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Cardiogenic Shock
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SHOCK= Inadequate Tissue Perfusion
Mechanisms: Inadequate oxygen delivery Release of inflammatory mediators Further microvascular changes, compromised
blood flow and further cellular hypoperfusion
Clinical Manifestations: Hypotension Multiple organ failure i.e. altered conscious level
and reduced urinary output
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Types
1. Cardiogenic shock (associated with cardiac pathology)
2. Hypovolemic shock (caused by inadequate blood volume)
3. Anaphylactic shock (caused by allergic reaction)
4. Septic shock (associated with infections)
5. Neurogenic shock(caused by damage to the nervous system)
6. Metabolic ( associated with metabolic acidosis, hypothyroidism,addisonian crisis)
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Cardiogenic shock
Cardiogenic shock is defined as sustained
hypotension with tissue hypoperfusiondespite adequate left ventricular fillingpressure, secondary to some cardiacpathology.
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Cardiogenic Shock Clinical
Parameters
Hypotension i.e., systolic BP less than 90
mm of Hg , weak and thready pulse Elevated JVP
Cold and clammy skin
Altered mental status
Reduce urine output
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Hemodynamic Parameters
Systemic Vascular Resistance (SVR)
Cardiac Output (CO) Mixed Venous Oxygen Saturation (SvO2)
Pulmonary Capillary Wedge Pressure
(PCWP)
Central Venous Pressure (CVP)
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Differentiating Types of Shock
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Cardiogenic Shock
Etiologies
Pathophysiology Clinical/Hemodynamic Characteristics
Treatment Options
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Etiologies
1. Acute extensivemyocardialinfarction/ischemia
2. VSR
3. Papillary muscle/chordalrupture- severe MR
4. Ventricular free wallrupture with subacutetamponade
5. RV infarction
Other conditions
Refractory sustained
tachyarrhythmias
Acute fulminant myocarditis
cardiomyopathies
Pulmonary embolism
Severe valvular heartdisease and acuteregurgitations
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Pathophysiology
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Initial evaluation
EKG
CXR Echocardiography
Blood biochemistry , biomarkers
Hemodynamic measurements (swan ganzcatheter)
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Treatment
Inotropes or vasopressors
Intra-aortic Balloon Pump (IABP) Fibrinolytics
Revascularization: CABG/PCI
Refractory shock: ventricular assist device,cardiac transplantation
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Inotropes do not change
outcome
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Dopamine
1 stimulant which increases myocardialcontractility through preferentialstimulation of myocardial B1-adrenergicreceptors
DOSE
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Dobutamine
Positive inotrope, peripheral vasodilater,arrhythmogenic at higher doses
synthetic catecholamine increases myocardialcontractility through preferential stimulation ofmyocardial B1-adrenergic receptors. Dobutaminehas less chronotropic effect than does dopamine and
typically does not cause significant changes in heartrate when the dose is less than 15 g/kg/min
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Norepinephr ine
vasoconstriction, inotropic stimulant.
Should only be used for refractoryhypotension with dec SVR. Norepinephrine is a powerful 1 stimulant
that results in arterial vasoconstriction and is
1-stimulant that increases inotropy.
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Other drugs
Phosphodiesterase inhibitors, such as
milrinone and amrinone Digoxin
Levosimendan, a calcium-sensitizing drugwith positive inotropic and vasodilating
properties Arginine vasopressin (AVP) a potent
vasopressor hormone
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Nitric oxide synthase inhibitors (LNNMA
and LNAME) block the synthesis of nitricoxide
Nesiritide
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IABP(Intraortic balloon pump) is
a bridging measure
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IABP
1. Augments coronary blood flow in diastole
2. Balloon collapse in systole creates avacuum effect decreases afterload
3. Decrease myocardial oxygen demand
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Indication for IABP
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Definitive treatment
PCI
Surgical revascularization Surgical repair of cardiac defect
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SHOCK trial
Hochman J et al. N Engl J Med 1999;341:625-634
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Copyright restrictions may apply.
Hochman, J. S. et al. JAMA 2006;295:2511-2515.
Kaplan-Meier Long-term Survival of All Patients and Those Discharged Alive FollowingHospitalization
SHOCK 6 years later
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Normal Values
Right Atrial
Pressure, CVP
Mean 0-6mmHg
PulmonaryArtery Pressure
Systolic
End-diastolic
mean
15-30mmHg
4-12mmHg
9-19mmHg
PCWP Mean 4-12mmHgCardiac Output 4-8 L/min
Mixed Venous
O2 Sat
>70%
SVR 800-1200