AMI- Presentation and Investigation Flashcards
What are the 4 most common presentation of coronary heart disease in the community?
- New exertional angina
- Acute MI
- Unstable angina
- Sudden cardiac death
Stable angina
If myocardial blood flow is reduced with increased demand then ischaemia occurs
What is the classic presentation of stable angina?
Central chest tightness often with radiation to neck and/or arms
What are aggravating factors of stable angina?
- Exertion
- Stress
What are relieving factors for stable angina?
- Stopping activity
- Rapid improvement with sublingual nitrate
What causes stable angina?
- Fatty streak becomes a non-obstructive plaque
- When it becomes an obstructive plaque >70% obstructed then stable angina occurs
What process is responsible for stable angina?
Atherosclerosis
When do acute coronary syndromes occur?
When there is spontaneous plaque rupture and local thrombosis with degrees of occlusion
What does plaque rupture lead to?
Plaque disruption leads to atherothrombosis formation
What 3 conditions make up ACS?
- Unstable angina
- NSTEMI
- STEMI
What is atherothrombosis caused by?
Unstable plaques
What type of plaques result in stable angina?
- Fibrous plaque
- Atherosclerotic plaque
Why do plaques rupture?
-Inflammation is important determinant in plaque stability, along with other mechanisms including shear stress
What is the main difference between the presentation of ACS and stable angina?
ACS symptoms will almost always give symptoms at rest in contrast to stable angina which is only on exertion
When taking a history, why is it important to establish the characteristics of the patients pain?
To differentiate from other causes of chest pain
What is the history of pain relating to ACS?
- Retrosternal pain
- Character is tight band/pressure/heaviness
- Radiates to neck and/or jaw and/or down arms
- Aggravated by exertion, emotional stress
- Relieved by, incomplete improvement with GTN or physical rest, remain ongoing
What are the non-modifiable risk factors for coronary artery disease?
- Age
- Gender
- Creed
- Family history
- Genetics factors
- Previous angina, cardiac events or interventions
- Race
What are the modifiable risk factors for coronary artery disease?
- Smoking
- Diabetes mellitus
- Hyperlipidaemia
- Hypertension
- Lifestyle
Unstable angina pectoris
Angina on effort, but of progressive increasing frequency and severity often provoked by less exertion and/or then at rest
NSTEMI
Starts with myocardial ischaemia symptoms occurring at rest
Examination of unstable angina and NSTEMI.
- May look very unwell
- May look completely fine
- Often no specific features to fins
- Ensure you check HR, BP, murmurs and crackles in the chest
ECG of unstable angina and NSTEMI.
May be normal but:
- Commonly ST depression, transient ST elevation and/or T wave inversion
- More often in UAP changes resolve after pain and in NSTEMI they tend to persist
- Serial ECGs to detect delayed changes is essential
What is important to remember when making a diagnosis of UAP or NSTEMI?
- Typical symptoms are not always present in ACS cases
- Atypical ACS presentation is more often seen in women: the elderly or diabetics, influenced by reduced pain sensation
What are some atypical symptoms of UAP and NSTEMI?
- Breathlessness alone +/- signs of heart failure
- Nausea+ vomiting +/- other autonomic symptoms
- Epigastric pain +/- recent onset indigestion
What is the main biomarker used in UAP and NSTEMI?
-Cardiac troponin
Why is troponin useful to look at when making a diagnosis?
- Helpful in risk stratification
- Elevated cTn suggest high risk of adverse events
- Not all troponin elevations are ACS and caused by atherothrombosis
What is cardiac troponin?
Contractile apparatus of myocytes thin filaments
When is cardiac troponin elevated?
With compromise of myocyte integrity
What is troponin a marker of?
Cardiac myocyte damage
When does myoglobin peak after AMI?
<0.5 days
When does cardiac troponin peak after AMI?
1-2 days
When does CK-MB peak after AMI?
Around 1 day
When does cardiac troponin peak after UAP?
Around 1 day
What is the immediate treatment for UAP and NSTEMI?
- ABCDE approach
- Followed by MONAC
What is the MONAC approach?
- Morphine
- Oxygen
- Nitroglycerine
- Aspirin (300mg orally)
- Clopidegrol
What anti-platelet therapy should all ACS patients receive?
Both aspirin and a ADP receptor blocker such as clopidegrol
What anti-thrombotic therapy should ACS patients receive?
IV unfractionated heparin or low molecular weight heparin
What are the advantages of low molecular weight heparin?
- Improved clinical outcome
- Easier to administer
- Given subcutaneously
- Does not need to be monitoredd
What other medications should ACS patients be put on?
- B blockers
- Statins
- ACE Inhibitors
Why is coronary revascularisation considered?
Clear evidence that high risk patients with UA/NSTEMI benefit from early invasive strategy compared to medical therapy alone
What types of coronary revascularisation are available?
- PCI
- CABG
What is the treatment path for UA and NSTEMI?
- Most patients stay in hospital for 2-7 days
- No all patients will have angiography and not all who have it will have revascularisation
- Decisions more difficult in the elderly and/or those with important co-morbidities
- Many not reviewed after hospital discharge
Why are STEMIs more severe?
- Plaques rupture leads to more complete, or complete thrombotic occlusion of coronary lumen and infarction of distal myocardium
- Proximal occlusion of main artery causes greater damage
- However, occlusion of distal or branch vessel which supplies critical structures can cause significant problems (rupture of papillary muscle, acute mitral regurgitation, occlusion of AV node artery)
What occurs in a time dependent manner following STEMI?
Necrosis of myocardial tissue
What increases the amount of cardiac tissue that can be salvaged?
