Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. Find a good presentation on Acute myocardial infarction here.
4. Distribution of coronary blood
supply
Right Coronary Artery Left Coronary Artery
Right atrium
Right ventricle
SA node (85%)
AV node
Inter-atrial septum
Portion of left atrium
Postero-inferior 1/3 of Inter-
ventricular septum
Portion of posterior part of left
ventricle
Left atrium
Left ventricle
Most of the Interventricular
septum
Atrio-ventricular bundle and its
branches
5. ACUTE MYOCARDIAL INFARCTION
• Cardiac muscle
necrosis secondary
to protracted lack
of coronary
perfusion
• Usual etiology:
Thrombus at site of
vascular injury
6. OTHER ETIOLOGIES OF ACUTE
MYOCARDIAL INFARCTION
• Coronary embolus
• Coronary spasm
• Coronary anomoly
• Primary in situ thrombosis
• Vasculitis
• Hypotension
7. DETERMINANTS OF EXTENT OF DAMAGE
• Territory supplied
• Duration of occlusion
• Existence of collaterals
• Oxygen demand at time of occlusion
• Vasospasm
8. RISK FACTORS
Risk factors for atherosclerosis are generally risk factors for
myocardial infarction
Diabetes (with or without insulin resistance) – the single
most important risk factor for ischaemic heart disease (IHD)
Tobacco smoking
Hypercholesterolemia
Low HDL
9. High blood pressure
Family history of ischaemic heart disease (IHD)
Obesity
Age: Men at age 45 & Women at age 55
Hyperhomocysteinemia (high homocysteine, a toxic
blood amino acid that is elevated when intakes of
vitamins B2, B6, B12 and folic acid are insufficient)
Stress
Alcohol
Males are more at risk than females
12. Presenting Signs in Acute MI
• Appearance: Pallor, diaphoretic, anxious
• Vital Signs: Normal or abnormal BP and P
– Hypertension and tachycardia: SNS
– Hypotension and tachycardia:
• Cardiogenic shock
• Myocardial rupture
• Tachyarrhythmia
– Hypotension and bradycardia
• vagal stimulation
• Bradyarhythmia
13. Presenting Signs in Acute MI (Cont.)
• Lungs: Rales - CHF
• Heart: Displaced LV impulse
–S3
–S4
–Murmur of mitral regurgitation
–Murmur of ventricular septal
rupture
–Pericardial rub
14. DIAGNOSIS
The diagnosis of myocardial infarction can be
made after assessing
Patient's complaints and physical status
ECG changes
Coronary angiogram
Levels of cardiac markers
15.
16. ORDER OF ECG CHANGES IN AMI
Earliest: Increased R and T wave amplitudes; giant R wave and
Hyperacute T waves
Progressive ST elevation
Q waves appear
Loss of R waves
“T wave” inversion (because of change in ventricular repolarisation)
and it persists
26. LATERAL AMI
STE in I, aVL
*Note the ST depression in II, III, aVF consistent
with reciprocal changes, as well as in V2-V3 which
may represent a posterior MI
27.
28. INFERIOR AMI
STE in II, III, aVF
*Note the ST depression in I, aVL consistent with
reciprocal change, as well as in V1-V4 representing a
posterior MI
29.
30. POSTERIOR WALL AMI
ST Segment Depression in V1-V3 and posterior thoracic
leads with STE
31.
32. PLASMA MARKERS
CK-MB
Increases at 4-6 hours
Peaks at 12 hours
Normalizes in 48-72 hours
TROPONIN T & I
Increases at 4-6 hours
Remains elevated for 2
weeks
34. Cardiac Specific Troponins (cTnT, cTnI)
• Rise within 4-8 hours, remain elevated 7-14
days (T>I)
• 30% of patients with UAP show ↑ levels cTnT
or I, indicating increased risk of adverse
outcome
35.
