Unit 12 Week 3

Question 1

What is an MI

Answer 1

Sudden ischaemic death of myocardial tissue (usually due tro ischaemia)

Question 2

pathophysiology of MI

Answer 2

Most commonly, a thrombus occludes a coronary artery (most often the Left Anterior Descneing) , leading to ischemia in the myocardium supplied by that artery.

Therefore, area loses function.

Due to low regenerative capacity of cardiac tissue, a scar forms and in turn, ejection fraction and cardiac output is reduced.

Question 3

who is most at risk of MI

Answer 3

Shares risk factors for atherosclerosis

Non-modifiable: older age, being male sex, being of South Asian descent, family history of premature CVD, premature menopause

Modifiable: smoking, diabetes mellitus, hypertension, hyperlipidaemia, obesity, having a sedentary lifestyle

Question 4

How does this link to angina

Answer 4

Narrowing of coronary arteries increases the likelihood of disrupted blood flow and haemostasis, therefore increasing likelihood of thrombosis and arterial occlusion

Question 5

what is angina

Answer 5

Chest pain/discomfort due to inadequate blood supply to myocardium. 2 types: stable and unstable.

Question 6

pathophysiology of angina

Answer 6

Manifestation of temporary myocardial ischemia.

Fixed angina - Atherosclerotic plaques build within the walls of coronary arteries and arterioles, impeding the flow of blood through to cardiomyocytes. This impediment of blood flow can often be counterbalanced by autoregulatory mechanisms (e.g. release of adenosine, prostaglandins.

Dynamic angina – coronary spasm occurs, impeding blood flow (can be triggered or spontaneous)

Question 7

what does arterioscelrosis mean

Answer 7

a general term that refers to thickened and stiffened blood vessels – atherosclerosis is a type of arteriosclerosis.

Question 9

what is atherosclerosis and what are the stages?

Answer 9

a disease of the large and intermediate arteries in which fatty lesions called atheromatous plaques develop on the inside of the vessel walls.

1. Damage occurs to vascular endothelium which increases expression of adhesion molecules on endothelial cells and decreases their ability to release substances that prevent adhesion (NO). Damage also recruits monocytes and lipids (LDLs).
2. Monocytes cross the endothelium into the tunica intima of the vessel wall and differentiate into macrophages which oxidise and digest the accumulated lipoproteins giving the macrophages a foam-like appearance.
3. The macrophage foam cells then aggregate on the blood vessel and form fatty streaks.
4. Overtime fatty streaks grow and coalesce. The surrounding fibrous and smooth muscle tissues proliferate to form larger plaques.
5. Macrophages also release cytokines that stimulate inflammation and further proliferation of smooth muscle and fibrous tissue inside the vessel wall.
6. The lipid deposits plus proliferation can become so large that the plaque projects into the lumen which can partially or fully occludes the vessel.

Question 10

shared risk factors for MI and atherosclerosis

Answer 10

These are the modifiable ones:

Tobacco – smoking and long-term exposure to second-hand smoke

Hypertension – can damage coronary arteries and increase risk at least twofold; particularly if occurs with other conditions such as obesity, high cholesterol or diabetes.

Hyperlipidaemia – the blood has too many lipids (cholesterol and triglycerides). One type is known as hypercholesterolemia which means there is a high level of LDL (bad) cholesterol in the blood.

Physical inactivity and obesity – both linked with high cholesterol levels, high triglyceride levels, and high blood pressure.

Diabetes – rise in blood sugar levels increases risk of MI; increases risk twofold.

Non-modifiable risk factors:

Age – men aged 45 or older and women aged 55 or older.

Family history – of CHD in first-degree relative age <50 (men) and age <60 (women).

Question 11

Coronary arteries arise from where?

Answer 11

aortic sinuses (beginning of the ascending artery)

Question 12

how many coronary arteries are there

Answer 12

2 a left and right that supply their respective sides of the heart although there is some crossover

Question 13

which aortic sinus does the right coronary artery arise from?

