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Pharmacy Stage 2 > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

during what phase does the heart extract most of its oxygen from the coronary arteries?

A

during diastole (so dependent on diastolic pressure)

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2
Q

If there is a greater demand of oxygen from the heart what happens to the rate of blood flow and the amount of O2 extracted?

A
  • increased blood flow

- no increase in amount of O2 extracted

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3
Q

what is the main cause of O2 demand?

A

-change in vascular resistance?

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4
Q

why does vascular resistance affect O2 demand?

A
  • oxygen demand is affected by (blood flow X O2 conc gradient b/w artery and vein)
  • but the conc gradient doesn’t change much, i.e. it’s always high
  • and blood flow is affected by (aortic pressure / coronary resistance)
  • if the aortic pressure remains unchanged, then the coronary resistance must reduce to increase blood flow hence increase O2 demand.
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5
Q

Explain how metabolic factors affect oxygen demand and blood flow?

A
  • O2 acts as a vasoconstrictor
  • Lack of O2 (hypoxia) = vasodilation
  • This prevents regeneration of ATP from AMP
  • Adenosine, a direct vasodilator that acts on A2 adenosine receptors on vascular muscle, levels rise in myocardium
  • Lactate, H+ and prostacyclin (PGI2) accumulate and cause vasodilation
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6
Q

Explain how endothelium-mediated factors affect oxygen demand and blood flow?

A
  • bradykinin, histamine and Ach release NO
  • NO diffuses into vascular muscle
  • cGMP levels rise activating protein kinase G
  • causes vascular relaxation
  • resulting in vasodilation, hence increased blood flow, therefore increased O2 demand.
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7
Q

Explain how neurohumoral factors affect oxygen demand and blood flow?

A
  • adrenaline and noradrenaline bind to alpha1-adrenoreceptors in the epicardial vessels causing vasoconstriction
  • adrenaline and noradrenaline bind to β-adrenoreceptors in the subendocardial vessels causing vasodilation
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8
Q

what is it called when the oxygen supply doesn’t meet the oxygen demand?

A

ischaemia

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9
Q

what is myocardial ischaemia?

A

when the oxygen supplied to the heart doesn’t meet the demand for oxygen

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10
Q

what is coronary reserve?

A

the capacity to increase perfusion more than the resting perfusion value

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11
Q

what is the effect of narrowing the large epicardial coronary artery?

A
  • increases blood resistance to flow
  • pressure falls below diastolic pressure
  • use up coronary reserve
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12
Q

what effect does narrowing the small arterioles e.g. by an atheroma developing?

A

increased resistance to blood flow but not as much as in the large arteries as the small ones can dilate.

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13
Q

what is the effect of lack of blood/oxygen to the heart?

A
  1. myocardial ischaemia
  2. chest pain (angina)
  3. myocardial infarction (MI)
  4. hypotension
  5. Anaemia
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14
Q

what is wall tension?

A

the force generated per unit myocardial area

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15
Q

What is Laplaces’ law?

A

Cardiac Wall Tension = (transmural pressure X radius) / (2 X wall thickness)

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16
Q

If the stroke volume and cardiac output decreases but there’s no change in wall thickness, what would happen?

A
  1. ventricular pressure rises
  2. ventricular radius increases
  3. wall tension increases
  4. Myocardial O2 demand rises
  5. Sympathetic counteractive stimulation (HR increases and Vasoconstriction occurs)
  6. ventricular myocardium hypertrophy therefore occurs
17
Q

Risk factors of coronary heart disease/myocardial ischaemia?

A 
Modifiable Risk Factors:
1. Hypertension
2. Diabetes
3. Hypercholesterolaemia(Total : HDL-C, LDL-C)
4. Smoking
5. Diabetes mellitus
6. Sedentary life-style
7. Obesity
Non-modifiable Factors:
8. Age
9. Male Gender
10. Family history
18
Q

what causes Angina Pectoris?

A
  • transient (shot-lasting) episodes of myocardial ischaemia

- which causes pain after the heart switches to anaerobic metabolism

19
Q

what is stable angina?

A
  • pain experienced on exertion of emotional stress
  • indication of significant artery narrowing
  • pain ends when rested
20
Q

what is unstable angina?

