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DS1102 > Week 3 - Additional Cardiovascular Stuff > Flashcards

Week 3 - Additional Cardiovascular Stuff Flashcards

1
Q

What are the 2 types of Acute coronary syndrome

A
  • STEMI - ST-Elevation Myocardial Infarction
  • NSTEMI - Non-ST-Elevation Myocardial Infarction event
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2
Q

What is NSTEMI

A

Non-ST Elevation Myocardial infarction event
Partial Blockage: NSTEMI is typically caused by a partial blockage of a coronary artery , which reduces blood flow to a portion of the heart muscle

Plaque Rupture: The blockage is usually due to the rupture of an atherosclerotic plaque leading to the formation of a blood clot

Subendocardial Infarction: The affected area often involves the inner layer of the heart muscle (subendocardium), unlike STEMI, which usually affects the entire thickness of the heart muscle.

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3
Q

How does the ECG of an NSTEMI differ from a normal ECG

A

There is a ST-segment depression and T-wave inversion characteristic of sub endocardial ischaemia

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4
Q

What is STEMI

A

ST-Elevation Myocardial Infarction

Complete Blockage: STEMI usually results from a complete blockage of a coronary artery, often caused by a blood clot that forms over an atherosclerotic plaque.

Transmural Infarction: This type of heart attack affects the full thickness of the heart muscle wall (transmural infarction), leading to more extensive damage compared to other types of myocardial infarctions.

Myocardial Damage: The lack of blood flow leads to ischemia and eventual necrosis (death) of the heart muscle in the affected area

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5
Q

What is the difference between an ECG of STEMI and a normal ECG

A

ECG is elevated at ST segment

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6
Q

What is the differences between STEMI and NSTEMI events

A

How much heart wall is affected - STEMI the whole wall, NSTEMI inside wall only
ECG trace - ST depressed in NSTEMI and elevated in STEMI
Severity of infarction and loss of cardiac function

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7
Q

What are the similarities between STEMI and NSTEMI

A
  • Both are caused by a thrombosis (blood clot)
  • Both cause chest pain (angina)
  • Both decrease cardiac output and stroke volume
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8
Q

What are the main pharmaceutical treatments for a myocardial infarction and their mechanisms of action

A

Short term: GTN (opens blood vessels very quickly) - dilate coronary vessels
Short term: opioids - for pain
Long term (targeting blood clot) - aspirin (or other anticoagulant/ blood thinner) - this can stop a blood clot from forming - but it can’t remove a blood clot
Long term - beta blocker to reduce cardiac workload - to stop heart failure and the heart wearing out

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9
Q

What is heart failure

A

Also known as congestive heart failure (CHF), is a chronic condition in which the heart is unable to pump blood effectively to meet the body’s needs for oxygen and nutrients. This results in inadequate blood flow and can cause a buildup of fluid in the lungs and other tissues.

  • in heart failure there is low cardiac output
  • It primarily occurs in the left ventricle
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10
Q

What are the 2 types of heart failure

A
  • Failure with preserved ejection fraction
  • Failure with reduced ejection fraction
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11
Q

What is the equation for ejection fraction

A

stroke volume/end diastolic volume

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12
Q

What are heart failure causes

A
  • Hypertension
  • Coronary artery disease
  • arrhythmias
  • Valvular heart disease
  • Excessive alcohol intake
  • Hyperthyroidism
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13
Q

What is a normal EF (ejection fraction)

A

50-60%

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14
Q

What is preserved ejection fraction

A
  • Where the heart does not relax enough and hence the heart doesn’t fill up with enough blood and therefore doesn’t pump out enough blood
  • Does not have adequate stroke volume because there is not enough blood getting into the heart
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15
Q

What is reduced ejection fraction

A
  • Where the heart is filling with enough blood but isn’t pushing all the blood out
  • Stroke volume is low
  • Means that ejection fraction is very low
  • Tells us that the heart muscle itself isn’t contracting very hard so it can’t push out the blood that it receives.

*means that the sympathetic system is over stimulating

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16
Q

What are the 2 things which the body does in compensation to heart failure resulting in low cardiac output

A
  • sympathetic activation
  • Activation of RASS
    both increases the workload of the failing heart which is bad
17
Q

What happens when sympathetic system is activated during heart failure

A
  1. Sympathetic activation
  2. Baroreceptor sense that the blood pressure has decreased
  3. Cardioaccelerator increases heart rate and contractility to increase CO
  4. Vasomotor center increases, increasing vasoconstriction

this increases the workload of the failing heart which is bad

18
Q

What happens when RAAS is activated during heart failure

A
  1. Activation of RAAS
  2. Kidneys have a reduced blood flow causing an increase in angiotensisn 2 (constricts blood vessels increasing BP) and aldosterone (causes Na+ and water retention to increase, increasing blood volume)
  3. Increases work load on the heart
19
Q

What are treatments for heart failure with reduced ejection fraction

A

Beta blockers and diuretics
to decrease further damage from overstimulating the heart. It reduce blood volume

20
Q

What is treatment for heart failure with preserved ejection fraction

A
  • usually treat cause
  • drugs for reduced ejection fraction not always useful for preserved ejection fraction
21
Q

What are signs and symptom of left sided heart failure

A
  • Fluid builds up in lungs because the blood is the heart isn’t being pushed out
  • Pulmonary hypertension - blood filling into the lungs
  • Little peripheral oedema - because fluid build up is in the lungs
22
Q

What are signs and symptoms of right side heart failure

A

Patient has fluid build up in the general circulation

  • fluid builds up in systemic system
  • Peripheral oedema
  • Right sided failure lead o low CO from left side also
23
Q

What is oedema

A

Oedema is a build up of fluid in the body which causes the affected tissue to become swollen

DS1102 (30 decks)

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