, and myocardial
dysfunction, allowing for recovery of stunned and
hibernating myocardium and reversal of neurohormonal
derangements.
Device-related complications and irreversible organ failure
remain major limitations.
 VAD with active circulatory support reverse
hemodynamic and metabolic parameters in cardiogenic
shock more effectively than with standard IABP
treatment alone.

The use of newer percutaneous devices is still in its

infancy.
 Tandem Heart LVAD-Extracorporeal devices
Left atrial-to-femoral arterial LVAD
Low speed centrifugal continuous flow
pump
21F venous transeptal cannula
17F arterial cannula
Maximum flow 4L/minute
 The TandemHeart (Cardiac Assist, Inc, Pittsburgh, Pa)
removes blood from the left atrium using a cannula placed
through the femoral vein and into the left atrium via
transseptal puncture.
Blood is then returned to a systemic artery, usually the
femoral, with retrograde perfusion of the abdominal and
thoracic aorta.
European Heart Journal (2005) 26, 12761283
 Intracorporeal devices

IMPELLA LP 2.5 & LP 5.0

Helical propellar-axial flow
Minimally invasive,percutaneous catheter
LVADs.
Insertion similar to IABP but device rests
across the aortic valve,with the tip in the LV
cavity.
Full anticoagulation needed.
FDA approved for high risk PCI,post
PCI,cardiogenic shock,myocarditis &bridge
to decision.
TandemHeart and Impella are currently available percutaneous LVAD
for hemodynamic support in cath lab.
 Impella
Axial flow pump
Much simpler to use
Increases cardiac output & unloads LV
LP 2.5
12 F percutaneous approach; Maximum 2.5 L flow
LP 5.0
21 F surgical cutdown; Maximum 5L flow

Blood Inlet

Blood outlet

Motor

Pressure Lumen
J Am Coll Cardiol 2008;52:15848
J Am Coll Cardiol 2008;52:15848
Impella outcome data
ISAR-SHOCK
26 patient RCT Impella vs IABP
Cardiac Index, MAP (by 10mmHg) vs IABP
Complications IABP
No difference in mortality

PROTECT-II
654 patients RCT IABP vs Impella in high-risk PCI
Stopped after n= 305 due to futility
Primary EP composite of 10 MAEs
Incidence 38% Impella vs 43% IABP
Management of Special Conditions
The treatment of certain conditions that lead to CS is marked
by important differences from management of CS due to LV
failure.
The recognition of LV outflow obstruction is critical in
patients with hypotension, because diuretics and inotropic
agents exacerbate obstruction.
Treatment of CS with hypertrophic obstructive
cardiomyopathy includes volume resuscitation and beta-
blockade.
 Outflow obstruction may also be seen in some cases of tako-
tsubo cardiomyopathy when extensive akinesis/ dyskinesis of
apical zones occurs with hyperkinesis of remaining
myocardium.
Therapy is guided by echocardiography and clinical response.
IABP may provide circulatory support.
Beta-blockade is often not indicated in this circumstance
because it exacerbates LV dysfunction.
Long-Term Survival and Quality of Life
Long-term survival data from the SHOCK trial were
reported recently.
Remarkably, the 3- and 6-year survival rates in the early
revascularization group were 41.4% and 32.8% with
persistence of treatment benefit.
These rates are similar to or better than 30-day survival rates
reported in studies in which patients did not routinely
receive invasive therapy and similar to 5-year survival rates
for many forms of cancer.

JAMA.
2006;295:25112515.
 At least as important as long-term survival is quality of life in
survivors.
Again, this is far better than many clinicians would suspect.
Already at 2 weeks after discharge, 75.9% of patients
assigned to revascularization and 62.5% of patients assigned
to medical stabilization in the SHOCK trial were in New
York Heart Association functional class I to II .
60 Among patients who were in functional class III to IV at 2
weeks, 55% of survivors improved to class I to II by 1 year.
2013 ACCF/AHA Guideline for the
Management of ST-Elevation Myocardial
Infarction

Developed in Collaboration with American College of Emergency Physicians and Society for
Cardiovascular Angiography and Interventions

American College of Cardiology Foundation and American Heart Association, Inc.

