Shock cardiogeno e rottura di setto interventricolare

Dott. Alessandro BrussaDott.ssa Daniela Comi

Scuola di Specializzazione in Anestesia, Rianimazione e Terapia IntensivaUniversità degli Studi di Udine

Dott. Paolo ChiarandiniClinica di Anestesia e RianimazioneDirettore Prof. Giorgio della Rocca

Caso clinico

26/10/2015, ore 17:19

L. F. 78 anni, giunge in PS per dolore addominale da qualche giorno, riacutizzatonelle ultime 2 ore (NRS 10).

In anamnesi: malattia di Alzheimer, ipertensione arteriosa non in terapiadomiciliare

In PS: pallida, sofferente, tachipnoica, ipotermica (TC 35°C). Ipotesa (AP 70/40mmHg) e tachicardica (FC 130 bpm), saturazione non rilevabile. Addome teso,molto dolente e dolorabile.

ECO fast: aorta addominale nei limiti, anse intestinali dilatate.

ECG (non refertato): tachicardia sinusale, abnorme deviazione assiale destra,blocco intraventricolare aspecifico, possibile infarto laterale, intervallo QT corto.

EGA venoso: pH 7.04, lattati 14.5 mMol/L, Creat 2.34 mg/dL. Si inizia infusionedi liquidi caldi, si somministra morfina 3 + 2 mg ev.

26/10/2015, ore 18:00 TC torace addome

Allertamento anestesista rianimatore.

Parametri vitali stabili durante la procedura, AP 130/80 mmHg, HR 130 bpm,SpO2% 98% in aria ambiente, RR 18 atti/min, GCS 15, TC 34°C

TC torace-addome: “[…] il quadro nel complesso potrebbe essere compatibilecon sofferenza vascolare delle anse su base di bassa portata – ipoperfusione.Il fegato presenta dilatazione delle vene sovraepatiche (15 mm) e densitàomogenea […]. Entrambi i reni presentano impregnazione corticale rallentatae disomogenea, con aree di ipoperfusione – ischemia […]. A livello toracicoversamento pleurico a destra di 18 mm ed a sinistra di 4 mm con distelectasiadel parenchima adiacente. Minimo versamento pericardico […]”

L’accesso in PS si chiude con il ricovero presso la Terapia Intensiva Clinica.

Caso clinico

Incannulamento vena giugulare interna destra con introduttore AVA.

TnI 10.0 ng/mL, BNP 2658 pg/mL

Deterioramento neurologico ed ipotensione (70/40 mmHg)Procedure:• IOT (somministrati Midazolam 3 mg e Propofol 20 mg)• Avviata Noradrenalina a 0.1 mcg/kg/min• Riempimento volemico con soluzione albuminata 4% 250 mL• Posizionato CV (paziente anurica)

Incannulamento arteria femorale dx con introduttore PiCCO.

18:40

18:45

19:10

Eco TT: Ventricoli dx e sn dilatati, ipocinesia diffusa, rilevazione di versamento pericardico, non variazioni respiratorie della VCI.Procedure:• Avviato Enoximone a 1.75 mcg/kg/min.

18:50

Inviato emocromo, PE complete, profilo ingresso, TnI, BNP. All’EGA-A:pH 7.23, PaO2 350, PaCO2 35, HCO3 15.3, BE -11.5, SaO2 98.8%, SvO2 59%, Lac 15, P/F 350

Ingresso TI Clinica, h 18:20

18:35

All’EGA-A:pH 7.27, PaO2 119, PaCO2 30.6, HCO3 15.4, BE -11.4, SaO2 97%, Lac 10, P/F 322

22:09

Posizionamento catetere Swan-Ganz, PAPm 25 mmHg, wedge pressure 18 mmHgTnI 13.9 ng/mL00:00

26/10/2015

Paziente analgosedata con Remifentanil 0.2 mcg/kg/min, intubata e ventilata in SIMV + PS(5+13), P/F 380. Emodinamica sostenuta da noradrenalina 0.08 mcg/kg/min ed enoximone2.5 mcg/kg/min, AP 100/60 mmHg, HR 140 bpm. Anurica.

