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Sudden cardiac death and cardiogenic shock a team approach to save heart and brain
1. Sudden Cardiac Death And Cardiogenic
Shock : A Team Approach To Save Heart
and Brain
Dr Han Naung Tun, MBBS, MD, FACTM
National Representative Heart Failure Specialist of Tomorrow for Myanmar in HFA and
Ambassador of Echocardiography in EACVI, ESC
Council of Clinical Practice and Working Groups of European Society of Cardiology ,
France
Twitter : @HanCardiomd
2. Preamble
Main Topic: Ventricular Arrhythmias and SCD
– Clinical
ESC Guidelines: Ventricular Arrhythmias and
the Prevention of Sudden Cardiac Death
3. Patient Presentation
A 35-year-old male patient presented with out-of-hospital cardiac arrest.
He received immediate bystander phone-guided CPR.
After 5 minutes the medical intervention team arrived.
The initial rhythm was ventricular fibrillation.
There was ROSC after five cycles of CPR.
General malaise and dyspnoea since a few days, no chest pain (heteroanamnesis)
and he was intubated on site
4. Past Medical History
1 year before admission: ‘palpitations’, ECG: first degree AV block normal
24h rhythm monitoring, exercise test and echocardiography
3 months before admission: ‘longstanding cough’, CT thorax: nodular
opacities
2 months before admission: total AV-block during bronchoscopy,
R/implantation DDD-pacemaker, Echo: moderately ↓ LVEF and↓ RVEF
5. Table from JACC V O L. 6 8 , NO . 4 , 2 0 1 6
Cardiac Sarcoidosis
David H. Birnie, MD, MBCHB,a Pablo B. Nery, MD,a
Andrew C. Ha, MD,b Rob S.B. Beanlands, MDa
7. No known allergies
Familial medical history - Grandfather died of unidentified pulmonary
disease
Medication at admission - Methylprednisolone 24 mg OD, Omeprazole
20 mg OD
Social history - Theatre director
8. BP 90/50 mm Hg; HR 95 bpm; T 35,9°C; SpO2 95%
Full sedation (GCS 3/15), intubated and mechanically ventilated with low
ventilatory settings
Cold and clammy extremities, no signs of congestion
Tachycardia, no murmurs
Soft abdomen, normal peristalsis
Physical examination
9.
10.
11.
12.
13. Quick look TTE: severely impaired LV and moderately impaired RV
function
Coronary angiogram: normal
Pacemaker: 90% ventricular pacing, normal sensing and capture
threshold
Arterial blood gas: mild metabolic acidosis
Labs: raised cardiac and liver enzymes, acute kidney injury KDIGO 1,
raised inflammatory markers
14. Haemodynamically unstable
Recurrent VT, high dose of vasopressors (norepinephrine
0,800 µg/kg/min)
Amiodarone continuous infusion
Insertion of IABP
→ transfer to our hospital
Further course
15. Initial management in tertiary hospital
• Admission to ICCU
• Correction of electrolytes
• DDD-pacing at 100 bpm
• Association of Milrinone 0,400 µg/kg/min
• Targeted temperature management
• Persistent ventricular arrhythmia
• R/ Methylprednisolone 40 mg IV
• Lidocaine
• → stabilisation of arrhythmia, noradrenalin
16.
17. Further course on ICCU
Day 3
Persistent severely depressed left ventricular function
Inotrope dependent (milrinone)
Progressive organ failure (AKI stage 2, raised liver enzymes)
19. Still in the ICCU ...
Heart team: pLVAD 5,0L/min via right subclavian artery
Removal of IABP
Complicated by retroperitoneal haemorrhage
R/vascular surgery, transfusion with stabilisation
20.
21.
22.
23. Day 5 and after
D5
Haematoma insertion site; DVT right subclavian vein due to
compression
Sedation hold – neurologically intact
Start mobilisation (cycling)
Start beta blocker
D8
Extubation
25. What is the most appropriate next step to consider in this
patient?
