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Phase 2a Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Name 6 things an ECG can identify

A
  • Arrhythmias
  • Myocardial infarction / ischaemia
  • Pericarditis
  • Chamber hypertrophy
  • Electrolyte disturbances
  • Drug toxicity
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2
Q

What is the SA node?

A

The dominant pacemaker with an intrinsic rate of 60-100bpm

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3
Q

What is the AV node?

A

The backup pacemaker with an intrinsic rate of 40-60bpm

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4
Q

What are the ventricular cells?

A

Backup pacemaker cells with an intrinsic rate of 20-45bpm

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5
Q

Describe the impulse conduction pathway

A 
> Sinoatrial node
> AV node 
> Bundle of His
> Bundle branches 
> Purkinje fibres
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6
Q

What is the P wave?

A

Atrial depolarisation - seen in every lead apart from aVR

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7
Q

What is the PR interval?

A

Time taken for the atria to depolarise and electrical activation to get through the AV node

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8
Q

What is the QRS complex?

A

Ventricular depolarisation

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9
Q

What is the ST segment?

A

Interval between depolarisation and repolarisation

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10
Q

What is the T wave?

A

Ventricular repolarisation

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11
Q

Define dextrocardia

A

Heart on the right side of the chest instead of the left

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12
Q

What does an ECG of an acute ANTEROLATERAL myocardial infarction look like?

A

ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads

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13
Q

What does an ECG of an acute INFERIOR MI look like?

A

ST segments are raised in inferior leads (II, III, aVF)

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14
Q

Why can’t you see atrial repolarisation on an ECG?

A

It happens at the same time as the QRS complex

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15
Q

On an ECG, how much should one small box across represent? How much should one large box across represent?How much should one large box vertically represent?

A

ACROSS;
One small box = 0.04s
One large box = 0.5

VERTICALLY;
One large box = 0.5mV

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16
Q

Where can you palpate the left ventricle?

A

5th left intercostal space in the mid-clavicular line - responsible for the apex beat

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17
Q

Define stroke volume

A

Volume of blood ejected from each ventricle during systole

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18
Q

Define cardiac output

A

Volume of blood each ventricle pumps out as a function of time

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19
Q

What is the equation for cardiac output?

A

CO (L/min) = Stroke volume (L) x Heart rate (BPM)

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20
Q

Define total peripheral resistance

A

Total resistance to flow in systemic blood vessels from beginning of aorta to vena cava

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21
Q

Define preload

A

Volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction

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22
Q

Define afterload

A

Pressure the left ventricle must overcome to eject blood during contraction

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23
Q

Define contractility

A

Force of contraction and the change in fibre length during systole

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24
Q

Define elasticity

A

Myocardial ability to recover normal shape after systolic shape

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25
Q

Define diastolic dispensibility

A

The pressure required to fill the ventricle to the same diastolic volume

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26
Q

Define compliance

A

How easily the heart chamber expands when filled with blood

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27
Q

What is Starling’s law?

A

Force of contraction is proportional to end diastolic length of cardiac muscle fibre

The more the ventricle fills, the harder it contracts

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28
Q

How does standing affect BP?

A

Standing decreases venous return due to gravity

> cardiac output decreases

> drop in blood pressure

> stimulating baroreceptors to increase blood pressure

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29
Q

What is heart sound S1?

A

Mitral and tricuspid valve closure

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30
Q

What is heart sound S3?What does it sound like?

A

Early diastole during rapid ventricular filling

It is normal in children and pregnant children, but is associated with mitral regurgitation and heart failure

KENTUCKY

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31
Q

What is heart sound S4?

A

“gallop” in late diastole, produced by blood being forced into a stiff hypertrophic ventricle

Associated with left ventricular hypertrophy

TENNESSEE

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32
Q

Which coronary arteries are prone to atherosclerosis?

A
  • Circumflex
  • Left anterior descending (LAD)
  • Right coronary arteries
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33
Q

What are the risk factors of atherosclerosis?

