Cardiogenic shock

» Case based symposium«Acute heart failure in the emergency room

Veli-Pekka HarjolaFHFA, FESCHelsinki University Hospital, Finland

Conflicts of interest

• none declared

Evaluation of starting point

A. I never see cardiogenic shock patients in ED

B. I see CS patients occasionally but I do not have 24/7 cath lab services in my hospital

C. I work in hospital with 24/7 cath lab services and cardiac ICU/CCU and see these patients often

D. Other

Past medical history • arterial hypertension (bisoprolol 2.5mg OD; losartan

50mg OD)• metastatic mammary cancer with lung metastases• irritating cough for some time• in April cataract surgery l.a. and dental therapy • 30.4. 2015 to ED: right-sided sharp chest pain; ECG

and CXR nothing relevant• hs-TnT 32-35 ng/L: ”no change, can be discharged

home”

74-yr old female with acute dyspnea arrived to ED 8.5.2015

• 8.5.2015 arrived to a community hospital ED at 20:20 because of dyspnea and mild fever

• Significant respiratory distress, respiratory rate 30/min• Blood pressure 140/70, HR 115/min• ECG sinustachycardia 112/min, spO2 90%• Cardiac auscultation normal• Widespread rales bilaterally• No peripheral oedema, feet cold, mild aching in both calfs • Arterial blood pO2 9.1 kPa (FiO2 40%), CO2 3.9 kPa, pH 7.46• Lactate 1.3 mmol/L

Clinical findings in ED

First ECG in ED

What would you do next

A. start bronchodilators and antibioticsB. wait for chest x-rayC. wait for more laboratory resultsD. do immediate ultrasound

What would you do next

A. salbutamol and cefuroxime startedB. chest x-ray requestedC. laboratory tests requestedD. ultrasound not done

Chest X-ray (recumbent position)

Points to consider• cardiac volume• aorta• signs of congestion• oedema• pneumonia• pleural fluid• cancer invasion

Chest X-ray (recumbent position)

Points to consider• cardiac volume: normal• aorta: normal• signs of congestion: yes• oedema: interstial, yes• pneumonia: no • pleural fluid: some• cancer invasion: yes

Rapid clinical deterioration in 3.5 hrs

• Non-invasive posite-pressure ventilation initiated due to progressive respiratory distress

• Yet no response: respiratory rate 37/min, spO2 85%

• HR 120/min, sinus rhythm• Blood pressure 90/50 mmHg• No mental disturbance• No limitation to care• Patient got intubated with propofol sedation

Thereafter progressive hypotension

• Noradrenalin was started and rapidly up-titratedLaboratory results • hs-TnT of 322 ng/L• WBC 5.0 E9/L, neutrophils 2.6 E9/L • C-reactive protein 10 mg/L• Creatinine 123 umol/L, eGFR 37 ml/min

Second ECG in ED (9.5. 01:30)

What is your hypothesis now?

A. Pericardial tamponade and cardiogenic shock (CS)

B. Pulmonary embolism & CSC. Acute coronary syndrome & CSD. Some other cause of CSE. Septic shock F. Hypovolemic shock

What would you do next ?

A. Request immediate bedside ultrasound B. Pulmonary CT-angiogramC. Transfer the patient to cath labD. Other

Bed-side echo

• Right side normal• Left side: wide spread antero-apicolateral hypokinesia

and inferior hyperkinesia• No pericardial effusion• No significant signs of valvular regurgation or aortic

stenosis• No structural disruptions• Inferior vena cava normal; No pleural fluid• No pictures saved, unfortunately• Lung US ??

What would you do next ?

A. Send the patient by ambulance to primary PCI center in 20 min distance with nurse

B. Stop active treatmentC. Continue with medical therapy and see

whether recovery will occurD. Other

Transfer to a PPCI center

• Before transfer: • Blood pressure was 110/80 mmHg, mean arterial

pressure 87 mmHg, heart rate 100/min, sinus• Periphery was cold, diuresis 20 ml/hour• Blood lactate 2.2 mmol/L• Patient was transferred by ambulance (20min) with

nurse without mechanical circulatory support

The diagnosis was confirmed with coronary angiogram

Dr Marjut Varpula is acknowledged

What is the diagnosis?

A. Aortic dissectionB. Rupture of mitral chordaeC. ACS with large hypokinesiaD. Takotsubo cardiomyopathyE. Other

Conclusion and clinical recovery • recent procedures may have provoked stress-induced

cardiomyopathy and lead to pulmonary oedema• patient developed CSin the ED• propofol aggreviated hypotension by vasodilation and

lead to pronounced hemodynamic collapse • angiogram showed open coronaries and confirmed

Takotsubo cardiomyopathy• levosimendan infusion was started 9.5

– patient was extubated– norepinephrine was weaned off

• discharged home 21.5.

Prediction of in-hospital mortality CardShock risk score

Variable Risk scoreAge > 75 years 1Confusion 1Previous MI or CABG 1ACS etiology 1LVEF <40% 1Blood lactate

2-4 mml/L 1> 4 mmol/L 2

eGFRCKD-EPI 30-60ml/min 1

<30 ml/min 2Maximum points 9

Harjola VP, Lassus J et al. Eur J Heart Fail, 2015, 17: 501

Publihed on-line 21.5.2015 simultaneously in Eur J HF and Eur H J

• hypotension (SBP <90 mmHg) despite adequate filling status AND

• signs of hypoperfusion– oliguria– cold peripheries– altered mental status– lactate >2 mmol/L– metabolic acidosis– (mixed venous oxygen saturation SvO2 >65%)

Definition of cardiogenic shock

Mebazaa A et al EJHF and EHJ 2015

Take home message• ECG and echocardiography immediately • Arterial line (no agreement on method of haemodynamic monitoring: PAC etc)

• Fluid challenge (saline or Ringer’s lactate, >200 mL/15–30 min)• Dobutamine to increase cardiac output; levosimendan especially in

CHF patients on oral beta blockade• Vasopressors to maintain systolic BP (norepinephrine is recommended)

• All rapidly transferred to a centre with 24/7 cath lab • Short-term MCS possibly in refractory CS

– depending on patient age, comorbidities and neurological function– no mode of short-term MCS is recommended over another– IABP not routinely recommended in CS

• Cardioversion of rapid arrhythmias

Mebazaa A et al EJHF and EHJ 2015

Thank you

Back-up slides

Take home message

1. Fluid challenge first (Ringers solution 200ml/15min)2. Bed-side echo3. Inotropic agent (dobutamine; levosimendan; PDEI)4. Vasopressor if needed to maintain systolic/mean BP

(noradrenaline) 5. Continuous monitoring of the signs of organ perfusion and

hemodynamics (noninvasive, invasive)6. Mechanical circulatory support rather than combination of

several inotropes