Managing Acute Cardiac

Emergencies in Special Population

Dr Ika Faizura Bt Mohd Nor

CASE 1

34 years-old woman.

Transferred from Hospital Klang with SOB (NYHA 11)

Previously well, Sedentary lifestyle.

2/12 SOB with housework and shopping

Denies any palpitation, chest pain and dizzy spell

No PMH of DM, HPT

G5P1+ 3, 32 weeks pregnant.

Physical Examination

Comfortable at rest

Afebrile

P=100 regular, BP 99/50, RR 20

JVP 6cm

Soft 1HS EDM loud P2

Lungs bi-basal crepitations

Mild pedal oedema

Transferred to HDU for monitoring.

IV frusemide

Mitral stenosis

90 % in CRHD ( 50% of patient has childhood history of RF)

Others:

Congenital

Calcification

Endocarditis with vegetation

PATHOPHYSIOLOGY OF MS

Begin with formation of tiny nodules

along valve leaflets

Fusion of the leaflet commissures

Thickening, fusion and shortening

of the chordae tendineae

Superimposed thickening, fibrosis,

and calcification of the leaflet

cusps

Cardiac hemodynamicsDevelopment of pressure gradient between the LA & LV in diastole.

In severe MS

leading to reductions in SV and CO

With mild to moderate MS

abnormalities are often only apparent with

exercise

other conditions that increase HR.

LAPulmonary

venousPulmonary capillary

Pulmonary arterial

Pulmonary vascular

resistanceRV failure

Severity of mitral stenosis

Degree of

MS

Mean gradient

(mmhg)

MVA (cm2 )PA press Symptoms

Normal 0 4 - 6 10-20

Mild MS <5 >1.5 <30 Exertional dyspnoea

Moderate

MS5 - 10 1.0 - 1.5 30-50

Symptom with minimal

exertion

Severe MS > 10 <1 >50 Symptom at rest

Natural progression Slow progressive disease.

Progression becomes more rapid after the onset of symptoms. Progression varies across geographical areas

The mean interval (rheumatic fever the onset of symptoms ) was 16.3 years.

At 25 years –

8 percent were asymptomatic,

9 percent were NYHA class II,

33 percent were NYHA class III,

50 percent were NYHA class IV or had undergone mitral valve surgery.

Progression from mild severe disability took an = 9.2±4.3 years.

34 years-old woman.

Transferred from Hospital Klang with SOB (NYHA 11)

Previously well, Sedentary lifestyle.

2/12 SOB with housework

Denies any palpitation, chest pain and dizzy spell

No PMH of DM, HPT

G5P2+ 2, 32 weeks pregnant.

Antepartum hemodynamic changes

The CO rises 30 to 50 % above

baseline during normal pregnancy

rise in blood volume

decline in SVR

maternal HR rises by 15 to 20

beats/min

Causes a 2 – 3 fold increase in the resting trans-mitral gradient.

Patient’s symptomatic status increase by about one NYHA class

Patient who is asymptomatic may develop mild symptoms.

Hemodynamic changes during labor and delivery

Marked fluctuations in CO

( increases up to 80 %)

Uterine contractions

Increased sympathetic tone due to

pain and anxiety.

The type of anesthesia

Relief of vena caval obstruction post

delivery.

Pregnancy in women with MS

Cardiac Disease in Pregnancy (CARPREG) index –Four predictors of cardiac events were identified:

Poor functional class (>NYHA class 11) or cyanosis

Previous cardiac events (eg, DHF,TIA, stroke) or arrhythmia

Left heart obstruction

MVA of <2 cm2,

AVA of <1.5 cm2,

peak LVOT >30 mmHg

Left ventricular systolic dysfunction (EF <40 )

1point = 3%, 30%,66%

CXR

ECG

The QRS amplitude and morphology are normal unless there is mitral regurgitation or coexistent aortic valve disease.

Left atrial hypertrophy and enlargement P wave that becomes broader (duration in lead II>0.12 sec), is of increased amplitude,

and is notched (due to the delay in left atrial activation). "P-mitrale.“

The left atrial changes also produce a prominent negative terminal portion of the P wave in lead V1.

