Myocardial Infarction
What is the WHO definition for Acute Myocardial Infarction
The answer
What is the characteristic history of pain of Acute MI ?
The answer
Can you have acute MI without any history of pain?
The answer
Yes.
It is called "silent" MI. If you take careful history there may have been prior episodes of discomfort, which the patient has passed it off as indigestion or trivial.
Diabetics with loss of sympathetic tone may also prone to have silent MI.
What are the enzyme changes associated with myocardial infarction?
The answer
The classic patterns enzymes may not be elevated very early in the course of the AMI.
The initial enzyme determination in the ER may be normal.
You should not depend on one set of enzyme determinations but must order a sequence of test over several days.
You should understand that the enzyme levels will vary depending on the amount of time between the onset of the infarct and when the test is performed.
| < 4hours | 24 hours | 72 hours | ||
| WBC | Non-specific | Normal | Increased | Normal |
| CK | Lack specificity and sensitivity | Normal | Peak increase | Normal |
| CK-MB | Less specific (skeletal injury, Hypothyroidism) | Normal | Peak increase | Normal |
| Troponin I and T | Specific Cardiac injury | Normal | Peak increase | Remains elevated (5-9 days) |
| Myoglobin | Not Cardiac specific | Increased (peak 8-12 hrs) | Normal | |
| AST(SGOT) | Non-specific | |||
| LDH | LDH-1 and LDH-2 "flip" | Normal | Increased | Returns to baseline in 8-12 days |
What are the EKG changes of acute myocardial infarction ?
The answer
Ischemia and infarction -
ST segment elevation.
Intracellular potassium leaks out of damaged cells and makes the resting membrane potential more positive. As a result, current of injury flows from damaged cells to normal cells during the diastolic period (T-QRS segment). This shifts the baseline of the EKG down, giving the impression that the ST segment is elevated.
ST segment depression
Reciprocal changes: In leads facing opposite the infarction ST segment can be depressed.
Elevation and depression can actually co-exist in the same EKG depending on the position of the recording lead.
New Q waves: From the dead tissue /absence of depolarization current in the dead tissue and receding currents from opposite side of Heart.
R wave progression: Loss of R wave is due to loss of muscle bulk.
Describe EKG changes in acute, recent and old Myocardial infarction.
The answer
Acute
Significant Q wave with typical ST segment elevation in the same lead.
Recent
- Significant Q wave
- Diminished R wave
- Twave inversion
- ST segment elevation
Old
Only characteristic abnormalities of the QRS are found.
- Significant Q wave
- Diminished R wave
When is ST segment elevation and Q wave are significant?
The answer
Does normal EKG at the initial presentation with chest pain rule out acute MI?
The answer
Correlate the site of infarction to coronary circulation i.e. location of Infarction/ occlusion of branch of coronary artery
The answer
| Location | QRS abnormalities | Vessel affected |
| Inferior | II, III, AVF | Terminal branches of LAD and or Right posterior descending |
| Anteroseptal | V1, V2 | Distal LAD |
| Anterior | V1, V2, V3, V4 | Proximal LAD |
| Anterolateral | I, AVL, V4-V6 | Distal circumflex |
| High lateral wall | Lead 1 and AVL | Proximal circumflex branch of LCA |
| True posterior | No Q waves. Leads showing reciprocal changes only: Tall R waves, tall T waves and ST depression in V1, V2 | Posterior descending |
What are the characteristics of subendocardial infarction?
The answer
Non Q wave infarctionDescribe the evolution of EKG changes over time in Acute Myocardial Infarction
The answer
| In the first few hours | Normal R waves | ST elevation | Peaked T wave | |
| Within 24 hours | Beginning of Q wave | R wave loss | ST beginning to return to baseline | T wave inversion |
| 24-48 hours | Deepening Q wave | R wave loss | ST segment returning to baseline | Continued T wave inversion. |
| After 48-72 hours | Deep Q waves | No R waves | ST usually back to baseline | |
| After several weeks | Deep Q waves | Small R wave may return | ST back to normal | |
From this information you should understand the need for obtaining sequential cardiac enzymes and EKG and learn to interpret them based on the latency between onset of pain and the time of evaluation.
What a re the conduction system defects with disruption of coronary circulation?
The answer
| SA Node | ||
| AV Node | 2nd degree heart block | |
| Left bundle | Left Bundle branch block | Conduction blocks alter the changes of MI and you should be aware of it. |
| Right bundle | Right bundle branch block | |
| Purkinge | Heart block |
Describe the patho-physiology of atherosclerotic plaque leading to thrombosis.
The answer
Describe the evolution of myocardial changes that occur following acute myocardial infarction.
The answer
What is the pathogenesis for transmural and subendocardial infarctions?
The answer
Describe the evolution of clot/thrombus over time.
The answer
Natural history of thrombus
What are the clinical consequences of acute myocardial infarction?
The answer
What are the goals of therapeutic strategy for MI?
The answer
What measures can you undertake to alter supply/demand of oxygen to Myocardium?
The answer
Limit all activities for a period of time to limit the oxygen demand.
Bedside commode for 24 hours
Bed rest in ICU for 3 days
Slow ambulation for next 4 days
Oxygen therapy: With a normal arterial pO2, probably has little effect on the supply/demand ratio of the myocardium. However it is better to keep the patient on oxygen in the acute stage even if the blood gases are normal, as the clinical status can change precipitously in the early stages of myocardial infarction.
