Cardiogenic Shock

Prof. dr. Harris Hasan SpPD,SpJP(K),FIHA

Departemen Kardiologi & Kedokteran Vaskular
FK USU RSUP H.Adam Malik

Cardiogenic shock one of the most serious

condition :
Mortality is in excess of 80% with treatment
Usually caused by pump failure due to massive MI
The recognition of cardiogenic shock, accurate
assessment of the patients haemodynamic status
and identification of the causes are the key to its
management.

Cardiogenic shock are life-threatening

conditions that should be treated as
medical emergencies.
The most common etiology is severe left
ventricular (LV) dysfunction, leading to
pulmonary congestion and or systemic
hypoperfusion.

Keypoints from the history :

Recent MI ? If so, which territory
(inferior/posterior associated with RV infarct)
Previous heart failure ?
Valve disease or prothesis or cardiomyopathy ?
Thrombolysis given ?Any symptoms of
internal/GI bleeding? Analphylaxis?

 Timing. Days 2-3 post MI, suspect myocardial

rupture.
Sudden onset when previously stable : suspect
rupture, VSD, acute mitral rupture.
Fluid balance. Is patient dehydrate/overdiuresed?
Drugs. Any negative inotropes, e.g.blocker,
verapamil, diltiazem? Excessive opiate analgesia.

Cardiogenic shock (CS) :

Systemic hypoperfusion due to severe
depression of the cardiac index(<2.2
(L/min)/m2
Sustained systolic arterial hypotension (<90
mmHg)
Elevated filling pressure (pulmonary capillary
wedge pressure (PCWP) >18 mmHg).
Hospital mortality rates > 50%

Definition :
A state of hypotension, with reduced end
organ perfusion due to low cardiac output.

Etiology / patophysiology :

Acute MI : >80% cases caused by extensive

LV infarction
Have three-vessel or left main stem disease,
associated with infarction
of at least 40% of the LV myocardium

Etiologies of Cardiogenic Shock (CS) and

Cardiogenic Pulmonary Edema
Acute myocardial infarction/ischemia
LV failure
VSR
Papillary muscle/chordal rupture-severe MR
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 cardiomyopathy
Hypertrophic cardiomyopathy with severe outflow
obstruction
Aortic dissection with aortic insufficiency or tamponade
Pulmonary embolus
Severe valvular heart disease
Critical aortic or mitral stenosis
Acute severe aortic or MR
Toxic-metabolic
Beta-blocker or calcium channel antagonist overdose

Other etiologies or cardiogenic shock

RV failure due to:
Acute myocardial infarction
Acute coronary pulmonale
Refractory sustained bradyarrhythmias
Pericardial tamponade
Toxic/metabolic
Severe acidosis, severe hypoxemia

Myocardial
dysfunction
Systolic

systemic
perfusion

Diastolic

Cardiac output

LVEDP

stroke volume

Pulmonary congestion

Hypotension
Hypoxemia

coronary perfusion
pressure
Ischemia
Compensatory
vasoconstriction;
Fluid retention

Progressive
myocardial
dysfunction
DEATH

Clinical diagnosis of cardiogenic shock

Blood pressure
Pulse
Peripheral circ.
End organ perfusion

Mixed venous O2
saturation
Lactic acidosis
Echo

hypotension, systolic BP
usually < 90 mmHg
sinus tachycardia
cool skin, low volume,
pulse, poor capillary
refill peripheral cyanosis
oliguria or anuria
confusion or impaired
concious level
abdominal pain
<70% (due to O2 extraction in
tissues)
if tissue perfusion very poor, may
occur
large ventricular motion abnormality
or other cause for shock evident

Hemodynamic Patterna

Normal values
MI without pulmonary edemab
Pulmonary edema
Cardiogenic shock
LV failure
RV failurec
Cardiac tamponade
Acute mitral regurgitation
Ventricular septal rupture

Hypovolemic shock
Septic shock

RA,
mmHg

RVS,
mmHg

RVD,
mmHg

PAS,
mmHg

PAD,
mmHg

PCW,
mmHg

CI,
(L/min)/m2

SVR,
(dyn.s)/cm5

<6

<25

0-12

<25

0-12

<6-12
13(5-18)

2.5
2.7(2.2-4.3)

(800-600)

PBF
SBF

There is a significant patient-to-patient variation. Pressure may be normalized if cardiac output is low

Forrester et al classified non-perfused MI patients into four hemodynamic subsets

isolated or predominant RV failure

PCW and PA pressure may rise in RV failure after volume loading due to RV dilation, right to left shift of
the interventricular septum, resulting in impaired LV filling, when biventricular failure is present, the
patterns are similar to those shown for LV failure
d

Haemodynamic features of cardiogenic shock :

Low cardiac index
Persistent hypotension
Elevated LV
filling pressure

( usually <1.81 min/m2)

(systolic BP < 90mmHg
for > 30 min)
( PCWP >20 mmHg)

Multiple organ dysfunction syndrome

Cardiovascular Catecholamine levels rise with
secondary increase in heart rate
and contractility
Myocardial oxygen demands rise
Systolic dysfunction: demand >
supply, depressant factors (sepsis)
Diastolic dysfunction
Arrhythmias: supraventricular,
ventricular

Examination : looking for signs of reduced

tissue perfusion and of potential causes of shock

General
examination
:
Concious level , confusion
Central or peripheral cyanosis
Tachypnoea
Dehydration
Cool peripheries, reduced capillary refill

Pulses :
Tachycardia, low-volume pulse, pulsus
alternans
Pulsus paradoxus (tamponade)
Unequal / absent pulses (aortic dissection
or peripheral atherosclerosis)

Blood pressure :
Equal or unequal between arms

JVP :
High in RV infarction, massive pulmonary
embolism, often in normal in LV infarction

