Cardiovascular 2 Flashcards

1
Q

In the heart, where is the Sinoatrial (SA) node located?

A

In the roof of the right atria

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2
Q

Where is the Atrioventricular node (AV) located?

A

Lies in the basement/floor of the atrial cavity

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3
Q

Describe how electrical activity travels through the heart to initiate contraction of the myocardium

A

Initial impulse in SA node , the dominant pacemakerwhich activates electrical activity in the atria.

Impulse spreads throughout the roof of the left and right atria, causing atria contraction

AV node transmits electrical impulses down the cardiac septum to the bundle of his, which branches into the left and right bundle branches, which divide further into the purkinje fibres.

This results in ventricular depolarisation = contraction.

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4
Q

Describe how the pacemaker locations relate to the ECG wave

A

P - SA node activation of atrial depolarization

PQ/PR - Depolarization along the atria; impulse delay at the AV node

QRS -Ventricular depolarization/contraction and atrial repolarisation

ST - Completion of ventricular depolarization

T - Ventricular repolarisation

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5
Q

Define: Stable Angina

A

One or more of the coronary arteries blocked by atherosclerotic plaque.

No pain at rest at blood flow is ‘adequate’. Chest pain on exercise or stress due to increased oxygen demand to myocardium which cannot be met due to plaque occlusion.

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6
Q

With regards to symptoms, what is the distinguishing feature between Stable Angina and Acute Coronary Syndrome?

A

In Stable Angina, the chest pain is relieved by rest or GTN spray

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7
Q

Describe the physiological changes in an unstable angina, (including ECG and Troponin levels)

A

Unstable Angina = Plaque ruptures and a thrombus forms around it, partially occluding the artery.
There is ischemia, but no infarction.

ECG may be normal or show an inverted T wave. Troponin normal.

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8
Q

Describe the physiological changes in an NSTEMI, (including ECG and Troponin levels)

A

In an NSTEMI, there is significant occlusion of the coronary artery which causes a distal infarction. Infarction of the subendothelial layer.

ECG shows ST Depression

Troponin elevated

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9
Q

Describe the physiological changes in an STEMI, (including ECG and Troponin levels)

A

In a STEMI, there is a complete occlusion of the coronary artery lumen, resulting in a distal infarction that is transmural.

ECG shows ST elevation

Troponin elevated

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10
Q

Peak time for troponin following Myocardial damage is…

A

3-6 hours post onset of chest pain is the accepted time for the best testing of troponin.

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11
Q

Describe the acute management of stable angina

A

Short acting Glyceral Trinitrate - GTN spray or tablet administered sublingually.

Repeated after 5 minutes if pain as not gone.

Call an ambulance if pain hasn’t gone 5 minutes after taking second dose.

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12
Q

MOA of Glyceral trinitrate (GTN) spray ?

A

Converted in the body to nitric oxide which causes arterial vasodilation, relieving chest pain.

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13
Q

(3) Side effects of GTN spray?

A

Flushing, headache, light-headedness

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14
Q

Describe the chronic management of stable angina

A

1stline = GTN (symptom control), BB or CCB.

If symptoms not controlled, 2ndline = Add Dihydropyridine CCB to BB– if not tolerated/contraindicated considerlong actingnitrates.

If symptoms not controlled refer to cardiology for consideration ofangio/revascularisation

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15
Q

Modifications used as primary prevention of cardiovascular events?

A

Lifestyle modifications

Aspirin 75mg OD

Lipid lowering therapy

ACEi or ARB in diabetes in HTN.

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16
Q

Describe the acute management of acute coronary syndrome

A

M - Morphine

O - Oxygen (if needed)

N - Nitrates (GTN spray)

A - Aspirin (ASAP)/Anti-platelets (in hospital) + Anti-coagulant

17
Q

Describe the chronic management of acute coronary syndrome

A

ACEi/ARB

Dual antiplatelet therapy (aspirin + second antiplatelet)

Beta blocker/Calcium channel blocker

Statin

18
Q

MOA of Aspirin

A

Irreversibly binds to COX, reducing the production of thromboxane; which reduces platelet aggregation and decreases the risk of arterial occlusion.

19
Q

Adverse effects of aspirin

A

GI Irritation, Peptic ulceration and haemorrhage

20
Q

MOA of Clopidogrel

A

Binds to ADP receptor on platelet cell surface, inhibiting granule release to recruit other platelets.

21
Q

MOA of Statins

A

Reduce serum cholesterol by inhibiting enzyme involved in making cholesterol and increasing LDL clearance by the liver