Ischaemic Heart Disease

Question 1

Define ischaemic heart disease (IHD).

Answer 1

IHD is a violation of delivery of blood to the myocardium due to atherosclerosis of coronary vessels fo the heart.

Question 2

What are the forms of IHD?

Answer 2

Stenocardia (angina pectoris); heart attack (MI) and acute coronary insufficiency.

Question 3

What is the painless form of IHD and how does it differ from the typical form of the disease?

Answer 3

Painless form is characterised by insufficiency of blood circulation or violation of heart rhythm; the typical form is characterised by sudden death with a background of atherosclerosis.

Question 4

What factors lead to IHD (aetiology)?

Answer 4

Arterial hypertension (70%); diabetes mellitus; smoking; genetics; hypercholesterolamia; obesity (all these factors contribute to the development of atherosclerosis).

Question 5

What are the pathoanatomical changes seen in stenocardia?

Answer 5

Single foci of cardiosclerosis (50% stenosis required); course is severe is multiple CA’s are affected.

Question 6

What are the pathanatomical changes seen in MI?

Answer 6

Necrosis of fibres (within 5 - 6 hours); new capillaries (8 - 10 days); connective tissue in area of necrosis; scarrring; corrugation of area due to fibrotic tissue (3 - 4 months); parietal thrombosis (is lesion is in endocardium).

Question 7

What are the causes of ischaemia in the myocardium (17)?

Answer 7

Decreased oxygen delivery; (permanent) obstruction of the CA’s; arteriosclerosis; spasm of arteries; system hypotension; severe anaemia; increased oxygen demand; hypertrophy; tachycardia; resistance of CVs; diastole duration; rate of heart contractions; rate of contractions; cavity call tension; diastolic pressure in the left ventricle due to pre-load; middle pressure in the aorta due to post-loading; contractility and defects of oxygen supply to the myocardium due to oxygen supply and diastolic pressure in the aorta.

Question 8

What basic changes are made to the function of myocardial cell during ischaemia and how does this change action potential in ventricular cells?

Answer 8

Electrical activity and contractility. Resting potential increases. The speed of the action potential decreases leading to intensification and shortening of the plateau phase. The difference in potential between normal and ischaemic cells leads to arrhythmias.

Question 9

What are the consequences of violation of contractility of the myocardium?

Answer 9

Reduced function of the left ventricle; weakening of diastole (4th heart sound); reduced systole (hypo/akinetic); due to MI dykinesia and paradoxical movement.

Question 10

What is the overall result of violation of contractility of the myocardium?

Answer 10

Diminished ejection fraction compensated by minute volume (Sterling’s law).

Question 11

What two factors determine the course of IHD?

Answer 11

Degree of obstruction and condition of left ventricle.

Question 12

What additional factor is considered to contribute to early mortality in patients with IHD?

Answer 12

Complex ventricular ectopia.

Question 13

What are the five forms of IHD according to the classification by the WHO (1970)?

Answer 13

(1) Primary arrest of circulation of blood; (2) Stenocardia (exertional stenocardia [first development, stable, progressive] and spontaneous stenocardia; (3) MI (acute or old); (4) cardiac insufficiency; (5) arrhythmias.

Question 14

What are the six forms of IHD according to the classification by SKRC AMS (1983)?

Answer 14

(1) Acute coronary death; (2) stenocardia; (3) MI (small or large foci); (4) post-infarction cardiosclerosis; (5) disturbance of rhythm; (6) cardiac insufficiency.

Question 15

What are the three forms of post-infarction aneurysm?

Answer 15

True; false and functional.

Question 16

What are the sub-types of true post-infarction aneurysm?

Answer 16

Diffuse; saccular and dissecting.

Question 17

What is a false post-infarction aneurysm?

Answer 17

Involving the walls of the myocardium and formed at rupture and are limited by pericardiac adhesions.

Question 18

What is a functional post-infarction aneurysm?

Answer 18

Areas of viable myocardium that have lost contractability and protrude during systole.

Question 19

What is the first type of aneurysm according to Stoney (1994) and what is the ejection fraction?

Answer 19

Normokinesis of LV. EF = 50%.

