Mechanical Complications of MI

1
Mechanical Complications of MI

• Victor Ghaborial, MD
• Temple UniversityMorning Report 1/20/00

2
HPI

• Male Pt 77yrs without prior history of heart
  disease
• Presented to ER C/O SOB for one day which became
  progressive and on presentation to ER he required
  intubation

3
History

• Emphysema, on OTC Primatene
• Rt Knee surgery
• No DM, HTN or CA
• MEDS Primatene
• Social Hx Smoker

4
Physical Exam

• B/P 90/70 Pulse 115
• Diaphoretic, intubated
• HEENT unremarkable
• Neck supple, no JVD
• Ht RRR S1S2 audible, no murmurs or gallops
• Lungs CTAs (anteriorly and laterally)
• Abdomen Soft, non tender without organomegally
• Ex No edema PP
• Neuro No apparent focal deficits

5
Labs

• TCPK CKMB CKI Troponin I
  307
  35.5 11.6 28.7
• HGB HCT WBCs Plat MCV
  13.6 43
  4.56 334 94
  
• Gluc Cr BUN Na K Cl CO2
  152
  2.0 18 129 5.0 100 19
• ABGs 7.12/61/385/99.9 IMV,100,750,12

6
EKG
7
Cardiac Cath

• Mid Lt Cx 70---0 stent
• LAD 80---5 stent
• OM2 99---0 stent
• RCA 100 Chronic occlusion?
• Pt in Cardiogenic Shock---IABP placed

8
Course

• E/D following AM
• Continues to be critically ill
• CABG and MVR
• Expired

9
Papillary Rupture
shock
Aneurysm
Mechanical Complications of MI
mural thrombi
mitral regurge
10
Cardiogenic Shock

• characterized by hypotension, tachycardia,
  reduced urine output, mental confusion,
  diaphoresis, and cold extremities, has a
  mortality of gt 65. It is most often associated
  with massive anterior infarction and gt 50 loss
  of LV functioning myocardium

11
Recurrent Ischemia

• Chest pain of MI subsides within 12 to 24 hours.
• Any residual or subsequent chest pain may
  represent pericarditis, pulmonary embolus, or
  other complications.
• Recurrent ischemia is accompanied on ECG by
  reversible ST and T-wave changes.
• Silent ischemia (ECG changes without pain) may
  occur in up to 1/3 of patients without recurrent
  pain.

12
Mitral Regurgitation

• occurs in about 35 of patients.
• In some patients, permanent mitral regurgitation
  is caused by papillary muscle or free wall scar.
• Frequent auscultation during the first few hours
  of infarction often reveals a transient late
  apical systolic murmur thought to represent
  papillary muscle ischemia with failure of
  complete coaptation of the mitral valve leaflets.

13
Myocardial rupture

• Occurs in three forms
• rupture of the papillary muscle
• rupture of the interventricular septum
• external rupture

14

• Rupture of the papillary muscle is most often
  associated with an inferior-posterior infarct due
  to right coronary artery occlusion.
• It produces acute, severe mitral regurgitation
  and is characterized by the sudden appearance of
  a loud apical systolic murmur and thrill, usually
  with pulmonary edema.

15
Rupture of the interventricular septum

• It is rare, 8 to 10 times more common than
  rupture of the papillary muscle.
• Sudden appearance of a loud systolic murmur and
  thrill medial to the apex along the left sternal
  border in the 3rd or 4th intercostal space,
  accompanied by hypotension with or without signs
  of LV failure, is characteristic

16
External rupture

• increases in incidence with age and is more
  common in women.
• It is characterized by sudden loss of arterial
  pressure with momentary persistence of sinus
  rhythm and often by signs of cardiac tamponade.
• It is almost always fatal

17
Pseudoaneurysm

• is a form of rupture of the free LV wall in which
  an aneurysmal wall containing clot and
  pericardium prevent exsanguination.

18
Ventricular Aneurysm

• is common, especially with a large transmural
  infarct (most commonly anterior) and good
  residual myocardium.
• Aneurysms may develop in a few days, weeks, or
  months.
• They do not rupture but may be associated with
  recurrent ventricular arrhythmias and low cardiac
  output.

19
An aneurysm

• may be suspected when paradoxical precordial
  movements are seen or felt, accompanied by
  persistent elevation of ST segments on the ECG or
  a characteristic bulge of the cardiac shadow on
  x-ray.

20
Echocardiography

• helps establish the diagnosis and determine the
  presence of a thrombus.
• Administration of ACE inhibitors during acute MI
  modifies LV remodeling and may reduce the
  incidence of aneurysm

21
Ventricula Asynergy

• An akinetic segment is noncontracting with no
  systolic inward motion.
• A hypokinetic segment has reduced contractile
  excursion and partial impairment of inward
  motion.
• A dyskinetic segment shows systolic expansion or
  bulging (paradoxical motion).

22
Mural Thombosis

• occurs in about 20 of acute MI patients (60 of
  patients with large anterior infarcts).
• Systemic embolism occurs in about 10 of
  patients with LV thrombus (best diagnosed by
  echocardiography)
• risk is highest in the first 10 days but persists
  at least 3 mo.

23
Pericarditis

• may cause a pericardial friction rub in about 1/3
  of patients with acute transmural MI.
• The friction rub usually begins 24 to 96 h after
  MI onset.
• Earlier onset is unusual and suggests other
  diagnoses (eg, acute pericarditis), although
  hemorrhagic pericarditis occasionally complicates
  the early phase of MI.
• Acute tamponade is rare.

24
Dresslers Syndrome

• develops in a few patients days to weeks or even
  months after acute MI, although the incidence
  appears to have declined in recent years.
• It is characterized by fever, pericarditis with
  friction rub, pericardial effusion, pleurisy,
  pleural effusions, pulmonary infiltrates, and
  joint pains.

25
Mitral Regurge

• Retrograde flow from the left ventricle through
  an incompetent mitral valve into the left atrium.
• The most common causes in adults in North America
  are myxomatous degeneration with or without MVP,
  papillary muscle dysfunction, rheumatic valve
  damage, and ruptured chordae tendineae.

26
Papillary Muscle Dysfunction MR

• It is secondary to recent or old MI with or
  without a ventricular aneurysm and papillary
  muscle fibrosis.
• Infarction of the ventricle at the base of the
  papillary muscles, or ischemia of this area
  during an anginal attack, can cause marked MR
  even with a normal papillary muscle.

27
Palpitations

• Severe MR may cause palpitations long before
  heart failure symptoms develop
• Probably caused by the frequency of ectopic beats
  and postextrasystolic hyperdynamic action of the
  enlarged LV.

28
Atrial fibrillation

• Atrial Fibrillation is common when the left
  atrium enlarges and is certain when it is
  extremely large.

29
Chest X-Ray

• of moderate to severe MR show an enlarged left
  atrium and ventricle.
• Pulmonary vascular congestion confined to the
  right upper lobe occurs in about 10 of patients
  with pulmonary congestion due to severe MR and
  can be confused with pneumonia.

30
EKG

• In MR, ECG shows various degrees of left atrial
  and ventricular hypertrophy with or without
  ischemia.
• Typically, the ECG shows increased left atrial
  and ventricular voltage.
• Sinus rhythm in the presence of symptomatic MR
  strongly suggests acutely ruptured chordae with
  inadequate time for atrial stretching to have
  occurred.

31
Valve Replacement

• If MR is the cause of heart failure, early valve
  replacement increases the chance of a good
  outcome and decreases the chance of worsening LV
  function.