ECG pathology and arrythmia

Question 1

define cardiac arrest

Answer 1

sudden cessation of cardiac activity so that the victim becomes unresponsive with no normal breathing and no signs of circulation

Question 2

what does BLS stand for

Answer 2

basic life support

Question 3

what is basic life support

Answer 3

( resuscitation system that u r tested on)

Question 4

what are shockable and non shockable rythems

Answer 4

shockable = ventricular fibrillation (irregular heartbeat of ventricles) and ventricular tachycardia (a heart rate over 100 beats a minute.
non-shockable = systole (no pulse) and pulseless electrical activity PEA

Question 5

define fibrilation

Answer 5

irregular, rapid contractions of muscles esp heart

Question 6

what is defibrillation

Answer 6

• external electrodes n chest apply current that simultaneously depolarise all cells in heart
• depolarised cells are ‘refractory’ (cant start another pulse) and then cannot sustain re-entrant arrhythmia

Question 7

what is tachycardia

Answer 7

heart rate above 100 bpm

Question 8

what are some symptoms of tachycardia

Answer 8

palpitations
light headedness
SOB
sweatiness/nausea

Question 9

why is tachycardia bad

Answer 9

• reduced filling time (of blood in heart)
• increased myocardial oxygen demand
• often associated with other effects e.g venoconstriction

Question 10

what is a syndromic approach

Answer 10

treatment given based on clinical symptoms without having clear diagnosis

Question 11

what does SVT stand for

Answer 11

supra ventricular tachycardia

Question 12

what are 3 main causes of SVT

Answer 12

• trigger e.g adrenaline
• ectopic focus e.g automaticity
• re-entrant arrhythmia (due to changed electrophysiological properties of damaged tissue)

Question 13

what is re-entrant arrythmia

Answer 13

when a cardiac impulse fails to stop and re-excites the tissues that have recovered from the refractory period.

Question 14

where does re-entrant arrythmia occur

Answer 14

AV node

Question 15

what is particular about the tissue that comes from atrial epitaphic tachycardia

Answer 15

generates its own action potentials at a faster rate than the SA node

Question 16

abnormal connections b/q the atria and ventricles can lead to re-entrant arrythmias

Question 17

‘sinus’ tachycardia is typically due to trigger e.g jogging

Question 18

what us the approximate conduction of the AV node

Answer 18

150 bpm

Question 19

what is cardioversion

Answer 19

Cardioversion is a medical procedure that uses quick, low-energy shocks to restore a regular heart rhythm

Question 20

what are vagal manoeuvres

Answer 20

techniques used to increase vagal parasympathetic tone in an attempt to diagnose and treat various arrhythmias.

Question 21

how can adenosine be used to help arrythmias

Answer 21

• adenosine stimulates A1 adenosine receptors in heart
• like acetyl choline, adenosine can hyperpolarize cells and prevent propagation of action potentials
• adenosine has an extremely short half life os 6 sends as it is rapidly taken up the tissue

Question 22

what is the cause of atrial fibrilation

Answer 22

• poor coronary blood flow leading to damaged myocardial tissue with altered electrophysiological properties
• disorganised depolarisation and hence disorganised contraction of left atria
  (acute stress can also be factor)

Question 23

what are some effects of atrial fibirlation

Answer 23

• predisposes static blood which can form thrombi
• thrombi can move out of heart to lodge in brain and cause stroke

Question 24

what are the 4 classifications of atrial fibrillation

Answer 24

acute
paroxysmal (recurrent over 7 days)
persistant ( lasts over a year)
permanent (cant be brought back to sinus rhythm)

Question 25

what is the long term management of atrial fibrilation

Answer 25

anticoagulation
- lowers risk of stroke by 60%
(blood close doesnt form)

Question 26

what is a negative to using anticoagulation meds for fibrilation

Answer 26

has increased risk of bleeding

Question 27

how can taking anticoagulant affect the elderly

Answer 27

can cause subdural haematomas which is where blood collects between skull and surface of brain

Question 28

what is the aim of rate control drugs

Answer 28

• limit symptoms but can also prevent development of heart filure

Question 29

why are rhythm control drugs less preferred

Answer 29

patients frequency dont stay in sinus rythm

Question 30

how would u diagnose acute partial fibrilation

Answer 30

ECG

Question 31

how does the time frame affect how you would treat someone with AF

Answer 31

• if onset within 48 hours can cardiovert electrically or pharmacologically
• if onset over 48 hours patient required anticoagulation to dissolve potential stroek

Question 32

what is a TOE

Answer 32

trans-oseophaeal ehochardiogram
- used to see if there are clots in left atrium

Question 33

what drug is used for fast AF

Answer 33

rate lowering drugs
(beta blockers and digoxin can be used too)

Question 34

what is bradycardia

Answer 34

heart rate below 60bpm

Question 35

what are some causes of bradycardia

Answer 35

• lack of stimulus
• conduction abnormality
• SA node damage
• AV node block
• bundle branch block
  fascicular block

Question 36

define AV block

Answer 36

represents delay/disturbance in transmission of impulse from atria to ventricles

Question 37

whats the difference between mobitz type 1 and 2 in an AV block (snd degree block)

Answer 37

type 1 = conduction progressively slower with each beat until impulse is completely blocked and cycle starts over

type 2 = fixed PR interval but some of the impulses are not conducted to ventricles

Question 38

what is a 1st degree AV block

Answer 38

impulses reach ventricle but conduction is slow

Question 39

what is a 3rd degree AV block

Answer 39

no atrial impulses reach the ventricles
- heart is reliant on escape rhythms which re typically slow
- no associate between P waves and QRS complexes

Question 40

what can stimulate beta 1 receptors to make heart beat faster and increase stroke volume

Answer 40

isoprenaline

Question 41

what is an emergency way to treat brachycardia

Answer 41

atropine blocks parasympathetic stimulation of SA and AV node, increasing heart rate

Question 42

when is temporary pacing favourable

Answer 42

for conditions that temporary pacing will resolve the issue
if it doesnt resolve then a permanent pacemaker is the go to
(prolonged pacemaker use can form dependency)

Question 43

what are 2 methods of temporary pacing and their negatives

Answer 43

transcutaneous (external) pacing
- can be difficult to capture and monitor
- can cause muscle stimulation

transvenous (endocardial) pacing
- bleeding
- infection
- myocardial damage
- pnemothorax
- technical difficulty

Question 44

what is hyperkalaemia

Answer 44

excess potassium in the blood

Question 45

what 3 things can cause yperkalaemia

Answer 45

• excess despotism into blood (over correction of potassium deficiency)
• reduced excretion capacity (renal failure)
• shift out of cells

Question 46

what are signs of hyperkalaemia on ECG waves

Answer 46

first: narrow, tall T-waves
later on: widening QRS and prolonged PR

Question 47

how can we manage hyperkalaemia

Answer 47

• calcium glutinate (protects myocardium by preventing ventricular fibrillation from occurring) (limited duration but buys time)
  or
• salbutamol nebuliser (can shift extracellular potassium into cells)
• insulin dextrose (can shift extracellular potassium into cells)
• treat underlying cause
• calcium resonium (mops up excess potassium in diet and ensures it isnt absorbed) and low potassium diet

Question 48

why should calcium gkutinate be given through a larger cannula

Answer 48

it can irritate tissues

Question 49

how does sodium bicarbonate help hyperkalaemia via chronic kidney disease

Answer 49

CKD causes acid to build up in blood and body exchanges protons for intracellular potassium
- this can worsen hyperkalaemia but helps keep blood pH stable and prevent potassium entering blood