Myocardial Infarction Flashcards

(19 cards)

1
Q

What were the patient’s (M) risk factors in the case study?

A

Non modifiable
*Age
*Male
*Family history

Modifiable
*Smoking (M) – scratching arteries and inflammation comes to fix but in the process it ends up blocking the arteries.
*Hyperglycemia - as above
*Hypercholesteremia – build up plaque in the arteries
*Hypertension – too high, BV change shape to cope
*Physical Inactivity

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2
Q

In the cardiac cycle, what do systole and diastole commonly refer to?

A

Ventricular contraction and relaxation

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3
Q

What part of the cardiac cycle is responsible for the heart sounds S1 & S2?

A

S1 = Closing of the AV valves and beginning of systole

S2 = Closing of SV valves marking the end of systole and beginning of diastole

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4
Q

What is a myocardial infarction?

A

AKA Heart attack

Blockage stops the blood flow to the heart = damage to myocardium or tissue ischemia

Ischemia associated with MI most common when a thrombus forms after an atherosclerotic plaque in the coronary artery ruptures

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5
Q

What are some of the symptoms of a MI? Relate these to the case study.

A

Angina (chest pain) - M thought it was indigestion and it was not responsive to nitrates

Diaphoresis (sweating)

Numbness/tingling to left arm – because the nerves down arm on this side join to the heart

Pallor – due to reduced blood flow

Dyspnoea – shortness of breath – because heart can’t pump blood hard enough so has to bring faster to get oxygen in

Anxiety – feeling of impending doom

Nausea/vomiting

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6
Q

What are some of the signs of a MI? Relate these back to the case study.

A

Tests for M:

ECG - measure electrical activity - T wave inversion, ST segment elevation/depression

Cardiac Enzymes - Elevated cardiac enzymes - Creatine phosphokinase (CPK), Troponin T and troponin I

Pain - did not subside with aspirin/GTN administration

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7
Q

Explain what happens when a MI occurs and the myocardial cells begin to die.

A

When these cells die, their contents—including enzymes and proteins—leak into the bloodstream. This can lead to inflammation and the release of substances like troponin, which are used as biomarkers to diagnose an MI

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8
Q

Explain what myocardial remodelling is.

A

Myocardial remodeling refers to the changes that occur in the structure and function of the heart muscle after an injury, such as a myocardial infarction.

Following damage, the heart tissue can undergo:
* Hypertrophy: The heart muscle thickens to cope with increased workload.
* Dilation: The heart chambers may enlarge to accommodate changes in blood flow and pressure.
* Fibrosis: Scar tissue forms, replacing healthy muscle tissue, which can affect the heart’s ability to contract and relax.

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9
Q

Explain the management of MI in pre-hospital or ED enviroments.

A

M – morphine – opens blood vessels = vasodilates

O – oxygen – saturate it so heart doesn’t work so heart

N – nitroglycerin – powerful vasodilator – route = sublingual

A – Aspirin – stop platelets sticking together

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10
Q

Explain what an NSTEMI is

A

NSTEMI (Non-ST-Elevation Myocardial Infarction): This type involves partial blockage of a coronary artery, leading to damage to the heart muscle. No S-T elevation on ECG

Involves the subendocardial tissues (tissue under the endocardial lining)

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11
Q

Explain what a STEMI is

A

THIS IS WHAT M HAD:

STEMI (ST-Elevation Myocardial Infarction): This is the more severe type of heart attack, where there is a complete blockage of a coronary artery. It affects a larger area of the heart muscle, leading to significant damage. Shows characteristic S-T elevation on an ECG

Involves the transmural tissue - full thickness of cardiac muscle

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12
Q

What other medical interventions could be used in hospital to manage an MI?

A

Tenecteplase (30-50mg/weight based)= clot buster

Enoxaparin = blood thinner and prevent clots from forming

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13
Q

What can be some complications of an MI? Note the one relating to the case study of M.

A

WHAT M HAD:

*ventricular fibrillation (VF) cardiac arrest
*VF is diagnosed through an ECG, which will show irregular, erratic electrical activity without distinct QRS complexes

TREATMENT FOR M:
Defibrillation: Delivering an electric shock to restore a normal rhythm.

M DEVELOPED ATRIAL FIBRILLATION - A FIB - atria only shaking – blood not moving so can clot. Might need to consider anticoagulant

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14
Q

Expected laboratory tests for chest pain/MI

A

*Cardiac Enzymes
*Urea and Electrolytes
*FBC
*BSL
*Thyroid function test

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15
Q

Expected investigations for chest pain/MI

A

*ECG
*Angiogram
*Chest Xray

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16
Q

What are the post discharge maintenance requirements usually?

A

*Aspirin and Clopidogrel
*Metoprolol - lower BP and strengthen heart
*Simvastatin - at night to lower cholesterol because we make the most cholesterol at night
*PRN Nitroglycerin spray - GTN works quickly to dilate blood vessels, improving blood flow to the heart and relieving chest pain.

17
Q

Explain why Aspirin and Clopidogrel are used together

A

Different Mechanisms of Action:

Aspirin: Inhibits the enzyme cyclooxygenase (COX), leading to reduced production of thromboxane A2, a substance that promotes platelet aggregation.

Clopidogrel: Blocks the ADP receptor on platelets, preventing activation and aggregation.

Dual antiplatelet therapy (DAPT)

18
Q

What other procedure did M have?

A

angiogram followed by PCI (angioplasty with stent)

Percutaneous coronary intervention (PCI) involves the use of coronary angiograms to visualize and assess the damage associated with coronary ischemia. Once the problem is located angioplasty can be performed to open up the affected vessel(s)

19
Q

What dietary changes did M have to consider post-discharge?

A

Dietary changes include a low-fat, low-salt diet with plenty of fruit and vegetables.

Reduce cholesterol - increase HDL by exercise, LDL can be effected by too much saturated fats

Soluble fibre can also help lower LDL cholestrol