Physiology of tachycardia Flashcards
WHY DO WE WORRY ABOUT TACHYCARDIA
i) what is included in AAGBI?
ii) what is the most important thing to ensure?
iii) name three red flags in awake patients
iv) name three red flags in asleep patients
v) name three things post op AF can cause? what CV event can tachycardia increase risk of intra op
i) standard anaesthiatist monitoring - ECG, HR, BP, SpO2, ETCO2
ii) vital organ perfusion and an adequate CO (CO = SV x HR)
iii) SOB, light headed, chest pain, syncope
iv) ECG change (ST change - ischaemia, rhythm change, ectopic), hypotension, change on O2 sats, change in end tidal CO2
v) post op AF is associated with increased CV events, MI, CCF, renal failure, ventricular dysrhythmias
- tachy - increased risk of intraop MI as it affects coronoary artery perfusion
CONTROL OF HEART RATE
i) what is it normally determined by? where is this found? what does this show as on ECG?
ii) which three ions determine this?
iii) how many bpm is the spontaneous firing rate of the heart if there are no neurohumoral factors affecting it? what does this decrease with?
iv) what are the two main neuro factors that affect heart rate? why is resting HR not the intrinsic 100-120bpm?
v) name three humoural factors that affect heart rate? which receptors in the SA node are stimulated?
i) determined by the SA node in the posterior wall of the RA
- sinus rhythm
ii) SA node exhibits automaticity > determined by changes in Ca, Na and K
iii) SA node spontaneously fires at 100-115bpm if unmodified by neurohumoral factors - decreases with age
iv) ANS
- sympathetic > inc HR via adrenergic receptors
- psym - predominates therefore resting HR is 60-80bpm
v) humoural - circulating catecholamines acting on B1 adrenoRs on SA node cells, thyroxine, temperature
ELECTROLYTES AND THE ECG
i) what does depolarisation of the heart muscle cause? what does repolarisation cause?
ii) why does hyperkalemia cause cardiac problems? (3)
iii) what does the P wave show?
iv) what is QRS complex?
v) what is the T wave?
vi) does ECG signal mean the heart is pumping?
i) depol > contraction
repol > relaxation
ii) lowers cell action potential > prevents repol > cardiac muscle paralysis and conduction blocks
iii) P wave = atrial depol therefore contraction
iv) QRS > ventric depol > ventric contraction
v) T wave > ventric repol > ventric relaxation
vi) no
CARDIAC CYCLE
i) how long does the whole cardiac cycle last normally?
ii) how long do systole and diastole last?
iii) how long may cardiac cycle last in tachycardia eg 180bpm? how are systole and diastole time affected? what is the consequence of this?
i) normally cardiac cycle is 0.85s
ii) systole - 0.3s, diastole 0.55s
iii) in tachy - cardiac cycle can last 0.3s
- systole and diastole both shorter but diastole reduces more than systole (so they are the same)
- coronary artery filling occ in diastole so less time for filling in tachy
BARORECEPTORS
i) what do they detect?
ii) name two places they are found
iii) what does a decrease in MABP lead to? (4) what may this lead to
i) detect arterial pressure
ii) carotid sinus and aortic arch (only responsive to an increase in arterial pressure)
iii) decrease in MABP > BR in the carotid sinus decrease firing > feed back to medulla via solitary nuc via GP nerve > inc HR to compensate > response quickly to maintain BP but this response dimishes with time
- therefore the patient may look stable and suddenly decompensate as the compensation mechanisms fail
NEGATIVE FLUID STATUS
i) name three sources of negative fluid status
ii) name three things that should be checked intra operatively
iii) what will detect a fall in BP/ blood volume? what will this cause?
iv) what is a late sign of hypovolaemia?
i) fluid loss from vomiting, lack of oral intake, blood loss
ii) check BP, feel peripheries, check blood gas (lactate and Hb), check urine output
iii) baroreceptors in carotid sinus will detect fall in BP > fire to increase HR and contractility to increase SV to compensate
iv) sustained low BP - compensation mechs will control for this for a while
PAIN AND SEPSIS
i) name two things that can represent pain in an asleep patient?
ii) what should be done if asleep patient may be in pain?
iii) how does sepsis affect vascular tone? what does the body do to compensate?
iv) do you need a high temp to confirm sepsis? name three things that may be seen
i) increasing BP and RR
ii) give analesgia > IV paracetamol > diclofenac > morphine
iii) reduction in vascular tone > vasodilation
- tachycardia is a compensation mech to aim to maintain CO
iv) dont need a high temp
- see tachy, hypotension, acidosis, high/low temp, rising lactate, low urine output
AWARENESS UNDER ANAESTHESIA
i) how may depth of anaes be assessed?
ii) name four signs of awareness?
iii) what can be given to stop patient moving?
iv) what response can intubation cause? what is released? what else may cause this?
i) entropy
ii) tachycardia, hypertension, increased RR, dilated pupils, sweating
iii) give a muscle relaxant eg rocuronium
iv) vasopressor response (widened pulse pressure, bradycardia, irregular respirations)
- big release in catecholamines
- may also be caused by short sharpe pain eg relocation of a bone - wait 15 mins to see if it resolves
DRUG INTERACTIONS
i) what reaction do most anaesthetic drugs cause? what is this similar to? name an agent that does this
ii) what always has to be considered in a tachy patient?
iii) name three signs associated with anaphylaxis? name two trigger agents
iv) what is given?
i) anaes > vasodilation (similar effect to hypovolaemia)
- propofol does this
ii) anaphylaxis > rel of histamine/vasoactive substances due to hyperactivated imm sys
iii) wheeze, hypotension, CV collapse
- trigger agents - muscle relaxants, anti biotics
iv) IM adrenaline
THYROID SUPPLEMENTS
i) which thyroid hormone will be increased?
ii) name four things that hyperthyroidism can cause
iii) what can happen if this is left untreated?
iv) what should be given to mitigate this
i) T3
ii) nervous, anx, sensitive to heat, irreg/fast HR
iii) thyroid storm > be aware and consider this as a cause of tachycardia
iv) beta blockers to aid reduction in HR plus iodine/carbimazole
ECG CHANGES
i) what does hyperkalemia this prevent?
ii) what is seen in hyperkalemia on ECG if mild? moderate? severe?
iii) where do SVTs arise from? name three treatments
iv) what underlying cardiac condition can cause SVT? what is specifically seen on ECG in this condition?
i) prevents repolarisation
ii) affects T waves initially then creates conduction blocks and a sinusoidal ECG
- mild - peak T wave and prolonged PR
- mod - loss of P wave, ST elevation, ectopic and escape rhythms
- severe - widening QRS, sin wave, VF, asystole, BBB
iii) arise from above the ventricle and is narrow complex
- treat with vagal manoevres, specific cardiac medication, may need cardioversion
iv) WPW - accessory electrical pathway > delta wave (sloped QRS)