• Episodio di TV ed FA trattati con bolo di amiodarone 300 mg e MgSO4 2 gr.

• Si invia ECG, si richiede consulenza cardiologica urgente• pH 7.38, PaO2 138, PaCO2 33.4, HCO3 20.7, BE -4.9, SaO2 98%, SvO2 90%, Lac 3.4, P/F 381• TnI 15.9 ng/mL, BNP 4418 pg/mL, AST 10157 UI/L, ALT 4527, LDH 26366 UI/L

06:30

12:00Referto ECG: nei limiti di norma.• Emodinamica mediante termodiluizione in cuore destro (C.O. 5.46, C.I. 3.16)• Stop noradrenalina• TnI 18.0 ng/mL

27/10/2015

18:00

Insorgenza di FA ad alta frequenza senza risentimento emodinamico.• Si esegue ECG e si invia a refertare con criterio di urgenza.• Bolo di amiodarone 300 mg ed avvio di infusione continua con 900 mg/24h• pH 7.39, PaO2 125, PaCO2 22.7, HCO3 17, BE -10.9, SaO2 97%, Lac 5.8, P/F 416• TnI 16.2 ng/mL

18:45

Valutazione cardiologicaEcocardioscopia: VS di normali dimensioni […] limitata area di acinesia a carico della paretebasale inferiore, funzione contrattile nei limiti di norma. VD normofunzionante. Nonpresenti vizi valvolari. Non versamento pericardico.ECG: FA, FC 142 bpm, lesione subepicardica inferiore con specularità anteriore.Diagnosi: shock cardiogeno con disfunzione multiorgano. Infarto miocardico inferiore.Conclusioni: considerato il ritardo dalla presentazione dei sintomi > 24 h e l’attuale stabilitàemodinamica in terapia (AP 100/70 mmHg, HR 100 bpm), si ritiene non indicato studiocoronarografico urgente. Da rivalutare in base all’andamento clinico.Programma: consiglio somministrazione di Flectadol 500 mg ½ fl, infusione di eparina sodicamantenendo aPTT compreso fra 1.5 e 2.5. Proseguire curva enzimatica della Troponina.

27/10/2015

19:20

22:45

23:30

Paziente analgosedata con Remifentanil 0.05 mcg/kg/min. Alla finestra neurologicarisvegliabile, collaborante, sofferente per forti algie addominali. Intubata e ventilata in SIMV+ PS (5 + 12), P/F > 400. Emodinamica sostenuta da enoximone 2.5 mcg/kg/min, AP 105/60mmHg, HR 125 bpm nonostante i. c. di amiodarone. Addome dolente alla palpazione,peristalsi assente. Anurica nonostante stimolo farmacologico con furosemide a 8 mg/h.• Somministrato acetilsalicilato di lisina 250 mg ev ed avviata eparina sodica i.c. come daconsulenza cardiologica (aPTT 1.5-2.5).• C.O. 3.52, C.I. 2.04

C.O. 1.9, C.I. 1.1Su episodio ipotensivo (AP 70/50 mmHg) si riavvia noradrenalina.

FA ad alta frequenza (HR 170 bpm), emodinamica instabile.• Cardioversione elettrica con 200J; iniziale ripresa RS (HR 90 bpm)• Nuovo episodio di FA, secondo tentativo di cardioversione con 200J fallito.• Si somministra amiodarone 200 mg in bolo con parziale controllo della frequenza cardiaca(HR 130 bpm).• pH 7.19, PaO2 131, PaCO2 17.3, HCO3 9.9, BE -20.4, SaO2 96%, SvO2 86%, Lac 14, P/F 437

