CARDIOGENIC SHOCK , SỐC TIM, ĐH Y DƯỢC TP HCM

Bài giảng dành cho sinh viên y khoa, bác sĩ đa khoa, sau đại học. ĐH Y Dược TP Hồ Chí Minh. Definition Etiology Pathophysiology Clinical manifestation Diagnosis Management Prevention

CARDIOGENIC

SHOCK

Vu Minh Phuc MD PhD.

04-2012

1 DEFINITION

Cardiogenic shock is a condition of inadequate tissue perfusion resulting from myocardial dysfunction.

The clinical definition of cardiogenic shock is decreased cardiac output and evidence of tissue hypoxia in the

presence of adequate intravascular.

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2 ETIOLOGY

(1) Congenital heart disease

(2) Myocarditis (virus, bacteria, sepsis, noninfectious inflammation)

(3) Poisoning or drug toxicity

(4) Myocardial injury (trauma, cardiac surgery)

(5) Cardiomyopathy

– inherited abnormality: DCM, HCM, RCM, NCCM

– acquired abnormality of pumping function

• Myocardial ischemia or infarction

• Secondary to valvular heart diseases

(6) Acute valvular heart diseases: AR, MR, AS, prosthetic valve thrombosis

(7) Arrhythmia

(8) Obstruction: tamponade, contrictive pericarditis, myxoma

(9) End stage of other kinds of shock

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2 PATHOPHYSIOLOGY

COMPENSATORY AND PATHOLOGIC MECHANISMS

  SVR (due to  cathecholamine) → redirect blood flow from

peripheral and splanchnic to the heart and brain.

  HR and SVR →  LV work & myocardial oxygen consumption.

  SVR →  SV when pumping function of the heart is poor.

 4  venous tone →  CVP (right atrial) and pulmonary capillary pressure

(left atrial).

(5) Renal perfusion  → activation of renin-angiotensin-aldosterol → renal

fluid retention

(4) + (5)  Pulmonary edema

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4 CLINICAL MANIFESTATIONSFindings consistent with cardiogenic shock

Cardiovascular Function

Assessment of

End-Organ Funtion

• Tachycardia

• Normal or low BP with a narrow pulse pressure

• Weak or absent peripheral pulses

• Delayed capillary refill with cool extremities

• Signs of congestive heart failure (eg, pulmonary edema, hepatomegaly, jugular venous distention)

• Cyanosis, low SpO 2 (caused by cyanotic CHD or pulmonary edema)

• Cold, pale, diaphoretic skin

• Changes in mental status

• Oliguria

D • Changes in mental status

E • Variable temperature

• Focal infection, hyper or hypothermia

• Systemic Inflammation Reaction Syndrome (SIRS)

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5 DIAGNOSIS

3 Diagnosis of causes

1 Congenital heart disease ECG, CXR, Echocardiography

2 Myocarditis (virus, bacteria,

5 DIAGNOSIS

4 Assessment of End-Organ Function and complications

(ABG), central venous oxygen saturation, plasma lactate, hemoglobinemia

– Kidney : urinary analysis, renal function

– Liver : liver function, coagulation test, blood glucose

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6 MANAGEMENTMain objectives

1 To improve the effectiveness of cardiac function

and overall cardiac output by increasing the efficiency of ventricular emptying

2 To minimize interventions or host responses that

increase metabolic demand

6 MANAGEMENT

AIRWAY SUPPORT

1 Monitoring of hypoxemia

2 Airway support

– High flow oxygen is indicated

– NCPAP or BiPAP or ventilator : pulmonary edema

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6 MANAGEMENT

EXCLUDE THE CAUSES OF CARDIOGENIC SHOCK

1 At the same time of treatment of shock

– CHD: specific procedures (BAS, balloon pulmonary valvar dilation,

PGE1, ) – Viral myocarditis : gamma globulin

– Bacterial myocarditis, sepsis : antibiotics

– Myocarditis in rheumatic diseases: corticosteroids

– Myocardial ischemia or infarction, poisoning or drug toxicity: specific

treatments – Treatment of other kinds of shocks

2 Before treatment of shock

Antiarrhythmia drugs (arrhythmia), pericardiocentesis (tamponade)

3 After treatment of shock

Cardiac surgery (CHD, valvular heart disease)

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6 MANAGEMENT

TREATMENT OF SHOCK

Preload

variable 1 Fluid administration?

Contractility 2 Inotropic agents?

decreased

Afterload

increased

3 Reduce afterload?

• Presence of risk factors of inadequate preload: poor intake,

fever, vomitting, diarrhea

• Low CVP, ventricle’s volume on echocardiogram.

∗ HOW? and WHAT?

• Cautiously and slowly give 5-10 mL/kg isotonic crystalloid

infusion over 10-20 minutes

• Frequently assess respiratory function during fluid therapy

→ respiratory distress, pulmonary edema?

• NCPAP, BiPAP, ventilator are ready.

- Fatal hypotension systoilc BP < 60 + 2n (< 70) mmHg

Fatal hypotension → MOD → irreversible shock → die

 Inotrope agents has strong vasoconstriction

(High dose Dopamine or Epinephrine or Norepinephrine)

Hypotension

 Inotrope agents can  SVR

(Dobutamine or Milrinone + Dopamine –renal dose)

Normal BP : Vasodilators (Nitroglycerin or Nitroprusside)

-  afterload #  pulmonary arterial resistance

- Milrinone, Dobutamine are preferred

Hypotension  Inotrope agents can  SVR

- gradually  then off Epi or Norepi

- and Dobutamine or Milrinone

(gradually  the dose if no response)

- and Dopamine-renal dose

(gradually  to renal dose)

Stable hemodynamics  Don’t change the drugs’ dose for ≥ 24 hours

Stable hemodynamics  Gradually  drugs’ dose then off

6 MANAGEMENT

TREATMENT OF COMPLICATIONS

1 Adjust electrolyte and acid-base balance

2 Acute renal failure

3 Digestive hemorrhagia due to stress

4 DIC

5 Acute pulmonary edema associated with cardiogenic

shock

• Give diuresis even patient in shock

• Morphine and Nitroglycerin are contraindicated

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Thanks for your attention