36. OTHER TESTS
BLOOD leukocytosis, ESR and CRP is elevated
Chest X-ray Pulmonary edema
Echocardiography
Mural thrombi
Cardiac rupture
VSD
MR
Pericardial effusion
37. DIAGNOSIS OF MYOCARDIAL
INFARCTION (American college of cardiology
and the Europeon society of cardiology)
Elevated Troponins or CK-MB above 99th
centile with
one of the following
Ischemic symptoms
Development of Q-waves on ECG
Ischemic ECG changes (ST elevation/depression)
Coronary artery intervention
38. A. IMMEDIATE
MANAGEMENT
B. MAINTAINING
VESSEL PATENCY
C. PREVENTION
OF FURTHER
COMPLICATIONS
D. LATE
MANAGEMENT
Defibrillation
services
Resuscitation
Reperfusion
Detection and
Management of
acute
complications
Drugs
Adjunctive
therapy
Arrythmias
Ischemia
Acute circulatory
failure
Pericarditis
Mechanical
complications
Embolism
Impaired
ventricular function
Ventricular
aneurysm
Risk stratification
and management
Life style
modification
Drug therapy in
Secondary
Prevention
Mobilization and
Rehabilitation
40. REPERFUSION
Primary PCI is the treatment of choice
Thrombolysis (Greatest benefits if in 2 hours)
Streptokinase 1.5 Million Units in 100ml of N/S over 1 hour
Alteplase 15mg bolus then 0.75mg/kg in 30 mins (50mg)
followed by 0.5mg/kg in 60 min (35mg)
Major hazard is Cerebral Haemorrhage
DETECTION AND MANAGEMENT OF ACUTE
COMPLICATIONS
Arrythmias
Ischemia
Heart failure
41. Major Contraindications To the Use of
Thrombolytic Therapy
• Any previous history of hemorrhagic stroke
• History of stroke, dementia, or central nervous system
damage within 1 year
• Head trauma or brain surgery within 6 months
• Known intracranial neoplasm
• Suspected aortic dissection
• Internal bleeding within 6 weeks
• Active bleeding or known bleeding disorder
• Major surgery, trauma, or bleeding within 6 weeks
• Traumatic cardiopulmonary resuscitation within 3 weeks
42. Relative Contraindications To the Use of
Thrombolytic Therapy
• Oral anticoagulant therapy
• Acute pancreatitis
• Pregnancy or within 1 week postpartum
• Active peptic ulceration
• Transient ischemic attack within 6 months
• Dementia
• Infective endocarditis
• Active cavitating pulmonary tuberculosis
• Advanced liver disease
• Intracardiac thrombi
• Uncontrolled hypertension (systolic blood Pressure >180 mm Hg, diastolic blood pressure >
110 mm Hg
• Puncture of noncompressible blood vessel within 2 weeks
• Previous streptokinase therapy
43. Risks of Coronary Angiography: (all
are rare)
• Stroke
• Myocardial infarction
• Arrhythmia
• Renal failure
• Allergic reaction to contrast agent
44. B. MAINTAINING VESSEL PATENCY
• Anti-platelets
Aspirin 75-300mg daily and/or Clopidogrel 75mg daily
• Anti-coagulants
S/C Heparin 12,500 units twice daily
IV Heparin (within 48-72 hrs of thrombolysis)
Warfarin in Persistant A.Fibrillation & Extensive anterior
infarction
• Adjunctive therapy
B-Blockers Atenolol 5-10mg to dec. pain and arrythmias but
should be avoided in HF, AV Block and severe bradycardia
Nitrates S/L GTN 300-500 mcg in threatened MI and IV nitrates
(Nitroglycerin 0.6-1.2mg/hour or Isosorbide dinitrate are
useful in treating LVF and Ischemic pain relief.
45. C. FURTHER COMPLICATIONS AND THEIR
PREVENTION
1. ARRYTHMIAS (VF, VT, AF, AT, Heart blocks and
Ventricular ectopics)
Can be avoided by Pain relief, Rest and Correction of
hypokalemia
• Vent. Fib….5-10% cases…..prompt defibrillation
• Atrial Fib….transient and rarely requires treatment
….DC cardioversion, Digoxin or B-Blocker are
TOCs…..Patient can go into LVF so give
Anticoagulants
• AV block….Atropine 0.6mg IV + Temporary
pacemaker
46. 2. ISCHEMIA 50% cases known as post-infarct Angina
Managed as Unstable Angina
• IV nitrates (0.6-1.2mg/hour)
• IV heparin (1000 units/hour)…dose adjusted to PT
• LMWH
• GP IIb/IIIa receptor antagonists…..selected cases
3. ACUTE CIRCULATORY FAILURE in extensive myocardial
damage
4. PERICARDITIS (on 2nd
and 3rd
day)
Opiod based analgesics
Also called Post-Infarction syndrome/Dressler’s
syndrome…..fever, pericarditis and pleurisy (due to
auto-immunity)….may require High dose Aspirin,
other NSAIDS and Cortico-steriods.