The P waves changes are not seen in patients with atrial fibrillation. The fibrillatorywaves are coarse, generally >0.1 mV in amplitude, reflecting left atrial hypertrophy.

Pulmonary hypertension and right ventricular hypertrophy. The frontal axis shifts to the right (S>R in lead I and aVL) and a tall R wave develops in V1

and V2 (R>S or R/S ratio >1).

ECHOCARDIOGRAPHY

ECHOCARDIOGRAPHY

LA thrombus- TOE.

ManagementMedical

Surgical

Obstetric

The 2006 ACC/AHA guidelines on the management of valvular heart disease

identified the following risk groups for adverse maternal and/or fetal outcomes in

patients with MS

High Risk : Prophylactic PTMC or open commissurotomy prior to becoming pregnant

34 years-old woman. G5P2+ 2, 32 weeks pregnant, SOB (NYHA 11),

Severe MS (MVA 0.9), Est PAP 82/23 mmhg

High risk —

Symptomatic MS(NYHA

class II to IV)

Severe PHT

PA press>75 % of

systemic press.

o Low risk

Mild MS

MVA >1.5 cm2 and a mean

gradient <5 mmHg

No severe pulmo HPT

Medical management Bed rest and oxygen therapy

IV diuretic

B blocker: propranolol

Avoidance of significant anemia

Treating infection early.

Medical management AF:

Digoxin/B Blocker

Cardioversion

Anticoagulant:

SC/IV heparin – up to 12 weeks

Oral warfarin -12 to 36 weeks

SC/IV heparin – after 36 weeks

Percutaneous Transluminal Mitral Commisurotomy

Cardiac catheterization and angiographynoninvasive tests are not conclusive

Direct measurement of intra-cardiac pressures – gradient across the MV

severity of MS

Pre Vs Post PTMC

Obstetric and labor management

Pulmonary oedema

Arrhythmia

Obstetric and labor management

Good labor analgesia (avoid tachycardia)

Mode of delivery:

Trans-vaginal with epidural analgesia -preferred

Shortened second stage

Invasive cardiac monitoring

Arterial BP

Pulmonary catheter

ANTIBIOTIC PROPHYLAXIS —

Routine endocarditis prophylaxis is not necessary for

either cesarean or vaginal delivery

However, continuation of antibiotics for secondary

prophylaxis of rheumatic fever is recommended

Obstetric and labor management

Surgical option

Closed commissurotomy,

Open commissurotomy,

Mitral valve repair,

Mitral valve replacement

Case 2

20/10/2013 – 10 pm

23 year old college student in MIRI

MVR(mechanical-carbomedic)in Pakistan in 2011

Well post MVR on warfarin

2/52: SOB . 3/7:cough and orthopnea

Noted cannot hear prosthetic click:-2 weeks

Admitted in Miri hospital; treated as CAP with IV

augmentin

Physical Examination

SOB at rest

Afebrile

P=105 regular, BP 104/59, RR 28

JVP 6 cm

No prosthetic click heard

Lungs bi-basal crepitations

Mild pedal oedema

Blood test

Wcc 13.9x10 (neu 91), hb 17.4, plt 324

Lft ; normal, Rp; normal

Inr 4.1

Crp; 36.6 and ESR 13

Differential diagnosis

Transfer to CCU- for invasive monitoring

Refer to CTS for redo MV

Keep NBM

FFP x 2

IV Frusemide

IV Rocephine

4 am 21/10/2013

Worsening SOB

Already had 2 unit of FFP

P; 130 bpm, BP 130/80

JVP: 8cm

I/O: -200

Intubation

Post

Intubation

at 4 am

7.30 am 21/10/2013 Intubated ventilated sedated

P: 131 bpm Bp 83/59 CVP 18, sat 100% on Fio2 65%

Dobutamin 2.5 mcg/kg/min

INR 2.5

By 2 pm: maximun3 inotrope and milrenone

IABP was inserted

Aneuric with worsening renal profile and metabolic

acidosis

CVVH was started

22/10/2013

Redo MVR

Prosthetic Heart Valve

As early as 1960s

The ideal valve substitute should mimic the characteristics of a normal

native valve.

