Cardiovascular Physiology 2 Flashcards
What ECG leads are referred to as bipolar?
The limb leads.
These record the potential difference between 2 active electrodes.
I, II, and III - these form the borders of Einthoven’s triangle
What are the unipolar limb leads?
The augmented (because they’re lower amplitude than the standard and chest leads) limb leads.
They record the potential difference between one active limb electrode and a “composite reference” electrode formed by an average of the signals from the other limb leads.
aVL = left arm
aVR = right arm
aVF = left leg
What are the unipolar chest leads?
These are the precordial leads.
They’re in a horizontal plane across the chest and are placed at anatomically defined positions, V1-6.
They record electrical activity perpendicular to the limb leads - ie view the heart from a horizontal plane.
V1-2 = right ventricle
V3-4 = interventricular septum
V5-6 = anterolateral aspect of LV
What changes on an ECG would indicate a posterior infarct?
- ST depression in V1-4
- R > S wave in V1-2
- upright T waves in V1-2
- reflection of the trace would produce the more expected ECG changes of an infarction
What is the CM5 ECG placement?
- provides an excellent view of the left ventricle
- very sensitive at detecting left ventricular ischaemia (>80%)
- lead I is displayed
- right arm electrode (red) over manubrium
- left arm electrode (yellow) in V5 position
- left leg electrode (green) is neutral and can be placed anywhere, but often placed on clavicle
- CM5 = clavicle, manubrium and V5
What are the characteristics of AF?
- irregularly irregular rhythm
- HR is variable and depends on how many atrial impulses are transmitted from the atria to the ventricles
- no P waves
- P waves replaced by fibrillatory waves ~f waves
What is this?
Atrial flutter
- usually regular but can be irregular
- HR is variable and depends on how many atrial impulses are transmitted from atria to ventricles
- no P waves
- P waves replaced by saw tooth flutter waves
What is this?
SVT
- narrow QRS complexes
- rate approaching 200bpm
- regular
- may be due to:
- AV nodal re-entry tachycardia (AVNRT) - re-entry circuit next to or within AV node
- AVRT (AVRT) AV re-entrat tachycardia - re-entry circuit formed from AV node and an abnormal accessory pathway linking atria and ventricles (eg Wolff-Parkinson-White with accessory pathway)
What is this?
Ventricular tachycardia.
Characterized by:
- monomorphic ventricular tachycardia
- may be pulsed or pulseless
- wide morphology as ventricular tachyarrhythmia
- can deteriorate into VF
What is this?
Torsades de pointes
Characterized by:
- polymorphic VT
- twisting axis
- may be due to SEs from drugs +/- structural heart disease
What is this?
2nd degree heart block, Mobitz 2
- PR interval is constant but not all beats are conducted
- repeating pattern of conducted: non conducted impulses (eg 2:1 conduction, a P-QRS-T will then be followed but just a P wave and alternate beats are conducted)
- may also see 3:1 block etc
- this can deteriorate into complete (3rd degree) heart block
What is this?
1st degree heart block
- PR interval > 0.2 seconds (5 small squares on ECG)
- PR interval is measured from start of P wave to start of QRS complex
- represents an AV conduction delay
What is this?
Complete heart block (3rd degree)
- dissociation between atrial and ventricular conduction
- regular atrial rate (some P waves concealed in QRS complexes)
- slow ventricular rate (~40 bpm) set by ventricular pacemaker cells as escape rhythm
- dangerous rhythm - needs immediate pacing
What is this?
2nd degree heart block, Mobitz type 1
- Wenckebach
- progressive lengthening of the PR interval until a QRS complex is not conducted and a P wave is seen with no QRS this then repeats
- seen in high vagal tone in athletes or post MI
What is the effect of regurgitant lesions?
- allow backflow of blood and hence increase volume load in the heart chamber preceding the valve
- this leads to distension and ultimately chamber dilatation
What is the effect of stenotic valves?
- reduces the cross-sectional area of the valve
- causes higher resistance against flow and hence increased pressure is required to eject blood past the narrowed valve
- this ultimately leads to hypertrophy
How common is mitral regurgitation?
5 in 10,000
What are the most common causes of acute MR?
- ruptured chordae tendinae
- post MI
- trauma
What are the most common causes of chronic MR?
- mitral valve prolapse
- rheumatic fever
- connective tissue diseases
- dilated cardiomyopathy
What are the effects of chronic MR on cardiac function?
- during systole, some blood flows back into the LA and LA volume increases
- LA dimensions can increased by 4x to accommodate the regurgitant volume - may lead to development of AF
- LA end diastolic volume increases, and hence a larger volume is delivered to the LV - progressive dilatation of left heart
- if cardiac muscle dysfunction develops then SV falls, this elevates end-systolic volue and end diastolic volume - this increases LA and LV pressure
What are the clinical features of chronic MR?
- initially asymptomatic
- as systolic dysfunction develops then symptoms of fatigue, SOB on exertion, orthopnoea and reduced exercise tolerance
- palpitations (if AF occurs)
- pansystolic murmur (max at apex, radiates to axilla) and 3rd heart sound
- ECG shows P mitrale, AF and voltage criteria for LVH
- CXR shows cardiac enlargement, straightened L heart border and pulmonary oedema
What are the ways of grading severity of MR?