A
  • Age
  • Tobacco
  • High serum cholesterol
  • Obesity (more pericardial fat -> increased inflammation)
  • Diabetes
  • Hypertension
  • FHx
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34
Q

How are atherosclerosis plaques generally distributed in the body?

A
  • Within peripheral and coronary arteries

- Focal distribution along artery length

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35
Q

Describe the structure of an atherosclerotic plaque

A

Complex lesion of;

  • lipids
  • necrotic core
  • connective tissue
  • fibrous “cap”
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36
Q

What will eventually happen to an atherosclerotic plaque?

A
  • Occlude the vessel lumen > ANGINA

- Rupture > THROMBUS FORMATION

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37
Q

Briefly describe the process of initial atherosclerosis formation

A
  1. Endothelial cell injury causing endothelial dysfunction
  2. Chemoattractants released from endothelium which attract leukocytes
  3. Leukocytes accumulate and migrate into vessel wall
  4. More chemoattractants released from injury site
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38
Q

What inflammatory cytokines are found in atherosclerotic plaques?

A
  • IL-1 (MAIN ONE)
  • IL-6
  • IFN-gamma
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39
Q

What are fatty streaks?

A
  • Earliest lesion of atherosclerosis
  • Begin forming <10yrs old
  • Consist of aggregations of lipid-laden macrophages and T lymphocytes within intimal layer of vessel wall
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40
Q

What are intermediate lesions?

A

Composed of layers of;

  • Lipid laden macrophages (foam cells)
  • Vascular smooth muscle cells
  • T lymphocytes

There is adhesion and aggregation of platelets to vessel wall

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41
Q

How does aspirin prevent thrombus formation?

A

Aspirin inhibits platelet aggregation

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42
Q

What is the fibrous cap of advanced atherosclerotic lesions made of?

A

Extracellular matrix proteins (e.g. collagen and elastin) laid down by smooth muscle cells that overlie the lipid core and necrotic debrisIt may be calcified

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43
Q

What makes up an advanced lesion / fibrous plaque?

A
  • Smooth muscle cells
  • Macrophages / foam cells
  • T lymphocytes
  • Red cells
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44
Q

Describe plaque rupture

A
  1. Plaque constantly growing and receding
  2. Fibrous cap needs to be resorbed and redeposited in order to be maintained
  3. If balance shifts (e.g. in favour of inflammatory conditions - increased enzyme activity), then the cap becomes weak and the plaque ruptures
  4. Basement membrane, collagen, and necrotic tissue is exposed
  5. Haemorrhage of vessel within plaque
  6. Thrombus formation and vessel occlusion
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45
Q

What is angina?

A

Chest pain or discomfort as a result of reversible myocardial ischaemia

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46
Q

What is usually meant by “reversible myocardial ischaemia”?

A

Narrowing of one or more of the coronary arteries

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47
Q

What are the three types of angina? Explain them

A

Stable
- Induced by effort, relieved by rest

Unstable

  • Angina of recent onset (< 24hrs)
  • Deterioration in previously stable angina, with symptoms occurring at rest

Prinzmetal’s angina
- Caused by coronary artery spasm (rare)

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48
Q

What causes mismatch between coronary blood supply and metabolic demand?

A
  • Atheroma / stenosis of coronary arteries
  • Valvular disease
  • Aortic stenosis
  • Arrhythmia
  • Anaemia (thus, less O2 is transported)
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49
Q

Why does ischaemia cause pain?

A

Ischaemic metabolites (e.g. adenosine) stimulate nerve ending and produce pain

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50
Q

Is angina more common in men or women?

A

Men

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51
Q

Name 9 risk factors for angina

A
  • Smoking
  • Sedentary lifestyle
  • Obesity
  • Hypertension
  • Diabetes mellitus
  • Family history
  • Genetics
  • Age
  • Hypercholesterolaemia
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52
Q

What are the 4 stages of angina?

