Cardiovascular physiology Flashcards
What is the difference between adequate blood flow and adequate blood pressure
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:
- The kidney (requires a certain perfusion pressure)
- A disease state that requires a high pressure to overcome an obstruction (carotid stenosis)
Explain the dichrotic notch in the arterial waveform
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.
Why is mean arterial pressure (87) approximately one third of the way between the diastolic (70) and systolic (120) pressures.
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
Why is the systolic RV pressure so much lower than the systolic pressure in the LV
Low pulmonary vascular resistance –> lower pressure needed to perfuse it
Cardiac muscle differs from other excitable tissues by having two specific requirements. What are these and how are these achieved
- Simultaneous contraction of all cells
- Prevention of tetany (sustained contraction)
Achieved through three factors:
- Specialized conduction system in the heart ensures contraction of all fibres.
- The myocardium is a functional syncitium
- 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
How much longer is the cardiac action potential than that of a nerve cell?
200 times longer (300ms vs 1-2ms)
What prevents tetanic contraction in the heart
Ion channel inactivation resulting in a prolonged refractory period
What is the natural firing rate of the SA node. Is this different to the resting heart rate? why?
100 - 120
resting rate is 70
Slower because of tonic PSNS activity
What makes pacemaker cells different from ordinary cardiac myocytes
- Automaticity - they fire without external stimulus
2. Rhythmicity - in a set rhythm
How is automaticity in pacemaker cells achieved?
- “Funny” currents - continuous slow leak of Na ions into the cell until the threshold potential of -40mV is reached.
- Main depolarization caused by Ca2+ influx (T-type and then L-type) rather than Na= influx
- Repolarization from K + outflow
How is the heart rate change
The slope of phase 4 is increased (Increased Na+ permeability) or decreased (increase K+ permeability). This causes a tachycardia and bradycardia respectively.
How much does the AV node slow conduction by
100ms
How does depolarization occur through the ventricles
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.
What are the advantages of delayed conduction of the AV node
- Allows time for atrial emptying
2. Protects the ventricles from atrial tachyarryhthmias
What happens when baroreceptors are stretched?
Their firing rate increases –> inhibits output from the vasomotor centre –> relative increase PSNS tone = vasodilation
What is the difference between the carotid body and the carotid sinus?
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
Where are high pressure baroreceptors found? How are these receptors stimulated and what are the effects of their stimulation?
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
Where are low pressure baroreceptors located and what is the effect of their stimulation?
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
When are both high and low pressure baroreceptors stimulated and what happens when they are not stimulated
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.
What are the major problems with massive blood transfusion
- Immune reaction
- Infection
- Dilutional coaguloathy (FFP + Plt required)
- Hypothermia
- Hyperkalaemia
- Hypocalcaemia
- Acidosis
Which cells regulate renin release in the kidney
Within the juxtaglomerular apparatus: macula densa cells sense reduced tubular Na delivery and stimulate neighbouring granular cells to release renin.
What are the effects of morphine, fentanyl and remifentanyl on the CVS
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
How long does it take for the peak effect of fentanyl (ie. during induction)
3 minutes
In which types of CVS disease is Neuraxial blockade (peripheral vasodilation) beneficial and in which is it contraindicated
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)
From which spinal segments do preganglionic efferents of the SNS arise?
T1 - L2
Which neurotransmitter is used in the SNS ganglia
Which neurotransmitter is used at the postganglionic nerve endings?
What is the exception to this?
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)
What is the sympathetic chain?
The sympathetic chain is a ganglionated nerve chain extending from the base of the skull to the coccyx
Where do all PSNS Preganglionic efferents emerge from
Cranial nerves: 3, 7, 9, 10
Spinal nerves: S2 - S4
What % of PSNS fibres are carried by the vagus nerve?
75%
What effects does the prone position have on the the CVS
- Raised intrathoracic pressure
- Reduced atrial filling
- Reduced LV compliance
Both lead to reduced stroke volume and hence reduced CO - 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
How are the adverse CVS effects of the prone position mitigated
Careful positioning of pillows under the patients chest/pelvis or a special frame to free the abdomen and allow easy movement of the abdomen.
How do the lithotomy (hips 90 knees 90) and Lloyd Davies positions (hips>90 knees>90) affect the CVS
Increased CO beginning of surgery
- Pool blood flows to the heart
Decreased CO end of surgery
- Peripheral redistribution of blood
When should Trendelenburg position be avoided
TBI and high risk of pulmonary oedema from fluid overload
When is reverse Trendelenburg used
Head and neck surgery to increase venous drainage reducing blood loss and intracranial pressure
List and describe the CVS effects of gas insufflation during laparoscopy
- Vagal response (bradycardia/asystole - Release pneumoperitoneum/Atropine/CA)
- Vascular injury (fluid/blood products until surgeon stops bleeding)
- 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
What are the CVS effects of increasing intra-abdominal pressure in laparoscopic procedures?
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
How can the consequences of raised IAP during laparoscopy be minimized
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)
What effects can absorbed CO2 during laparoscopy cause
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)
How are the affects of absorbed CO2 minimized during anaesthesia?
ETT –> control Ve
What stimulates the ‘stress response to surgery’
Cytokine (release of local inflammatory mediators)
Neuroendocrine (painful stimuli reaching the CNS)
Increase myocardial oxygen demand
What surgical stimuli are most commonly produced pronounced vagal response
Traction on extraocular muscles
Cervical dilatation
Perineal stimulation
Stretching of peritoneum during laparoscopic surgery
How can the cardiovascular effects of the sympathetic responses to surgery be minimised?
Mitigate the cytokine response –> minimally invasive surgery
Mitigate the neurohumoral response –> Regional anaesthesia
At the end of surgery the tourniquet is deflated. What effects do you think this has on the cardiovascular system?
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.
What volume of autotransfusion would occur if both legs were exsanguinated prior to torniquet inflation?
±800 ml
When does increasing BP due to torniquet pain commonly occur
When the torniquet has been on for > 90 mins
How could you minimise the cardiovascular consequences of surgical tourniquets?
Fluid bolus prior to release
Adjust minute ventilation for hypercapnoea
One leg should be exsanguinated at a time
What happens to the CVS when an aortic cross clamp is applied and released?
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.
What treatments are used to mitigate the effects of aortic cross clamping application and release
Application:
- Increase VA, epdiural, GTN, BB
Release
- Fluids, Inotropes, vasopressors
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
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)
What is the ideal way to monitor blood loss during surgery?
Suction losses
weighed swabs
Combine this with
- haemodynamic variables
- Urine Output
- Hb