Precordium :
Apex dyskinetic in anterior MI/LV aneurysm
Apex hyperdinamic in VSD and mitral regurgitation
Thrills/murmurs of mitral regurgitation/VSD
S3 when LA pressure high

Chest :
Combination of pulmonary oedema +
shock heralds very poor prognosis chest
infection can cause or exacerbate shock

Transthoracic echo in suspected cardiogenic

shock :
LV function
- usually extensive wall motion
abnormality in infarcts territory
RV function
- hypokinetic free wall in RV
infarct, dilated, poor function
in massive pulmonary embolism
Pericardial effusion - sign of RV compress / tamponade
VSD
- colour and continous wave doppler

of septum in all views ; can be ;

; can
be easy to miss an be
- pulmonary systemic flow
>1,5
Valves
- flail, prolaps mitral valve
- coexsistig valve
stenosis/regurgitation
Aortic root
- dilated in type A (proximal dissection)
- TOE, fast CT or MRI scan if
suspicious

CXR :
Coexisting pulmonary oedema /chest infection
Position of Swan Ganz catheter, identify
iatrogenic pneumothorax
Aortic root and mediastinal diameter

Laboratory test :
Arterial blood analysis (acid base balance, blood
gases). If thrombolytic has been given, defer to
avoid arterial bleeding or use pressure bandage
U & Es, creatinine, LFTs(renal failure and shock
liver may develop) FBC

ECG :
Confirm ischaemia or infarct zone / infarct
extension
Arrhythmias, especially atrial fibrillation,
excacerbate shock

Shock

Admit to ICU
Large bore/central IV
Arterial line

Initial steps

Intubation
Severe hypoxemia, acidosis
Restore circulation

Stabilization

Volume expansion (IVF,

PRBC)
Goal : CVP 10 mmHg,
PCWP 15 mmHg

Positive BP response

Negative BP response
Vasopressor therapy
Dopamine, phenylephrine, NE
Inotropic therapy (if LV dysfunction)
Dobutamine (avoid milrinone)

Defenitive theraphy

Consider intra-aortic balloon pump

Cardiogenic shock (MI)

RV infarct

Myocarditis

Valvular heart disease

Distributive Shock

Obstructive shock

Intra-aortic balloon pump

insertion

Maintain pre-load

Immunosuppresiv
e Rx

Slow HR for MS

Septic

Pulmonary embolism

Nitrates, beta blockers, ASA,

heparin
Monitor with PA catheter
Restore perfusion

Avoid nitrates
AV pacing
Dobutamine

Ventricular
support IABP,
LVAD Consider
OHT

Primary PTCA/stent
CABG (failed PTCA/stent)

MI Complications

Lytics

(VSD, free-wall rupture)

Support LV

Therapy = surgical

LVAD-bridge to OHT, recovery

Surgical Rx

Antibiotics

Lytics (acute)

severe AS

Identify source

Thrombectomy

Acute AI

Support BP, CO,

Acute MR

peripheral perfusion

volume support

and pO2 (ventilation)

(temp)

Tamponade

Anaphylactic

pericardiocentesis

Epinephrine

Pericardial window

Antihistamine
Addisons disease
Steroid Rx
Neurogenic
Supportive Rx

Vasopressors and inotropes used in shock

Agent

Dopamine

Dose
(g/kg/min)

HR /
contractility

Vasoconstrict
/vasodilate

Order of use
Cardiogenic shock
Restore
BP

Cardiac
output

1-4

+/+

0/+

n/a

n/a

4-20

++/++-+++

++-+++/0

2.5-20

++/++++

0/++

n/a

Norepinephrine

2-20

+/++

++++/0

n/a

Epinephrine

1-20

++++/++++

++++/+++

Avoid

Avoid

Dobutamine

Comments

Improves renal blood

flow via dopaminergic
stimulation
First-line agent to
restore BP
First-line agent to
improve cardiac
output but
arrhythmogenic
Purer vasoconstrictor
than dopamine
Potent inotrope;
significant increase in
myocardial oxygen
requirements;
equipotent
vasoconstrictor and
vasodilator

MANAGEMENT
Rapid correction of haemodynamic compromise is essential
to avoid organ damage from hypoperfusion : acute tubular
necrosis, myocardial infarct extension, shock liver.

Oxygenation : high flow (100% O2 via mask)

Monitoring
ECG/blood pressure
Urinary catheter
Swan-Ganz catheter allows
CVP measurement
PCWP measurement
Central administration of drugs
Mixed venous O2 saturation measurement
Confirmation of VSD
Thermodilution catheters especially if suspected
mixed picture (sepsis and LV impairment)

MANAGEMENT (continued)
Optimize filling pressures (assessed as PCWP)
Improve cardiac output : Dobutamine, low-dose
dopamine
Treat reversible myocardial ischaemia
Thrombolysis
Emergency cardiac catheterization
Intra-aortic ballon pump (IABP)
Treat other reversible causes
Surgical repair of VSD and flail mitral leaflet
Arrhythmias should be corrected to optimize
cardiac output
Pericardial aspiration

Conclusion
The history, physical examination and laboratory
data offer critical insight into the underlying cause of
shock. Although coronary artery disease remains the
most common cause of cardiac dysfunction and
shock, other causes should be excluded by a careful
review of all data.
The clinical presentation is similar regardless of the
cause, with the constellation of hypotension,
tachycardia, tachypnea, clouded sensorium and
oliguria.

 The pulmonary artery catheter remains an

important tool for patients with shock and
should be used to optimize outcomes.
The use of intra-aortic balloon pumps and
left ventricular assist devices continues to
increase, with emerging results of clinical
trials and improved device sign.