Acute MI Flashcards
Heart risk examples?
Smoking and stress Alcohol - Hypertension Drug abuse- High cholesterol Age - Obesity Gender - Family history
Process of Atherogenesis?
Normal | } Clinically silent Fatty streak | Atheromatous plaque | } Angina and claudication Atherosclerotic plaque
Describe chronic stable angina?
Predictable Fixed stenosis Demand led ischaemia Safe
How to treat chronic stable angina?
Stop Sit Spray (GTN)
Ways of describing chest pain?
Heavy feeling Weight on chest Pressure Tightness
In depth description of the atherosclerotic process?
T-he development of atheroma begins with the deposition of a fatty streak within the wall of a vessel. -Over time, this initial lesion develops firstly into an atheromatous plaque and subsequently to an area of atherosclerosis. These two stages are often completely asymptomatic, although the lesion may occlude the vessel lumen sufficiently to give rise to symptoms such as angina or claudication during exercise or to transient ischaemic attacks. - The atherosclerotic plaque, particularly when it is mature and calcified, is a relatively inflexible structure and is prone to fissuring and rupture. These events in turn may trigger the development of a thrombus which can cause acute vascular stenosis, leading to local ischaemia and possibly to infarction. Depending on the vessel involved, this can become manifest as a myocardial infarction, stroke, critical leg ischaemia, or even cardiovascular death.
What is a STEMI?
ST elevation MI
What is an NSTEMI?
Non ST elevation MI
What is an NSTEMI?
Non ST elevation MI
Detailed Process of atherothrombosis?
- The arterial endothelium is damaged initially by uneven or high ‘shear forces’ in the blood (related to abnormal pressure/flow relationships and enhanced by hypertension, hypercholesterolaemia, smoking, diabetes, inflammation and immune processes). - Lipids accumulate within the intima of the artery at a site of damage. - Over the years, fatty streaks grow towards the media of the artery and may become fibrous because of the production of collagen. Plaques are formed. - If the plaque grows into the arterial lumen, it causes further uneven blood flow and increased shear stress. This increases the build-up of plaque and stenosis of the artery. - The first symptom of arterial stenosis may be pain or cramps at times when the blood flow cannot keep up with the body’s demand for oxygen. Typically, these symptoms develop gradually as the plaque slowly narrows the artery. - At some point, plaques with a high lipid content, which are soft and unstable, may rupture and cause an acute blockage. - During plaque rupture, the lipid core and underlying endothelium is exposed to platelets in the blood. These adhere to the injured surface and release mediators, such as adenosine diphosphate (ADP) and thromboxane A2 (TXA2), that trigger platelet aggregation. - Circulating platelets aggregate at the site of injury forming a platelet-rich thrombus through further platelet activation and recruitment. This process is known as atherothrombosis.
Acute coronary syndromes?
Unstable angina MI sudden Cardiac death
What is an acute coronary syndrome?
Acute presentation of CAD
Describe acute coronary syndrome?
Dynamic stenosis - subtotal or complete occlusion Supply led ischaemia Unpredictable Dangerous
Factors that affect plaque rupture (fissure)
Lipid content of plaque (higher = more likely to burst) Thickness of fibrous cap Sudden changes in intraluminal pressure or tone Bending/twisting of an artery in each heart contraction Plaque shape Mechanical Injury
Process of a platelet cascade?
Initiation - spontaneous plaque rupture Adhesion- Platelet recruitment and adhesion at the sit of injury - forming monolayer Activation- adhesion leads to this Release of activators- ADP etc is released through degranulation Surface receptors- ADP binds to receptors Amplification of platelet activation - this accelerates and leads to platelet aggregration Inflamattory cascade triggered-
Description of an acute MI?
Severe crushing central chest pain Radiating to jaw and arms especially left Similar to angina but more sever and prolonged- not relieved by GTN spray Sweating, nausea and vomiting
Angina attack vs. Acute MI details
Angina MI - 10 mins -30 mins or longer - Onset=exertion -At rest - Severity usual pain -More severe - GTN= Relief -No effect - No associated symptoms -Sweating, nausea & vomiting
ECG changes in an acute STEMI?
ST elevation T wave inversion Q wave formation
Detailed description of an ECG in STEMI?
