Cardiovascular physiology Flashcards

1
Q

What is the difference between adequate blood flow and adequate blood pressure

A

Flow and pressure are different entities closely related by the Hagan-Poiseuille equation. It should be considered that all tissues require adequate blood flow for adequate nutrient delivery and waste removal. However, in some situations pressure at which the blood is delivered is also critical:

  1. The kidney (requires a certain perfusion pressure)
  2. A disease state that requires a high pressure to overcome an obstruction (carotid stenosis)
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2
Q

Explain the dichrotic notch in the arterial waveform

A

The interruption in the decline in arterial pressure waveform is called the dichrotic notch and is thought to be caused by elastic recoil of the aortic wall immediately after aortic valve closure.

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3
Q

Why is mean arterial pressure (87) approximately one third of the way between the diastolic (70) and systolic (120) pressures.

A

At rest the cardiac cycle spends about 2 thirds of the time in diastole and one third of the time in systole

MAP = 1/3 SBP + 2/3 DBP

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4
Q

Why is the systolic RV pressure so much lower than the systolic pressure in the LV

A

Low pulmonary vascular resistance –> lower pressure needed to perfuse it

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5
Q

Cardiac muscle differs from other excitable tissues by having two specific requirements. What are these and how are these achieved

A
  1. Simultaneous contraction of all cells
  2. Prevention of tetany (sustained contraction)

Achieved through three factors:

  1. Specialized conduction system in the heart ensures contraction of all fibres.
  2. The myocardium is a functional syncitium
  3. Cardiac action potential is prolonged via slow Ca2+ inflow through L-type channels, thus ensuring total ventricular depolarization.

Ion channel inactivation results in a prolonged refractory period, thus preventing repeated tetanic contraction

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6
Q

How much longer is the cardiac action potential than that of a nerve cell?

A

200 times longer (300ms vs 1-2ms)

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7
Q

What prevents tetanic contraction in the heart

A

Ion channel inactivation resulting in a prolonged refractory period

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8
Q

What is the natural firing rate of the SA node. Is this different to the resting heart rate? why?

A

100 - 120

resting rate is 70

Slower because of tonic PSNS activity

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9
Q

What makes pacemaker cells different from ordinary cardiac myocytes

A
  1. Automaticity - they fire without external stimulus

2. Rhythmicity - in a set rhythm

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10
Q

How is automaticity in pacemaker cells achieved?

A
  1. “Funny” currents - continuous slow leak of Na ions into the cell until the threshold potential of -40mV is reached.
  2. Main depolarization caused by Ca2+ influx (T-type and then L-type) rather than Na= influx
  3. Repolarization from K + outflow
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11
Q

How is the heart rate change

A

The slope of phase 4 is increased (Increased Na+ permeability) or decreased (increase K+ permeability). This causes a tachycardia and bradycardia respectively.

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12
Q

How much does the AV node slow conduction by

A

100ms

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13
Q

How does depolarization occur through the ventricles

A

The AP descends therough the AV node into the bundle of His where it then divides into the left and right bundles and finally into the purkinje fibers which branch into the ventricles. the ventricles depolarize from inside to out.

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14
Q

What are the advantages of delayed conduction of the AV node

A
  1. Allows time for atrial emptying

2. Protects the ventricles from atrial tachyarryhthmias

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15
Q

What happens when baroreceptors are stretched?

A

Their firing rate increases –> inhibits output from the vasomotor centre –> relative increase PSNS tone = vasodilation

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16
Q

What is the difference between the carotid body and the carotid sinus?

A

Carotid body is a chemoreceptor situated at the bifurcation of the common carotid artery sensitive to O2, CO2 and H+

Carotid sinus is the initial dilatation of the internal carotid that contains baroreceptors sensitive to stretch

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17
Q

Where are high pressure baroreceptors found? How are these receptors stimulated and what are the effects of their stimulation?

A

In the carotid sinus. They are stretch receptors. Distension –> inhibition of SNS stimulation to the heart and circulation and increase in PSNS stimulation to the heart.

Bradycardia
Peripheral vasodilation

Reduced SNS also reduces release of adrenalin and noradrenalin from the adrenal medulla into the circulation

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18
Q

Where are low pressure baroreceptors located and what is the effect of their stimulation?

A

Location: Right atrium.