27/10/2015

09:00

09:10

09:45

Paziente analgosedata con remifentanil 0.1 mcg/kg/min, soporosa ma risvegliabile, muove iquattro arti. Emodinamica in FA supportata da noradrenalina 0.16 mcg/kg/min edenoximone 2.5 mcg/kg/min, AP 85/43 mmHg, HR 127 bpm. Intubata e ventilata in SIMV +PS (5 + 11), FiO2 0.5, P/F 366. Anurica nonostante stimolo farmacologico con furosemide a 8mg/h. In corso terapia anticoagulante con eparina 25000 UI i. c.• EGA-A: pH 7.3, PaO2 183, PaCO2 24.7, HCO3 13.8, BE -14.3, SaO2 98.3%, SvO2 90%, Lac 18• TnI 27.9 ng/mL, AST 8295 UI/L, ALT 5352, LDH 23052 UI/L• Si richiede consulenza cardiologica

Ecocardio transtoracicoVS di normali dimensioni con lieve ipertrofia concentrica. […] Funzione sistolica ventricolaresinistra normale in ventricolo ipercinetico. Presenza di dropout di echi a livello delsegmento medio del setto muscolare configurante DIV di 15 mm di diametro con shuntsn/dx emodinamicamente significativo. […] VD di dimensioni ai limiti superiori di normacon normale funzione di pompa. Non versamento pericardico. FE 82%

Consulenza cardiologica: in accordo con il dott. Proclemer si concorda trasferimento dellapaziente in sala di emodinamica.

10:2012:15

Emodinamica (14 h e 20 minuti dal First Medical Contact)STEMI inferiore subacuto in shock complicato da DIV a livello del setto medio• Coronarografia Coronaropatia calcifica trivascolare: occlusione recente di IVP,occlusione cronica di ramo diagonale e MO, patologica critica diffusa di IVA media e stenosicritica di Cfx medio-prossimale.• Cateterismo cardiaco destro lieve ipertensione polmonare• Posizionamento IABP per via femorale sinistra (introduttore arterioso 8 Fr 11 cm,introduttore venoso 7 Fr 11 cm)

28/10/2015

19:00

22:00

00:00

Paziente analgosedata con remifentanil 0.1 mcg/kg/min, apre gli occhi alla chiamata.Intubata e ventilata in SIMV + PS (5 + 11), FiO2 0.5, P/F 258. Ipotesa e tachicardica, in corsonoradrenalina 0.22 mcg/kg/min, IABP e amiodarone 900 mg/die, AP 65/45 mmHg, HR 135bpm. Anurica. TC 38.1°C. In corso terapia anticoagulante con eparina 25000 UI i. c.• EGA-A: pH 7.23, PaO2 129, PaCO2 30.2, HCO3 14, BE -13.7, SaO2 97%, Lac 17• TnI 40.0 ng/mL, BNP 3602 pg/mL

Condizioni cliniche in peggioramento, mAP 45 mmHg con noradrenalina 0.25 mcg/kg/min econtropulsazione aortica. Scambi respiratori compromessi. Anurica.• Si avvia adrenalina 0.06 mcg/kg/min• EGA-A: pH 7.29, PaO2 87.7, PaCO2 27, HCO3 15, BE -12.4, SaO2 94.5%, Lac 15, P/F 175

Si avvia Diazepam 5 mg/h

07:50

29/10/2015

Progressiva ipotensione e bradicardia non responsiva al supporto rianimatorio massimale e contropulsazione aortica fino ad arresto cardiocircolatorio . Si constata l’exitus.

28/10/2015

Accertamento diagnostico

Cuore (gr 560)

Forma conservata, volume aumentato con marcato ispessimento. Presenza disevera aterosclerosi subocclusiva della coronaria di destra e della coronaria disinistra (discendente anteriore). Presenza di marcata area di necrosiinterventricolare con parziale rottura.

Conclusioni

– Arteriosclerosi generalizzata di grado lieve con coronarosclerosimultifocale subocclusiva.

– Infarto miocardico acuto del setto interventricolare

Cardiogenic Shock

• Definition

• Causes

• Incidence

• Treatment

Cardiogenic shock is a state of end-organ hypoperfusion due to cardiacfailure.