-ST elevation 1mm< in 2 adjacent limb leads - >2mm ST elevation in at least 2 contiguous precordial leads -New onset bundle branch block
What does an old MI look like on an ECG?
Q waves +- inverted T waves
What a change in the ECG at leads 2,3 and AVF say about its anatomical position?
Inferior
What leads are affected in an anterior MI?
V1-V6
What leads are affected in anteroseptal MI?
V1-V4
What a change in leads 1, AVL and V1-V6 say about the anatomical position of the MI?
Anterolateral
What is troponin?
Protein Marker Highly specific for cardiac muscle damage Can detect tiny amounts of cardiac necrosis
Mode of action of aspirin and thienopyridines
ASA inhibits COX, preventing the production of prostaglandin and thromboxane A2 (TxA2) from arachidonic acid. TxA2 aids the expression of the GP IIb/IIIa binding site on the platelet, allowing fibrinogen to bind. Clopidogrel is a potent inhibitor of ADP-induced platelet aggregation, irreversibly inhibiting the binding of ADP to its platelet membrane receptors. ADP binding is necessary for activation of the GP IIb/IIIa receptor, which is the binding site for fibrinogen. Clopidogrel thus ultimately inhibits the activation of the GP IIb/IIIa receptor and its binding to fibrinogen. Due to the different mode of action of aspirin and clopidogrel, the initial interest was to determine which antiplatelet was most effective at reducing vascular events
Indications for reperfusion therapy?
Chest pain suggestive of acute MI ECG changes No contraindications
Risks of thrombolytic therapy?
-Failure to perfuse - Haemorrhage - Hypersensitivity +
Early treatment of STEMI?
Analgesia - diamorphine (IV) Anti-emetic Aspirin GTN if BP is above 90mmHg Oxygen if hypoxic Primary angioplasty Thrombolysis if angioplasty not available within 2 hours
Complications of acute MI?
Death Arrhythmic complications Structural complications Functional complications
Examples of structural complications from an MI?
Cardiac rupture Ventricular septal defect Mitral valve regurgitation Left ventricular aneurysm formation Mural thrombus Inflammation Acute pericarditis
Functional complications of an MI?
Acute ventricular failure - left, right or both Chronic cardiac failure Cardiogenic shock
Killip classification for heart failure?
1- no signs of heart failure (6%) 2- Crepitations <50% of lung fields (18%) 3- Crepitations >50% of lung fields (38%) 4- Cardiogenic shock (81% of CCF)
Routine observations for heart failure?
Cardiac monitor - rhythm How does patient feel Pulse and BP Hear sounds especially added sounds Murmurs Pulmonary crepitations Fluid balance especially fluid output
The most important thing to remember about in an acute NSTEMIs?
The ECG may be normal
What does troponin C bind?
Calcium (for both cardiac and skeletal muscles)
What does troponin 1 do?
In the absence of Ca++ it binds to actin which inhibits actin-myosin ATPase induced contraction - cardiac specific isoforms Short= Inhibits actin-myosin interactions
What is Troponin 1 specific to?
Cardiac muscle
What does Troponin T do?
Links troponin complex to tropomyosin which facilitates contraction - cardaic specific isoform Short= Binds with tropomyosin and facilitates contractions
Where are troponin T and 1 located?
Integral components of the myofibrillar contractile apparatus of the heart
Which are the preferred biomarkers for heart attacks?
Troponin T & 1 (TnT & Tn1)
Why are troponins the gold standard biomarkers?
Nearly absolute myocardial specificity-highly sensitive They reflect the microscopic zone of myocyte necrosis Suggestion that any amount of Myocardial ischaemia should be labelled as MI
What are we measuring with troponin?
Embolization Microvascular circulation Myonecrosis `
What is serial Tn testing used for?
To discriminate between acute and chronic events
Diagram of adhesion, activation and aggreggation?
What is the final common pathway leading to platelet aggregation and thrombus formation?
GP-IIb-IIIa
What happens in GP IIb-IIIa?
The expression of GP IIb-IIIa and the cross-linking of platelet receptors GP IIb-IIIa by fibrinogen molecules
What is a GRACE calculator?
Risk calculator for death or MI from admission to hospital to 6 months after discharge
How are stents inserted?