A
  • incomplete occlusion causing pain on minor exertion
  • can also cause pain when at rest due to blockage
  • blood flows through other vessels or small arteries dilate to allow more blood supply (aka collateral blood supply). This happens to meet O2 demand
21
Q

what is variant angina?

A
  • Focal Coronary Vasospasm (Localised spasm of the coronary artery causing vasoconstriction)
  • pain experienced due to lack of O2 supplied at rest
22
Q

During non-aerobic respiration what is produced and what does it dissociate into?

A
  • Lactic acid is produced

- Dissociates into Lactate and H+

23
Q

what is the consequence of low ATP and high H+ concentrations?

A

causes abnormal ventricular contraction

24
Q

what can happen as a result of persistent ischaemia?

A
  • acidosis (due to inhibited glycolysis)

- Myocardial Infarction

25
Q

What are the Consequences of Myocardial ATP Deficiency?

A
  1. Impairment of ventricular systolic pumping action
  2. Decreased compliance of myocardium during diastole
  3. Pulmonary congestion and dyspnoea (difficulty breathing)
26
Q

explain how ATP deficiency causes an impairment in ventricular systolic pumping?

A
  • No ATP = reduced ability to contract
  • therefore, increased demand on the heart from other organs
  • end systolic volume increases and stroke volume decreases
  • therefore reduced ejection fraction
27
Q

explain how ATP deficiency causes a decreased compliance of the heart during diastole?

A
  • hypertrophy of the heart (increased heart size due to increased cell size) causes a lack of ATP (not sure how!!!)
  • this therefore reduces actin-myosin separation.
  • therefore diastolic filing is impaired as less volume to fill
28
Q

what is myocardial infarction?

A

heart attack resulting from prolonged chest pain

29
Q

what promotes the development of a myocardial infarction?

A
  1. Thrombocyte activation (build of atheroma) causing vasoconstriction
  2. abnormal function of endothelium (lack of vasodilators and anti-thrombotic substances)
  3. systemic nervous stimulation increasing the cardiac work
30
Q

What does the ECG wave tell us about myocardial infarction?

A
  • If the Q-wave is abnormal, then signs of transmural infarction (MI) but doesn’t say if acute
  • Elevation/Depression of ST region/interval and reversal of T wave indicates ischaemia, but not yet necrosis
  • the ST region may return to normal few days after an MI but T-wave may remain inverted for weeks
31
Q

what enzymes help to detect an MI?

A
  1. Myocardial creatinekinase (CK-MB)
  2. Cardiac Troponin-T (cTnT)
  3. Cardiac Troponin-I (cTnI)
  4. Aspartate aminotransferase (ASAT)
  5. Myocardial lactate dehydrogenase (LDH1)
32
Q

what are the two principles of angina therapy?

A
  1. reduce oxygen demand by decreasing cardiac work load

2. increase oxygen supply by improving coronary blood flow

33
Q

explain the process of smooth muscle relaxation?

A

1) ACh binds to G protein receptors causing IP3 production.
2) IP3 releases Ca2+from ER.
3) Ca2+and calmodulin form complex which stimulates NO synthase to produce NO.
4) NO diffuses from endothelial cell into adjacent smooth muscle cells.
5) NO activates guanylylcyclase to make cyclic GMP (cGMP).
6) cGMP activates protein kinase G which phosphorylates several muscle proteins to induce muscle relaxation.

34
Q

what do nitrates do to treat myocardial ischaemia (mainly angina and acute coronary syndrome)

A

-reduces venous return, cardiac size and myocardial O2 consumption

35
Q

explain the mechanism of action of nicorandil?

A
  1. it donates NO to promote the relaxation of venous vasculature. also maximises coronary blood flow and reduces pre-load and afterload
  2. another mechanism it does is opening ATP-dependent potassium channels causing hyperpolarisation therefore causing aterial dilation. And also causes cardiac repolarisation leading to reduced cardiac work.
36
Q

how do beta-blockers work in treating angina?

A
  1. block cardiac β1-Adrenoreceptor, and reduce the generation of intracellular cAMP.
    - this decreases heart rate and force of cardiac contraction. Consequentially reduces blood pressure and myocardial O2 demand.
    - it also increases diastole period and coronary perfusion (pushing blood out)
37
Q

what effect does calcium channel blocker have on the heart?

A

-causes peripheral vasodilation and reduces cardiac work

Pharmacy Stage 2 (85 decks)

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