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Cardiovascular System > Session 6- When things go wrong > Flashcards

Session 6- When things go wrong Flashcards

1
Q

QT interval

A

QT interval time taken for depolarisation and repolarisation ventricle

  • varies with heart rate
  • calculation to correct for heart rate
  • start of the Q wave and the end of the T wave

0.44-0.45 seconds 11 small boxes

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2
Q

what does a prolonged QT interval indicate

A

indicates prolonged ventricular repolarisation

associated risk for dangerous arrythmias

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3
Q

characteristics of normal sinus rhythm

A
  • regular rhythm at a rate of 60-100 bpm
  • each QRS complex id preceded by a p wave
  • normal p wave axis: p waves should be upright in leads I and II inverted aVR
  • the PR interval remains constant
  • QRS complexed are < 100ms wide
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4
Q

what causes heart block

A

degeneration electrical conducting system with age- sclerosis and fibrosis

acute myocaridal ischaemia

medications

valvular heart disease

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5
Q

first degree AV/heart block

A

1st-degree AV block: conduction is slowed without skipped beats. All normal P waves are followed QRS complexes, but PR interval is longer than normal

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6
Q

second degree heart block

A

mobitz type 1

also called wenkebach

successively longer PR interval until one QRS is dropped- is electrical signal not conducted through to ventricles- then cycle starts again

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7
Q

second degree AV block- Mobitz type 2

A

PR intervals do not lengthen- sudden dropped QRS complex without prior PR changes

atrial rhythm is regular

ventricular rhythm is irregular

HIGH RISK PROGRESSION TO COMPLETE HEART BLOCK

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8
Q

third degree AV block

A

atria and ventricles are depolarising independently- complete failure of AV conduction

  • ventricular pacemaker takes over- slow 20-4- bpm
  • typically too slow to maintain blood pressure
  • usually wide QRS complex
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9
Q

bundle branch block

A

delayed conduction within the BB

  • can be RBBB and LBBB
  • p wave and PR intervals are normal
  • wide QRS complex because ventricular depolarisation takes longer
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10
Q

supraventricular arrhythmia

A

sinus node
atrium itself
AV node

normal (narrow) QRS complex-when conducted ventricles depolarise normally

arises from multiple atrial folci
rapid chaotic impulses 
no p waves- wavy baselines
irregular R-R intervals
impulses AV node at rapid irregular rate 
not all conducted
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11
Q

ventricular arrhythmia

A

wide and bizarre QRS complex

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12
Q

Afib

A

slow- ventricular response- <60 bpm
fast- ventricular response >100 bpm
normal- 61-99 bpm

Afib with coarse fibrillation- amplitude >0.5mm
fine fibrillation amplitude <0.5mm

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13
Q

haemodynamic effects of atrial fibrillation

A

• Loss of atrial contraction leads to increased blood stasis c/w normally
contracting atria - stasis most evident in left atrium - flow velocity
markedly reduced concomitantly with impaired contractility of left
atrial appendage; leads to small clots in LA – therefore atrial
fibrillation well-established risk factor for ischaemic stroke
secondary to emboli

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14
Q

premature ventricular ectopic beats

A
  • Ectopic focus in ventricle muscles
  • Impulse does not spread via fast
    His-Purkinje system -
  • Therefore much slower
    depolarization ventricular muscle
    Therefore Wide QRS
  • Premature because occurs earlier
    than would be expected for the next
    sinus impulse
  • May be ASx or cause palpitations
    without haemodynamic
    consequences
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15
Q

VTACH

A 
Run of ≥
3 Consecutive PVC
-VTACH is broad
complex tachycardia
-Persistent VTACH is
a dangerous rhythm
requiring urgent
treatment
-High risk progression
to Ventricular
fibrillation
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16
Q

venricular fibrillation

A 
-Abnormal, chaotic,
fast ventricular
depolarisation
- Impulses from
numerous ectopic
sites in ventricle
- No coordinated
contraction
- Ventricles quiver
- No cardiac output
- If sustained –
cardiac arrest
17
Q

myocardial infarction

A

muscle necrosis present- therefore blood tests will be positive

18
Q

STEMI

A

ST segment elevation myocardial infarction

Due to complete occlusion of coronary artery
• “Full thickness” of myocardium involved
• Sub-epicardial injury causing ST Segment elevation in leads facing
affected area is the earliest sign

19
Q

Non- STEMI

A

non ST elevation MI

20
Q

in anterior cardiac wall necrosis. Which artery?

which leads?

A

left anterior descending artery- also known as Anterior Interventricular branch of left coronary artery

widow maker

major ECG changes will be seen precordial/chest leads- V3 and V4. If septum involved also V2 and sometimes in limb leads

21
Q

unstable angina

A

•
“Unstable angina (UA) is an acute coronary syndrome that is defined
by the absence of biochemical evidence of myocardial damage…
characterised by specific clinical findings of prolonged (>20
minutes) angina at rest; new onset of severe angina; angina that
is increasing in frequency, longer in duration, or lower in threshold;
or angina that occurs after a recent episode of myocardial
infarction.”

22
Q

ECG Changes in Non-STEMI and

Ischaemia: ST segment

A

• ECG changes due to subendocardial injury
• ST segment DEPRESSION and T wave inversion
• On ECG tracing behaves as if abnormal current traversing
damaged tissue is moving AWAY from recording electrode

23
Q

ECG Changes in Non-STEMI and Ischaemia: T waves

A

Acutely, there is either a depressed ST segment or there is an inverted T wave.

Within hours there is raised troponin I and T on a blood test (indicating myocyte death).

After a few weeks the ST segment and T wave return to normal.

No pathological Q wave develops because the infarction is not the entire thickness of the myocardium.

24
Q

ECG changes- stable angina

A

• ST depression during exercise because of coronary disease – but
“stable” atherosclerotic plaque causing fixed narrowing
• ECG changes will REVERSE at rest
• ECG: down sloping of ST-segment depression or elevation

25
Q

hypokalaemia

A

– Moderate hypokalaemia is a serum level of < 3.0
mmol/L
– Severe hypokalaemia is defined as a level < 2.5
mmol/L
• Decreased extracellular potassium causes
myocardial hyperexcitability
• Palpitations, Arrhythmia, Cardiac arrest

26
Q

hypokalaemia - ECG

A

ECG:
• Increased amplitude and width of the P wave
• Prolongation of the PR interval
• T wave flattening and inversion
• ST depression
• Prominent U waves (best seen in the precordial leads)

27
Q

Hyperkalaemia

A
  • Hyperkalaemia: >5mmol/L (5.2 mmol/L in some labs)
  • Problems usually develop at higher levels - 6.5 mEq/L to 7 mEq/L -

• Resting membrane potential becomes less negative
• Causes some voltage gated Na+ channels to be
inactivated
• Heart becomes less excitable
• Conduction problems occur
• Can lead to
– Palpitations, Arrhythmia, Cardiac arrest

28
Q

what can be seen on an ECG with hyperkalaemis

A

TENTED T WAVES
LOSS OF P WAVE
WIDENING QRS
QRS contiues to widen approaching sine wave

Cardiovascular System (18 decks)

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