 Primary PCI in STEMI
I IIa IIb III
Primary PCI should be performed in patients with STEMI and ischemic symptoms
of less than 12 hours duration.

I IIa IIb III

Primary PCI should be performed in patients with STEMI and ischemic symptoms
of less than 12 hours duration who have contraindications to fibrinolytic therapy,
irrespective of the time delay from FMC.

I IIa IIb III

Primary PCI should be performed in patients with STEMI and cardiogenic shock
or acute severe HF, irrespective of time delay from MI onset.
Indications for Coronary Angiography in Patients
Who Were Managed With Fibrinolytic Therapy or Who Did Not
Receive Reperfusion Therapy

*Although individual circumstances will vary, clinical stability is defined by the absence of low output,
hypotension, persistent tachycardia, apparent shock, high-grade ventricular or symptomatic
supraventricular tachyarrhythmias, and spontaneous recurrent ischemia.
 Indications for PCI of an Infarct Artery in Patients Who Were
Managed With Fibrinolytic Therapy or Who Did Not Receive
Reperfusion Therapy

*Although individual circumstances will vary, clinical stability is defined by the absence of low output, hypotension, persistent
tachycardia, apparent shock, high-grade ventricular or symptomatic supraventricular tachyarrhythmias, and spontaneous
recurrent ischemia.
 CABG in Patients With STEMI

I IIa IIb III

Urgent CABG is indicated in patients with STEMI and coronary anatomy not
amenable to PCI who have ongoing or recurrent ischemia, cardiogenic shock,
severe HF, or other high-risk features.

I IIa IIb III

CABG is recommended in patients with STEMI at time of operative repair of
mechanical defects.
 CABG in Patients With STEMI

I IIa IIb III

The use of mechanical circulatory support is reasonable in patients with STEMI
who are hemodynamically unstable and require urgent CABG.

I IIa IIb III

Emergency CABG within 6 hours of symptom onset may be considered in
patients with STEMI who do not have cardiogenic shock and are not candidates
for PCI or fibrinolytic therapy.
 Complications After STEMI

Treatment of Cardiogenic Shock

 Treatment of Cardiogenic Shock
I IIa IIb III
Emergency revascularization with either PCI or CABG is recommended in
suitable patients with cardiogenic shock due to pump failure after STEMI
irrespective of the time delay from MI onset.

I IIa IIb III

In the absence of contraindications, fibrinolytic therapy should be administered
to patients with STEMI and cardiogenic shock who are unsuitable candidates for
either PCI or CABG.
 Treatment of Cardiogenic Shock
I IIa IIb III
The use of intra-aortic balloon pump counterpulsation can be useful for patients
with cardiogenic shock after STEMI who do not quickly stabilize with
pharmacological.

I IIa IIb III

Alternative LV assist devices for circulatory support may be considered in
patients with refractory cardiogenic shock.
 PCI in Specific Clinical Situations:
Cardiogenic Shock
I IIa IIb III PCI is recommended for patients with acute MI who
develop cardiogenic shock and are suitable candidates.

A hemodynamic support device is

I IIa IIb III recommended for patients with cardiogenic
shock after STEMI who do not quickly stabilize
with pharmacologic therapy.
 My ideal approach to a STEMI Cardiogenic Shock
Emergency angiography and revascularisation: Primary PCI preferably

On-table echo to rule out mechanical defects

Stabilise the patient in the lab before revascularisation

IABP

Pressors if required (Norepinephrine/dopamine)

Anaesthetic support

Consider calling the surgeon for true surgical disease

PCI of culprit artery. Other vessels if shock persists

Use abciximab for PCI

Consider percutaneous LVAD if shock persists with IABP + multi-vessel revascularisation

Conclusions
CS is a treatable illness with a reasonable chance for full
recovery.
The CS literature has traditionally focused on the very high
mortality associated with this diagnosis.
It is important to recognize that although patients with CS
are at very high risk for early death, great potential exists for
salvage.
Recent evidences challenges the notion that patients with CS
are a lost cause.
 Shock
Pathophysiology, Classification, and
Approach to Management
Shock