In particular, it should have excellent hemodynamics, long durability,

high thromboresistance, and excellent implantability

Figure 1. Different types of prosthetic valves.

Pibarot P, Dumesnil J. Circulation 2009;119:1034-1048 Copyright © American Heart Association, Inc. All rights reserved.

Bileaflet mechanical

(St Jude)Monoleaflet mechanical

(Medtronic Hall)

Caged ball valve

(Starr-Edwards)

Stented porcine

bioprosthesis

Stented pericardial

bioprosthesis

Stentless porcine

bioprosthesis

Percutaneous bioprosthesis

expanded over a balloon Self-expandable

percutaneous bioprosthesis

(Edwards Sapien) (CoreValve)

Figure 2. Algorithm for the selection of the optimal prosthesis in the individual patient.

Pibarot P, Dumesnil J. Circulation 2009;119:1034-1048 Copyright © American Heart Association, Inc. All rights reserved.

Long term managementAnti-thrombotic

Risk of Thromboembolic event

Mechanical > bioprosthetic valves

Mitral > aortic prosthetic valves

Early (<3 months)> late (> 3months)

Concomitant risk factors:

Atrial fibrillation

LV dysfunction

Left atrial dilation??

Previous thromboembolism

Hypercoagulable condition.

Aortic Valve

Mechanical

Mitral Valve

Bioprosthetic

< 3 months

> 3 months< 3 months

Mitral Valve +

Risk factor

Aortic Valve +

Risk factor

> 3 months

Aortic Valve

Mitral Valve

Figure 6. Prosthetic valves explanted for severe dysfunction.

Pibarot P, Dumesnil J. Circulation 2009;119:1034-1048 Copyright © American Heart Association, Inc. All rights reserved.

Obstructive thrombosis

Pannus ingrowth

Rupture of the outlet strut

and leaflet escape

Leaflet calcific degeneration and tear

Figure 7. Algorithm for the management of patients with left-sided prosthetic valve thrombosis.

Pibarot P, Dumesnil J. Circulation 2009;119:1034-1048 Copyright © American Heart Association, Inc. All rights reserved.

Thrombolysis:-

urokinase,

streptokinase,

Rtpa

Long term managementEndocarditis Prophylaxis

Patients with prosthetic valves are at high risk for endocarditis

because of the foreign valve surface and sewing ring.

Lifelong requirement for antibiotic prophylaxis

Dental

Endoscopic

surgical procedures

Patients and their treating physicians/dentists should be aware

of the importance of:

Dental hygiene

Blood cultures for any febrile illness before starting antibiotic therapy.

Long term managementProsthetic Valve Endocarditis

The incidence ≈0.5% per patient-year

High mortality rates (30% to 50%).

Diagnosis:

Positive blood cultures

Echocardiographic evidence of prosthetic infection:

Vegetations

Paraprosthetic abscesses

New paravalvular regurgitation

TEE is essential because of its greater sensitivity in detecting these

abnormalities.

Prosthetic valve endocarditis will eventually require surgery.

Case 3

42 years old Malay man Diagnosed with Non Ischemic Dilated Cardiomyopathy in

2005

CRT-D implanted in 2006

Ventricular Assist Device in planted July 2012

Well post Implantation. F class 1

End stage Heart Failure

Despite recent advancement in the management of heart failure, the quality of life and the survival rate of patients with severe heart failure remains limited.

The one-year mortality rate of those with advanced disease exceeded 50 % and the occurrence of sudden death is frequent.

For those patients who are suitable candidates, cardiac transplantation is the gold standard with proven benefit.

But worldwide shortages of donor hearts have resulted in the development of Ventricle Assist Device (VAD) to bridge patients to heart transplant.

Survival for the LVAD vs. OMM groups at 1 year were 52% vs. 25%, respectively.