A
  1. Initiation
  2. Adaptation
  3. Clinical stage
  4. Pathological stages
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53
Q

Describe the initiation stage of atherosclerosis

A
  • Endothelial injury results in lipid accumulation in the intimal layer of the vessel
  • Endothelial cells secrete chemoattractants
  • Monocytes arrive and proliferate into macrophages in the presence of oxidised LDL
  • Macrophages ingest oxidised LDL and turn into foam cells, forming a lipid core in the intimal layer
  • Mural thrombus forms and subsequent healing takes place
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54
Q

Describe the adaptation stage of atherosclerosis

A
  • Plaque progresses to 50% of lumen size, and vessel can no longer compensate by remodelling
  • Drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix
  • Progresses to unstable plaque
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55
Q

Describe the clinical stage of athersclerosis

A
  • Plaque continues to grow but runs risk of haemorrhage or exposure of tissue HLA-DR (which might stimulate T cell accumulation)
  • Drives inflammatory reaction against plaque
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56
Q

What is an intimal cell mass?

A

Collection of muscle cells and connective tissue without lipids

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57
Q

Describe the composition of an atheromatous plaque

A
  • Distorted endothelial surface containing lymphocytes, macrophages, smooth muscle cells, and damaged endothelial cells
  • Local necrotic and fatty matter with scattered foam cells
  • Evidence of local haemorrhage with iron deposition and calcification
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58
Q

Name four complications of plaque rupture

A
  • Acute occlusion due to thrombus
  • Chronic narrowing of vessel lumen with healing of the local thrombus
  • Aneurysm change
  • Embolism of thrombus +/- plaque lipid content
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59
Q

What is the clinical presentation of angina?

A
  • Central chest tightness / heaviness
  • Provoked by exertion, especially after;
    > eating
    > cold windy weather
    > anger / excitement
  • Relieved by rest or GTN spray
  • Pain may radiate to arms, neck, jaw, or teeth
  • Dyspnoea, nausea, sweatiness, faintness
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60
Q

How do you score angina?

A

1 point = central / tight / radiation
2 points = precipitated by exertion
3 points = relieved by rest / GTN spray

1/3 = non-anginal pain
2/3 = atypical pain
3/3 = typical angina
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61
Q

What are the differential diagnoses for angina?

A
  • Pericarditis / myocarditis
  • Pulmonary embolism
  • Chest infection
  • Dissection of aorta
  • GORD
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62
Q

Name five methods of diagnosing angina

A
  • 12 lead ECG
  • Treadmill test / Exercise ECG
  • CT scan calcium scoring
  • SPECT / myoview
  • Cardiac catheterisation
63
Q

How do you use a 12 lead ECG to diagnose angina?

A
  • Often normal
  • May show ST depression
  • Flat or inverted T waves
  • Look for signs of past MI
64
Q

Describe the treadmill test for diagnosing angina

A
  1. Put an ECG on a patient, then make up run on an incline treadmill (try to induce ischaemia)
  2. Monitor how long patient is able to exercise for

If you see ST segment depression, this is diagnostic of late-stage ischaemia

65
Q

What is the problem with the treadmill test / exercise ECG?

A

Many patients are unable to use it

E.g. can’t walk, unfit, young females, bundle branch block

66
Q

Describe the CT scan calcium scoring

A

CT the heart and if there is atherosclerosis in the arteries, the calcium will light up white

  • Significant calcium = angina
67
Q

Describe the SPECT / myoview for diagnosing angina

A
  1. Radio-labelled tracer injected into patient
  2. Taken up by coronary arteries
  • Lights up = good blood supply
  • Doesn’t light up = little blood supply
  • No light after exercise = myocardial ischaemia diagnosis
68
Q

Name four methods of treating angina

A
  • Modify risk factors
  • Treat underlying conditions - Pharmacologically
  • Revascularisation
69
Q

How can you modifiy risk factors to improve angina symptoms?

