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Cardiovascular Block > End of block key points > Flashcards

End of block key points Flashcards

1
Q

NSTEMI vs STEMI

A

NSTEMI

  • plaque ruptures, thrombus, partial occlusion to vessel
  • injury to subendocardial myocardium

STEMI
- complete occlusion of BV, transmural injury and infarct to myocardium

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2
Q

which symptom will increase the risk of sudden cardiac death in patient with hypertrophic cardiomyopathy?

a) chest pain
b) peripheral oedema
c) oedema
d) headache
e) breathlessness
f) syncope

A

syncope

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3
Q

role of furosemide?

A
  • diuretic

- inhibits [Na+ / K+ / 2Cl-] carrier in thick ascending loop of henle

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4
Q

whats open in plateau phase of action potential in cardiomyocytes?

A
  • voltage gated calcium channels
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5
Q

what removes calcium from cardiac myocytes to the extracellular space?

A
  • sodium / calcium exchanger
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6
Q

what channels plays an important part in repolarising cardiac myocytes?

A
  • voltage gated potassium channel (Delayed rectifier)
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7
Q

what ion channel causes the rapid upstroke of the action potential in cardiac myocytes?

A
  • voltage gated sodium channel
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8
Q

what channel is blocked by local anaesthetics?

A
  • voltage gated sodium channels
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9
Q

what ion channel is blocked by drugs causing pharmacologically acquired long QT syndrome?

A
  • voltage gated potassium channel
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10
Q

In adulthood, what are common complications of an untreated atrial septal defect?

A
  • atrial arrhythmias and right heart failure
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11
Q

Which phase of the ECG corresponds to beginning of the rapid passive ventricular filling?

A
  • The ST segment

* think after QRS, blood in aorta and PA, blood from RA and LA gonna enter RV and LV

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12
Q

Action of bisoprolol?

A
  • heart rate slowed
  • acts on beta receptors of heart
  • can reduce mortality in HF patients
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13
Q

what happens as a result of angiotensin 2 production and where does it act?

A
  • v. constriction

- acts on efferent arterioles

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14
Q

23 y/o pregnant female, gripping chest pain on exertion. known to have systolic murmur. ECHO revels severe aortic stenosis. cause of chest pain?

A
  • her circulating volume increased (pregnancy)

- increasing oxygen demand in the myocardium

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15
Q

in penetrating chest trauma what chamber of heart most likely to be affected?

A

right ventricle

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16
Q

third heart sound?

A
  • beginning of isometric relaxation
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17
Q

what common valvular heart disease would result in systolic crescendo-descrendo murmur?

A
  • aortic stenosis
18
Q

what when activated causes a reduction in circulating volume?

A

BNP

19
Q

tetralogy of fallot

A
  • aortic override
  • pulmonary regurgitation
  • atrial septal defect
  • right sided aortic arch
20
Q

what would be associated with normal pulmonary artery pressures and large A waves in JVP?

A
  • tricuspid stenosis
21
Q

What happens normally in depolarisation?

A
  • in normal heart

- RV and LV depolarise together, contract simultaneously

22
Q

Describe what occurs in bundle branch block?

A
  • unaffected ventricle depolarises first
  • electrical impulses through myocardium to other side
  • delayed, slowed depolarisation
  • broader QRS complex
23
Q

Describe position of the V1, V6 leads?

A

V1 - RHS

V6 - LHS

24
Q

Describe what may happen if LHS bundle depolarises first?

A
  • LHS initiated
  • signal towards RHS through depolarising the interventricular septum
  • away from V6 to V1
  • v1 small positive deflection
  • small negative in V6
  • depolarisation of septum from LHS to RHS
  • signals move in both directions however LV larger, so overall net movement to LHS
  • thus positive V6 and negative v1
25
Q

What occurs in RBBB?

A
  • initial septal activation is unchanged
  • LHS depolarises normally, thus positive V6, negative V1
  • then reversed to RHS
  • thus V1 positive, M shaped
  • V6 negative, broader S shape
26
Q

Describe what occurs in LBBB?

A
  • septal depolarisation reversed from right to left
  • RV activation 1st, then depolarisation to LHS
  • V1 negative , v6 positive
  • V6 characteristic bunny ears
27
Q

Describe significance of right internal jugular vein?

A
  • communicates directly with RA via SVC thus gives indication of central venous pressure
28
Q

Most important points to remember when reading JVP?

A
  1. Blood flows from high to low pressure
  2. contraction increases pressure
  3. relaxation decreases pressure
29
Q

A wave

A

atrial contraction, some pressure goes back up to RIJv causing slight distension

30
Q

x descent after A wave

A

right atrium relaxation

31
Q

C wave

A

bulging of blood against closed tricuspid valve.

rv contracts against closed tricuspid

32
Q

V wave

A

atrial filling

33
Q

Y descent

A

opening of tricuspid valve thus allowing ventricular filling

34
Q

no A waves

A

atrial fibrillation

35
Q

giant regular uniform A waves

A
  • ventricles contract against higher pressure

- RV hypertrophy, tricuspid stenosis, pulmonary hypertension

36
Q

cannon intermittent A wave

A
  • cardiac arrhythmia, RV contracts against closed tricuspid
37
Q

large V wave

A
  • increased ventricular filling
  • tricuspid regurgitation
  • often joins with C wave to form CV wave
38
Q

Steep X, Y descent

A

Friedrich’s sign

reduced elasticity of pericardial sac e.g. constructive pericarditis

39
Q

S1 and S2 sound

A

S1 - LUB, AVV closure after blood from atria to ventricles

S2 - DUB, aortic and pulmonary valve closes after ventricles eject blood

40
Q

third heart sound

A
  • rapid ventricular filling

Cardiovascular Block (16 decks)

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