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Ischaemic heart disease > Pathophysiology and treatment of Ischaemic heart disease > Flashcards

Pathophysiology and treatment of Ischaemic heart disease Flashcards

1
Q

list, in order of increasing severity, the types of acute coronary syndromes

A
  1. stable angina
  2. unstable angina
  3. NSTEMI
  4. STEMI
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2
Q

How does stable angina develop

A
  1. angina pain develops when there is increased demand in the setting of a stable athersclerotic plaque
  2. the vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial demand
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3
Q

how does unstable angina occur

A
  1. the plaque ruptures and a thrombus forms around the ruptured plaque, causing partial occlusion of the vessel
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4
Q

how does an NSTEMI occur

A
  1. the plaque rupture and thrombus formation causes partial occlusion to the vessel
  2. results in injury and infarct to the subendocardial myocardium
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5
Q

how does a STEMI occur

A
  1. characterised by complete occlusion of the blood vessel lumen
  2. results in transmural injury and infarct to the myocardium, which is reflected by ECG changes and a rise in troponin
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6
Q

define ischaemic heart disease

A

narrowing of the lumen of the coronary arteries resulting in an imbalance between the supply of oxygen and the myocardial demand
- resulting in myocardial ischaemia and chest pain

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7
Q

what are involved in the regulation of coronary blood flow

A
  1. adenosine
  2. beta agonists
  3. acid
  4. EDRF- nitric oxide
    - endothelium derived relaxing factor
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8
Q

describe the process of atherogenesis

A
  1. damage to endothelium- LDLs, tobacco smoke, diabetes, hypertension
  2. activation of toll receptors initiate inflammatory response
  3. monocytes drawn into intima by TNFa, MCP and VCAM-1, ICAM
  4. LDLs enter the endothelium and become oxidised
  5. monocytes mature into macrophages and engulf cholesterol and turn into foam cells and secrete other inflammatory mediators (IL-1, TGF)
  6. attract and stimulate smooth muscles to proliferate
  7. fatty streaks develop into soft plaques, then hard plaques
  8. foam cells release tissue factor (thrombogenic)
  9. necrotic core and lipid core also thrombogenic
  10. thrombus that kills
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9
Q

what determines when the plaque ruptures

A

the combination of the development of the plaque and the degree of inflammation

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10
Q

give examples of risk factors of IHD

A

smoking, diabetes, hypertension, hypercholesterolaemia

- other potential markers that relate to cardiovascular risk (C reactive protein, Il-6)

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11
Q

give examples of the causes of stable angina

A
  1. atherosclerosis
  2. hypotension
  3. lung infection
  4. valve problems
  5. heart failure
  6. anaemia
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12
Q

what is Prinzmetals or invariant angina

A
  1. spontaneous or irregular spasms of coronary vessels

2. mechanisms: stress/exercise, cold, cocaine, decongestants, triptans

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13
Q

what are the symptoms of stable/prinzemetals angina

A
  • pain
  • tachycardia
  • nausea and sweating
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14
Q

how can angina be diagnosed

A
  1. exercise ECG
  2. echocardiography
  3. coronary angiography
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15
Q

how can angina be treated

A
  1. mixture of drug therapy and non pharmacological intervention
    - reduce body weight, smoking and stress
  2. drug treatment designed to decrease work done by the heart and increase blood supply
  3. prevent progression of disease
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16
Q

what is reflex tachycardia

A
  1. side effect caused by treatment of stable angina
  2. due to activation of sympathetic nervous system
    - if treatment causes reflex tachycardia, should look to block effects of sympathetic nervous system using a beta blocker
    - eg. bisoprolol.
17
Q

what do beta blockers inhibit

A

inhibit renin release from kidney and so inhibit RAAS

  • decrease frequency and force of contraction
  • so decrease cardiac output
18
Q

how do Ca2+ channel antagonists have an effect on cardiac workload

A
  1. reduce frequency and force of contraction
  2. increase dilation of arterioles
    - leading to reduced cardiac workload
19
Q