Small increases in atrial pressure distend the low pressure baroreceptors which lead to the release of atrial natriuretic peptide –> increase sodium and water excretion by the kidneys
ANP
1. Natriuresis
–> Increase GFR: Afferent VD and efferent VC
–> reduced tubular Na reabsorption
2. Inhibits renin release from kidney
3. Inhibits aldosterone release from adrenal cortex

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19
Q

When are both high and low pressure baroreceptors stimulated and what happens when they are not stimulated

A

Increase in pressure, distension and stretch –> bringing about their effects. The response to hypovolaemia and hypotension is therefore brought about by the fall in activity of these systems and abolition of the responses that they generate.

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20
Q

What are the major problems with massive blood transfusion

A
  1. Immune reaction
  2. Infection
  3. Dilutional coaguloathy (FFP + Plt required)
  4. Hypothermia
  5. Hyperkalaemia
  6. Hypocalcaemia
  7. Acidosis
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21
Q

Which cells regulate renin release in the kidney

A

Within the juxtaglomerular apparatus: macula densa cells sense reduced tubular Na delivery and stimulate neighbouring granular cells to release renin.

22
Q

What are the effects of morphine, fentanyl and remifentanyl on the CVS

A

Morphine –> H release –> decr. SVR –> hypotension

Fentanyl –> More CVS stable –> may cause vagal bradycardia

Remifentanyl –> 20% decrease in HR and BP with some decrease in myocardial contractility

23
Q

How long does it take for the peak effect of fentanyl (ie. during induction)

A

3 minutes

24
Q

In which types of CVS disease is Neuraxial blockade (peripheral vasodilation) beneficial and in which is it contraindicated

A

Reduced SVR is beneficial in CCF, HPT, IHD –> Afterload reduction.

Peripheral vasodilation may also impair preload which would be contraindicated in patients with fixed or low CO state (AS)

25
Q

From which spinal segments do preganglionic efferents of the SNS arise?

A

T1 - L2

26
Q

Which neurotransmitter is used in the SNS ganglia
Which neurotransmitter is used at the postganglionic nerve endings?
What is the exception to this?

A

Acetylcholine in the ganglia (released by pre-ganglionic efferents) and in the adrenal medulla

Noradrenalin is released by postganglionic nerve endings with exception of the eccrine sweat glands (acetylcholine) versus apocrine sweat glands (noradrenalin)

27
Q

What is the sympathetic chain?

A

The sympathetic chain is a ganglionated nerve chain extending from the base of the skull to the coccyx

28
Q

Where do all PSNS Preganglionic efferents emerge from

A

Cranial nerves: 3, 7, 9, 10

Spinal nerves: S2 - S4

29
Q

What % of PSNS fibres are carried by the vagus nerve?

A

75%

30
Q

What effects does the prone position have on the the CVS

A
  1. Raised intrathoracic pressure
    - Reduced atrial filling
    - Reduced LV compliance
    Both lead to reduced stroke volume and hence reduced CO
  2. Obstruction of IVC
    - Poor prone positioning leads to abdominal compression - obstructing the inferior vena cava.

a) Decreased VR to heart –> decreased CO
b) Distension of the paravertebral venous plexus of Batson –> increase blood loss and obscure surgical field

31
Q

How are the adverse CVS effects of the prone position mitigated

A

Careful positioning of pillows under the patients chest/pelvis or a special frame to free the abdomen and allow easy movement of the abdomen.

32
Q

How do the lithotomy (hips 90 knees 90) and Lloyd Davies positions (hips>90 knees>90) affect the CVS

A

Increased CO beginning of surgery
- Pool blood flows to the heart

Decreased CO end of surgery
- Peripheral redistribution of blood

33
Q

When should Trendelenburg position be avoided

A

TBI and high risk of pulmonary oedema from fluid overload

34
Q

When is reverse Trendelenburg used

A

Head and neck surgery to increase venous drainage reducing blood loss and intracranial pressure

35
Q

List and describe the CVS effects of gas insufflation during laparoscopy

A
  1. Vagal response (bradycardia/asystole - Release pneumoperitoneum/Atropine/CA)
  2. Vascular injury (fluid/blood products until surgeon stops bleeding)
  3. Venous gas embolism: rare CO2 soluble so less severe versus air embolism
    - Release pneumoperitoneum
    - Resuscitate/Supportive
    - Senior help
    - Left lateral position for aspiration via CVP
36
Q

What are the CVS effects of increasing intra-abdominal pressure in laparoscopic procedures?