Answer 13

anterior

Question 14

route that the right coronary artery takes

Answer 14

It passes BETWEEN THE PULMONARY TRUNK and the RIGHT AURICLE, to descend along the atrioventricular groove where it starts to branch

Question 15

sinoatrial branch

Answer 15

the first branch of the right coronary artery

passes betyween the ASCENDING aorta to form a ring around ther vena cava

it supplies the SA node- damage here can cause arrhythmias

variation is that this artery arises from the left circumflex artery

Question 16

conus branch artery

Answer 16

branch of the RCA

it supplies the anterior ventricular surface and the anterior pulmonary conus (area just below the pulmonary trunk)

this artery often anastamoses with its corresponding left version

Question 17

right marginal artery

Answer 17

runs on the inferior aspect of the heart and supplies the inferior and apex

Question 18

Posterior interventricular artery (PDA- descending)

Answer 18

ON THE POSTERIOR ASPECT OF HEART

may anastamose with the anterior descending

Question 19

What happens to the right coronary artery as it keeps travelling

Answer 19

usually peters out

occasionally continues and anastmoses with the left circumflex artery

Question 20

left coronary artery

Answer 20

shorter but much larger

arises from the posterior aortic sinus

passes between the pulmonary trunk and the left auricle

has 2 main branches

Question 21

what are the 2 main branches of the left coronary artery

Answer 21

Anterior interventricular/descending artery (LADA)

Left circumflex artery (LCX)

Question 22

LAD artery

Answer 22

runs along the interventricular groove where a number of branches arise

• left conus
• in 50% the large diagonal branch

as it continues it may anastamose with the posterior interventricular

Question 23

left circumlex branch

Answer 23

continues to the diaphragmatic surface of the heart.

As it approaches the left margin of the heart, the left marginal artery will arise to continue towards the apex. As the left marginal artery continues to the diaphragmatic surface, it may anastomose with the right coronary artery.

Question 24

coronary artery dominance

Answer 24

-determined by which coronary artery gives rise to the posterior descending artery (interventricular)

Right dominant- (~85% of the population): posterior descending artery (PDA) supplied by the RCA

Left dominant- (~8% of the population): PDA supplied by the left circumflex artery (LCX)

Codominant- (balanced; ~7% of people): PDA supplied by both RCA and LCX

Question 25

why is th heart prone to infarction

Answer 25

• Coronary blood flow peaks during early diastole at a point when the pressure differential between the aorta and the ventricle is greatest.
• Anastomoses occur between a number of the branches of the coronary arteries, however these are not sufficient to adequately perfuse the heart if one of the main branches becomes occluded.
• The LAD is the most commonly occluded artery and is often referred to as the “widow maker” due to its high mortality rate associated with LAD infarction.

Question 26

sympotms of an MI

Answer 26

Chest pain (may or may not be central chest pain) that can radiate to the arms, shoulders, neck or jaw.

• Pain is described as pressure, squeezing, aching, burning or sharp pain.
• Common complaint is radiation to the left arm or neck.
• Caused by the lack of oxygen to the cardiac myocytes and creates a hypoxic state which can lead to ischemic tissue death and therefore, ischemic pain.

Pain may be associated with sweating, vomiting, dyspnea, fatigue or palipitations

Overwhelming feeling of doom

Coughing

Question 27

signs of an MI

Answer 27

• Low grade fever, pale and cool, clammy skin
• Hypotension/hypertension depending on the extent of MI.
• Dyskinetic cardiac impulse (forceful impulse that signifies overload)
• S3 and S4 are normally present in myocardial dysfunction.
• Signs of congestive heart failure may be present including peripheral oedema and an elevated jugular venous pressure.
• ECG can be conducted and show signs of heart muscle dysfunction.

Question 28

What is an anterior ST elevation MI and what changes would you see on an ECG

Answer 28

Anterior ST elevation: This is when the anterior myocardial tissue of the heart suffers injury or death due to a lack of blood supply. This tends to be due to a thrombus or lesion in the left anterior descending coronary artery.

Uusally results in complete coronary artery occlusion so it is transmural

may get T wave inversion

ST elevation (QRS is actually depressed) this is due to local electrolyte leakage and myocytes being starved of oxygen

Question 29

what is heart block and some examples of causes

Answer 29

A condition where the heart beats more slowly or with an abnormal rhythm. It’s caused by a problem with the electrical pulses that control how your heart beats

Birth defect

· Autoimmune diseases such as lupus

· Surgery may affect the heart’s electrical system

· Genes

· Heart attack

· Some medicines

· Muscle disorders or other diseases

· Heart issues like clogged arteries, inflammation of the heart muscle and heart failure

Question 30

How would a first degree heart block look on an ECG

Answer 30

Partial block between the SA node and AV node

consistent prolonged PRI

Question 31

second degree type 1 heart block

Answer 31

Complete block between the SA node and AV node (A progression of first degree). Progressively growing PRI segment until there is no QRS complex present. Then the ECG returns to normal only to repeat that action.

long, long , drop QRS

Question 32

Second Degree Type 2:

