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Introduction
Heart failure: hypotension. Periferic signs of shock oliguria Altered consciousness Dyspneea See massive PAO. Lactate level elevation.
Most frequent: Myocardic infarction Obstructive causes: Tamponade Pulmonary embolysm Other causes: Myocardiopathy Severe myocarditis Valvulopathy : IA => EI, dissection IM RA Post CEC
Etiology
Physiopathology
Preload determinants
Diastola diminuation Acceleration of cardiac rate Loss of atrial contraction Extraparietal pressure augumentation: tamponade PEP Compliance issues: ischemic Hypertrophic cardiomiopathy
Expands easily because of its thinness Its expansion may limit LV filling Systo-diastolic perfusion
Spontanious respiration
Bronchial edema => increase resistance to gas flow => increased inspiratory depression Increased venous return Increase in the transparietal gradient of the LV => disconfort in the systolic ejection of LV.
Ventilation Interactions
In spontanious ventilation: inspiration increases the venous return and therefore the rate of RV The increase in lung volume increases lung resistance In assisted ventilation: Increased intrathoracic pressure
Decreases venous return Increases postload of the RV Increases vascular resistence of the lungs
The increased intrathoracic pressure decreases venous return and therefore preloads VG the increased intrathoracic pressure reduces afterload by decreasing LV - transmural LV pressure Decrease in the systolic stress of VG the increase in intrathoracic pressure by PEEP increases these effects
Hemodynamic table
Cardiac debit decrease Oxygen transportation decrease DO2 decrease Increase in extraction Absence of inflammatory syndrome Secondary appearance of an inflammatory syndrome Especially in post CPB
Monitoring of cardiac output and filling pressures Approximation PAOP => POG => LVEDP => ventricular volume Error causes: PEP, decreased LV compliance Pulmonary embolysm Mitral pathology, IA Respiration interference
If PAOP <12 => filling is usefull If PAOP is between 12 and 18: In the abscence of pulmonary edema => fill In case of pulmonary edema => do not fill If PAOP is over 18 => probably no filling Variation of PAOP and cardiac output should be monitored during filling.
Measurement of right and left ventricular surfaces A surface of the LV <7 cm2/m2 is in favor of hypovolemia evolution of the surface of the LV during filling surface of the RV, risk of expansion
During filling with 3L of crystaloids: parallel increase in the surface and measured pressures Systolic volume increase End of filling process: increased filling pressures without increasing the ventricular surface
Medication Treatment
1
Isoprenaline Dopexamine Dobutamine Dopamine Adrenalin Noradrenalin
0 0 0 ++
0 + 0 +++ 0 0
Treatment
Hemodynamic Filling Oxigenation Pain treatment Ethiological Thrombolysis is uneffective Thrombolysis and counterpulsation Percutaneous dilation Emergency coronary surgery Search for an VSD or IM
Drug treatments
With caution when blood pressure is borderline Not to be used when PA is already low
Vasodilators increase cardiac output by decreasing afterload Vasodilators have a limited role in acute : Risk of aggravating hypotension Only the nitro-derivates are sometimes used: low dose: vassodilutant => decreased venous return High dose: arterial vasodilation Diuretics should not be used in acute cardiogenic shock outside of the PAO.
Volemic expansion
Hemodynamic effects: Decrease in the VA preload Decrease in LV afterload Respiratory effects: Hypoxemy correction Acidosis correction Decrease in oxygen consumption Respiratory work decrease sedation
Non-invasive ventilation
The non-invasive ventilation allows: Rapid correction of hypoxemia with shunt reduction A decrease in respiratory frequence and therefore a decrease in respiratory workload Reduces the need for intubation during severe PAO Most often: CPAP, PEP from 7.5 to 10 cmH2O.
an increase in diastolic blood pressure => improved perfusion VG a decrease in blood pressure in late diastole => facilitates the left ventricular ejection
Counterpulsation mechanism
Increased diastolic pressure Assisted sistolic pressure Non-assisted sistolic pressure
Treatment
ACFA Bradycardia
LV infarctus
Shock complicating 10% of IDM Mortality remains very high Installation of an ischemic vicious circle
Hypotension Sympathetic stim.
Ischemic aggravation
LVEDP increase
Mechanical complications of MI
Mitral inssuficience Pillar disruption or disfunction CIV Secondary pain Ecocardiography Surgery LV rupture 3/5 day
RV infarction
Very rare Most often associated with a posterior/inferior myocardial infarction Low-speed + increase in CVP + no sign of respiratory signs Treatment : Filling Inotropes IABP SEA
Myocarditis
State of shock in a viral context Diffuse alteration of systolic function on echocardiography TTT : Symptomatic Corticoides +- Immunosupressors Circulatory assistence Frequent recovery
Rao => LV hypertrophy, and late dilation On examination: breath mitigated by the low flow At echocardiography: gdt decreased by low-speed => Area Measurement Dangers of drug treatments: VD => decreased preload => lower ESR and lower BP => myocardial ischemia -antagonists poorly supported Counterpulsation awaiting surgery
Etiology: endocarditis, aortic dissection Clinical : Somewhat increased P differential Wheezing PTDVG > POG Dg => echocardiography
Tamponade
Pericardial effusion => increased pressure => discomfort filling Dg : KT : egalisation of POD/PAPD/POG Echocardiography
Conclusions
Cardiogenic shock requires diagnosis and etiologic treatment whenever possible treatment is not limited to dobutamine a complete hemodynamic assessment is necessary in case of failure of initial treatment
Bibliography
Choc cardiognique : Encycl Med Chir, Anesthsie-Ranimation, 36-840-c-10, 1999, M Shaller, P Eckert, D Tagan, Lausanne Choc Cardiognique : Anesthsie Ranimation Chirurgicale K Samii Infarctus aigu du myocarde avec sus-dcalage du segment ST : 48heures Encycl Med Chir, Anesthsie-Ranimation 36-725 F10