eLFH - Cardiovascular Physiology Part 2 Flashcards
12 Lead ECG electrode placement
ECG lead categorisation
Limb leads (Bipolar)
Augmented limb leads (Unipolar)
Chest leads (unipolar)
Limb leads
Read potential difference between 2 active electrodes
Form borders of Einthoven’s triangle
Augmented limb leads
Record potential difference between one active limb electrode and a composite reference electrode formed by the average of signals from the other limb leads
Readings have lower amplitude so are augmented
Chest leads
Aka precordial leads
Record electrical activity perpendicular to limb leads in ‘horizontal plane’
Standard ECG recording speed
25 mm/s
Standard ECG calibration
1 mV/cm
Normal cardiac axis
- 30 degrees to + 90 degrees
Time represented by one small ECG square
0.04 s
ECG changes associated with Posterior STEMI
ST depression V1-4
Upright T waves in V1-2
R>S wave in V1-2
ECG electrode position to pick up posterior STEMI
V7-9 continue posteriorly along same horizontal plane from V6
CM5 electrode position
Red over Manubrium
Yellow in V5 position
Green is neutral and can go anywhere, but often placed on left clavicle
Hence name CM5:
Clavicle
Manubrium
V5
CM5 use
Good view of left ventricle and very sensitive at detecting left ventricular ischaemia (>80%)
Most common Atrial flutter ventricular rate
150 bpm
2:1 conduction ratio most common with atrial rate of 300
Ways in which valvular lesions result in increased work for the heart
Volume
Pressure
Volume changes leading to increased work for the heart in valvular lesions
Regurgitant lesions allow backflow
Increase volume load in the heart chamber preceding the valve
Leads to distension and dilatation
Pressure changes leading to increased work for the heart in valvular lesions
Stenotic pathology reduces cross sectional area of valve
Therefore higher resistance against flow and pressure load
Chamber preceding the valve develops higher pressure to eject blood past the narrowed valve
Leads to hypertrophy
Two most common valvular pathologies
Aortic stenosis
Mitral regurgitation
Most common causes of acute mitral regurgitation
Ruptured chordae tendinae
Post MI
Trauma
Most common causes of chronic mitral regurgitation
Mitral valve prolapse
Rheumatic fever
Connective tissue diseases
Dilated cardiomyopathy
Effects of chronic mitral regurgitation on cardiac function
LA volume increases due to backflow during systole
Can lead to AF
Progressive dilatation of left heart as LAEDV increases so greater volume delivered to LV
If muscle fails and stroke volume falls, LA and LV pressure increases as LVESV and LVEDV increase
Clinical features of chronic MR
Initially asymptomatic
As left heart failure develops then get symptoms of SOB, orthopnoea, etc
Palpitations if AF develops
Cardiac auscultation with MR
Pansystolic murmur
Maximal at apex
Radiation to axilla
3rd heart sound
ECG changes with MR
P mitrale due to LA enlargement
AF
LVF
CXR findings with MR
Cardiac enlargement
Straightening of left heart border
Pulmonary oedema
Grading of MR severity
Functional capacity of pt - NYHA functional class III or IV
Measurement of regurgitant fraction
Degree of LV dysfunction
Measurement of regurgitant fraction in MR
Measures flow into left atrium : Flow into aorta
Value > 0.3 indicates mild MR
Value > 0.6 is severe MR
Anaesthetic management changes for patient with MR for optimal cardiac output
Avoid bradycardia - bradycardia increases time for regurgitation
Minimise vasoconstrictor use - dilated peripheral system needed for good forward flow
Avoid large preload increase - can decompensate the heart
Aide memoir of anaesthetic management changes in MR
‘Fast and Loose’
Higher HR, Avoid vasoconstrictors
Categories of Aortic Stenosis
Congenital
Acquired
Most common causes of congenital Aortic stenosis
Bicuspid or Unicuspid valve
Most common causes of acquired aortic stenosis
Rheumatic heart diseases
Degenerative calcification
Risk factors for degenerative calcification of aortic valve
HTN
High cholesterol
Diabetes
Smoking
Effects of Aortic Stenosis on cardiac function
Valve area decreases
Outflow obstruction leads to increased LV systolic pressure
Compensatory concentric LV hypertrophy - initially preserves function but leads to decreased compliance and diastolic dysfunction
Reduced passive filling due to reduced compliance - increased LA systole contribution
Increased myocardial O2 demand
Increased LV pressure reduces coronary blood flow due to transmitted LV diastolic pressure acting as a Starling resistor