Answer 32

Intermittent complete block between the SA node and AV node. Therefore the QRS ‘drops’ intermittently.

normal normal drop

Question 33

third degree heart block

Answer 33

n complete heart block is caused when there is complete block at the AV node, therefore the atria and ventricles are no longer synchronized and are working independently. As seen by the ECG below, P waves are still visible but do not relate to QRS complexes. QRS complexes may be wide or narrow but the key point is that the rate is still regular. Each P wave is the same distance from each other and so are the QRS Complexes. 3rd degree heart block is also bradycardic

Question 34

what is stable angina

Answer 34

It is caused by an imbalance in coronary perfusion due to chronic stenosing coronary atherosclerosis relative to myocardial demand. Stable angina does not occur at rest, but in a given patient can be reliably induced by activities that increase the energy requirements of the heart including:

pysical activity

emotional excitement

psychological stress

Question 35

Unstable or crescendo Angina

Answer 35

This refers to a pattern of increasingly frequent, prolonged (>20 min), or severe angina, precipitated by progressively lower levels of physical activity or even occurring at rest. Unstable angina is associated with:

§ Plaque disruption

§ Superimposed thrombosis

§ Distal embolization of thrombus

§ Vasospasm

Question 36

Explain mechanism of referred pain- MAKE IT RELEVANT TO A HEART ATTACK

Answer 36

Referred pain, also known as reflective pain, is pain perceived at a different location than the site of stimuli

The example in this case is due to angina pectoris (chest pain) which is brought about by a myocardial infarction which has cause ischemia to cardiac myocytes

pain from heart attacks can be felt in the

Neck

o Left Shoulders

o Left arm

mechanism:

dorsal horn and brain stem neurons receive convergent sensory inputs from various tissues.brain can’t correctly identify the actual input source

The Spinal level that receives visceral sensation from the heart (C8, T1-T4) simultaneously receives cutaneous sensation from the parts of the skin supplied by that spinal nerve’s dermatome.

· The multiple primary sensory neurons converge on a single ascending tract.

· There is no ability to discriminate between the two.

· This results in confusion as to where the sensation is coming from.

· This results in pain being located along the related dermatome of the same spinal segment.

Question 38

What is a primary coronary angioplasty

Answer 38

Angioplasty is the procedure of inserting, then inflating, a small balloon in the blocked coronary artery, leaving a rigid support to restore blood flow

Angioplasty is the primary treatment for heart attack patients reduces complications and improves recovery rates

Question 39

what is cardiac catherterisation

Answer 39

Cardiac catheterization is an invasive diagnostic procedure which involves taking x-rays of the coronary arteries using a technique called coronary angiography or arteriography – this provides important information about the structure and function of the heart

A catheter is passed through the peripheral arteries/veins into cardiac chambers, the pulmonary artery, and coronary arteries and veins

Left heart catheterization is commonly u

Question 40

what is a cardiac angiogram and how does it show occlusions

Answer 40

An angiogram is a type of x-ray which uses contrast dye to allow doctors to look at blood vessels. The dye is injected into the blood first which then highlights the blood vessels.

Question 41

what blood tests are used in the diagnosis of MI

Answer 41

serum troponin- Ctoponin T and I– When myocyte injury takes place, Troponin is released. Whilst elevated levels indicate myocardial damage, absolute values differ.

AST (aspartate aminotransferase)- High concentrations found in the heart and muscles. Only a small amount of AST is typically in the bloodstream. Elevated levels may indicate an injury to one of the organs which contains AST.

FBC- Used to rule out anaemia as a cause of decreased oxygen supply. Leucocytosis is also common in the case of acute MI.

Creatinin kinase- Found in the heart, muscles and other organs. Elevated in instances of a heart attack since injured heart muscle cells release CK-MB into the blood.

Lipid profile-Cholesterol levels fall within 24 hours of an acute MI and return to pre-infarction levels over following three months. It is also to generally assess risk of CVD; however it is not the most reliable as around half of people with heart attacks have normal cholesterol levels.

