CARDIOGENIC SHOCK

Faculty of Medicine

University of Brawijaya

DEFINITION of SHOCK
Disorder of tissue perfusion as a result of imbalance
between oxygen supply to and oxygen demand of
the cells.
All types of shock result in tissue perfusion disorder,
which may develop acute circulatory failure or it is
also called shock syndrome

IT IS NOT LOW BLOOD

PRESSURE !!!
IT IS HYPOPERFUSION..

TYPES OF SHOCK*
Type

of Shock

Clinical

causes

Hypovolemic

Volume loss

Cardiogenic

Distributive

Obstructive

Pump failure
Increased venous
capacitance or
arteriovenous
shunting
Extra-cardiac
obstruction of
blood flow

Primary

mechanism
Exogenous blood,

plasma, fluid or
electrolyte loss
Myocardial
infarction, cardiac
arrhythmias, heart
failure
Septic shock,
spinal shock,
autonomic
blockade, drug
overdose
Vena caval
obstruction, cardiac
tamponade,
pulmonary embolism,
aortic compression or
dissection

*MORE THAN ONE TYPE MAY BE PRESENT

DEFINITION OF CARDIOGENIC
SHOCK
Systolic

BP < 90 mm Hg, or 30 mm
Hg below baseline for at least 30
mins, evidence of poor tissue
perfusion and persistence of shock
after correction of non-myocardial
factors (eg hypovolaemia, hypoxia,
acidosis, arrhythmias)

CRITERIA FOR CARDIOGENIC

SHOCK DIAGNOSIS

<90 mmHg

<2.2 li/min.m2
>15 mmHg

SHOCK REGISTRY JACC SEPT. 2000, SUPP. A

SPECTRUM OF CLINICAL
PRESENTATIONS
Mortality

Respiratory
Distress

Hypotension Hypoperfusion

21%
22%

1.4%

5.6%

70%
60%

28%

65%

RISK FACTORS FOR CARDIOGENIC SHOCK DUE TO

AMI [ACUTE MYOCARD INFARCT]-MEDIATED LV
DYSFUNCTION

Age

> 65
Female gender
Large infarction
Anterior infarction
Prior infarction
DM (diabetes mellitus)
Prior HTN (hypertension)

POST-MORTEM STUDY OF SHOCK

HEARTS

At least 40% of the myocardium infarcted in the

aggregate (old and new injury)
80% have significant LAD (left anterior descendent)
disease
2/3 have severe 3Vdz (three vessel disease)

OUTCOMES OF CARDIOGENIC
SHOCK

Historic
More

67%

mortality 60-80%

recently reported mortality numbers

in the SHOCK trial registry

56% in GUSTO-I
(v.s. 3% in Pts. without shock)

OUTCOMES OF CARDIOGENIC
SHOCK
The

ST pattern in Cardiogenic shock:

15-30 % Non-ST elevation MI

Older
Mortality: 77%

70-85%

ST elevations MI/ New LBBB

Mortality: 53-63%

OUTCOMES OF CARDIOGENIC
SHOCK

The SHOCK registry

Similar

groups

mortality in the two

62.5% in non-ST elevation

60.4% with ST elevation

AETIOLOGY OF CARDIOGENIC
SHOCK
myocardial infarction including complications of
myocardial infarction (eg acute mitral regurgitation,
VSD, free wall rupture, LV aneurysm)
end-stage cardiomyopathy
myocardial contusion
myocarditis
LV outflow obstruction (HOCM, aortic stenosis)
LV inflow obstruction (mitral stenosis, LA myxoma)
sequela of cardiopulmonary bypass

ETIOLOGIES OF CARDIOGENIC
SHOCK

Acute myocardial
infarction/ischemia
LV failure
VSR(ventricular septal
rupture)
Papillary
muscle/chordal
rupture- severe MR
(mitral regurgitation)
Ventricular free wall
rupture with subacute
tamponade