Area particularly vulnerable to ischaemia with AS causing reduced coronary blood flow
Subendocardium
Clinical features of chronic AS
Develops gradually - often 10-15 year asymptomatic period
Triad of:
-Exertional SOB
- Chest pain
- Syncope
Why are exertional symptoms classical for AS
Heart is unable to adequately increase cardiac output during exercise due to outflow tract obstruction
Auscultation of AS
Coarse ejection systolic murmur
Maximal over aortic area
Radiation to carotids
Quiet 2nd heart sound
Clinical examination finding with AS
Narrow pulse pressure
CXR findings for AS
Cardiac enlargement
Aortic valve calcification
ECG findings for AS
LVH
Can develop 1st or 2nd degree HB if calcification extends to conducting system
ECG findings with LVH
Voltage criteria
Left axis deviation
T wave inversion in V5 or V6 +/- ST depression (this indicates a ‘strain’ pattern)
Can also get widened QRS
Voltage criteria for LVH on ECG
R wave in either V5 or V6 exceeds 25 mm
OR
Sum of tallest R wave in V5 or V6 and deepest S wave in V1 or V2 exceeds 35 mm
Grading of AS severity
Functional capacity
Echo assessment - mean gradient and aortic valve area
Mean gradient and Aortic valve area grading of AS severity
Aortic valve area in healthy adult
2.5 - 3.5 cm^2
Anaesthetic management changes for patient with AS for optimal cardiac output
Avoid tachycardia as it shortens diastolic time for coronary flow
Maintain SVR - preserves gradient for coronary filling
Maintain preload
Maintain sinus rhythm - onset of AF will decompensate
Avoid vasodilation with induction drugs as can create negative spiral
Negative spiral that can be seen in AS patients if vasodilation not avoided with induction of anaesthesia
Reduced SVR
Reduced aortic diastolic pressure
Reduced coronary perfusion
Myocardial ischaemia
Further reduction in cardiac output
Cardiogenic shock
Aide memoir of anaesthetic management changes in AS
‘Slow and tight’
Effect on BP of moving from supine to standing
Initial increased pooling of blood to legs
Reduces Preload / venous return to heart
Immediate drop in stroke volume by Frank-Starling mechanism
Cardiac output and BP therefore fall
Mechanisms to restore cardiac output to compensate for drop in BP from standing from supine
1) Baroreceptors
2) Afferent pathways
3) Vasomotor centres
4) Sympathetic tone
5) Efferent pathway
6) Effect of sympathetic stimulation
Baroreceptor pathway
Stretch receptors which increase or decrease firing rate according to stretch detected
Negative feedback mechanism to vasomotor centre
I.e. High firing rate, inhibits vasomotor centre vs Low firing rate, less inhibition of vasomotor centre
Baroreceptor location
Walls of carotid sinus, aorta and heart
Carotid sinus baroreceptors most sensitive to BP alterations
Afferent pathway
From carotid sinus baroreceptors to the CNS
Via Hering branch of Glossopharyngeal nerve (CN IX)
Aortic and cardiac baroreceptors relay signals to CNS via vagus nerve
Sensory nucleus for CN IX and CN X that connects baroreceptor afferent pathways to vasomotor centres
Nucleus tractus solitarius
Vasomotor centre pathway
Pressor centre:
Tonic output to maintain background vascular smooth muscle tone
Depressor centre:
Inhibits the pressor centre and directly inhibits sympathetic outflow at spinal level
Pressor centre of vasomotor centre location
Ventrolateral medulla
Depressor centre of vasomotor centre location
Caudal and medial to pressor centre in medulla
Sympathetic tone pathway
Set by balance of pressor centre and depressor centre signals
Also affected by central and peripheral chemoreceptors triggered by changes to PaCO2 and pH
Location of central chemoreceptors
Medulla
Location of peripheral chemoreceptors
Carotid and aortic bodies
Have more effect on respiratory centre but some effect on BP
Cushing reflex
Hypertension
Bradycardia
Irregular breathing
Triggered by massive sympathetic outflow in aim of maintaining cerebral perfusion pressure
Efferent pathway
Sympathetic outflow is via pre-ganglionic nerves
Majority of these nerves synapse in paravertebral chain with long post-ganglionic nerves
Efferent pathways go to heart and blood vessels
Pre-ganglionic nerve fibres also stimulate adrenal medulla using cholinergic transmission
Features of pre-ganglionic sympathetic nerves
Short
Myelinated
ACh neurotransmitter
Features of post-ganglionic sympathetic nerves
Long
Unmyelinated
Noradrenaline neurotransmitter
Effect of sympathetic stimulation
Peripheral vasoconstriction - increases SVR
Peripheral venoconstriction - increases venous return to heart