A

IAP < 10 mmHg
- Increase VR and SV due to transient autotransfusion from pooled blood in the splanchnic circulation

IAP 10 - 20 mmHg

  • IVC obstruction occurs reducing VR and SV –> SNS activation to increase SVR which is often greater than increase the reduction of CO and hence hypertension results
  • Tachycardia, hypertension, increase SVR (afterload) markedly increases myocardial workload and may result in cardiac ischaemia

IAP > 20 mmHg
- Reduced VR overwhelms SNS compensation –> hypotension

37
Q

How can the consequences of raised IAP during laparoscopy be minimized

A

Automatic limit on IAP on insufflation equipment of 15 mmHg
Avoid intraoperative hypovolaemia

Mediate SNS compensation with short acting opioids and volatile anaesthetic concentration

(very occasionally beta blockade may be required)

38
Q

What effects can absorbed CO2 during laparoscopy cause

A

Hypercapnoea

  • -> Dysrhythmia (SNS from vasomotor centre)
  • -> Hypoxia [AGE = FiO2(PB-PH20) - PCO2/RQ]
  • -> Hypertension (Peripheral chemoreceptor - respiratory center adjacent and connected to vasomotor center)
  • -> Peripheral vasodilation (vascular smooth muscle relaxation)
39
Q

How are the affects of absorbed CO2 minimized during anaesthesia?

A

ETT –> control Ve

40
Q

What stimulates the ‘stress response to surgery’

A

Cytokine (release of local inflammatory mediators)
Neuroendocrine (painful stimuli reaching the CNS)

Increase myocardial oxygen demand

41
Q

What surgical stimuli are most commonly produced pronounced vagal response

A

Traction on extraocular muscles
Cervical dilatation
Perineal stimulation
Stretching of peritoneum during laparoscopic surgery

42
Q

How can the cardiovascular effects of the sympathetic responses to surgery be minimised?

A

Mitigate the cytokine response –> minimally invasive surgery

Mitigate the neurohumoral response –> Regional anaesthesia

43
Q

At the end of surgery the tourniquet is deflated. What effects do you think this has on the cardiovascular system?

A

When the tourniquet is released there is a return of acidotic, hypercapnic, hypoxic blood into the circulation. This can produce a transient hypotension and tachycardia.

44
Q

What volume of autotransfusion would occur if both legs were exsanguinated prior to torniquet inflation?

A

±800 ml

45
Q

When does increasing BP due to torniquet pain commonly occur

A

When the torniquet has been on for > 90 mins

46
Q

How could you minimise the cardiovascular consequences of surgical tourniquets?

A

Fluid bolus prior to release

Adjust minute ventilation for hypercapnoea

One leg should be exsanguinated at a time

47
Q

What happens to the CVS when an aortic cross clamp is applied and released?

A

APPLIED (hypertension)
- Sudden increase BP due to increase SVR

RELEASE (hypotension)
When the cross clamp is released, cardiovascular instability may ensue secondary to the return of cold, acidotic, hypercapnic blood to the heart which may cause myocardial stunning leading to decreased contractility.

The sudden reduction in systemic vascular resistance causes hypotension.

48
Q

What treatments are used to mitigate the effects of aortic cross clamping application and release

A

Application:
- Increase VA, epdiural, GTN, BB

Release
- Fluids, Inotropes, vasopressors

49
Q

How much maintenance fluids are required to compensate for the third space losses, evaporative losses during open intra-abdominal surgery and compare this to normal

A

Normal maintenance
1st 10 kg - 4 ml/kg/hr (40 ml/hr max)
2nd 10 kg - 2 ml/kg/hr (20 ml/hr max)
Thereafter - 1 ml/kg/hr (60 ml/hr + additional weight after 20 kg)

70 kg man –> 110 ml/hour maintenance fluid

Maintenance fluid during intra-abdominal surgery
10 ml/kg/hour

70 kg man –> 700 ml/hour maintenance fluid due to increase evaporative losses and sequestration (omentum and bowel wall)

50
Q

What is the ideal way to monitor blood loss during surgery?

A

Suction losses
weighed swabs

Combine this with

  1. haemodynamic variables
  2. Urine Output
  3. Hb