CARDIOGENIC SHOCK

Prof. Dr Dhiman Banik

D Card, MD(Card), FACC
Prof. and Consultant, Cardiology, NHFH&RI
Definition of SHOCK

Widespread hypoperfusion of tissue due to

reduction of the blood volume or cardiac output
or redistribution of blood, resulting in an
inadequate effective circulating volume.
Shock or Circulatory failure

(A)Low flow(reduced stroke volume)

(B)Low peripheral arteriolar resistant(vasodilatation)
 Low stroke volume

HYPOVOLAEMIA: Major reduction in blood

volume, e.g. internal and external haemorrhage,
severe burn, salt and water depletion.
CARDIOGENIC:Severe mechanical impairment,
e.g.myocardial infarction, acute MR.
OBSTRUCTIVE: Obstruction of blood flow
arround the circulation, e.g. pulmonary
embolism, cardiac tamponade, tension
pneumothorax
 Vasodilatation

 SEPTIC/SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME(SIRS):Infection and
SIRS which may causes widespread endothelial
damage with vasodilatation, microvascular
occlusion, capillary leak, tissue damage.
 ANAPHYLACTIC: Vasodilatation triggered by
an allergen.
 NEUROGENIC: Major brain and spinal injury
which disrupts vasomotor control.
 Clinical features of LOW FLOW
SHOCK
 Rapid, shallow respiration.
 Cold, clammy skin.
 Tachycardia(>100/min)
 Hypotension(SBP<100mm of Hg)
 Drowsiness, confusion and irritabiliy.
 Oliguria
 Multi-organ failure
 Clinical features of vasodilated
shock,e.g. sepsis, anaphylaxis
 Rapid, shallow respiration.
 Warm peripheries.
 Tachycardia(>100/min)
 Hypotension(SBP<100 mm of Hg)
 Drowsiness, confusion and irritability.
 Oliguria.
 Multi-organ failure
 Cardiogenic Shock

 Systemic hypoperfusion secondary to severe

depression of cardiac output and sustained
systolic arterial hypotension despite elevated
filling pressures.
 Some Notes
 Develops in 10% to 20% of patients hospitalized AMI
 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
Fig: Updated SCAI SHOCK classification pyramid
Table 1: Descriptions of shock stages: physical examination, biochemical
markers and hemodynamics
Hemodynamics
 Risk Factors for Cardiogenic Shock Due to
AMI-mediated LV Dysfunction…
 Age > 65
 Female gender
 Large infarction
 Anterior infarction
 Prior infarction
 DM
 Prior HTN
Fig: The proposed 3-axis conceptual model of cardiogenic shock evaluation and prognostication
 Etiology

 Left ventricular systolic dysfunction:

› AMI/ Ischemia
› Valvular disease
› Myocardial depressant drugs
 Etiology (Cont.)

 Left ventricular diastolic dysfunction

› Ischemia
› Ventricular hypertrophy
› Restrictive cardiomyopathy
› Consequence of prolonged hypovolemic or septic
shock
› pericardial tamponade
 Etiology (Cont.)

 Increased afterload
› Aortic stenosis
› Hypertrophic cardiomyopathy
› Coarctation of the aorta
 Etiology (Cont.)

 Valvular or structural abnormality

› Mitral stenosis
› Endocarditis
› Mitral/ aortic regurgitation
› Obstruction due to atrial myxoma or thrombus
› Papillary muscle dysfunction or rupture
› Ruptured septum or free wall arrhythmias
 Etiology (Cont.)
 Right ventricular dysfunction
› Right ventricular infarction
› Pulmonary embolism
› Pulmonary vascular disease
› Hypoxic pulmonary vasoconstriction
› Acute respiratory distress syndrome
› Pulmonary fibrosis
› Sleep disordered breathing
› Chronic obstructive pulmonary disease
 Etiology (Cont.)

 Arrhythmias
› Atrial and ventricular arrhythmias (tachycardia-
mediated cardiomyopathy)
› Conduction abnormalities (eg, atrioventricular blocks,
sinus bradycardia)
 Reversible Myocardial
Dysfunction
 Large areas of nonfunctional but viable
myocardium can also contribute to the
development of cardiogenic shock in patients
after myocardial infarction. This reversible
dysfunction can be described in two main
categories.