Cardiogenic shock - a major component of the the mortality

associated with cardiovascular disease (the #1 cause of U.S.
deaths)
Hypovolemic shock - the major contributor to early mortality
from trauma (the #1 cause of death in those < 45 years of age)
Septic shock - the most common cause of death in American ICUs
(the 13th leading cause of death overall in US)
Shock: Definitions

Kumar and Parrillo (1995) - The state in which profound and

widespread reduction of effective tissue perfusion leads first to
reversible, and then if prolonged, to irreversible cellular injury.
Shock: Classification
Hypovolemic shock - due to decreased circulating blood volume in relation to
the total vascular capacity and characterized by a reduction of diastolic filling
pressures
Cardiogenic shock - due to cardiac pump failure related to loss of myocardial
contractility/functional myocardium or structural/mechanical failure of the
cardiac anatomy and characterized by elevations of diastolic filling pressures
and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in the
cardiovascular circuit and characterized by either impairment of diastolic filling
or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid resuscitation) by
increased cardiac output and decreased SVR
Classification of Circulatory Shock
HYPOVOLEMIC
Hemorrhagic
Trauma
Gastrointestinal
Retroperitoneal
Fluid depletion (nonhemorrhagic)
External fluid loss
- Dehydration
- Vomiting
- Diarrhea
- Polyuria
Interstitial fluid redistribution
- Thermal injury
- Trauma
- Anaphylaxis
Increased vascular capacitance (venodilatation)
Sepsis
Anaphylaxis
Toxins/drugs

Kumar and Parrillo, 2001

Classification of Circulatory Shock
CARDIOGENIC
Myopathic
Myocardial infarction (hibernating myocardium)
Left ventricle

Right ventricle
Myocardial contusion (trauma)
Myocarditis
Cardiomyopathy
Post-ischemic myocardial stunning
Septic myocardial depression
Pharmacologic
Anthracycline cardiotoxicity
Calcium channel blockers

Mechanical
Valvular failure (stenotic or regurgitant)
Hypertropic cardiomyopathy
Ventricular septal defect

Arrhythmic
Bradycardia Kumar and Parrillo, 2001
Tachycardia
Classification of Circulatory Shock
EXTRACARDIAC OBSTRUCTIVE
Impaired diastolic filling (decreased ventricular preload)
Direct venous obstruction (vena cava)
- ntrathoracic obstructive tumors
Increased intrathoracic pressure
- Tension pneumothorax
- Mechanical ventilation (with excessive pressure or volume depletion)
- Asthma
Decreased cardiac compliance
- Constrictive pericarditis
- Cardiac tamponade
Impaired systolic contraction (increased ventricular afterload)
Right ventricle
- Pulmonary embolus (massive)
- Acute pulmonary hypertension
Left ventricle
- Saddle embolus
- Aortic dissection
Kumar and Parrillo, 2001
Classification of Circulatory Shock

DISTRIBUTIVE
Septic (bacterial, fungal, viral, rickettsial)
Toxic shock syndrome
Anaphylactic, anaphylactoid
Neurogenic (spinal shock)
Endocrinologic
Adrenal crisis
Thyroid storm
Toxic (e.g., nitroprusside, bretylium)

Kumar and Parrillo, 2001

Shock Hemodynamics
CO SVR PWP EDV
Hypovolemic
Cardiogenic
Obstructive
afterload
preload
Distributive
pre-resusc
post-resusc
Hypovolemic Shock

Degree of volume loss response

10% well tolerated (tachycardia)
20 - 25% failure of compensatory mechanisms (hypotension, orthostasis, decreased
CO)
> 40% loss associated with overt shock (marked hypotension, decreased CO, lactic
acidemia)
 Clinical Correlates of Hemorrhage
Class I ClassII Class III Class IV
Blood loss (mL) > 750 750 - 1500 1500 - 2000 > 2000

