Myocardial Infaction Flashcards

(22 cards)

1
Q

What is MI

A

Cell death of heart muscle - heart attack

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2
Q

Clinical signs of MI

A
  • low BP
  • high HR
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3
Q

Symptoms of heart attack

A

Sweatiness
Nausea
Excruciating chest pain
Breathlessness
ANGINA/acute coronary syndrome

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4
Q

Angina - what is it

A

Crushing central chest pain
Radiate to jaw or teeth
Or either arm

Brought on by stress, and lowered by rest and stopping physical exertion

Relieved by rest or GTN within 5 minutes

Also known as chronic coronary syndrome

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5
Q

Why does angina happen?

A
  • chest pain due to myocardial ischaemia
  • due to flow limiting atherosclerosis or anaemia etc..
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6
Q

What are most heart attacks caused by?
Describe mechanism

A

Coronary artery disease when coronary arteries narrow due to atheroma in their walls

  • if atheroma is unstable and pieces break off this can lead to blood clot forming
  • clot can block coronary arteries
  • can starve heart of oxygen = damaged heart muscle (HEART ATTACK!!)

Also called acute soronayr syndroe

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7
Q

What is primary angioplasty

A

Where a stent is put in coronary artery after a heart attack to open up coronary artery to prevent new heart attack

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8
Q

What lifestyle changes to make to decrease heart attack?

A
  • decrease alcohol
  • decrease smoking
  • weight loss
  • exercise
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9
Q

Type 1 MI

A

Atherosclerotic plaque rupture in the coronaries, causing an occlusive thrombus (clot which forms over the atherosclerosis)

Or partial occlusion!!!

Most common!!

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10
Q

Type II MI

A

No plaque rupture and thrombus

  • extreme atherosclerosis on both sides of vessel
  • vasospasm of coronary arteries (eg: after cocaine ingestion)
  • non-atherosclerotic coronary dissection
  • oxygen supply and demand mismatch
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11
Q

What happens in heart attack?

A

Ischaemia
Impaired contraction of myocardium
Abnormal electrical activity can cause dangerous arrhythmias

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12
Q

What is the key aspect of virchows triad in MI

A

Changes to the vessel wall which causes changes to blood flow (makes it more turbulent), which cuuld rupture

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13
Q

Risk factors in risk calculators

A

Dyslipidaemia
Smoking
Diabetes
Hypertension
Male
Age
Family history

(Obesity, sedentary lifestyle, renal failure, inflammatory disease, south Asian ethnicity, low birth weight and socioeconomic status are also risk factors but nor on calculators)

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14
Q

What investigations are needed for heart attack

A

First - gold standard = ECG (determines whether to go for coronary angiography - elevates ST)
- coronary angiogram
- echocardiology
- serum troponing level

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15
Q

What is troponin

A
  • cardiac protein involved in actin and myosin interaction and contractility
  • released due to myocardial damage
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16
Q

What is the difference between a STEMI and NSTEMI

A

STEMI = ST elevation MI
- has ST elevation on heart attack
- raised troponin due to cardiac muscle damage

NSTEMI = non ST elevation MI
- may nor have ST elevation on ECG
- raised troponin due

If no ST elevation and no raised troponin = = unstable angina

17
Q

Echocardiogram

A

Ultrasound showing which part of the heart may or may not be contracting

May indicate which coronary artery is blocked depending on which cardiac muscle not contracting

May show scarring

18
Q

What is coronary angiography

A

Dye in coronary arteries
Injected
Opacities the vessels

19
Q

Management of MI

A

Immediate:
- morphine pain relief
- high flow oxygen
- oral aspirin

  • thrombocytes drugs (OLD) replaced with:
    Surgical intervention:
  • primary percutaneous intervention - vessel in arm or leg , balloon to expand narrowed artery and put stent in

Simvastatin - to reduce death by Conor’s heart disease - inhibits HMG CoA reductase - to decrease cholesterol levels

20
Q

Key drugs for prevention of MIs

A
  • beta blockers - bisoprolol
  • antiplatelet drugs: aspirin, P2Y12 inhibitors (prasugrel, ticagrelor, clopidogrel) - reduce platelet activation on stent clots
  • ACE inhibitors - ramapril
  • glyceryl trinitrate
21
Q

Why are beta blockers used in MI

A

Decrease death rates in weeks afterwards:

  • protects against arrhythmia
  • negatively chronotropic, makes heart go slower, allowing for increased coronary artery filling.
  • Reduces sympathetic over activity (and therefore hypertrophic remodelling). - Negatively ionotropic - reduce O2 demand as makes contract less/
22
Q

Glyceryl trinatrate use and how it helps

A
  • glyceryl trinitrate - spray for angina to increase nitric oxide level
  • potent vasodilator for coronary dilatation, decreases preload and after load so heart doesn’t meed to contract as much , allowing for drcreased oxygen consumption!