A
  • Stop smoking
  • Encourage exercise
  • Weight loss
70
Q

Name 5 types of drugs used to treat angina

A
  • Aspirin
  • Statins
  • Beta-blockers
  • GTN spray
  • Ca2+channel antagonists / blockers
71
Q

How does aspirin help treat angina?

A
  • COX inhibitor - reduces prostaglandin synthesis (inc. thromboxane A2) resulting in reduced platelet aggregation
  • Reduces angina events
    e. g. SALICYLATE
72
Q

What are the side effects of aspirin?

A

Gastric ulceration

73
Q

How do statins help treat angina?

A
  • HMG-CoA reductase inhibitors - reduces cholesterol produced by liver
  • Reduces angina events and LDL-cholesterol
  • Anti-atherosclerotic
74
Q

What are the first line anti-anginal medicines?

A
  • Betablockers

- GTN spray

75
Q

How do beta blockers help treat angina?

A
  • Reduce force of contraction of heart (e.g. BISOPROLOL and ATENOLOL)
  • Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway
  • B1 activation > Gs > cAMP to ATP > contraction
76
Q

What do beta blockers ‘reduce’?

A

Reduce;

  • Heart rate (negatively chonotropic)
  • Left ventricle contractility (negatively inotropic)
  • Cardiac output
77
Q

What are the side effects of beta blockers?

A
  • Tiredness
  • Nightmares
  • Bradycardia
  • Erectile dysfunction
  • Colds hands and feet
78
Q

What are the contraindications for beta blockers?

A
  • Asthma
  • Heart failure / block
  • Hypotension
  • Bradyarrhythmias
79
Q

How does GTN spray help treat angina?

A
  • Venodilator (nitrate)
  • Dilates systemic veins, thereby reducing venous return to right heart
  • Reduces preload
  • Thus reduces work of heart and O2 demand
  • Also dilates coronary arteries
80
Q

What are the side effects of GTN spray?

A

Strong headache immediately after use

81
Q

How do Ca2+ channel antagonists / blockers help treat angina?

A
  • Primary arterodilators
  • Dilates systemic arteries, resulting in BP drop
  • Thus reduces after load on the heart
  • Thus less energy required to produce same cardiac output
    e. g. VERAPAMIL
82
Q

When do you perform revascularisation to treat angina?

A
  • When medical fails

- High risk angina

83
Q

What two methods are there of revascularising a patient to improve symptoms of angina?

A
  • Percutaneous coronary intervention (PCI)

- Coronary artery bypass graft (CABG)

84
Q

Describe percutaneous coronary intervention

A
  • Dilating coronary atheromatous obstructions by inflating balloon within it
  • Expands plaque = makes artery bigger
85
Q

What are the pros and cons of PCIs?

A

Pro;

  • Less invasive
  • Convenient
  • Short recovery
  • Repeatable

Cons;

  • Risk of stent thrombosis
  • Not good for complex disease
86
Q

Describe coronary artery bypass graft

A

Left internal mammary artery (LIMA) used to bypass proximal stenosis in LAD coronary artery

87
Q

What are the pros and cons of CABG?

A

Pros;

  • Good prognosis
  • Deals with complex disease

Cons;

  • Invasive
  • Risk of stroke or bleeding
  • One time treatment
  • Long recovery
88
Q

What is ‘acute coronary syndrome’?

A

An umbrella term that includes;

  • ST-elevation myocardial infarction (STEMI)
  • Unstable (crescendo) angina (UA)
  • Non-ST elevation myocardial infarction (NSTEMI)
89
Q

What is an ST-elevation myocardial infarction (STEMI)?

A

Complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis

It causes full thickness damage of heart muscle

90
Q

How can you diagnose a STEMI?

A

ECG

  • Tall T waves
  • ST elevation
  • Subsequent pathological Q wave
    May present as new left bundle branch block (LBBB) on ECG
91
Q

What is a non-ST-elevation myocardial infarction (NSTEMI)?