Increased heart rate - accelerates pre-potential decay in cardiac pacemaker cells
Increased cardiac contractility - increased Ca2+ release from sarcoplasmic reticulum in cardiac myocyte
All the above ultimately increase cardiac output
Classification of haemorrhage
Class I
Class II
Class III
Class IV
Class I haemorrhage blood loss
< 15%
750 ml
Class I haemorrhage signs
Minimal signs of shock
HR slightly raised possibly
BP stable
Class II haemorrhage blood loss
15 - 30%
750 - 1500 ml
Class II haemorrhage signs
Tachycardia
Tachypnoea
Narrow pulse pressure
UO < 0.5 ml/kg/hour
Class III haemorrhage blood loss
30 - 40%
1500 - 2000 ml
Class III haemorrhage signs
Marked tachycardia
Fall in BP
CNS impairment
UO severely compromised
Class IV haemorrhage blood loss
> 40%
2000 ml
Class IV haemorrhage signs
Life threatening
Weak thready pulse
Significant hypotension
Anuria
Mottled with CRT > 5s
Compensatory mechanisms to sudden loss of circulating volume
(detected by baroreceptors and volureceptors in RA and great veins)
Immediate responses:
- Redistribution of CO
- Catecholamine release
- Recruitment of effective circulating volume
Later responses
Redistribution of cardiac output following sudden loss in circulating volume
Maintains blood flow to key organs
Muscle blood flow decreases
Renal vasoconstriction reduces CO to kidneys (usually 25%) - also reduces fluid lost in urine
Cerebral blood flow preferentially maintained
Catecholamine release following sudden loss in circulating volume
Sympathetic outflow increases and adrenal medulla releases catecholamines into circulation
Increases:
- HR
- Cardiac contractility
- Vasoconstriction
- Venoconstriction
Recruitment of effective circulating volume following sudden loss in circulating volume
Venoconstriction mobilises blood from liver, muscle and lung reservoirs
Fluids translocated from interstitium to plasma
Renin secretion due to reduced renal perfusion - RAAS activated
ADH released from pituitary following fall in atrial stretch receptor stimulation
Mechanism by which fluid translocates from interstitium to plasma in response to haemorrhage
Haemorrhage leads to drop in hydrostatic pressure in capillaries
Generates Starling forces gradient favouring translocation of fluid from interstitium into intravascular space
Ultimately fluid will shift from intracellular space to replenish interstitium and then into plasma again
Volume of fluid that can be re-absorbed from interstitium into plasma following haemorrhage
0.25 ml/kg/min
Later response mechanisms to compensate for fall in circulating volume following haemorrhage
Increased plasma protein synthesis - takes few days
Increased erythropoietin production - initially results in high reticulocyte count before Hb and RBCs restored
Compensatory mechanisms following rapid IV crystalloid infusion in euvolemic patient
Venodilation
Fluid redistribution - increased hydrostatic pressure so fluid moves to interstitium via Starling forces mechanism
Diuresis - inhibition of ADH release
Valsalva manoeuvre definition
Forced expiration against a closed glottis
Intrathoracic pressure change with Valsalva manoeuvre
Rise in intrathoracic pressure by 40 mmHg
Graph with phases of autonomic changes in BP and HR during Valsalva manoeuvre
Phase 1 - onset of strain
Phase 2 - continued strain
Phase 3 - release of strain
Phase 4 - strain still off
Phase 1 of Valsalva - Onset of strain
Squeeze on intra-pulmonary vessels
Return of more blood to left atrium
Increased preload results in increased stroke volume
Direct transmission of intra-thoracic pressure onto aorta
Phase 2 of Valsalva - Continued strain
Impaired return of blood to thorax
Reduced CO and BP
Baroreceptors sense reduced BP
Sympathetic compensation increases HR and peripheral vasoconstriction
Phase 3 of Valsalva - Release of strain
Loss of squeeze on intra-pulmonary vessels
Calibre of intra-pulmonary vessels increases
Temporarily reduces return of blood to heart - BP falls
Too brief an interval for any HR changes
Phase 4 of Valsalva - Strain still off
Venous return to LA normalises
CO now delivered to vasoconstricted peripheral circulation
Overshoot of BP sensed by carotid sinus baroreceptors
Reflex vagal slowing of HR
Clinical uses of Valsalva manoeuvre
Assess autonomic function
Cardiovert SVT
Valsalva ratio calculation
Use of Valsalva ratio
Ratio > 1.5 indicates competent functioning of autonomic cardiac control
Effect of age on Valsalva ratio
Ageing blunts baroreceptor response
Therefore reduced Valsalva ratio
