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*
Primary
Type of Shock Clinical causes 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

Hypovolemic

Volume loss

Cardiogenic

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

Distributive

Obstructive

*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
1.4%

21%
22% 70%
5.6%

28%

60%
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

mortality 60-80%

More

recently reported mortality numbers

67% 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

mortality in the two

groups
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:

LVEDP (mm Hg)

on coronary flow
Elevated LVEDP

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 preexisting 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).