Cardio & Anaes Flashcards

1
Q

Oxygen dissociation curve

A

**Go look at a diagram
Right shift vs Left shift

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2
Q

Right shift of O2 dissociation curve

A

gives off oxygen easier
- Hyperthermia
- Mild hypercarbia
- Mild acidosis
- Increase in 2,3 DPG

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3
Q

Left shift of O2 dissociation curve

A

doesn’t give off oxygen easily
- Hypothermia
- Low carbon dioxide
- Alkalosis
- Decrease in 2,3 DPG

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4
Q

Formula for CO

A

Cardiac output = stroke volume x heart rate

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5
Q

Factors influencing stroke volume

A
  1. Preload
  2. Contractility
  3. Afterload
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6
Q

Discuss preload and resultant CO

A
  • Frank-Starling’s law of the heart
  • If you increase the preload, you will increase the
    stroke volume up to a certain point & this will lead to
    an increased cardiac output (and increased BP)
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7
Q

Discuss contractility and the heart muscle

A

o If the contractility decreases, and the afterload and diastolic volume stay the same = decreased stroke volume (decreased CO)
o If preload & afterload stay the same, and
you only increase the contractility =
increased stroke volume (increased CO)

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8
Q

Discuss Afterload and the CO

A

Afterload = impedance against which the ventricle delivers SV
- The afterload that affects the stroke volume is the resistance of the peck arteries .. not the same as
peripheral vascular resistance!
- If we increase the afterload (& nothing else changes) = decreased stroke volume (decreased CO & BP)

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9
Q

Discuss the correlation between CO and the heart rate

A
  • If patients’ HR goes below 60 bpm or above 160 bpm,
    the cardiac output becomes impaired & the BP will decrease
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10
Q

Coronary blood flow:

A
  • Most of the coronary blood flow happens during diastole , this is determined by the coronary perfusion pressure
  • If patient become tachycardic ) we reduce the time that is available for coronary perfusion to take place
  • Similarly, if the aortic blood pressure drops it will negatively affect coronary perfusion
  • Thus, if we want to maintain coronary perfusion > monitor the heart rate of the patient and the BP
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11
Q

Coronary Perfusion Pressure formula

A

CPP = Aorta Pressure - L ventricular pressure

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12
Q

Electrophysiology of the heart during anaesthesia **

A
    • Increasing catecholamines = increasing the stress of the patient = cause a tachycardia by increasing the slope of hyperpolarization.
    • surgical procedures can increase the vagal stimulation = significant bradycardia by slowing down / shortening the action potentials (decreasing the hyperpolarisation)
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13
Q

Describe the correlation of Hb concentration and perfusion

A

There is an optimal Hb whereby oxygen will optimally be given off by RBCs = this is ± 10 g/dl.

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14
Q

What effect does blood viscosity have on Ox delivery?

A

an increase in blood viscosity (which happens when RBC count incr) will impair the RBC’s ability to fit through the capillaries = impaired O2 delivery

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15
Q

How does the body compensate for anaemic patients

A

body maintains oxygen delivery by increasing the cardiac output

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16
Q

Effects of spinal anaesthesia on cardiovascular system

A
  • Our elastance will decrease thus, if our preload stays the same, we will actually increase the stroke volume
  • What we actually get though, is a bit of a venous dilatation / venous pooling .. thus, our stroke volume doesn’t increase as much as it theoretically should because the preload also changes
  • Depending on how high the spinal moves, you expect some decrease in blood pressure (NB) if you do a saddle block, you don’t expect any change in BP
17
Q

Effects of ventilation on CVS

A

When we start ventilating a patient (especially if they are slightly fluid behind), we can significantly decrease the preload & thus decrease the stroke volume > intrathoracic pressure increases with ventilation and blood flow into thorax may be reduced

18
Q

Effects of IAA and IV and Opiate and BNZ on CVS

A

Some of the inhalational agents, IV agents, opiates, and benzodiazepines we use can decrease contractility

19
Q

Effects of IAA and IV and Opiate and BNZ and ventilation on CVS

A

We now combine agents that decrease the contractility with ventilation which decreases the preload. Resultantly, you have a significant decrease in stroke volume and cardiac output (and BP).

20
Q

Effects of ketamine on CVS

A

Unlike the other IV anaesthetic agents
Ketamine increases the sympathetic outflow > incr BP (because there is an incr SVR and an incr SV). Unfortunately, ketamine directly decreases the contractility of the heart. This is however completely overshadowed by the sympathetic effects

21
Q

Effects of propofol on CVS

A

Propofol reduces sympathetic outflow > decr BP (because there is a decr SVR and a normal / decr HR). Furthermore, it also slightly decreases the contractility of the heart. If there is a decrease in contractility, there will be a decrease in stroke volume. In our bodies, we expect a compensatory increase in heart rate, but in this case it doesn’t occur.

22
Q

Effects of thiopentone on CVS

A

dose-dependent hypotension
Thiopentone decreases sympathetic outflow > decr BP (because there is a decr SVR and a decr contractility). There is however an increase in HR to compensate for the decreased stroke volume caused by the decreased contractility.

23
Q

Effects of etomidate on CVS

A

Etomidate is the most cardiovascularly stable IV agent, however not in all cases

Etomidate reduces the sympathetic outflow > decr BP (because there is a decr SVR). No other effects noted. If you have a patient in theatre who is hypovolaemic, their body will compensate by increasing the HR (sympathetic effect). Thus, if you now give that same patient Etomidate, they will become cardiovascularly unstable

24
Q

Effects of IAA on CVS

A

They all vasopress everything. Halothane’s main effect is on the contractility, however all of them can affect the contractility in a dose-dependent way. Isoflurane, sevoflurane, and enflurane mainly have an effect on the SVR but may also affect contractility. All these agents will give you a dose-dependent drop in BP.

25
Effects of suxamethonium and other muscle relaxants on CVS
Suxamethonium has the potential to decrease HR (stimulates parasympathetic pathway). Pancuronium decreases parasympathetic pathway and results in incr BP by incr the HR > avoid in IHD! Neostigmine can cause a severe bradycardia because it stops acetylcholinesterase which will increase acetylcholine in all NMJs and thus cause parasympathetic stimulation. This paragraph is very NB! ***
26
Effects of alpha 2 agonists on CVS
Clonidine & Dexmedetomidine decrease the BP by decreasing the SV and the HR. However, this only occurs when given via rapid IV administration. Thus, give IV slowly over 10 minutes in paediatric patients
27
Effects of other drugs on CVS
Anticholinergics will decrease parasympathetic pathway and incr HR. Adrenaline will incr BP by incr HR, SVR, and [ ]. Dobutamine has beta-1 and beta-2 stimulation > beta-2 stimulation causes peripheral vasodilatation. Thus, if your patient has enough fluids / bloods, their BP can incr, but if they are hypovolaemic, their BP may decr. Phenylephrine is an alpha-receptor agonist > causes vasoconstriction & incr peripheral resistance. It is the main drug that is currently used for that expected hypotension as a big part of hypotension during spinals & GA, is that there is a decrease in SVR. A consequence is that BP incr, SVR incr, your baroreceptors become activated, and this leads to a reflex bradycardia.