Unit 6 - Cardiovascular system 6 Flashcards

1
Q

What is myocardial oxygen balance?

A

Ratio of oxygen supply to oxygen demand

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2
Q

What is oxygen supply increased by?

A

Either increasing arterial oxygen content or increasing coronary blood flow

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3
Q

What is an increase in blood pressure or heart rate met with?

A

A proportionate increase in coronary blood flow

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4
Q

When does myocardial ischaemia develop?

A

When blood supply to the myocardium is inadequate to meet the metabolic demands of the tissue

  • absolute reduction at rest
  • supply ischaemia
  • relative reduction in face of increased muscle work
  • demand ischaemia
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5
Q

What percentage of cases is myocardial ischaemia associated with critical stenosis of one or more coronary arteries?

A

95%

- practically unknown in absence of coronary artery disease

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6
Q

What is chronic stable angina?

A

Critical stenosis (narrowing) of one or more epicardial coronary arteries due to atherosclerosis

  • advanced and stable plaques in one or more multiple locations
  • fixed stenosis
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7
Q

What is the main symptom of chronic stable angina?

A

Typical pattern of demand ischaemia
- angina pain develops on exertion
reproducibly relieved by rest or nitrovasodilator

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8
Q

What is the characteristic pain pattern of chronic stable angina?

A

Referred pain

referred pain to the chest and upper left arm

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9
Q

What is silent ischaemia?

A

Evidence of myocardial ischaemia in the absence of chest discomfort

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10
Q

What percentage of transient ischaemic episodes in stable coronary artery disease are NOT associated with pain?

A

70%

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11
Q

Which group of patients is silent ischaemia particularly seen in?

A

Diabetic patients

- sensory neuropathy

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12
Q

What can be used to diagnosis silent ischaemia?

A

Exercise or stress testing along with ambulatory ECG

- Holter monitor

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13
Q

What are the three other types of ischaemia?

A
  • Prinzmetal’s (variant) angina
  • cardiac syndrome X
  • unstable (crescendo) angina
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14
Q

What is Prinzmetal’s (variant) angina?

A

Occurs at rest due to coronary artery spasm/constriction

- rare

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15
Q

What is Cardiac syndrome X?

A

Angina without epicardial coronary arteries

  • more likely to be a microvascular disease
  • more common in women
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16
Q

What is unstable (crescendo) angina?

A
Sudden onset
- at rest
- exercise
An acute coronary syndrome
- thrombosis leads to occlusion at site of plaque
17
Q

What can chronic coronary disease lead to?

A

Cardiomyopathy resulting in reduced left ventricle output

18
Q

What does chronic hypoperfusion lead to?

A

Reduced output in viable myocardium
- hibernating myocardium
Reversible with revascularisation

19
Q

What is an acute coronary syndrome?

A

Umbrella term

  • blood supply to the heart is suddenly blocked
  • unstable angina
  • acute myocardial infarction (AMI)
20
Q

What is the difference between unstable angina and acute myocardial infarction?

A

Unstable angina - obstruction typically incomplete
Acute myocardial infarction - usually fully occluded vessel
- rendering distal myocardium ischaemic

21
Q

What process precipitates coronary thrombosis?

A

Fissuing

Atheromatous plaque rupture

22
Q

What is a coronary thrombosis?

A

Formation of a blood clot in a coronary artery

23
Q

What can the formation of a coronary thrombosis be related to?

A
Increase in emotional or physical stress
Circadian rhythm
- sympathetic nervous system
- temperature changes
- heart rate in the morning
24
Q

What are the symptoms of acute coronary syndromes?

A
Chest pain
- tightness
- pressure
- discomfort
Pain or discomfort in one or both arms
Shortness of breath
Feeling dizzy or lightheaded
Nausea and/or diaphoresis
Anxiety
Symptoms steadily worsen
- unrelieved by rest or nitrates
25
How is an acute coronary syndrome diagnosed?
Symptoms ECG Biomarkers
26
What is STEMI?
ST elevation myocardial infarction
27
What is NSTEMI?
Non-ST elevation myocardial infarction
28
What biomarkers appear in plasma in hours post onset of symptoms indicative of muscle damage, both for NSTEMI and STEMI?
- troponins | - creative kinase isoforms
29
When is treatment initiated for muscle damage seen in NSTEMI or STEMI?
Before results of bloods | - especially if diagnostic ECG present
30
What is the molecular pathology of Myocardial infarction?
Deprivation of an area of the myocardium of oxygenated blood flow - hypoxia - cessation of mitochondrial oxidative phosphorylation - reduction in source of ATP Anaerobic glycolysis attempts to compensate - demand outweighs supply - only 7% requirement produced H+ and lactate build up - production of ROS - impaired contraction - impaired contracture Cell death by oncosis, apoptosis and autophagy - coagulation necrosis at tissue level - infarct progress from endocardium to epicardium - little or not collateral circulation
31
What is a major determinant of irreversible injury following an MI?
Time
32
What are the complications following an MI?
Cardiogenic shock Heart failure Arrhythmia
33
Where is the majority of cholesterol produced?
Liver | - contribution from diet