Other conditions complicating

large MIs
Hemorrhage
Infection
Excess negative inotropic or
vasodilator medications
Prior valvular heart disease
Hyperglycemia/ketoacidosis
Post-cardiac arrest
Post-cardiotomy
Refractory sustained
tachyarrhythmias
Acute fulminant myocarditis
End-stage
cardiomyopathyHypertrophic
cardiomyopathy with severe
outflow obstruction
Aortic dissection with aortic
insufficiency or tamponade
Pulmonary embolu
Severe valvular heart
disease-Critical aortic or
mitral stenosis, Acute severe
aortic or MR

PATHOPHYSIOLOGY
Compensatory

mechanisms such as salt &

water retention and peripheral
vasoconstriction tend to exacerbate LV
dysfunction.
Also decreased perfusion pressure,
especially in the presence of multi-vessel
coronary disease leads to further
depression of myocardial contractility.

PATHOPHYSIOLOGY OF SHOCK

Effect of:

on
coronary flow
Elevated LVEDP

LVEDP
(mm Hg)

PATHOPHYSIOLOGY OF SHOCK

Hypotension + LVEDP and critical stenosis

Myocardial Hypoperfusion LV dysfunction
Systemic lactic acidosis Impairment of nonischemic myocardium worsening hypotension.

SCHEMATIC
LVEDP elevation
Hypotension
Decreased coronary

perfusion
Ischemia
Further myocardial
dysfunction
Neurohormonal
activation
Vasoconstriction
End-organ hypoperfusion

CLINICAL FINDINGS

Physical Exam: elevated JVP, +S3, rales,

oliguria, acute pulmonary edema
Hemodynamics: decreased CO (cardiac
output), increased SVR (systemic vascular
resistance), decreased SvO2 (oxygen
saturation)
Initial evaluation: hemodynamics (PA
[pulmonary artery] catheter),
echocardiography, angiography

INVESTIGATIONS
Echo

for all patients to exclude

surgically correctable lesion and
tamponade and to look for RV
infarction
ECG: normal ECG virtually excludes
possibility of cardiogenic shock
caused by MI (myocardial infarction)

DIFFERENTIAL DIAGNOSIS OF
CARDIOGENIC SHOCK
AMI

(acute myocard infarct)

PE (pulmonary embolism)
COPD (chronic obstructive pulmonary disease)
Pneumonia
Aortic dissection
Tamponade
Acute valvular insufficiency
Hemorrhage
Sepsis
Drug OD (over dosage) of negative
inotropic/chronotropic agent

4 POTENTIAL THERAPIES
Pressors
Intra-aortic Balloon Pump (IABP)
Fibrinolytics
Revascularization: CABG (coronary artery
bypass grafting)/PCI (Per Cutaneous Coronary
Intervention)

Refractory shock: ventricular assist device,

cardiac transplantation

TREATMENT OF CARDIOGENIC
SHOCK
optimize preload and afterload.
Vasodilators should be given with extreme
caution.
Nitroprusside may cause coronary steal.
Vasodilators particularly important when
mitral regurgitation is a major contributing
factor

TREATMENT (CONTINUED.)
inotropes. Dobutamine unless shock is
profound in which case drugs with
vasoconstrictor actions preferable.
Phosphodiesterase inhibitors should be
reserved for those in whom catecholamines
have failed to improve cardiac performance
or those in whom arrhythmia or ischaemia
limits catecholamine dose
intra-aortic balloon pump. Only of value if
subsequent revascularization is possible

TREATMENT (CONTINUED)

thrombolysis. No definite evidence that this

alters prognosis. May be less effective in
patients with cardiogenic shock because of
poor coronary blood flow. Combination of
thrombolysis and IABP may be more
effective. Mortality higher in those treated
with t-PA compared to those treated with
streptokinase

TREATMENT (CONTINUED..)

PTCA (Percutaneous transluminal coronary

angioplasty). Probably treatment of choice
in cases due to IHD (ischemic heart disease).
Both PTCA and CABG need to be performed
within first few hours (ideally within 2-4 h)
of onset of symptoms. Result in improved
survival at 6 months and 1 year although
not at 30 days

TREATMENT (

CABG (coronary artery bypass grafting).

