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ESA 2 SK > CVS 10 Ischaemic Heart Disease > Flashcards

CVS 10 Ischaemic Heart Disease Flashcards

1
Q

What are some common causes of chest pain from lungs and pleura?

A

Pneumonia, Pulmonary embolism, pneumothroax

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2
Q

What are some common causes of chest pain from the GI system?

A

Oesophagus-reflux, peptic ulcer disease, gall bladder- biliary colic, cholecystitis

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3
Q

What are some common causes of chest pain from the chest wall?

A

Ribs- fractures, bone metastases, muscles, skin

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4
Q

What are some common causes of chest pain from the CVS?

A

Myocardium- MI, angina
Pericardium- pericarditis
Aorta- aortic dissection

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5
Q

What are the non-modifiable risk factors for coronary atheroma?

A

Increasing age
Male gender (females catch up after menopause)
Family history

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6
Q

What are the 4 important modifiable risk factors for coronary atheroma and what 3 others are there?

A

Hyperlipidaemia, smoking, hypertension, diabetes mellitus (x2 risk)
obesity, stress, exercise

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7
Q

Where does IHD cause pain?

A

Central, retrosternal or left sided

Can radiate to shoulders and arms, left side being most common, jaw, neck, epigastrium and back

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8
Q

What kind of pain is felt in IHD?

A

tightening, heavy, crushing, ocnstricting, pressure

occasionally described as burning epigastric pain particularly in inferior MI

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9
Q

How much of the lumen is blocked by atheroma for angina to occur?

A

over 70%

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10
Q

What kind of pain occurs with stable angina, when does it occur and how long does it last?

A

Typical of ischeamic chest pain in brief episodes, going upon resting for about 5 mins. Mild to moderate pain, occurs on exertion, emotion, after meals and in cold weather

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11
Q

How are acute stable angina episodes treated?

A

Sub-lingual nitrate spray/ tablet

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12
Q

What kinds of drugs are used to reduce myocardial oxygen demand?

A

Nitrates- reduce wall tension by reducing preload as venodilator allowing more blood to pool in legs
Ca2+ channel blockers- reduce wall tension by reducing afterload by peripheral vasodilation
Beta-blockers- reduce heart rate and contractility

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13
Q

What drugs are used to prevent cardiac events due to atheroma causing reduced coronary blood flow?

A

Aspirin- reduced platelet aggregation so less likely to have thrombus formation if plaque disrupted
Statins- lower LDL levels so slow progression of atherosclerosis, increasing plaque stability
Revascularisation- mechanically restores blood flow

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14
Q

What is unstable angina classified as?

A

Ischaemic chest pain that OCCURS AT REST or with minimal exertion, described as severe pain occurring in a crescendo pattern ( distinctly more sever, prolonged or frequent than before)

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15
Q

What is an MI?

A

Complete occlusion of a coronary vessel leading to death of the myocardium it supplies

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16
Q

What happens to a plaque for a clot to form?

A

`The fibrous cap undergoes erosion or fissuring, exposing blood to the thrombogenic material in the necrotic core. Platelets aggregate followed by a fibrin thrombus which can either block whole or most of vessel or break off to form an embolism

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17
Q

What methods of revascularisation are there?

A

Percutaneous Coronary Intervention and stenting (PCI)

Coronary artery bypass grafting

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18
Q

Where can grafts be taken from for coronary bypass grafting?

A

Radual artery, Internal mammary artery, saphenous vein (using reversed segment)

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19
Q

What 3 outcomes can plaque fissure and thrombus formation have?

A

(total occlusion)STEMI, (partial occlusion)NSTEMI, unstable angina

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20
Q

In which type of MI is there most necrosis?

A

STEMI

21
Q

Are biomarkers positive in untable angina?

A

No as no necrosis

22
Q

Where is the injury in STEMIs and how does it show on ECG?

A

Sub-epicardial (outside) surface causing ST elevation in leads facing injured area

23
Q

Where is the injury in NSTEMI and unstable angina and how does it show on ECG? What is the difference?

A

Injury limited to more vulnerable sub endocardial areas and shows as ST depression in leads facing injured area
No cell necrosis in unstable angina so biomarker tests negative

24
Q

What kind of occlusion occurs with NSTEMIs and unstable angina?

A

Partial/brief occlusion or occlusion with adequate collateral circulation

25
Q

What type of occlusion occurs in STEMIs?

A

Persistent complete occlusion of an artery supplying a significant area of myocardium without adequate collateral circulation

26
Q

What are the features of an MI history?

A

Central, crushing chest pain with typical radiation (shoulders, arms, jaw, back, epigastrium)
Severe pain, patient distressed, feeling of impending death
Pain at rest, often no precipitant
Not relieved by rest or nitrate spray
Sympathetic overdrive causing vasoconstriction so sweating and pallor
(LV dysfunction) Nausea, vomiting, breathlessness, faint
Risk factors present

27
Q

What will be found upon examination of a patient with an MI?