The sooner the occlusive thrombus is dissolved/removed and the vessel opened
What results in better survival of a STEMI?
Less LV damage
What are the choices in how to open infarct related artery?
- Fibrinolysis
- Primary PCI
Why is primary PCI considered superior over fibrinolysis?
- Reduces mortality
- Reduces recurrent MI
- Reduced risk of haemorrhagic stroke
When is PCI most effective?
Between 120-150 minutes after event
What is the treatment of choice for STEMI when PCI cannot be performed?
Fibrinolytic therapy
When is fibrinolytic therapy most effective?
Within 90 minutes of event or 30 minutes on arrival to hospital
What does fibrinolytic treatment increase the risk of?
Bleeding and intra-cranial haemorrhage in some patients
Who is at increased risk of bleeding with firbrinolytic therapy?
- Age>75
- Female
- Previous stroke
- Low body weight
- SBP>160mmHg
- INR>4
- Chronic kidney disease and elevated creatinine
What treatment is used as secondary prevention treatment for STEMI?
-General measures (stop smoking, diet, exercise)
-Co-morbidities (control BP, glycaemic control)
-Aspirin and clopidegrol for 1 year
-B blockers to slow heart rate
Statins
ACE inhibitors
When are ACE inhibitors always given after a STEMI?
Left ventricular dysfunction
What inpatient investigations are carried out following a STEMI?
-ECHO
What are the most important determinants of MI survival?
- Age
- LV ejection fraction
What is the survival of patients resuscitated following SCD?
~2%
What is the primary causes of SCD in those resuscitated?
80% VT or VF
What causes ventricular arrhythmia in SCD?
The atherthrombotic event causes acute myocardial ischaemia and subsequent sufficient electrical distubance
What is the only effective treatment for VF?
Defibrillation
What does VF rapidly deteriorate into?
Asystole
When does the best chance of success in resuscitation occur?
In the first 3-4 minutes
What are the 2 main groups of immediately life threatening complications of AMI?
- Mechanical complications
- Ventricular arrhythmic complications
What is a later complication of AMI?
LV thrombus
What are the most dramatic complications of MI?
Mechanical complications
What are the 3 main mechanical complications of MI?
- Free wall rupture
- Papillary muscle rupture
- Rupture of IVS
Where does free wall rupture occur?
At the edge of the infarcted area
What does free wall rupture lead to?
- Haemopericardium
- Acute tamponade
What can prevent EMD death falling free wall rupture?
False aneurysm or adhesions containing pericardial infusion
Who is free wall rupture most common in?
- Elderly
- Females
- HBP
- Anterior MI
What should be carried out urgently following free wall rupture?
- ECHO
- Pericardiocentesis
- Drainage with pigtail catheter
Who is septal wall rupture more common in?
- Elderly
- Females
- HBP
- Those not thrombolysed
What type of septal wall rupture is anterior MI associated with?
Apical VSD
What type of septal wall rupture is inferior MI associated with?
Basal VSD
What type of papillary muscle rupture is inferior MI associated with?
Posterior and medial muscle
What type of papillary muscle rupture is associated with anterior/lateral MI?
Anterior/lateral muscle
When do papillary muscle rupture and VSD usually occur?
Within the first week following an MI
What are the symptoms of papillary muscle rupture and VSD?
- Sudden sever breathlessness
- Autonomic activation including sweating, nausea and vomiting
- Chest pain
What are the signs of papillary muscle rupture and VSD?
- Shock
- Tachycardia
- Pulmonary oedema
- New harsh systolic murmur
- Right parasternal heave
- Palpable thrill
- Elevated JVP
How is papillary muscle rupture and VSD differentiated?
- MV rupture causes more SOB and oedema
- JVP usually more elevated with VSD
- Inferior MI associated with MR
- Anterior MI associated with VSD
- ECHO used
What might be seen on ECHO when investigating mechanical complications of MI?
- Prolapsing mitral leaflet +/- chunk of muscle
- Broad MR jet into normal size LA
- VSD easily missed
- RV size, function and pressure is a strong predicator of outcome with VSD
Other than ECHO what other investigation would be performed when investigating the mechanical complications of MI?
-Cath lab
Why is a right heart cath performed?
- Step up in O2 sats with VSD
- Confirms Dx and quantifies shunt
- Large v waves on wedge with acute MR
Why is a left cath performed?
- Establish coronary anatomy
- Better localisation of pathology
How should papillary muscle rupture and VSD be monitored?
- IV nitrates if SBP>90mmHg
- Inotropes if SBP<90mmHg
- IABP
- Call cardiac surgeons
What surgery can be performed for papillary muscle rupture or VSD?
- Mitral valves are usually replace rather than repaired
- VSD repair with pericardial or synthetic patch
- Coronary artery bypass
Ventricular tachycardia
Broad complex, regular generally rapid tachycardia
-Initiated by ventricular premature beat, sustained by re-entry loop
When does VT occur in relation to MI?
Any time following MI
What can drive VT?
-Ischaemic and/or myocardial damage
What is required if VT is sustained?
- Urgent cardioversion
- Electrically
- Amiodarone or pacing
What is the treatment for VT?
Medical therapy +/- ICD with anti-tachycardia pacing
Ventricular fibrillation
- Irregular ineffectual ventricular fibrillating activity
- Multiple wavelets of electrical activity
Where are LV thrombus typically seen?
Apical/anteri-apical MI resulting in significant LV dysfunction
When are LV thrombus seen in relation to MI?
After 48 hours
How are LV thrombi treated?
Anticoagulation for 6 months with warfarin and repeated ECHOs