Cardiogenic Shock

Dr M. Durand Anesthesia Department II CHU Grenoble

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

Cardiac performance determinants Preload Postload Contractility Cardiac frequence

Preload determinants

Diastola diminuation Acceleration of cardiac rate Loss of atrial contraction Extraparietal pressure augumentation: tamponade PEP Compliance issues: ischemic Hypertrophic cardiomiopathy

Diastolic and sistolic cardiac inssuficience

Sistolic : Ventricular contraction alteration Diastolic Abnormal ventricular filling:

Decreased distensibility ventricular fibrosis LV wall thickening.

causes : miocardic hypertrophy/ischemy.

Right heart failure

Right ventricule Very sensible at postload

cardiac output maintained up to a systolic pressure of 40 mmHg Less sensitive to preload

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

Increase in pulmonary volume

VG Interactions / Mechanical Ventilation

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

DC PA PVC PAPO DO2 ErO2

Cardiogenic Septic shock shock

Fundamental anomalies in shock states

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 : the Swan Ganz

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

PAOP - guiding filling value

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.

Evaluation for echocardiography

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

Swan Ganz and/or Ecocardiography

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

Study of variation in blood pressure during mechanical ventilation

Normal Function Abnormal Function

Medication Treatment
1
Isoprenaline Dopexamine Dobutamine Dopamine Adrenalin Noradrenalin

0 0 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

Phosphodiesterase inhibitors: Positive inotrope Peripheric vassodilutant They most be used:

With caution when blood pressure is borderline Not to be used when PA is already low

Diuretic and vassodilutant treatments

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

The existence of hypovolemia is not exceptional in cardiogenic shock: Administrated treatments:

sedation diuretics nitros

Prudent volemic expansion

Mechanical treatments - Ventilation

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.

Mechanical treatment: intra-aortic counterpulsation

Diastolic swelling of intra-aortic balloon:

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

Assisted tele-diastolic pressure Non-assisted tele-diastolic pressure

Treatment

Etiological : Tamponade => evacuation of the effusion Rhytm problems

ACFA Bradycardia

Pulmonary embolism Valvulopathies IDM

LV infarctus

Shock complicating 10% of IDM Mortality remains very high Installation of an ischemic vicious circle
Hypotension Sympathetic stim.

Ischemic aggravation
LVEDP increase

Perfusion pressure decrease

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

Cardiogenic shock of aortic stenosis

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

Cardiogenic shock from acute aortic insufficiency

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

Effusion Signs of tamponade

Treatment Effusion evacuation Attention at anesthesy/ventilation

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