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
Q

How is an acute coronary syndrome diagnosed?

A

Symptoms
ECG
Biomarkers

26
Q

What is STEMI?

A

ST elevation myocardial infarction

27
Q

What is NSTEMI?

A

Non-ST elevation myocardial infarction

28
Q

What biomarkers appear in plasma in hours post onset of symptoms indicative of muscle damage, both for NSTEMI and STEMI?

A
  • troponins

- creative kinase isoforms

29
Q

When is treatment initiated for muscle damage seen in NSTEMI or STEMI?

A

Before results of bloods

- especially if diagnostic ECG present

30
Q

What is the molecular pathology of Myocardial infarction?

A

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
Q

What is a major determinant of irreversible injury following an MI?

A

Time

32
Q

What are the complications following an MI?

A

Cardiogenic shock
Heart failure
Arrhythmia

33
Q

Where is the majority of cholesterol produced?

A

Liver

- contribution from diet