Question 42

Sildenafil

Answer 42

Selective phosphodiesterase type 5 inhibitor

cGMP

1* target- phosphodiesterase-5

activity- inhibitor

• cGMP activates PKG which activates myosin phosphatase which leads to release of Ca2+ from SR
• NO also activates the pathways via paracrine signalling
• inhibits PDE5 so stops degradation of cGMP
• this action relaxes and dilates these blood vessels allowing more blood to flow through
• general decrease in PVR and a decrease in BP as a result

used to trrat erectile dysfunction and pulopmary arterial hypertension– decreases systemic BP

Question 43

Glyceryl trinatrate

Answer 43

synthetic nitrate compound– needs to be broken down into its active form NO first to start working

• 1* target= mitochondrial aldehyde dehydrogenase
• activity- substrate— becomes NO (vasodilator)
• • 2* target= guanylate cyclase
• activity= agonist

following conversion to nitric oxide:

1. activation of guanylate cyclase
2. increse of cGMP synthesis in sm muscle (release of Ca2+)
3. relaxation of sm muscle, increased BF in veins, arteries and myocardium
4. means that the hert doesnt have to work as hard and this helps reduce the symptoms of chest pain

Question 44

why should nitrates and sildanefil be avoided together?

Answer 44

it can produce significant hypotension and is potentially fatal.

Question 45

Statins

Answer 45

selective, competitive inhibitor of HMG-CoA reductase, which is the enzyme responsible for the conversion of HMG-CoA to mevalonate in the cholesterol synthesis pathway.

inhibits cholesterol in 3 ways:

1. Inhibiting cholesterol synthesis

By inhibiting HMG-CoA reductase, statins block the pathway for synthesizing cholesterol in the liver. This is significant because most circulating cholesterol comes from internal manufacture rather than the diet.

2) Increasing LDL uptake

Liver cells sense the reduced levels of liver cholesterol and seek to compensate by synthesizing LDL receptors to draw cholesterol out of the circulation.

Increased transcription of various proteins occurs but most notably, LDL receptor. The LDL receptor is transported to the liver cell membrane and binds to passing LDL and VLDL particles, mediating their uptake into the liver, where the cholesterol is reprocessed into bile salts and other byproducts.

3) Decreasing protein prenylation

Question 46

clopidogrel

Answer 46

Class = antiplatelet antithrombotic drug

Chemistry = small molecule

PD= irreversibly inhibits binding of ADP receptor on platelets thus inhibiting ADP-mediated platelet activation and interfering with GpIIb/ IIIa-mediated platelet aggregation

Physiology = Prevents platelet activation

Desired use = prevention and treatment MI, other vascular disorders and often given with aspirin

Undesired = bleeding, GIT discomfort, rashes, rarely neutropenia.

Question 47

atenolol

Answer 47

Class: A B1 Antagonist, B blocker

Structure: Small molecule

Pharmacodynamics: Blocks of action of endogenous and exogenous agonists on B1 receptors

Physiology: Reduces bp in hypertensive patients by: decreasing CO, decreasing renin release, decrease NS—mediated sympathetic activity. In Angina it slows heart and reduces metabolic demand.

Clinical:

Desired – Hypertension, Angina, prevention of dysrhythmias in MI

Undesired – Cold extremities, fatigue.

Dangerous: bronchoconstriction in asthma, in emphysema, potential heart block or heart failure in those with coronary disease, decreased sympathetic warning to hypoglycaemia in diabetic patients

Question 48

atorvastatin

Answer 48

Atorvastatin is indicated alongside lifestyle changes (e.g. dietary modification) to prevent cardiovascular events such as MI and other health disorders associated with atherosclerosis such as stroke and angina. It is considered standard practice to prescribe atorvastatin following any cardiovascular event.

mechanism: Competitively inhibits HMG CoA reductase (Involved in Cholesterol metabolism by converting HMG-CoA to mevalonate). This results in lower total cholesterol, Low-density lipoprotein-cholesterol, and others. High LDL-C is associated with atherosclerosis leading to CV disease.

Question 49

atropine

Answer 49

Indication: Can be used to treat bradycardia, reduce salivation and bronchial secretions before surgery and is also used as an antidote for cholinergic drugs or mushroom poisoning.

Mechanism: Binds to and inhibits muscarinic acetylcholine receptors which causes a variety of effects, namely, inhibiting parasympathetic activity on the heart which increases heart rate

Question 50

WHILE waiting for an ambulance for an mi what tablet might someone chew on? why would they do this?

Answer 50

aspirin (as long as theyre not allergic)

Aspirin helps to thin the blood (chewing it speeds up the anti-blood-clotting properties) and improves blood flow to the heart, slowing the clot development before it causes permanent damage to the heart.

acetylsalicyclic acid

Pharmacology = prostaglandin G/H synthase 1 and 2 inhibitor

ASA blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2. Inhibition of COX-1 results in the reduction of platelet aggregation It does this by binding with a serine residue of the cyclooxygenase-1 enzyme leading to irreversible inhibition. This prevents the conversion of arachidonic acid to thromboxane A2 which is a potent inducer of platelet aggregation