Catheter inserted
Balloon inflated
Stent remains
Troponin-itis?
When clinicains diagnose patients with acute MI only on the fact that they have elevated troponin
What other conditions are troponin elevated in?
CCF
Hypertensive crisis
Renal failure
Pulmonary embolism
Sepsis
Stronk (TIA)
Peri/myo carditis
Post arrhythmia
Detailed diagnostic process for an MI?
- Detect rise/fall of cardiac biomarker values (preferably cardiac Tn with atleast one value above the 99th percentile upper refernce limit [URL])
- One of these other criteria
- Symptoms of ischaemia
- New or presumed new signif ST segment- T wave changes or new left bundle branch block. Development of pathological Q waves in the ECG
- Imgaing evidence of new loss of viable myocardium or new regional wallmotion abnormality
- ID of an intracoronary thrombus by angiography or autopsy
Diagnosis of an AMI simple explanation?
Troponin measurement is central and tested before symptoms
HOWEVER
You need atleast 1 of 4 additional criteria to diagnose an AMI
Definition of an MI classification 1?
Spontaenous MI related to ischaemia due to primary coronary event such as plaque erosion and/or rupture, fissuring or dissection
Definition of an MI classification 2?
MI secondary to ischaemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolism, anaemia, arrhythmias, hypertension or hypotension
Definition of an MI classification 3?
Sudden unexpected cardiac death. including cardiac arrest often with symptoms suggesting ischaemia with new ST- segment elevation, new left bundle branch block: or pathollogic/ angiographic evidence of fresh coronary thrombus
What is a type 2 myocardial infarction?
Secondary to ischaemic imbalance
Increased myocardial oxygen demand or reduced myocardial oxygen
Example’s of conditions causing increased myocardial oxygen demand are?
Sustained tachycardia
Significant hypertension
Mared left ventricular hypertrophy
Hypertrophic cardiacmyopathy
Valvular disease
Conditions causing reduced myocardial blood flow include?
Anaemia
Hypoxia (resp failure)
Bradychardia
Hypotension
Vasospasm
Coronary embolism
Causes of type 2 MI?
It is an MI due to ischaemic imbalance
Causes:
Increased myocardial O2 demand
Decreased myocardial 02/Blood flow
Typical features of a type 1 MI?
Sudden symptoms
Major ECG changes
No other obvious causes
Higher trop with rise then fall
Severe CAD on angiography
Typical features of a type 2 MI?
Less chest pain
Minor ECG changes
Tach/ BP low / illness
Smaller more static trop
Mild moderate coronary disease
What is non-ischaemic myocardial injury with necrosis?
Not technically a Type II MI but often labelled as such due to difficulties with classification
Usually occurs in complex patients with significant medical or surgical issues
Seriously unwell patients or chronic disease patients but without evidence of significant coronary artery disease absence of ischemic symptoms or ECG changes
Within this group it becomes much harder when patients develop some ischaemic features or minor ECG changes where the diagnosis might revert to Type I or II MI
Examples of cardiac injury not related to myocardial ischaemia?
Cardiac contusion
Ablation
Pacing
AICD shocks
Myocarditis
Cardiotoxic chemotherapy
Conditions associated with non-ischaemic myoardial injury with necrosis?
Cardiac inury not related to myocardial ischaemia
Multifactorial or indetreminate myocardial injury
Examples of multufactorial or indeterminate myocardial injury?
Severe sepsis or renal failure
Pulmonary embolus, pulmonary hypertension, cor pulmonale
Chronic severe heart failure, chronic renal failure
Seveer acute neurological diseases- stronk
Excercise, burns
Stress cardiomyopathy (takotsubo)
Seconday prevention methods?
Healthy lifestyle
Smoking cessation
Good control of BP, cholesterol and diabetes
4 phases of rehabilitation?
In- patient
Early post-discharge period
Structured excercise programme - hospital based
Long term maintenance of physical activity and lifestyle change (community based)
Targets for secondary cardiac MI prevention?
Avoid smoking
Healthy diet
Regular aerobic exercise
Optimal drug therapy
Cholesterol ,4.0 mmol/l
BP <140/85 mmHg
Heart attack tablets?
- Aspirin/clopidogrel
- Ateno