May be of benefit if facilities immediately
available. Operative mortality is high

TREATMENT

Patients with RV infarction leading to

cardiogenic shock particularly sensitive to
volume depletion and prone to deterioration
from bradycardia and loss of AV synchrony
due to advanced heart block. Focus of
therapy should be immediate restoration of
adequate LV filling pressure, maintenance of
sinus rhythm or synchronized pacing and
use of dobutamine to stimulate RV systolic
function

PRESSORS DO NOT CHANGE

OUTCOME

Dopamine

<2 micro - gram /kg BW/ minutes, renal vascular dilation

<2-10 micro - gram /kg BW/ minutes +chronotropic/inotropic (beta effects)
>10 micro - gram /kg BW/ minutes : vasoconstriction (alpha effects)

Dobutamine positive inotrope, vasodilates,

arrhythmogenic at higher doses
Norepinephrine (Levophed): vasoconstriction,
inotropic stimulant. Should only be used for
refractory hypotension with decreased SVR.
Vasopression vasoconstriction
VASO and LEVO should only be used as a last
resort

IABP (INTRA AORTIC BALLOON

PUMP) IS A TEMPORIZING MEASURE

Augments coronary blood flow in diastole

Balloon collapse in systole creates a vacuum
effect decreases afterload
Decrease myocardial oxygen demand

Intra-Aortic Balloon Pump

INDICATION FOR IABP

CONTRAINDICATIONS TO IABP
Significant aortic regurgitation or significant
arteriovenous shunting
Abdominal aortic aneurysm or aortic dissection
Uncontrolled sepsis
Uncontrolled bleeding disorder
Severe bilateral peripheral vascular disease
Bilateral femoral popliteal bypass grafts for
severe peripheral vascular disease.

COMPLICATIONS OF IABP
Cholesterol Embolization
CVA (cerebro vascular accident)
Sepsis
Balloon rupture
Thrombocytopenia
Hemolysis
Groin Infection
Peripheral Neuropathy

HOCM (HYPERTROPHIC
OBSTRUCTIVE CARDIOMYPATHY)
usual methods used to treat cardiogenic
shock exacerbate obstruction
plasma volume expansion and IV titration of
beta-blockers reduce ventricular outflow
obstruction and improve cardiac output

PROGNOSIS OF PATIENTS WITH

CARDIOGENIC SHOCK
poor
only about 1/3 of patients actively treated
survive initial episode and many of the
survivors have continuing angina, CCF and
decreased exercise tolerance
approximately 1/2 with a surgically
correctable lesion leave hospital
RV function usually returns to normal in
survivors of cardiogenic shock associated
with RV infarction

PROGNOSIS
50% of patients who require maximal
therapy and IABP to come off bypass die. If
ventricular assist device also required then
only 35-45% survive. Functional prognosis
for these survivors quite good
Mortality without aggressive highly
technical care is 70-90%. Hospitals without
the facilities for IABP or high-risk
angioplasty and surgical intervention
should begin initial resuscitative measures
and then make a rapid decision about
transfer to a hospital with the necessary
resources

Myocardial
stunning and
hibernation

MYOCARDIAL STUNNING

Mechanical dysfunction of myocardium which persists

despite absence of irreversible damage and
restoration of normal or near-normal coronary flow
and which recovers spontaneously.
Clinically important in 3 settings:

- after MI (especially after thrombolysis or primary

angioplasty)
- after complicated coronary interventions (when
myocardium may be ischaemic for long periods, particularly
if there is pre-existing LV dysfunction)
- after cardiac surgery

Mechanical circulatory support may be preferable to

inotropes for patients with stunned myocardium as
inotropes may adversely influence recovery of
potentially ischaemic segments

HIBERNATING MYOCARDIUM
Myocardium with impaired function that is
persistently impaired at rest due to decreased
coronary blood flow but which demonstrates
improved function when balance between oxygen
supply and demand is improved.
Dobutamine echocardiography can be used to
differentiate between stunned myocardium with a
patent artery ( function that persists during
infusion) from stunned myocardium with a
stenosed artery or hibernation (initial followed
by deterioration).