The definition of cardiogenic shock includes hemodynamic parameters:

• persistent hypotension (systolic blood pressure < 80 to 90 mmHg or meanarterial pressure 30 mmHg lower than baseline)

• severe reduction in cardiac index (< 1.8 L/min/m2 without support or < 2.0to 2.2 L/min/m2 with support)

• adequate or elevated filling pressure (left ventricular [LV] end-diastolicpressure > 18 mmHg or right ventricular [RV] end-diastolic pressure > 10 to 15mmHg)

NB: The diagnosis is usually made with the help of pulmonary artery (PA) catheterization;however, Doppler echocardiography may also be used to confirm elevation of LV fillingpressures

Circulation (2008); 117: 686-697

Definition

• Miocardial infarction

- STEMI

- nSTEMI

• Aortic dissection

• Acute myopericarditis

• Takotsubo cardiomyopathy

• Hypertrophic cardiomyopathy

• Cardiac tamponade

• Acute valvular regurgitation

• Massive pulmonary embolism

Circulation (2008); 117: 686-697

- endocarditis- trauma- degenerative disease

- ST elevation- release of cardiac markers- absence of significant CAD

Causes

Cardiogenic shock complicates approximately 5-8% of STEMI and 2.5% of nSTEMI cases

(incidence is on decline in parallel with increasing rates of use of primary PCI)

Mechanical complications (rupture of ventricular septum, free wall, or papillary muscles) cause 6-12% of cardiogenic shock cases(timely repair of myocardial rupture associated with CS is critical for survival)

Incidence

Circulation (2008); 117: 686-697

ESC Guidelines European Heart Journal (2012) 33, 2569–2619

Recommendations for initial diagnosis

Atypical ECG presentations

AMI Diagnosis

ESC Guidelines European Heart Journal (2012) 33, 2569–2619

STEMI algorithm

ESC Guidelines European Heart Journal (2016) 37, 267–315

NSTEMI algorythm

Treatment

• Reperfusion therapy

• Hemodynamic management

• Pharmacological treatment

• Mechanical support

• Surgical treatment ofcardiogenic shock (due tomechanical complications)

ESC Guidelines European Heart Journal (2012) 33, 2569–2619

NB: Routine use of IABP (in patients without shock) is not recommended.

Fibrinolysis(where primary PCI cannot be offered to STEMI patients within the recommended timelines)

Primary Percutaneous Coronary Intervention (PCI)

Reperfusion therapy

Emergency revascularization with either PCI or CABG is recommended insuitable patients with cardiogenic shock due to pump failure after STEMIirrespective of the time delay from MI onset (Class I, LoE: B)

In the absence of contraindications, fibrinolytic therapy should beadministered to patients with STEMI and cardiogenic shock who areunsuitable candidates for either PCI or CABG (Class I, LoE: B)

The use of intra-aortic balloon pump (IABP) counterpulsation can be usefulfor patients with cardiogenic shock after STEMI who do not quickly stabilizewith pharmacological therapy (Class IIa, LoE: B)

Step 1

Step 2

Step 3

ACCF/AHA STEMI Guideline Circulation (2013) 127:e362-e425

RCT, multicentrico, 300 pazienti

Emergency revascularization VS

Initial medical stabilization in patients with shock due to left ventricular failure complicating

myocardial infarction

At 30 days there was no significant overall benefit of early revascularization for patients with myocardial infarction who had cardiogenic shock due to left ventricular dysfunction. However, early revascularization resulted in lower mortality from all causes at six months.

Hochman et al. N Engl J Med (1999); 341:625– 634

Hemodynamic management

J Am Coll Cardiol. (2004) 44:340 –348.

Am Heart J. (2006) 151:890 e9–e15.

Clinical assessment with echocardiography is a reasonable alternative: thefinding of a short mitral deceleration time (< 140 ms) is highly predictive ofpulmonary capillary wedge pressure > 20 mm Hg in CS

PA (Swan-Ganz) catheterization is frequently performed to confirm thediagnosis of cardiogenic shock, to ensure that filling pressures areadequate, and to guide changes in therapy

Pharmacological treatment

The American College of Cardiology/ American Heart Association (ACC/AHA)guidelines recommend norepinephrine for more severe hypotensionbecause of its high potency.