A

Complete occlusion of a MINOR, or partial occlusion of a major, coronary artery previously affected by atherosclerosis

Causes partial thickness damage of heart muscle

92
Q

How do you diagnose an NSTEMI?

A
  • Retrospective diagnosis made after troponin results (and sometimes other)
  • No ST elevation or Q wave
  • Will see ST depression and / or T wave inversion
93
Q

What is the difference between a UA and NSTEMI?

A

In an NSTEMI, there is an occluding thrombus which leads to myocardial necrosis and a rise in serum troponin or creatine kinase-MB

In UA, there is an occluding thrombus that leads to myocardial ischaemia

94
Q

Link myocardial infarction to myocardial ischaemia

A

Cardiac myocytes dying due to myocardial ischaemia

95
Q

How many types of MI are there?

A

5

96
Q

Describe MI type 1

A

Spontaneous MI with ischaemia due to a primary coronary event

e.g. plaque erosion / rupture, fissuring, or dissection

97
Q

Describe MI type 2

A

MI secondary to ischaemia, due to increased O2 demand or decreased supply, such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension

98
Q

Describe MI type 3, 4 and 5

A

MI due to;

Type 3 = sudden cardiac death
Type 4 = PCI
Type 5 = CABG

99
Q

Describe the epidemiology of STEMI in the UK

A
  • 5/1000 deaths per annum

- Worse prognosis in elderly and those with left ventricular failure

100
Q

What are the risk factors for a heart attack?

A
  • Age
  • Male
  • FHx of IHD
  • Hx of premature CHD
  • Premature menopause
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Hyperlipidaemia
  • Obesity & sedentary lifestyle
101
Q

Describe the pathophysiology of a myocardial infarction

A
  • Rupture / erosion of fibrous cap of a coronary artery plaque
  • Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction, and distal thrombus embolism
  • Resulting in prolonged complete arterial occlusion within 15-30mins
102
Q

Describe the pathophysiology of a STEMI (specifically with regards to the Q wave)

A

Sub-endocardial myocardium is initially affected but, with continued ischaemia, the infarct zone extends through the sub-epicardial myocardium, producing a transmural Q wave MI

103
Q

What is the progression from fatty streak to cardiac event?

A 
> Fatty streak 
> Fibrotic plaque
> Atherosclerotic plaque
> Plaque rupture / fissure 
> Thrombosis
> MI / Ischaemia stroke / critical leg ischaemia, sudden CVS death
104
Q

What is the difference between the thrombi in unstable angina and myocardial infarction?

A 
UA = partial occlusion by thrombus 
MI = total occlusion by thrombus
105
Q

What is the clinical presentation of an ACS?

A
  • Unstable angina
  • New onset angina
  • Acute central chest pain
  • Sweating
  • Nausea
  • Vomiting
  • Dyspnoea
  • Fatigue
  • Shortness of breath
  • Palpitations
  • Distress and anxiety
  • Pallor
  • Tachycardia OR bradycardia
  • Hypotension
  • Reduced heart sound S4
  • May be signs of heart failure
  • Peripheral oedema
106
Q

What are the differential diagnoses for ACS?

A
  • Angina
  • Pericarditis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism
  • Oesophageal reflux/spasm
107
Q

Name 2 ways of diagnosing an MI

A
  • 12 lead ECG

- Biochemical markers

108
Q

Describe how you can use an ECG to diagnose a NSTEMI

A
  • ECG may be normal, should use biochemical markers for certain diagnosis
  • ST depression
  • T wave inversion
109
Q

Describe how you can use an ECG to diagnose a STEMI

A
  • Persistent ST elevation
  • Hyperacute T waves
  • Possible LBBB
  • May see pathological Q waves and T wave inversion a few days after an MI
110
Q

Which biochemical markers can you use to diagnose an MI?

A
  • Troponin T & I
  • CK-MB
  • Myoglobin
  • CXR
111
Q

How can you use troponin (T & I) to diagnose a heart attack?

