ECG Flashcards

1
Q

ECG - V2/V3 ST elevation (tombstoning)

A

anterior STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ECG - II/III/AvF ST elevation with reciprical depression in I/AvL

A

inferior STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ECG criteria to diagnose a posterior MI

A

ST segment depression v1-v4

R:S ratio in V1/V2 > 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ECG differentiate LBBB and RBBB

A

Positive V1 = right
Positive V6 = left

Both = broad QRS complex!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Example of 1 loop and 1 thiazide diuretic

A

Loop - frusemide

Thiazide - hydrochlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diuretic monotherapy in treatment of heart failure…

A

Do not improve prognosis or mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Frusemide and loop diuretic action/outcome

A

increase excretion of sodium, water and potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is spironolactone?

A

competitive antagonist of aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MOA spironolactone and a potential outcome

A

increases sodium and water excretion, decreases potassium excretion

may produce hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aldosterone receptors heart: normal vs pathological (3 effects)

A

Normal: low levels and minimal effect

Pathological: elevated aldosterone causes activation leading to detrimental effects on the heart - fibrosis, hypertrophy and dysrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What dosage of spironolactone has been shown to be beneficial in the treatment of severe systolic heart failure (improved survival)?

A

25mg daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Combined therapy with what other drug and spironolactone should be taken with extreme caution? Why?

A

ACE inhibitors and angiotensin II antagonists

Severe hyperkalaemia and may lead to death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Findings of beta adrenergic antagonists (beta blockers) and systolic heart failure

A

reduced…
- total mortality
- sudden death
- hospitalisation
and improved QOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List:
2: beta 1 blockers
1: beta 1 blocker with vasodilating properties
1: nonselective beta blocker with alpha 1 receptor blocking activity

A

b1
- bisoprolol
- metaprolol

b1 + vasodilating
- nebivolol

beta blocker + a1
- carvedilol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Possible MOA of beta blockers in systolic HF (3)

A
  • reduced SNS activity
    leading to reduced cardiac ischaemia and arrhythmias
  • reduced renin release
  • apart from beta blockade, some vasodilate e.g. carvediol, nebivolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Beta blocker treatment regime

A
  • start low and go slow
  • 4-8wks symptoms may worsen
  • up to 4 months before benefit seen
  • beta blocker therapy added to ACEi has additional mortality and morbidity benefits in HFrEF
17
Q

What is a predictor of adverse outcomes in patients with HFrEF?

A

HR
- increased HR is associated with increased mortality

18
Q

MOA of Ivabradine

A

Reduces HR by selectively inhibiting the current in the SA node responsible for spontaneous depolarisation - If current

19
Q

What is the If current in the heart? Site? When is it activated? What regulates its activity? What ions are involved? Describe their movement through the channel?

A

Responsible for spontaneous depolarisation - helps regulate HR

SA node

Activated when the heart hyperpolarizaes

cAMP

K+ and Na+

Both move in to the cell - overall effect is depolarization

20
Q

What is digoxin? Effect (2)? MOA (2)? Clinical impact on patients with HF?

A

naturally occurring cardiac glycoside found in the plant species Digitalis (foxglove)

1 Slows HR (increased parasympathetic activity)
2 Exerts +ve inotropic effect on heart (contractility)

1 increases vagal activity, decreased AV conduction = decreased HR
2 Inhibits Na+/K+ ATPase pump = increased intracellular Na+ = reduces Ca+ extrusion from the cell by the Na+/Ca+ pump = results in increased intracellular concentration of Ca+

Reduces hospitalisations but does not improve mortality + limited role in treatment

21
Q

Outline characteristics of Digoxin that lead to toxicity? What increases its toxicity? ADRs?

A

Low TI - may produce significant toxicity and death

Long T1/2 - 36-48 hrs

Primarily excreted in urine as unchanged drug

Hypokalaemia increases toxicity

Nauseau, vomiting, diarrhoea, green/yellow vision, bradycardia, ectopic beats, dysrhythmias

22
Q

Pharmacological treatment of systolic HF (HFrEF)? (8)

A
  • ACEi / angiotensin II antagonists
  • neprilysin inhibitors (breaks down BNP)
  • diuretics (fluid overload)
  • beta blockers
  • aldosterone antagonists e.g. spironolactone
  • ivabradine (I(f) current)
  • digoxin (increased contractility)
  • SGLT2 inhibitors

+ treatment of co-morbidities/disease states e.g. hypertension, IHD etc.