1. Myocardial stunning
2. Hibernating myocardium
 Myocardial stunning

 Represents post-ischemic dysfunction that

persists despite restoration of normal blood flow.
Myocardial dysfunction from stunning eventually
resolves completely.
 Hibernating myocardium

 State of persistently impaired myocardial

function at rest, which occurs because of the
severely reduced coronary blood flow.
Revascularization of the hibernating (and/or
stunned) myocardium generally leads to
improved myocardial function
Myocardial Pathology
 Cellular Pathology
Tissue
Cellular Hypoxia
Hypoperfusion

Anaerobic
Glycolysis

Lactic Acidosis

Intracellular Acidosis

Failure of energy dependent ion

transport pump

Intracellular accumulation of
sodium, calcium

Myocyte swelling

Cellular ischaemia and intracellular Ca ++

accumulation activates intrcellular proteases

Irreversible myocardial cellular injury

Mitochondrial swelling, accumulation of denatured proteins

and chromatin in cytoplasm, lysozomal breakdown,
mitochondrial fracture.
 Investigations
 Biochemical profile:
 CBC count: A CBC count is generally helpful to exclude anemia; a high
WBC count may indicate an underlying infection, and the platelet count may
be low because of coagulopathy related to sepsis.
 Cardiac enzymes
› The rapid release and metabolism of myoglobin occurs in persons with MI
› Cardiac troponins T and I are widely used for the diagnosis of myocardial
injury. Troponin elevation in the absence of clinical evidence of ischemia
should prompt a search for other causes of cardiac damage, such as
myocarditis. Troponin I and T can be detected in serum within the first
few hours after onset of acute myocardial infarction.
 Arterial blood gases: Arterial blood gas values indicate overall acid-base
homeostasis and the level of arterial blood oxygenation. A base deficit
elevation (reference range is +3 to -3 mmol/L) correlates with the occurrence
and severity of shock. A base deficit is also an important marker to follow
during resuscitation of a patient from shock.
 Lactate:
 Investigations (Cont.)
 Imaging Studies
 Echocardiography should be performed early to establish the cause of cardiogenic
shock.
› Echocardiography provides information on global and regional systolic
function and on diastolic dysfunction.
› Echocardiography findings can also lead to a rapid diagnosis of mechanical
causes of shock, such as papillary muscle rupture causing acute myocardial
regurgitation, acute ventricular septal defect, free myocardial wall rupture, and
pericardial tamponade.
 Chest radiography findings are useful for excluding other causes of shock or chest
pain.
› aortic dissection.
› Tension pneumothorax or pneumomediastinum
› Most patients with established cardiogenic shock exhibit findings of left
ventricular failure. The radiological features of left ventricular failure include
pulmonary vascular redistribution, interstitial pulmonary edema, enlarged hilar
shadows, the presence of Kerley B lines, cardiomegaly, and bilateral pleural
effusions; alveolar edema manifests as bilateral perihilar opacities in a so-called
butterfly distribution.
 Lactate
 An elevated serum lactate level is an indicator of
shock.
 Serial lactate measurements are useful markers of
hypoperfusion and are also used as indicators of
prognosis.
 Elevated lactate values in a patient with signs of
hypoperfusion indicate a poor prognosis.
 Rising lactate values during resuscitation portend a
very high mortality rate.
 4 Potential Therapies

 Pressors
 Intra-aortic Balloon Pump (IABP)
 Fibrinolytics
 Revascularization: CABG/PCI
 Refractory shock: ventricular assist device,
cardiac transplantation
 Management
 Detailed history
 Rapid recognition of the condition
 Rapid exclusion or treatment of readily reversible
causes.
 Oxygenation and airway protection
 12 lead ECG (occasionally right sided leads)
 Prompt stabilization of clinical and
haemodynamic status.
 Continuous ECG monitoring
 Relief of pain and anxiety
 Dopamine

 1-5mcg/kg/min: vasodilatation of renal,

mesenteric and coronary beds.
 5-10mcg/kg/min: increase in heart rate and
cardiac contractility.
 >10mcg/kg/min: arterial vasoconstriction and an
elevation of blood pressure.
 Dobutamine

 Increase in myocardial contractility and cardiac

output without markedly changing in heart rate or
systemic vascular resistance.
 Dose:5-10mcg/kg/min.
 Potent B2 stimulant, should be used when SBP
>90mm of Hg.
 Epinephrine/Adrenaline
 Epinephrine can increase the MAP by increasing the cardiac index and
stroke volume, as well as systemic vascular resistance (SVR) and heart
rate.
 Epinephrine decreases the splanchnic blood flow and may increase
oxygen delivery and consumption.
 Administration of this agent is associated with an increase in systemic
and regional lactate concentrations. The use of epinephrine is
recommended only in patients who are unresponsive to traditional
agents.
 The undesirable effects are an increase in lactate concentration, a
potential to produce myocardial ischemia, the development of
arrhythmias, and a reduction in splanchnic flow.
 Norepinephrine/Noradrenaline
 Norepinephrine is a potent alpha-adrenergic agonist
with minimal beta-adrenergic agonist effects.
 Norepinephrine can increase blood pressure
successfully in patients who remain hypotensive
following dopamine.
 The dose of norepinephrine may vary from 0.2-1.5
mcg/kg/min, and large doses, as high as 3.3
mcg/kg/min.
Intra-Aortic Balloon Pump (IABP)
Indications :
I. Hemodynamic compromise
1. Cardiogenic shock secondary to AMI with
continuing ischemia, VSR or MR
2. Cardiogenic shock due to transient ischemia,
myocarditis, sepsis, drug toxicity.
3. Failure to wean from cardiopulmonary bypass.
4. Hemodynamic support while awaiting
transplantation.
5. Severe arrhythmia owing to refractory ischemia.
II. Medically refractory ischemia
1. Medically refractory unstable angina.
2. Failed PTCA with refractory ischemia.
III. Prophylactic high-risk intervention
1. High risk PTCA owing to LV dysfunction and / or
large territory at risk.
2. PTCA during acute myocardial infarction.
3. Stabilization in patients with severe aortic
stenosis.
4. Severe multivessel or left main CAD requiring
urgent cardiac or non-cardiac surgery.
5. Large myocardial infarction.
Contraindications :
I. Absolute
1. Severe aortic insufficiency
2. Dissecting aortic aneurysm
3. Malignant arrhythmias
Asystole
Ventricular fibrillation
Pulseless electrical activity
II. Relative
1. Aortic aneurysm
2. Severe peripheral vascular disease
3. Mild aortic insufficiency
Active bleeding
Patients with contraindication to anticoagulation
Thrombocytopenia (<50,000)
Acute stroke
PDA
 Positioning
 The end of the balloon should be just distal to the
takeoff of the left subclavian artery
 Position should be confirmed by fluoroscopy or
chest x-ray
 IABP