Question 20

What is the second type of aneurysm according to Stoney (1994) and what is the ejection fraction?

Answer 20

Hypokinesis of the posterior wall and normokinesis of the anterior wall. EF > 30%.

Question 21

What is the third type of aneurysm according to Stoney (1994) and what is the ejection fraction?

Answer 21

Expressed hypokinesis. Normokinesis of anterior wall and akinesia of posterior wall. EF < 30%.

Question 22

What is the basis of division of stenocardia into classes according to the Canadian society of heart and vessels?

Answer 22

Four classes of stenocardia ranging from: class 1 (no stenocardia upon everyday physical loading and stenocardia during tense physical loading) to impossibility of everyday physical loading activities. There is gradual decrease of tolerance to everyday loading activities in between.

Question 23

Describe the clinical presentation of stenocardia.

Answer 23

Episodic radiating retrosternal pain (5 - 15 minutes) that is alleviated when nitroglycerine is administered.

Question 24

What are the secondary symptoms of stenocardia?

Answer 24

Dizziness; accelerated palpitations; sweating; SOB; nausea or vomiting.

Question 25

What are the notable changes upon auscultation of a patient with stenocardia?

Answer 25

Transitory S - sound; systolic noise on apex.

Question 26

What changes would you see on an ECG of a patient with stenocardia?

Answer 26

Depressed ST segment (or ST elevation but is rare).

Question 27

What is unstable stenocardia?

Answer 27

It is increasing stenocardia or pre-infarction. It is a condition between stenocardia and myocardial infarction.

Question 28

What are the three categories of unstable stenocardia?

Answer 28

(1) exertional stenocardia; progressive stenocardia; rest stenocardia.

Question 29

What causes unstable stenocardia?

Answer 29

An increase in the severity of atherosclerosis; spasm of coronary arteries or haemorrhage from unthrombosed plaques (later occlusion due to thrombosis).

Question 30

What is prinzmetal stenocardia?

Answer 30

Provocation of attacks at rest and is random spasming of the epicardial CAs.

Question 31

What changes might you see on the ECG of a patient with prinzmetal stenocardia?

Answer 31

Raised ST segment (transmural myocardial ischaemia); tachyarrhythmia; blockade of Gid crura; atrioventricular blockade.

Question 32

What factors contribute to acute myocardial infarction?

Answer 32

The progress of atherosclerosis; embolism or spasm of CA; thrombosis.

Question 33

Describe the types of arrhythmia that one may expect in a patient with a myocardial infarction?

Answer 33

Tachyarrhythmia and ventricular ectopia. Bradarrhythmia and atrioventricular blockade are also possible due to increased tone of the vagus nerve or as a direct onfluence of the myocardial infarction on the conducting system.

Question 34

What are the effects of mitral regurgitation?

Answer 34

Acute pulmonary oedema and hypotension due to the poor condition of papillary muscles.

Question 35

What structures are at risk of rupturing as a result of autolysis during myocardial infarction?

Answer 35

The wall of ventricles; intraventricular septum and papillary muscles.

Question 36

What are the result of congestion during myocardial infarction?

Answer 36

Thrombosis of veins; embolism of pulmonary artery branches; parietal thrombosis; system embolisation of arteries.

Question 37

What are the symptoms of myocardial infarction?

Answer 37

Anginal pain (retrosternal radiating pain); dizziness; SOB; sweating; accelerated palpitations; nausea or vomiting. In elderly patients that symptom of pain behind the breastbone may be absent). A mild fever may develop (does not exceed 39 degrees).

Question 38

What is the increase of arterial pressure dependent on?

Answer 38

Severity of pain and degree of activation of the sympathetic nervous system,

Question 39

Which area of the heart is connected to bradycardia ?

Answer 39

Posterior wall.

Question 40

What changes can you hear on auscultation of a patient with myocardial infarction?

Answer 40

Weakened S sound; splitting of S2 (after contraction of the LV); S4/3 sound (due to reduced compliance of the ventricular walls).

Question 41

What additional noises can be heard upon auscultation of a patient with myocardial infarction?

Answer 41

Mitral regurgitation; rupture of interventricular septum; pericardial friction.

