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CAM201 Clinical Skills > Myocardial ischaemia > Flashcards

Myocardial ischaemia Flashcards

1
Q

Factors which determine myocardial oxygen supply

A
  1. Diastolic perfusion pressure
  2. Coronary vascular resistance
    • _​​_External compression
    • Intrinsic regulation: local metabolites endothelial factors, neural innervation.
  3. O2 carrying capacity
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2
Q

Factors which determine myocardial oxygen demand

A
  1. Wall tension
  2. Heart rate
  3. Contractility
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3
Q

Coronary blood flow

A

LV myocardial flow principally diastolic.

RV myocardial flow both systolic and diastolic.

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4
Q

LV perfusing pressure

A

ADP-RAP or LVEDP.

Coronary perfusion pressure = aortic diastolic pressure - higher of LVEDP or RAP.

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5
Q

RV coronary perfusion pressure

A

Mean arotic pressure - higher of RVEDP or RAP

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6
Q

Autoregulation of coronary arteries

A

Metabolic control:

  • Oxygen
  • Adenosine, ADP
  • NO (nitric oxide)
  • Lactate, H+
  • Histamine, bradykinin
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7
Q

Oxygen in autoregulation

A

Acts as a vasoconstrictor.

As O2 levels drop during ischaemia: pre-capillary vasodilationa nd increased myocardial blood supply.`

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8
Q

Adenosine in autoregulation

A
  • Potent vasodilator.
  • Prime mediatory of coronary vascular tone.
  • Bind to receptors on vascular smooth muscle, decreasing calcium entry into cell.
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9
Q

Autoregulatory resistance

A

Involves three different cells

  1. Myocardial muscle cells: produces byproducts of aerobic metabolism (lactate, adenosine etc.)
  2. Vascular endothelial cell (arteriole): reacts to metabolic byproducts
  3. Vascular smooth muscle cell (arteriole): signaled by endothelial cell to contract (vessel constriction) or relax (vessel dilation).
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10
Q

Causes of reduced LV coronary flow

A

Global: reduced aortic diastolic pressure, increased RAP, increased LVEDP.

Local:

  1. Coronary artery disease (very common)
  2. Coronary artery spasm (perhaps global as well) rare.
  3. Coronary artery embolism (also rare)
  4. Microvascular disease
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11
Q

MVO2

A

Myocardial oxygen demand.

Determined by:

  • Heart rate
  • Contractility
  • Wall tension
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12
Q

What causes an increase in MVO2

A

Increases directly in proportion to HR

Increases with increased contractility

Increases with increased wall tension (i.e. increases with increasing preload or afterload).

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13
Q

Wall tension

A

Pressure x radius / wall thickness

Defined as: force per unit area generated in the LV throughout the cardiac cycle.

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14
Q

Afterload

A

LV systolic pressure.

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15
Q

Preload

A

LV end-diastolic pressure or volume.

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16
Q

Effects of myocardial ischaemia

A

Diastolic function: relaxation slowed reducing compliance causing dyspnoea

Systolic function: contractility impaired.

Alterations in electrical potential promoting dysrhythmias.

Possible papillary muscle dysfunction which may cause mitral regurgitation.

17
Q

Consequences of ischaemia

A

Chest pain

Systolic dysfunction (loss of contraction)

  • Decreased CO
  • Decreased coronary perfusion pressure

Diastolic dysfunction (loss of relaxation)

  • high pressure (LVEDP and PCWP) for any given volume
  • Dyspnea, decrease pO2, decrease O2 delivery
  • Increased wall tension (increased MVO2)

All three give rise to stimulation of sympathetic nervous system with subsequence catecholamine release - increased HR and BP (increased MVO2).

18
Q

Chronic angina presentation

A
  • Chest tightness to thorat, jaw, arms, epigastrium, back
  • Often accompanied by hydpnoea.
  • Effort related adn relieved by rest.
  • Can occur with significant ‘stress’.
  • Accentuated walking in the cold or walking into a strong wind.
19
Q

Sing sin chronic stable angina

A
  • Generally non in particular.
  • BP may be raised
  • Possible signs of atherosclerotic disease elsewhere: cartodi bruit(s), impalpable pedal pulses, xanthelasma.
20
Q

ECG in chronic angina

A

Likely to be normal at rest

21
Q

When is computer tomography coronary angiography used?

A
  1. Not used for asymptomatic patients.
  2. Used in patients with chest pain, as it is reliable in ruling out significant CAD.
  3. It is being used more and more in ED setting as a negative test reliable enough to allow early discharge from ED.
22
Q

Requirements for CTCA

A
  • Patients in SR (rate <65)
  • Tolerant of betablockers and nitrated(?)
  • Able to hold breath for 10sec
  • Able to hold arms above head during scan
  • Nomal renal function
23
Q

How do you stratify risk?

A

Using exercise echo or nuclear perfusion scan.

High risk: low exercise capacity, BP not rising or falling is worse, marked ST depression, a large area or multiple areas of ischaemia.

If the above: coronary angiography to look for left main stenosis and/or equivalent or triple vessel disease with impaired LV function.

24
Q

Stratifying risk in coronary stenosis

A

Fractional flow reserve (FRR) is a new technique enabling comparison of blood flow post a specific stenosis to blood flow in normal coronary artery.

FFR is the ratio of flow distal to stenosis to normal flow.

FFR = 1.0 is normal

FFR >0.8 ishcaemia very unlikely

FFR < 0.75 ischaemia will be caused by that stenosis

25
Q

Ivabradine

A

Anti-anginal

Selectively inhibits an ionic current (lf) in SA node slowing heart rate.

26
Q

Ranolazine

A

Inhibits late Na influx across sarcolemma thus reducing i/c Ca levels and minimizing delay in relaxation

27
Q

PCI

A

percutaneous coronary intervention.

Mainly ‘pallative’ only. Good at reducing symptoms but minimal evidence improves outcome.

28
Q

CABG

A

Coronary artery bipass graft.

Improves outcomes. Left main stenosis and TVD with impaired LV function. Good at improving ischaemic syndroms.

29
Q

Pathophysiology of acute coronary syndrome

A

Plaque vulnerability and extrinsic triggers result in plaque rupture.

Platelet adherence, aggregation and activation of the coagulation cascade with polymerization of fibrin.

Thrombosis with sub-total (UA, NTMI) or total coronary artery occlusion (AMI).

30
Q

Unstable angina symptoms

A
  • New nset angina
  • Increase in frequency, duration or severity
  • Decrease in exertion required to provoe
  • Any prolonged episode (>10-15 mins)
  • Failure to abate with >2-3 sublingual NTG
  • Onset at rest or awakening from sleep
31
Q

Signs of unstable angina

A

No specific signs: vary depending whether symptoms or not at time of exam.

ECG: ST depression, T changes, may be normal

Troponin: important discriminator

32
Q

ACS on discharge

A
  • Action plan and definitive follow-up.
  • All patients fo home with aspirin +/- clopidogrel, statin, beta blocker, and S/L GTN with appropriate instructions on how to use.
  • Ace inhibitors (ramipril or perindopril)
  • Emphasise importance of phoning 000 if ischaemic symptoms recur and perists 10’ despite GTN

CAM201 Clinical Skills (14 decks)

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