Mechanical Circulatory Support as a Bridge to Transplant tor for Destination Therapy. Curr Heart Fail Rep (2010) 7:159–166..DOI 10.1007/s11897-010-0026-4

Long Term use of a left ventricular assist Device for End stage Heart Failure. N Engl J Med, Vol. 345, No. 20, November 15, 2001

Mechanical Cardiac Support Device Dream and Develish Detail N Engl J Med, Vol. 345, No. 20.November 15, 2001

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive SummaryJ. Am. Coll. Cardiol. 2001;38;2101-2113

Long-Term Destination Therapy With the HeartMate XVE Left Ventricular Assist Device: Improved Outcomes Since the REMATCH Study Congestive Heart Failure.Volume 11, Issue 3, pages 133–138, May/June 2005

Since 2010, the smaller and streamlined design of axial (HM II) and centrifugal flow pumps

(Heartware) has been implanted instead of the pulsatile pumps (PVAD and IVAD) which were much larger.

Ventricular Assist Device

Why Do We Need VADs?

Malaysia Data 1995-2014

90 people were waiting for a heart

23 received one

48 died waiting

19 were taken out

21 VAD implanted in 2005-2014

IJN Heart Transplant Data

0

2

4

6

8

10

12

14

1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013

Chart Title

Listed Transplant

0

2

4

6

8

10

12

14

1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013

Transplant and patient on waiting list

Listed Transplant

Indications for VAD

Bridge to transplant (BTT)

most common

allow rehab from severe CHF

while awaiting donor

Bridge to recovery (BTR)

unload heart, allow “reverse

remodeling”

can be short- or long-term

“Destination” therapy (DT)

permanent device, instead of transplant

currently only in transplant-

ineligible patients

Bridge to candidacy (BTC)/

Bridge to decision (BTD)

when eligibility unclear at implant

not true “indication” but true

for many pts

2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults :

Circulation 2009, 119:1977-2016

21/06/2013

Worsening SOB and oedema

Admitted for decompensated heart failure

Respond to IV diuretic

Noted on echo:

Worsening LV dilatation

Worsening AR

25/06/2013

Sudden onset of SOB

Pulse: not palpable ( monitor 150 bpm )

BP: mean 45 mmhg

Sat 94% in RA

Chest: bibasal crepitation

CASE 4

23 y/o malay female

Diagnosed with idiopathic dilated cardiomyopathy

Had a heart transplant for six years previously.

Post-transplant course has previously been

uncomplicated.

Very compliant with medical follow up.

Last surveillance heart biopsy 3 months ago showed no

rejection

His last cath was 2 years ago and normal

2 day H/O generally feeling unwell with nausea and mild

dyspnea at rest.

Immunosuppressive regimen has been stable and

consists of cyclosporin and mycophenolate mofetil.

Other medications include Ramipril, ASA, pravastatin.

Clinical examination

On exam he appears restless,

BP 105/60, pulse 110 regular, O2 sat 99%.

No signs of CHF

Cardiac exam is only significant for an S3 gallop

Investigations CXR is unremarkable.

ECG reveals sinus tachycadia with IRBBB unchanged

from previous but new T inversion in the ant leads.

A bedside echocardiogram reveals mild generalized LV

hypokinesis.

Screening labs, including cardiac enzymes is

unremarkable

Differential diagnosis Early / Subclinical opportunistic pulmonary

infection.

Cardiac allograft rejection

.

Myocardial ischemia.

Anxiety.

Recurrent cardiomyopathy.

.

Myocardial ischemia

The transplanted heart remains denervated.

incapable of experiencing the subjective symptom of

angina pectoris.

The cardiac allograft is prone to develop a very diffuse

form of coronary vasculopathy

independent of the usual coronary risk factors

prevalent with time after transplantation, and can be

rapidly progressive.

Cardiac allograft rejection

A long-term transplant recipient who is on a stable low-

dose immunosuppressive regimen

Unlikely to develop allograft rejection or opportunistic

infection, although both are within the realm of possibility.

Anxiety

Patient is relatively hypotensive and to write his symptoms

off to anxiety or an upper respiratory infection would be

a great disservice.

Thank You

Dr Ika Faizura Bt Mohd Nor