A
  • Sensitive and specific markers of myocardial necrosis
  • Serum levels increase within 3-12 hours from the onset of chest pain, and peak at 24-48 hours
  • Fall back to normal over 5-14 days
  • Act as a prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation
112
Q

How can you use CK-MB to diagnose a heart attack?

A
  • Marker for myocyte death, but has low accuracy since it can be present in serum of normal individuals and in patients with significant skeletal muscle damage
  • Can be used to determine re-infarction as levels drop back to normal after 36-72 hours
113
Q

How can you use myoglobin to diagnose an MI?

A

Becomes elevated very early in MI but the test has poor specificity since myoglobin is present in skeletal muscle

114
Q

How can a CXR help identify an MI?

A

Look for cardiomegaly, pulmonary oedema, or a widened mediastinum (aortic rupture)

115
Q

What are the various methods of treating an MI?

A
  • Pain relief
  • Anti-emetic
  • Oxygen
  • Anti-platelets
  • Beta blockers
  • Statins
  • ACE inhibitors
  • Coronary revascularisation
  • Risk factor modification
116
Q

What do you use for pain relief following an MI?

A
  • GTN spray
  • MORPHINE!

Remember: MONA (M = morphine)

117
Q

What oxygen saturation should you aim for in a normal patient?

A

94-98%

118
Q

What oxygen saturation should you aim for in a patient with COPD?

A

88-92%

119
Q

Why do you give anti-platelet medication to someone who has just had an ACS?

A
  • Atheromatous plaque rupture results in platelets being exposed to ADP / thromboxane A2 / adrenaline / thrombin / collagen tissue factor
  • This results in platelet activation / aggregation via IIb/IIIa glycoproteins binding to fibrinogen
  • Then thrombin is able to enzymatically convert fibrinogen to fibrin resulting in the formation of a fibrin mesh over platelet plug, and the formation of a thrombotic clot
  • Anti-platelet drugs help prevent this
120
Q

What anti-platelet drugs can you give to someone who has just had an ACS?

A
  • Aspirin (oral)
  • P2Y12 inhibitors (oral)
  • Glycoprotein IIb/IIIa antagonists (IV)
121
Q

What is the mechanism of action of aspirin?

A

COX-1 inhibitor - blocks formation of thromboxane A2, thus prevents platelet aggregation

122
Q

What is the mechanism of action of P2Y12 inhibitors?

A

Inhibits ADP-dependent activation of IIb/IIIa glycoproteins, thereby preventing amplification response of platelet aggregation

e.g. CLOPIDOGREL, PRASUGREL, TICAGRELOR

123
Q

When should you use P2Y12 inhibitors?

A
  • Allergic to aspirin

- Alongside aspirin as a dual anti-platelet therapy

124
Q

What are the side effects P2Y12 inhibitors?

A
  • Neutropenia
  • Thrombocytopenia
  • Increased risk of bleeding
125
Q

What are the contraindications of P2Y12 inhibitor use?

A

If a CABG is planned

126
Q

When do you use glycoprotein IIb/IIIa antagonists to treat an ACS?

A

Used (in combination with aspirin and oral P2Y12 inhibitors) in patients with ACS undergoing percutaneous coronary intervention

127
Q

What are the side effects of glycoprotein IIa/IIb antagonists?

A

Increases risk of MAJOR bleeding

128
Q

Give some examples of glycoprotein IIb/IIa antagonists

A
  • ABCIXIMAB
  • TIROGIBAN
  • EPTIFBATIDE
129
Q

What beta blockers should you give to a patient who has just had an ACS?

A

ATENOLOL or METOPROLOL (IV then oral)

130
Q

What are the side effects and contraindications of beta blocker use?

A

Avoid with asthma, heart failure, hypotension, and bradyarryhthmias

131
Q

Which statins do you give to a patient to treat a recent ACS?

A

HMG-CoA reductase inhibitors (e.g. SIMVASTATIN, PRAVASTATIN, ATORVASTIN)

132
Q

Which ACE inhibitors do you give a patient to treat a recent ACS?