A

anxiousness, swesting, pallor, tachycardia/arrhythmias. low BP, signs of heart failure (s3/s4, crackles in lung bases)

28
Q

What are the initial investigations for Acute Coronary syndrome?

A
  1. ECG

2. Cardiac biomarkers

29
Q

What is the priority when a patient shows up with ACS?

A

Differentiate whether its a STEMI or NSTEMI/UA as treatment different

30
Q

Does a normal ECG mean there is no problem?

A

No, both UA and NSTEMI can present with no ECG changes

31
Q

What must be seen in the ECG to classiify event as a STEMI?

A

ST elevation in 2 or more leads facing same area
1mm in limb leads
2mm in chest leads

32
Q

What is troponin and how does it act as a biomarker (peaks etc)?

A 
Protein which blocks actin binding site in muscles 
Released in myocyte death
Very specific and sensitive
Starts to rise 3-4 hrs after pain onset
Peaks at 18-36hrs
Declines slowly over 10-14 days
33
Q

What is creatine kinase and how does it act as a biomarke (peaks etc)?

A

Enzyme present in skeletal muscle, heart and brain
3 iso enzymes, CK-MB is cardiac iso enzyme
rise 3-8hrs after onset
Peak at 24 hours
Back to normal 48-72hrs

34
Q

What are the ECG changes in a fully evolved STEMI and which areas of tissue cause them?

A

Big Q wave- necrosis
ST elevation- injured
T wave inversion- ischeamic area

35
Q

What is a pathological Q wave and how do they occur?

A

Wide, deep Q waves
Occur in leads facing transmural dead tissue. In normal heart Q wave quite small as nearest wall depolarises towards lead and far wall away. With dead transmural tissue there is now an electrical hole and only depolarisation away from lead giving a bigger downward peak

36
Q

If there is an inferior infarction, what leads will be abnormal and what artery occluded?

A

II, III, aVF

RCA

37
Q

If there is an antero septal infarction, what leads will be abnormal and what artery occluded?

A

V1-V2

LAD

38
Q

If there is an antero apical infarction, what leads will be abnormal and what artery occluded?

A

V3-V4

distal LAD

39
Q

If there is an antero-lateral infarction, what leads will be abnormal and what artery occluded?

A

I, aVL, V5-V6

Circumflex

40
Q

If there is an extensive anterior infarction, what leads will be abnormal and what artery occluded?

A

I, aVL, V2 to V6

Proximal LCA

41
Q

If there is a true posterior infarction, what leads will be abnormal and what artery occluded?

A

Tall R wave in V1

RCA

42
Q

In what two major ways are STEMIs treated to re-establish perfusion?

A

if within 90-120mins PCI (stent etc)

If after that fibrinolytic therapy and subsequent revascularisation

43
Q

What drugs are used in ACS to affect thrombosis, haemostasis and fibrinolysis?

A

Antiplatelet drugs like aspirin to prevent thrombosis
Anticoagulants like heparin
Fibrinolytic agents to dissolve thrombus

44
Q

How are STEMIs treated?

A

GOAL save myocardium
Re-establish perfusion
Monitoring, pain control, O2 if needed
anti-platelet agents- aspirin and clopidogrel
IV nitrates, beta blockers (anti ischaemic therapy)
Ace inhibitors (esp if LV dysfunction) reducing harmful remodelling of heart
statins

45
Q

How are NSTEMIs and unstable angina treated?

A

GOAL prevent MI and muscle loss
Prevent thrombosis progression with antiplatelet agents e.g aspirin, clopidogrel
Anticoagulants- LMW heparin
(note thrombolytics not used)
Risk assessment: High- PCI/CABG
Low- medical treatment, elective angio
General measures, antiplatelet, anti-ischaemic therapy, statins, ACEI

46
Q

What is the long term treatment after MIs?

A

Aspirin- reduced mortality and reinfarction
Beta blocker- reduced mortality and reinfarction
ACEI- improved survival
Statin
Manage risk factors, life style mods
weight loss, diet, stop smoking, exercise, less alcohol

47
Q

What complications can arise from MIs?

A

Sudden cardiac death- ventricular fib/asystole
Arrhythmias- sinus tachycardia- pain anxiety heart failure
sinus bradycardia (SA node ischaemia)
Heart block (2o and 3o may need temp pacemaker)
Ventricular tachycardia, ventricular fib
atrial fib
heart failure
cardiogenic shock

48
Q

What is cardiogenic shock?

A

When over 40% myocardium infarcted
Severely lowered cardiac output
SBP <90mmHg with inadequate tissue perfusion

ESA 2 SK (35 decks)

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