CVS 10 Ischaemic Heart Disease

Question 1

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

Answer 1

Pneumonia, Pulmonary embolism, pneumothroax

Question 2

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

Answer 2

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

Question 3

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

Answer 3

Ribs- fractures, bone metastases, muscles, skin

Question 4

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

Answer 4

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

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

Where does IHD cause pain?

Answer 7

Central, retrosternal or left sided

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

Question 8

What kind of pain is felt in IHD?

Answer 8

tightening, heavy, crushing, ocnstricting, pressure

occasionally described as burning epigastric pain particularly in inferior MI

Question 9

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

Answer 9

over 70%

Question 10

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

Answer 10

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

Question 11

How are acute stable angina episodes treated?

Answer 11

Sub-lingual nitrate spray/ tablet

Question 12

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

Answer 12

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

Question 13

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

Answer 13

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

Question 14

What is unstable angina classified as?

Answer 14

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)

Question 15

What is an MI?

Answer 15

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

Question 16

What happens to a plaque for a clot to form?

Answer 16

`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

Question 17

What methods of revascularisation are there?

Answer 17

Percutaneous Coronary Intervention and stenting (PCI)

Coronary artery bypass grafting

Question 18

Where can grafts be taken from for coronary bypass grafting?

Answer 18

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

Question 19

What 3 outcomes can plaque fissure and thrombus formation have?

Answer 19

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

Question 20

In which type of MI is there most necrosis?

Answer 20

STEMI

Question 21

Are biomarkers positive in untable angina?

Answer 21

No as no necrosis

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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

Question 24

What kind of occlusion occurs with NSTEMIs and unstable angina?

Answer 24

Partial/brief occlusion or occlusion with adequate collateral circulation

Question 25

What type of occlusion occurs in STEMIs?

Answer 25

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

Question 26

What are the features of an MI history?

Answer 26

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

Question 27

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

Answer 27

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

Question 28

What are the initial investigations for Acute Coronary syndrome?

Answer 28

1. ECG | 2. Cardiac biomarkers

Question 29

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

Answer 29

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

Question 30

Does a normal ECG mean there is no problem?

Answer 30

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

Question 31

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

Answer 31

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

Question 32

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

Answer 32

``` 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 ```

Question 33

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

Answer 33

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

Question 34

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

Answer 34

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

Question 35

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

Answer 35

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

Question 36

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

Answer 36

II, III, aVF | RCA

Question 37

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

Answer 37

V1-V2 | LAD

Question 38

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

Answer 38

V3-V4 | distal LAD

Question 39

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

Answer 39

I, aVL, V5-V6 | Circumflex

Question 40

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

Answer 40

I, aVL, V2 to V6 | Proximal LCA

Question 41

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

Answer 41

Tall R wave in V1 | RCA

Question 42

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

Answer 42

if within 90-120mins PCI (stent etc) | If after that fibrinolytic therapy and subsequent revascularisation

Question 43

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

Answer 43

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

Question 44

How are STEMIs treated?

Answer 44

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

Question 45

How are NSTEMIs and unstable angina treated?

Answer 45

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

Question 46

What is the long term treatment after MIs?

Answer 46

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

Question 47

What complications can arise from MIs?

Answer 47

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

Question 48

What is cardiogenic shock?

Answer 48

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