 Augments coronary blood flow in diastole.

 Balloon collapse in systole creates a vaccum
effect- decrease in afterload- decrease in
myocardial oxygen demand
 ECMO
 Extracorporeal membrane oxygenation (ECMO), also known
as extracorporeal life support (ECLS), is an extracorporeal
technique of providing prolonged cardiac and respiratory
support to persons whose heart and lungs are unable to
provide an adequate amount of gas exchange or perfusion to
sustain life. The technology for ECMO is largely derived
from cardiopulmonary bypass, which provides shorter-term
support with arrested native circulation.
 TYPES
 VV = veno-venous
 VA = veno-arterial: peripheral or central
 Veno-pulmonary artery ECMO (provides short-term right
ventricular and respiratory support following LVAD insertion)
 high (2 venous cannulae) vs low flow (1 venous cannula
 Indications for ECMO
 Primary diagnoses associated with
primary pulmonary hypertension of the newborn (PPHN), including
idiopathic PPHN,
 Meconium aspiration syndrome,
 Respiratory distress syndrome,
 Group B streptococcal sepsis, and
 Asphyxia
 Congenital diaphragmatic hernia (CDH)
 Selection criteria for neonates include the following:
 Gestational age of 34 weeks or more
 Birth weight of 2000 g or higher
 No significant coagulopathy or uncontrolled bleeding
 No major intracranial hemorrhage (grade 1 intracranial hemorrhage)
 Mechanical ventilation for 10-14 days or less
 Reversible lung injury
 No lethal malformations
 No major untreatable cardiac malformation
 Failure of maximal medical therapy
 Failure to meet these criteria is a relative contraindication for
ECMO.
INDICATIONS IN ADULT
 Preparation

 Equipment for ECMO

 The extracorporeal membrane oxygenation (ECMO) apparatus consists of a blood
pump with raceway tubing, a venous reservoir, a membrane oxygenator, and a
countercurrent heat exchanger, as shown in the image below
 Complications

 Neurologic- intracerebral hemorrhage, subarachnoid hemorrhage,

ischemic infarctions in susceptible areas of the brain, hypoxic-ischemic
encephalopathy, unexplained coma, and brain death
 Blood-Heparin induced thrmobocytopenia
 Mechanical ventilation-The CESAR study has shown an improvement in 6
month survival without severe disability in patients getting ECMO versus
conventional ventilation in ARDS

 Preterm infants are at unacceptably high risk for intraventricular hemorrhage

(IVH) if administered ECMO at a gestational age less than 32 weeks
Fig: Cardiogenic shock is a dynamic process. CA, cardiac arrest; MCS, mechanical circulatory support; SCAI, Society for Cardiovascular
Angiography and Interventions.
 Epidemiology
 The incidence rate of cardiogenic shock ranges from
5-10% in patients with acute myocardial infarction
(MI).
 Cardiogenic shock occurs in 8.6% of patients with
ST-segment elevation MI (STEMI), with 29% of
those presenting to the hospital already in shock.
 It occurs only in 2% of patients with non ̶ ST-
segment elevation acute coronary syndrome
(NSTACS).
Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM. Temporal trends in cardiogenic shock
complicating acute myocardial infarction. N Engl J Med. Apr 15 1999;340(15):1162-8.
 Prognosis

 If the precipitating cause and the accompanying

circulatory failure are dealt promptly before
significant organ failure (EARLY SHOCK) the
prognosis is good.
 Progressive deterioration in organ function and
MOF ensues (LATE SHOCK).
 Failure of four or more organs is associated with
a mortality >80%.
 TAKE HOME MESSAGE

 All forms of shock require early identification

and treatment.
 If inadequate regional tissue perfusion and
cellular dysoxia persist, MOF will develop
leading to very high mortality.
THANK YOU