A

RAMPIRPIL, LISONOPRIL

133
Q

What must you do if you prescribe ACE inhibitors?

A

Monitor renal function

134
Q

What is the clinical presentation for an AMI?

A
  • Chest pain > 20mins
  • Severe central ongoing pain
  • Pain radiating to left arm, jaw or neck
  • Does not usually respond to GTN spray
  • Pain = substernal pressure, squeezing, aching, burning, sharp
  • Sweating
  • Nausea
  • Vomiting
  • Dyspnoea
  • Fatigue
  • Palpitations
  • Breathlessness
  • Distress / anxiety
  • Pale, clammy
  • Significant hypotension
  • Brady/tachycardia
135
Q

What are the differential diagnoses for acute myocardial infarction?

A
  • Stable / unstable angina
  • NSTEMI
  • Pneumonia
  • Pneumothorax
  • Oesophageal spasm
  • GORD
  • Acute gastritis
  • Pancreatitis
  • MSK chest pain
136
Q

In a STEMI with infarction of the anterior border of the heart, what will you see on an ECG?

A

ST elevation in V1-V3

137
Q

In a STEMI with infarction of the inferior border of the heart, what will you see on an ECG?

A

ST elevation in II, III, aVF

138
Q

In a STEMI with infarction of the lateral border of the heart, what will you see on an ECG?

A

Change in I, aVL, V5-V6

139
Q

In an MI with infarction of the posterior border of the heart, what will you see on an ECG?

A
  • ST depression in V1-V3
  • Dominant R wave
  • ST elevation in V5-V6
140
Q

In a STEMI with infarction of subendocardium of the heart, what will you see on an ECG?

A

Changes anywhere on ECG

141
Q

Describe the evolution of a STEMI ECG

A

First few minutes;

  • T wave becomes tall, pointed, and upright
  • ST elevation

First few hours;

  • T waves invert
  • R wave voltage decreases
  • Q waves develop

Few days later;
- ST segment returns to normal

Weeks / months;

  • T wave may return upright
  • Q wave remains
142
Q

Describe the biochemical changes following a heart attack

A
  • Trop I & T increase

- Myoglobin increases

143
Q

What is the pre-hospital treatment for an MI?

A
  • Aspirin 300mg chewable
  • GTN (sublingual)
  • Morphine
144
Q

What is the hospital treatment for an MI?

A
  • IV morphine
  • Oxygen (if sats <90% or SOB)
  • Beta-blocker (ATENOLOL)
  • P2Y12 inhibitor (CLOPIDOGREL)
145
Q

Who is offered a PCI?

A

Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 MINUTES of first medical contact

146
Q

What happens if a patient cannot get a PCI?

A

Fibrinolysis, and then transfer to PCI after infusion

147
Q

What are the complications of myocardial infarction?

A
  • Sudden death
  • Arrhythmias
  • Persistent pain
  • Heart failure
  • Mitral incompetence
  • Pericarditis
  • Cardiac rupture
  • Ventricular aneurysm
148
Q

What tends to cause sudden death after an MI?

A

Ventricular fibrillation a few hours after MI

149
Q

What causes persistent pain after an MI?

A

Progressive myocardial necrosis

150
Q

What is heart failure?

A

When cardiac output is insufficient to meet body’s metabolic demands

151
Q

What causes mitral incompetence following an MI?

A

Myocardial scarring preventing valve closure

152
Q

What causes pericarditis following an MI?

A

Due to transmural infarct resulting in inflammation of pericardium

153
Q

What causes cardiac rupture after an MI?

A

Early rupture - result of shearing between mobile and immobile myocardium

Late rupture - due to weakening of wall following muscle necrosis and acute inflammation

154
Q

What causes ventricular aneurysm after a heart attack?

A

Stretching of newly formed collagenous scar tissue

Phase 2a Medicine (5 decks)

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