Morphine
venodilator effects which may cause a reduction in preload
reduction of ventricular wall stress and oxygen demand.
the central effects of morphine to increase vagal tone and reduce the pain-mediated rise in sympathetic tone may also reduce myocardial oxygen demands
Nitroglycerine and metropolol would both decrease oxygen demands
Beta-blockers have been shown to reduce mortality for at least one year following a MI
initiate beta-blocker therapy prior to hospital discharge
What measures can you undertake to prevent further progression of Thrombus/clot
The answer
aspirin and heparin will not lyse a coronary thrombus, however these drugs are essential in preventing re-occlusion.
Even during the administration of fibrinolytic agents, episodes of transient reperfusion followed by re-occlusion often precede sustained coronary reperfusion.
What is the rationale for re-establishing coronary perfusion?
The answer
Our job is to abort the infarct. Decide (with Cardiology consultation) on the method of reperfusion and "Just do it"
What are the available options to re-establish coronary perfusion?
The answer
What are the advantages and disadvantages of Thrombolytic therapy?
The answer
What are the advantages and disadvantages of Percutaneous transluminal coronary angioplasty (PTCA) ?.
With experienced hands , PTCA may have slight advantage in mortality and complications over Thrombolytic therapy in the short run.
At this point PTCA is equal to not better than thrombolytics.
What are the advantages and disadvantages of Coronary artery bypass graft (CABG)?
How does thrombolytic therapy work? How do you evaluate its success?
The answer
Tissue plasminogen activator (t-PA) converts plasminogen to plasmin which acts to digest the fibrin clot that is occluding one of the major coronary arteries.
A decrease in chest pain or reduction in the magnitude of ST-segment elevation in the ECG would suggest that reperfusion had been achieved.
Unfortunately, these markers are rather imprecise and coronary angiography is the only definitive method for recognizing successful reperfusion.
If reperfusion is not accomplished after 90 minutes of IV thrombolytic therapy, patient should be transferred to the cardiac catheterization laboratory for rescue angioplasty.
How would the latency from the onset of symptoms to the start of t-PA therapy influence the effectiveness of therapy?
The answer
First 6 hours
In order to salvage reversibly injured cardiac muscle, thrombolytic therapy should be initiated within the first six hours after the onset of symptoms.
Beyond 6 hours
Beyond six hours cardiac myocytes are irreversibly injured and reperfusion probably does not reduce the ultimate amount of necrosis.
There is evidence however, that reperfusion after six hours may help in the healing process with less thinning of the scar and less chance of aneurysm formation.
Beyond 12 hours
The lack of any benefit after 12 hours may be due in part to the ineffectiveness of thrombolytics in lysing older thrombi.
As clots age they are stabilize by factor XIIIa and there is cross-linking of fibrin and the beginning of collagen deposition.
| 0-6 hours | 6-12 hours | >12 hours | |
| Clot | Lysable | Collagen deposition. Not lysable | |
| Myocyte | Still viable |
irreversibly injured/does not reduce extent of necrosis/May facilitate healing process |
Risk of hemorrhagic transformation in the infarcted territory with very little muscle to salvage |
List thrombolytic agents. What are the advantages and disadvantages of each agent?
The answer
Streptokinase
Advantage
Since streptokinase costs only 1/5 to 1/10 as much as t-PA, it is used more often to treat acute myocardial infarction.
Disadvantage
Diffuse undesirable thrmbolytic process
Antigenicity . can be given only once for fear of reaction
T-PA
Advantage
T-PA binds to fibrin with greater affinity than does urokinase or streptokinase and activated plasmin on the fibrin surface.
more localized (clot specific) effect and less systemic fibrinolysis.
T-PA also has no antigenicity.
Disadvantage
Expensive
Urokinase
Anisoylated plasminogen streptokinase activator complex (APSAC).
Streptokinase and t-PA are thought to produce similar results in terms of vessel patency and overall mortality.
What are the major risk factors associated with the use of thrombolytic therapy? Are there any contra-indications for its use?
The answer
Intracrainal hemorrhage and bleeding are the main risk associated with thrombolytics.
Lysis of a preformed thrombus at a site of recent stroke or surgery allow for bleeding.
Thrombolytic agents should be avoided within 10 days of surgery and 6 weeks of a stroke.
Extremely low fibrinogen levels can also result in bleeding as well as impaired platelet function due to lysis of the surface glycoproteins.
What are the complications of myocardial infarction and describe the principles of management of each.
The answer
| Ventricular dysfunction | Hypotension/Cardiogenic Shock | IABP, Re-perfusion strategy |
| Ventricular dysfunction | Congestive Heart failure | |
| Papillary muscle ischemia/necrosis | Mitral regurgitation. Acute valvular dysfunction./Flash pulmonary edema | Emergency Valvular surgery |
| Irritable focus: | Dysrhythmias | Based on arrhythmia ( Atropine, Lidocaine) |
| Sudden death | ||
| Ischemia/necrosis of bundle of HIS: | Heart block | Pace maker |
| Elevated catecholamine release | Hypertension | |
| Pericarditis | High dose ASA 650 mg q 4-6 hour | |
| Rupture if interventricular septum | VSD | Requires Surgery |
| Thinning of Myocardium | Ventricular aneurysm | Requires Surgery |
What should be the management strategy when you suspect that the patient may have Myocardial infarction in the Emergency room ?
The answer
What is the period when the mortality for MI is highest? What can you do about it?
The answer
Who are the people at high risk for development of coronary atherosclerosis?
The answer
People at risk for coronary atherosclerosis are
How can we prevent or modify development of coronary atherosclerosis in people with high risk?
The answer
Appropriate treatment of