47. 5. MECHANICAL COMPLICATIONS
Papillary muscle damage…..acute onset pulmonary
edema due to severe MR (PSM + S3)…..diagnosed by
doppler’s echocardiography and treated by
emergency mitral valve replacement
Ruptured IV septum…..Left to right shunt (PSM
radiating to right sternal border difficult to
distinguish from MR) …..diagnosed on doppler’s
echocardiography …..fatal condition
Ventricular rupture…..cardiac tamponade…..fatal
6. EMBOLISM risk is decreased by prophylactic ani-
coagulants and early mobilization
48. 7.IMPAIRED VENTRICULAR FUNCTION
Due to infarct expansion…..lead to progressive
dilataion of the infarcted area and hypertrophy of
the rest of the portion
8. VENTRICULAR ANEURYSM 10% cases
Leads to HF, Ventricular arrythmias, Mural thrombus
and systemic embolism
Echocardiography is diagnostic
Surgical removal improves the chances of survival
49. D. LATE MANAGEMENT
1. RISK STRATIFICATION
LV FUNCTION ISCHEMIA ARRYTHMIAS
•Physical findings …
tachycardia, S3,
Crackles at lung
bases and elevated
venous pressure
•ECG changes
•Size of heart and
Pulmonary edema
on CXR
•Post-infarct angina …
treat like unstable angina
•CABG
•Implantable cardiac
defibrillators
50. 2. LIFE STYLE MODIFICATION
Quit smoking (5 year mortality twice if you don’t
quit)
Regular exercise (20min/day for 3 days/week)
Diet control to decrease weight and lipid lowering
51. 3. DRUG THERAPY (Secondary prevention)
Statins…best results when level of LDL is greater than 3.2
mmol/L….Atovstatin 80mg OD
Anti-platelets…Aspirin/Clopidogrel
B-Blockers….but contra-indicated in Bradycardia, AV block,
hypotension and Asthma
ACE inhibitors….Enalapril 10mg BD, Ramipril 2.5-5mg BD
Angiotensin receptor antagonists….valsartan 40-160mg OD,
Candesartan 4-16mg OD
Control of HTN and DM
4. MOBILIZATION AND REHABILITATION start working in 4-6
weeks
55. ABCs of Treatment and Secondary
Prevention of AMI
• Aspirin-prophylactic Rx for recurrent ischemic events;
give for at least 3 mo. after AMI, probably indefinitely
• Beta blockers-prophylactic, for reduction of cardiac
mortality; Rx for 2 yr-indefinitely
• Converting enzyme inhibitors-all pts with LV
dysfunction to reduce risk of progressive heart failure
and death.
• Diet and lipid lowering Rx-statins have been shown to
reduce risk of subsequent MI, need for
revascularization and mortality (4S, Care)
• Exercise and rehabilitation-essential in restoration of
confidence and improvement in quality of life
56. PROGNOSIS
• 1/4th
of the patients suffering acute MI die in few
min due to any arrythmia
• Half of the MI deaths occur in 1st
24 hours
• 40% of the rest die in 1st
Month
• Anterior infarcts are worse than Inferior infarcts
• BBB and increased enzymes reflects that the
damage is extensive
• Increased mortality is associated with old
age,depression and social isolation
57. SURVIVAL CHANCES
After surviving an acute attack….
• 80 % Survive the 1st
year
• 75 % Survive upto 5 years
• 50% Survive upto 10 years
• 25% survive upto 20 years
Notes de l'éditeur
NOTES FOR PRESENTERS
The key recommendation on cardiac rehabilitation says that:
‘Cardiac rehabilitation should be equally accessible and relevant to all patients after an MI, particularly people from groups that are less likely to access this service. These include people from black and minority ethnic groups, older people, people from lower socioeconomic groups, women, people from rural communities and people with mental and physical health comorbidities.’ (page 6, NICE guideline)
‘Healthcare professionals, including senior medical staff involved in providing care for patients after an MI, should actively promote cardiac rehabilitation’ (page 12, NICE guideline)
NOTES FOR PRESENTERS
‘A home based programme validated for patients who have had an MI that incorporates education, exercise and stress management components with follow-ups by a trained facilitator may be used to provide comprehensive cardiac rehabilitation’ (such as ‘The Edinburgh heart manual’; see www.cardiacrehabilitation.org.uk/heart_manual/heartmanual.htm) (page 12. NICE guideline)
Education should include issues such as:
when to return to work
driver and vehicle licensing agency guidelines
when it is safe to travel by air
sexual activity
how to use a perceived exertion scale to help monitor physiological demand
advice on competitive sport when relevant
advice to contact Civil Aviation Authority if the patient holds a pilot’s licence.
The exercise component should be designed to meet the needs of older patients or patients with significant comorbidity.
NOTES FOR PRESENTERS
The key recommendation on cardiological assessment says that:
‘All patients should be offered a cardiological assessment to consider whether coronary revascularisation is appropriate. This should take into account comorbidity.’ (page 7, NICE guideline)
The Guideline Development Group concluded that there was evidence of effectiveness of coronary revascularisation for secondary prevention in selected stable patients with non-acute coronary disease, and thus patients after MI who had not been considered for coronary revascularisation during the acute phase of management should be considered for further specialist cardiological assessment.