Blood loss (% > 15% 15 - 30% 30 - 40% > 40%

total)
Pulse rate < 100 > 100 > 120 > 140

Blood pressure Normal Normal

Pulse pressure Normal or

Orthostasis Absent Minimal Marked Marked

Capillary refill Normal Delayed Delayed Delayed

Resp rate 14 - 20 20 - 30 30 - 40 > 34

UO (mL/hr) > 30 20 - 30 5 - 15 <5

CNS mental status Slight anxiety Mild anxiety Anxious/confuse Confused/lethargi

d c
CI (L/min) 0-10% 20-50% 50-75% >75%
American College of Surgeons, 1989
Hypovolemic Shock

Rate of volume loss and pre-existing cardiac reserve response:

Acute 1L blood loss results in mild to moderate hypotension with decreased CVP and
PWP
Same loss over longer period may be tolerated without hypotension due to increased fluid
retention, increased RBC 2,3 DPG, tachycardia, and increased myocardial contractility
Same slow loss in patient with diminished cardiac reserve may cause hypotension or
shock.
Cardiogenic Shock

#1 cause of in-hospital mortality from Q-wave MI

Requires at least 40% loss of functional myocardium (single MI or
cumulative damage) - stunned, nonfunctional, but viable myocardium
may contribute to post-MI cardiogenic shock
Usually involves left main or left anterior descending obstruction
Historically, incidence of cardiogenic shock post-Q wave MI has run 8 -
20%with mortality 70 - 90% (? reduced incidence with thrombolytics 4
- 7%)
Cardiogenic Shock

Mortality substantially better for cardiogenic shock due to surgically

remediable lesions:
aortic valve failure (endocarditis, occasionally prosthetic valve failure or aortic dissection)
papillary muscle rupture (infarct, post-blunt chest trauma, endocarditis, prosthetic valve
failure)
- ischemic form seen 3 - 7 days post-LAD territory infarct (often preceded by new MR murmur)
- v wave of > 10 mm often seen in PWP trace
VSD (post-infarct, rarely traumatic)
- post-infarct seen 3 - 7 days post-LAD occlusion
- 5 - 10% oxygen saturation step-up
Cardiogenic Shock

RV infarction with cardiogenic shock seen in only 10 - 20% largest

inferior wall MIs
Isolated RV infarcts rare - almost all have some degree of LV
involvement
DX includes cardiac tamponade, restrictive cardiomyopathy,
constrictive pericarditis, and PE - Kussmauls sign, pulsus paradoxus,
filling pressure equalization may be seen in all
Rx fluids and inotropes rather than pressors
Good prognosis relative to LV infarct + shock
Obstructive Shock

Rate of development of obstruction to blood flow response:

acute, massive PE involving 2 or more lobar arteries and 50% pulmonary bed can cause
shock (sPAP max 50 mm Hg) but chronic PE can cause > 75% obstruction without shock
(sPAP 100 + mm Hg)
acute cardiac tamponade can occur with 150 mL fluid, but over 2L can be well tolerated if
slow accumulation

Similar variability based on presence of pre-existing cardiopulmonary

disease
Distributive Shock

Defining feature: loss of peripheral resistance

Dominantly septic shock, anaphylactic and neurogenic shock less
common
Clinical form of shock with greatest contribution of other shock
elements - i.e., hypovolemia, cardiac failure
Distributive Shock

Anaphylactic shock: immediate hypersensitivity reaction mediated

by the interaction of IgE on mast cells and basophils with the
appropriate antigen resulting in mediator cascade
Anaphylactoid reactions involve similar release of mediators via
non-immunologic mechanisms.
Primary mediators include histamine, serotonin, eosinophil
chemotactic factor, and proteolytic enzymes.
Secondary mediators include PAF, bradykinin, prostaglandins, and
leukotrienes.
Distributive Shock