Question 42

What does it mean for a myocardial infarction to the Q positive or negative?

Answer 42

It refers to whether the MI is transmural or subendocardial due to the presence or lack of Q wave.

Question 43

What makes a Q-positive myocardial infarction worse?

Answer 43

More extensive - higher level of creatinephosphokinase; reduced EF.

Question 44

What factors increase the risk of developing complete (III) antrioventricular blockade in MI patients?

Answer 44

The location of MI; presence of new disturbances of the conducting systmem.

Question 45

In which two groups of patients is there a greater risk of developing complete (III) AV blockade?

Answer 45

In those where there is a confirmed disturbance of the AVN which is superimposed leading to infranodal block. The second group are those with MI of the anterior wall.

Question 46

What is Venkebakh / Mobitz I AVB? What if the typical location of the MI in this case? What changes can be seen on an ECG? What is the typical treatment?

Answer 46

Disturbance of the AVN due to increased vagus tone. Usually affects posterior wall. Stable rhythm, narrow QRS, 50bpm. Usually treated with atropine.

Question 47

What is Mobitz II AVB? What if the typical location of the MI in this case? What is the typical treatment?

Answer 47

Disturbance in rhythm due to structural damage to the infranodal conducting system. Anterior wall. Treated using rhythm drivers / pacemakers.

Question 48

What are the effects of rupture of the heart?

Answer 48

Renewal of retrosternal pain; hypotension; pericardiac tamponade; heart arrest; dissociation of electrical and mechanical processes.

Question 49

Which patients are most at risk of experiencing rupture of the heart?

Answer 49

First MI; arterial hypertension; the elderly.

Question 50

What is the treatment for rupture of the heart?

Answer 50

Pericardiotomy and removal of tamponade.

Question 51

How does rupture of the interventricular septum present?

Answer 51

Pulmonary oedema; rough systolic noises on the left margin of the breast bone.

Question 52

How do you treat rupture of the interventricular septum?

Answer 52

Nitroprusside to reduce post-loading or intra-aortic balloon counterpulsation of ineffective.

Question 53

What are the clinical features of dysfunction of papillary muscles and how are they treated?

Answer 53

Transitory systole noise but become worse when pulmonary oedema develops. Treated by reducing post-loading and treating the ischaemia. Svan - Ganz catheter may be required if an entire papillary muscle is torn.

Question 54

What major complication can occur as a result of cirulatory stasis and how is it diagnosed and treated?

Answer 54

Thromboembolism (venous thrombosis and pulmonary embolism). Diagnosed using ECHO. Treated using anticoagulant therapy (intravenous heparin).

Question 55

What drug is used to counteract heparin?

Answer 55

Protamine.

Question 56

Describe the presentation of pericarditis.

Answer 56

Pain; friction of the pericardium.

Question 57

What are the causes of pericarditis?

Answer 57

Inflammation due to the necrosis of the myocardium joining to the pericardium.

Question 58

What are the characteristics of Dressler syndrome?

Answer 58

Retrosternal pain; fever; pleuropericarditis; effusion in the pleural cavity; causes an immunological reaction due to the myocardium antigens that appear during MI.

Question 59

What are the features of RV MI?

Answer 59

Due to occlusion of the RV; often related to lesion of the LV; mostly transmural.

Question 60

What are the symptoms of RV MI?

Answer 60

Hypotension (with increased pressure in the right auricle and decreased pressure in the left auricle); swelling of the jugular vein; increased transparency of pulmonary tissue; Kussmaul breathing.

Question 61

What conditions are often masked by RV dysfunction? How can RV MI be diagnosed?

Answer 61

Constrictive pericarditis; pericardiac tamponade; restrictive cardiomyopathy. Diagnosis requires simultaneous measuring of pressure in the RV, pulmonary artery; right auricle are needed by radioisotope scan.

Question 62

What should be considered in the treatment of RV MI?

Answer 62

If there is increased pressure of filling in the RV then minute volume should be supported (but only in this situation so diuretics and nitrates should be avoided). Minute volume can be increased by volume infusion; inotrope support in the form of Dobutamine should be used.