1. Inotropes

2. Vasopressor agents

Inotropes increase myocardial ATP consumption such that short-termhemodynamic improvement occurs at the cost of increased oxygen demandwhen the heart is already failing and supply is already limited.Levosimendan, a calcium-sensitizing agent, has so far shown little additionalvalue in randomized heart failure trials.

Circulation (2008); 117: 686-697

DobutamineEnoximoneLevosimendan

Norepinephrinevs

Dopamineas first-line vasopressor therapy to restore and maintain

blood pressure

Multicenter, randomized trial, 1679 patients

De Backer et al. N Engl J Med. (2010); 362:779–89

Although there was no significant difference in the rate of death between patientswith shock who were treated with dopamine as the first-line vasopressor agent andthose who were treated with norepinephrine, the use of dopamine was associatedwith a greater number of adverse events.

De Backer et al. N Engl J Med. (2010); 362:779–89

Randomized, double-blind trial, 1327 patients

SURVIVE randomized trial, JAMA (2007); 297:1883–1891

Despite an initial reduction in plasma B-type natriuretic peptide level in patients inthe levosimendan group compared with patients in the dobutamine group,levosimendan did not significantly reduce all-cause mortality at 180 days or affect anysecondary clinical outcomes.

SURVIVE randomized trial, JAMA (2007); 297:1883–1891

Mechanical support

Circulation (2008); 117: 686-697

• Intra-aortic balloon counterpulsation (IABP)

Use of an IABP provideso coronary and peripheral perfusion via diastolic balloon inflationo augments LV performance via systolic balloon deflation with an acute decrease in afterload.

NB: accurate timing of inflation and deflation is necessary to provide optimal support.

Not every patient has a hemodynamic response to IABP response predicts better outcome

• VA-ECMO

In patients with cardiogenic shock refractory to conventional medical therapies

o provides temporary cardiac and respiratory life support allowing myocardial recovery

o bridging to heart transplantation or the implantation of a left ventricular assist device (LVAD)

Mechanical support

Intensive Care Med (2016); 42:370–378

Journal of Critical Care (2015); 30: 949–956

Retrospective, observational cohort study125 patients

• Survival rates of those weaned from ECMO at 3months, 12 months, and 2 years were 87%, 79%,and 71%, respectively

• Ischemic heart disease, higher lactate and higherbilirubin at initiation of VA-ECMO, and a longerduration of renal replacement therapy duringECMO were all independently associated withdecreased length of survival LOVE score

• Good long-term survival can be achieved inpatients who have been successfully weaned fromVA-ECMO

Two-center retrospective study138 patients

Intensive Care Med (2016); 42:370–378

The ENCOURAGE score might be a useful tool to predict mortality of severe cardiogenic shock AMI patients who received VA-ECMO

Intensive Care Med (2016); 42:370–378

Surgical treatment of cardiogenicshock due to mechanical complications

Repair of ventricular septum rupture (VSR) and free wall rupture present technicaldifficulties to the surgeon because of the need to suture in an area of necroticmyocardium (mortality 87%). Repair of papillary muscle rupture does not involvenecrotic myocardium in suture lines, and mortality associated with this repair is lower.

The unpredictability of rapid deterioration and death with VSR and papillary musclerupture makes early surgery necessary even though there may be apparenthemodynamic stabilization with IABP.

A subgroup of patients with VSR exists for whom surgery is futile because mortalityapproaches 100% very elderly and patients with poor RV function.RV function is a more important determinant of outcome in VSR than LV function

Circulation (2008); 117: 686-697

Retrospective study on 34 consecutive patients who had undergone surgical repair for ventricular septum defects following acute myocardial infarction

The 30 days operative mortality was 65%. Mortality within the posterior VSDs group was 74% and the anterior VSDs group was 46%

A.Cinq-Mars et al. International Journal of Cardiology (2016); 206: 27–36

A.Cinq-Mars et al. International Journal of Cardiology (2016); 206: 27–36

A.Cinq-Mars et al. International Journal of Cardiology (2016); 206: 27–36