Anaphylactic shock Anaphylactoid shock

insect envenomations ionic contrast media
antibiotics (beta-lactams, protamine
vancomycin, sulfonamides) opiates
heterologous serum (anti-toxin, anti- polysaccharide volume expanders
sera) (dextran, hydroxyethyl starch)
blood transfusion muscle relaxants
immunoglobulins (esp IgA deficient) anesthetics
Egg-based vaccines
latex
Hypodynamic Shock: Perfusion

Extrinsic regulatory mechanisms dominate in most vascular beds except

brain and heart
Blood flow to other organs decreased via sympathetic vasoconstrictive
effects
Post-resuscitation, perfusion abnormalities may persist for days
(decreased perfusion of brain, kidneys, liver, splanchnic organs) with
potential persistent ischemia
? irreversible hypodynamic shock
Hyperdynamic Shock: Perfusion
Organ blood flow disturbed at higher pressures suggesting a primary
microvascular regulatory defect
Cerebral perfusion decreased by 33% while coronary vascular
resistance is significantly increased in septic shock - i.e., coronary and
cerebral autoregulatory mechanisms are relatively intact in sepsis
All other vascular beds exhibit similarly decreased vascular resistance
suggesting active vasodilatory process and failure of extrinsic control
mechanisms
Microvascular studies also show aberrant distribution of perfusion
within tissues and organs.
 Determinants of Effective Tissue Perfusion

Cardiovascular Performance
Cardiac Function
Venous Return
Vascular Performance
Microvascular Function
Oxygen Unloading and Diffusion
Cellular Energy Metabolism
 Cardiac Performance

Left Peripheral
Preload ventricular resistance
size
Stroke Arterial
volume pressure
Myocardial
Cardiac
Contractility fiber
output
shortening
Heart
rate

Afterload
Organ Blood Flow in Shock

Dependent on maintenance of blood pressure within an acceptable

range
For humans, good overall auto-regulation of blood flow between
60 - 100 mm Hg
However, experimental data in animals shows brain and heart have
wider ranges while skeletal muscle has a significantly narrow auto-
regulatory range.
Vascular Failure: Potential Causes

1) Tissue acidosis
2) Catecholamine depletion and resistance
3) Endogenous vasoactive substances
4) Decreased central sympathetic tone
5) Pathophysiologic nitric oxide generation
Microvasculature in Shock

Vessels of 100 to 150 um diameter

Precapillary vs. postcapillary sphincters
Intrinsic control (autoregulation)
stretch receptors
chemoreceptors (CO2, H+)

Extrinsic control via autonomic nervous system

 Determinants of Effective Tissue Perfusion (cont)

Oxygen unloading and diffusion

Oxyhemoglobin affinity
- RBC 2, 3 DPG
- Blood pH
- Temperature

Cellular Function
Cellular energy generation/substrate utilization
- Citric acid (Krebs) cycle
Oxidative phosphorylation
Other energy metabolism pathways

RBC = Red blood cells DPG = Diphosphoglycerate

Mechanisms of Cellular Injury in Shock

1) Cellular ischemia
2) Free radical reperfusion injury
3) Inflammatory mediators (local and circulating)
 Physiologic Oxygen Supply Dependency
Oxygen Consumption

Critical Delivery
Threshold

Oxygen Delivery

Mizock BA. Crit Care Med. 1992;20:80-93.

 Pathologic Oxygen Supply Dependency

Pathologic
Oxygen Consumption

Physiologic

Oxygen Delivery

Mizock BA. Crit Care Med. 1992;20:80-93.

Cellular Ischemia in Shock
Evidence

Oxygen supply-dependent oxygen consumption

Washout of organic acids (from ischemic tissues) in patients with
sepsis and MODS after vasodilator Rx
Elevated ATP degradation products with decreased
acetoacetate/hydroxybutyrate ratio (suggestive of altered hepatic
mitochondrial redox potential)
Kumar and Parrillo, 2001
Diagnosis and Evaluation
Clinical Signs
Primary diagnosis - tachycardia, tachypnea, oliguria, encephalopathy
(confusion), peripheral hypoperfusion (mottled, poor capillary refill
vs. hyperemic and warm), hypotension
Differential DX:
JVP - hypovolemic vs. cardiogenic
Left S3, S4, new murmurs - cardiogenic
Right heart failure - PE, tamponade
Pulsus paradoxus, Kussmauls sign - tamponade
Fever, rigors, infection focus - septic
Diagnosis and Evaluation
Laboratory
Hgb, WBC, platelets
PT/PTT
Electrolytes, arterial blood gases
BUN, Cr
Ca, Mg
Serum lactate
ECG
Diagnosis and Evaluation
Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF, oximetry)
MVO
DO and VO
2