how can Calcium channel blockers reduce heart rate

A

can reduce heart rate by blocking L type channels in the SA and AV nodes

  • this will slow the rate of depolarisation and therefore reduce the rate of action potential generation
  • they also decrease the force of contraction of the ventricles by reducing calcium entry through L type channels
20
Q

what is ivabradine

A

blocks the pacemaker current (Ih/f) in the nodal tissue of the heart

21
Q

what are the side effects of ivabradine

A

phosphenes, blurred vision, dizziness

22
Q

what does a blockade of Ih/f result in

A
  1. ivabradine will reduce Na+ entry through If channels and slow rate of depolarisation of the SA node cells
    - reducing firing frequency and therefore heart rate
    - won’t directly alter the force of contraction of the heart
23
Q

give examples of alternatives that can be used instead of ivabradine

A
  1. long acting nitrates- isosorbide mononitrate
    - decrease preload
  2. nicorandil
  3. ranolazine
24
Q

what can be used for secondary prevention of IHD

A
  1. aspirin- prevents platelet activation/aggregation
  2. ACE inhibitors- useful for diabetics
  3. statins- decreases inflammation and reduce cholesterol levels
25
Q

how can blood pressure be controlled

A

may be controlled by beta blocker/CCB or ACE inhibitor

- if not, add in additional agents as required

26
Q

what surgical interventions can be used in IHD

A
  1. percutaneous transluminal angioplasty
  2. coronary bypass graft
  3. stents
27
Q

why are nitrates useful in treatment of stable angina

A
  1. nitrates can dilate venous smooth muscle
  2. this decreases end diastolic volume, reduces stroke volume and therefore cardiac workload
  3. nitrates can also dilate some of the collateral coronary blood vessels
  4. can also have an effect on the arterioles, decreasing total peripheral resistance
    - therefore decreasing after load and the work done by the heart
28
Q

what is the molecular mechanism by which cardiac selective calcium channel blockers are useful in treating angina

A
  1. CCBs will slow the frequency of the heart beat by blocking L type channels in the SA node
  2. they will also slow conduction velocity and increase the refractory period of AV nodal cells by blocking L type calcium channels
    - this reduces ventricular rate
  3. they decrease the force of contraction of ventricular muscle by blocking L type calcium channels
29
Q

why are ACE inhibitors useful for secondary prevention

A
  1. they decrease workload of the heart by:
    - dilating veins and reducing EDV and therefore decreasing stroke volume
    - dilating arterioles and reducing total peripheral resistance and therefore decreasing after load
30
Q

why are statins useful in treating stable angina

A
  1. decrease serum LDL cholesterol
  2. also have anti inflammatory actions
  3. may decrease reactive oxygen species
  4. improve NO production by the endothelium and so cause vasodilation
31
Q

why is ivabradine useful in treatment of angina

A
  1. blocks If
  2. slows the depolarisation of the nodal cells
  3. reduces automaticity in the SA node
  4. increases the refractory period in the AV node
  5. reduces the work done by the heart
32
Q

why can a patient suffering a MI present with tachycardia, sweating and cold clammy skin

A
  1. this is caused through a combination of anxiety brought on by the pain associated with an MI and also the response to a reduction in cardiac output and therefore blood pressure
  2. in both cases, the sympathetic nervous system is activated either through anxiety or to try to maintain blood pressure in the face of decreased CO
    - leads to tachycardia as BP= CO X TPR
33
Q

why is morphine given as pain relief to someone having an MI

A
  1. morphine will reduce the pain associated with the MI
  2. this will decrease stress and anxiety and reduce the stimulation of the sympathetic nervous system
  3. morphine can also dilate some coronary blood vessels
    - so has the ability to increase oxygen supply to the heart muscle
34
Q

why might you have pulmonary congestion if you are having an MI

A
  1. reduced cardiac output will activate the sympathetic nervous system
  2. this will increase EDV
  3. weak left ventricle will not be able to clear all of the blood so it will back up in the atria
  4. this increases the pressure in the pulmonary capillaries preventing fluid from being reabsorbed
  5. this fluid passes into alveoli causing congestion

Ischaemic heart disease (8 decks)

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