(A) Weaning of mechanical circulatory support without other
measures
(B) Upgrade from DDD-pacemaker to CRT-D
(C) Insertion of long term left ventricular assist device
26.
27. Since the cardiac disease was
potentially reversible, LVAD as
bridge to heart transplant was
not yet considered. If no recovery
occurred, LVAD could be
considered since the patient
recovered from multiple organ
dysfunction but was still
dependent on temporary
mechanical support.
28. Since the cardiac disease was potentially reversible, LVAD as bridge to heart
transplant was not yet considered.
If no recovery occurred, LVAD could be considered since the patient recovered
from multiple organ dysfunction but was still dependent on temporary
mechanical support.
29. Because of the persistent very poor left ventricular systolic function, weaning
without other measures was not feasible.
Since there was persistent RV pacing with severely impaired left ventricular
ejection fraction and the need for a defibrillator in secondary prevention, the
pacemaker was upgraded to a CRT-D device with immediate positive
hemodynamic effect.
Milliez et al. Cardiac resynchronisation as a rescue therapy in patients with
catecholamine-dependent overt heart failure: Results from a short and mid-
term study European Journal of Heart Failure 2014
30. Because of the persistent very poor left
ventricular systolic function, weaning
without other measures was not feasible.
Since there was persistent RV pacing with
severely impaired left ventricular ejection
fraction and the need for a defibrillator in
secondary prevention, the pacemaker was
upgraded to a CRT-D device with
immediate positive hemodynamic effect
31.
32.
33.
34. D12
• Upgrade to CRT-D device because of persistent RV-pacing and septal dyskinesia
• Levosimendan
D14-16
• Gradual reduction of pLVAD flow – stable hemodynamics and biochemistry
• Sitting in a chair – cycling
D17
• Removal of pLVAD device
• Ischemic stroke (right ACM) – urgent thrombectomy
• Recuperation of left hemiparalysis
Day 12 and after ...
36. A multidisciplinary team approach is recommended in a patient with
cardiogenic shock and neurological complications to improve neurological
and cardiac outcome.
When a patient is 'sliding' on inotropes, temporary mechanical circulatory
support should be considered.
Bleeding and thrombotic complications of temporary mechanical
circulatory support (MCS) are frequent and should be monitored closely.
The risks of MCS should be balanced against benefits.
37. A percutaneous left ventricular assist device through the subclavian
artery permits early mobilisation and could buy time allowing cardiac
recovery.
Early sedation hold in patients with temporary MCS is useful to reveal
neurological complications and to facilitate appropriate management
and rehabilitation.
Early CRT-D implantation might have a beneficial hemodynamic effect
in acute heart failure, especially in the presence of high ventricular
pacing demands and dyssynchrony.
38. ESC guidelines:
Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death 2015
Acute and chronic heart failure 2016
Cardiac pacing and cardiac resynchronization therapy 2013
Alviar et al. Positive pressure ventilation in the cardiac intensive care unit JACC 2018.
Thiele et al. Management of cardiogenic shock complicating myocardial infarction
European Heart Journal 2019
Crespo-Leiro et al. Advanced heart failure: a position statement of the Heart Failure
Association of the European Society of Cardiology. European Journal of Heart Failure
2018
Milliez et al. Cardiac resynchronisation as a rescue therapy in patients with
catecholamine-dependent overt heart failure: Results from a short and mid-term study
European Journal of Heart Failure 2014
Birnie et al. Cardiac manifestations of sarcoidosis: diagnosis and management. EHJ 2016
Okada et al. Ventricular Arrhythmias in Cardiac Sarcoidosis. Circulation 2018
References
39. The best care of patients with
acute cardiovascular
syndromes relies on
immediate diagnosis and
decisions on treatment, some
of them life-saving.
The Clinical-Decision Making
Toolkit is THE tool to help all
practitioners make the best
bedside clinical decisions,
when managing patients with
acute cardiovascular diseases.
40. Acknowledgment
A clinical case form Dr. Schaubroeck Hannah
Subspecialty communities - Association for Acute
CardioVascular Care Education
Association for Acute CardioVascular Care
European Society of Cardiology