2 2
A Clinical Approach to Shock
Diagnosis and Management
Initial Diagnostic Steps
CXR
Abdominal views*
CT scan abdomen or chest*
Echocardiogram*
Pulmonary perfusion scan*
 A Clinical Approach to Shock
Diagnosis and Management
Initial Therapeutic Steps
Admit to intensive care unit (ICU)
Venous access (1 or 2 wide-bore catheters)
Central venous catheter
Arterial catheter
EKG monitoring
Pulse oximetry
Hemodynamic support (MAP < 60 mmHg)
Fluid challenge
Vasopressors for severe shock unresponsive to fluids
 A Clinical Approach to Shock
Diagnosis and Management

Diagnosis Remains Undefined or

Hemodynamic Status Requires Repeated Fluid
Challenges of Vasopressors
Pulmonary Artery Catheterization
Cardiac output
Oxygen delivery
Filling pressures

Echocardiography
Pericardial fluid
Cardiac function
Valve or shunt abnormalities
 A Clinical Approach to Shock
Diagnosis and Management

Immediate Goals in Shock

Hemodynamic support MAP > 60mmHg

PAOP = 12 - 18 mmHg
Cardiac Index > 2.2 L/min/m2
Maintain oxygen delivery Hemoglobin > 9 g/dL
Arterial saturation > 92%
Supplemental oxygen and mechanical
ventilation
Reversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L)
Maintain urine output
` Reverse encephalopathy
Improving renal, liver function tests
MAP = mean arterial pressure; PAOP = pulmonary artery
occlusion pressure.
 A Clinical Approach to Shock
Diagnosis and Management

Hypovolemic Shock
Rapid replacement of blood, colloid, or crystalloid
Identify source of blood or fluid loss:
Endoscopy/colonoscopy
Angiography
CT/MRI scan
Other
 A Clinical Approach to Shock
Diagnosis and Management

Cardiogenic Shock
LV infarction
Intra-aortic balloon pump (IABP)
Cardiac angiography
Revascularization
- angioplasty
- coronary bypass

RV infarction
Fluid and inotropes with PA catheter monitoring

Mechanical abnormality
Echocardiography
Cardiac cath
Corrective surgery
 A Clinical Approach to Shock
Diagnosis and Management

Extra-cardiac Obstructive Shock

Pericardial tamponade
pericardiocentesis
surgical drainage (if needed)

Pulmonary embolism
heparin
ventilation/perfusion lung scan
pulmonary angiography
consider:
- thrombolytic therapy
- embolectomy at surgery
 A Clinical Approach to Shock
Diagnosis and Management

Distributive Shock
Septic shock
Identify site of infection and drain, if possible
Antimicrobial agents (key rules)
ICU monitoring and support with fluids, vasopressors, and inotropic agents
Goals:
- SV02 > 70%
- improving organ function
- decreasing lactate levels
 Fluid Therapy

Crystalloids
Lactated Ringers solution
Normal saline

Colloids
Hetastarch
Albumin

Packed red blood cells

Infuse to physiologic endpoints
 Fluid Therapy

Correct hypotension first (golden hour)

Decrease heart rate
Correct hypoperfusion abnormalities
Monitor for deterioration of oxygenation
Therapy: Resuscitation Fluids

Crystalloid vs. colloid

Optimal PWP 10 - 12 vs. 15 - 18 mm Hg

20 mL/kg fluid challenge in hypovolemic or septic shock with

re-challenges of 5 - 10 mL/kg
100 - 200 mL challenges in cardiogenic
Terima kasih
Ass Wr WB