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kuliah patofisiologi syok kardiogenik dan terapi tentang syok kardiogenik
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CARDIOGENIC SHOCKFaculty of Medicine
University of Brawijaya
DEFINIDEFINITIONTION of SHOCK of SHOCK
IT IS NOT LOW BLOOD PRESSURE !!!IT IS HYPOPERFUSION…..
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
TTYPES OF SHOCKYPES OF SHOCK**
Type of Shock Clinical causes Primary mechanism
Hypovolemic
Volume loss
Exogenous blood, plasma, fluid or electrolyte loss
CardiogenicPump failure
Myocardial infarction, cardiac arrhythmias, heart failure
Distributive
Increased venous capacitance or arteriovenous shunting
Septic shock, spinal shock, autonomic blockade, drug overdose
Obstructive
Extra-cardiac obstruction of blood flow
Vena caval obstruction, cardiac tamponade, pulmonary embolism, aortic compression or dissection
**MORE THAN ONE TYPE MAY BE PRESENTMORE 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
MortalityRespiratory
DistressHypotension Hypoperfusion
21%
22%
70%
60%
5.6%
28%
65%
1.4%
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
OlderMortality: 77%
70-85% ST elevations MI/ New LBBBMortality: 53-63%
OUTCOMES OF CARDIOGENIC SHOCK
The SHOCK registry
Similar mortality in the two groups62.5% in non-ST elevation60.4% 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:
Elevated LVEDP on coronary flow
LVEDP(mm Hg)
PATHOPHYSIOLOGY OF SHOCK
Hypotension + LVEDP and critical stenosis Myocardial Hypoperfusion LV dysfunction Systemic lactic acidosis Impairment of non-ischemic myocardium worsening hypotension.
SCHEMATIC
LVEDP elevationHypotensionDecreased coronary perfusionIschemiaFurther myocardial dysfunctionNeurohormonal activation VasoconstrictionEnd-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)PneumoniaAortic dissectionTamponadeAcute valvular insufficiencyHemorrhageSepsisDrug 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 Myocardial stunning and stunning and hibernationhibernation
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).