- functional capacity of patient (NYHA functional class)
- measurement of regurgitant fraction (flow into LA: flow into aorta) - value of >0.3 indicates mild regurg, value >0.6 = severe regurgitation
- degree of left ventricular dysfunction
How should you anaesthetise patients with MR?
To optimise CO:
- avoid bradycardia - this increases the time for regurgitation, aim for faster HR to minimize this
- minimize use of vasoconstrictors (to achieve good forward flow, a dilated peripheral circulation is required)
- avoid a large increase in preload, this can decompensate the heart
Fast and loose
What are the congenital causes of AS?
- bicuspid
- unicuspid valve
What are the acquired causes of AS?
- rheumatic heart disease
- degenerative calcification (progressive calcification of valve leaflets can extend and involve the conduction system leading to conduction defects)
- associated with hypertension
- hypercholesterolaemia
- diabetes mellitus
- smoking
What are the effects of AS on cardiac function?
- as valve area decreases, resistance to systolic ejection increases and a systolic pressure gradient develops between LV and aorta
- this outflow obstruction causes increased LV systolic pressure
- as a compensatory mechanism LV wall thickness increases by concentric hypertrophy
- this leads to decreased compliance and diastolic dysfunction
- decreased compliance reduces passive filling of LV, so atrial systole makes a significant contribution
- myocardial O2 demand is increased
- increased LV pressure reduces blood flow through the coronary arteries
- the subendocardium is particularly vulnerable to iscahemia
What are the clinical features of chronic AS?
- 10-15 yr asymptomatic period
- exercise induced symptoms are classic, because the heart can’t increase it’s CO during exertion due to the outflow obstruction
- exertional dyspnoea/fatigue most common initial complaint
- classic triad - chest pain, heart failure, syncope eventually
What findings would you expect on examination of an AS patient?
- coarse ejection systolic mumur
- max over aortic area and radiates to carotid arteries
- quiet 2nd heart sound
- narrowed pulse pressure on BP measurement
What findings would you expect on CXR of aortic stenosis?
- enlarged heart
- aortic valve calcification (usually from 65yrs unless congenital biscuspid - 30yrs)
How do you find the aortic valve on a lateral CXR?
Draw a line from the carina to the junction of the diaphram with the anterior chest wall the aortic valve will be above this, mitral valve below.
What would you expect to find on an ECG of someone with aortic stenosis?
LVH in 85% of patients with aortic stenosis.
If calcification extends into the conduction system, you might see 1st or 2nd degree heart block.
What are the features of LVH on ECG?
- if an R wave in either V5/6 exceeds 25mm or if the sum of the tallest R wave in V5/6 with the deepest S wave (in V1/2) exceeds 35mm
- left axis deviation
- T wave inversion in V5-6 with or without ST depression indicates “strain” pattern
- prolonged QRS interval
What size is a normal adult aortic valve area?
2.5 - 3.5cm2
How is aortic stenosis graded with respects to the transvalve gradients?
Mild - <25 mmHg
Moderate - 25-40 mmHg
Severe - >40 mmHg
Critical - >80 mmHg
How is aortic stenosis graded based on aortic valve area?
Mild - >1.5 cm2
Moderate - 1 - 1.5 cm2
Severe - <1 cm2
Critical - < 0.5cm2
How should you anaesthetise a patient with aortic stenosis?
Slow and tight
- avoid tachycardia - this shortens diastolic time for coronary flow
- avoid significant bradycardia- this decreases CO
- maintain SVR to preserve gradient for coronary filling
- maintain preload
- maintain SR -onset of AF will cause decompensation, will need cardioversion
- avoid vasodilation caused by anaesthetic induction agents - this can create a negative spiral
What is the normal cardiac axis?
Between -30 degrees to +90
(0° is taken as the lead I viewpoint). Anything <-30° represents left axis deviation. Anything >+90° is termed right axis deviation.
What are J waves associated with?
Hypothermia - characterized by a dome in the terminal portion of the QRS complexes
The size of J wave usually corresponds to degree of hypothermia.
Also seen in hypercalcaemia, massive head injury and SAH.
Why does the pulse pressure become wide in aortic regurgitation?
Because regurgitant flow across the aortic valve into the LV causes a reduced diastolic pressure.
Aortic stenosis is associated with a narrowed pulse pressure.
What are the degrees associated with Leads I, II and III in the axial referencing system?
Lead I = 0°
Lead II = 60°
Lead III = +120°
What is NYHA functional class IV?
Symptoms occur at rest and the patient can’t carry out any physical activity without discomfort.
Implies severe heart failure.
What is Class III NYHA heart failure?
Moderate - marked limitation of physical activity and les than ordinary activity causes fatigue, palpitations or dyspnoea
Why do 30% of patients with aortic stenosis and normal coronary arteries have angina?
Because there’s an increased myocardial O2 demand due to increased wall tension - coronary blood flow doesn’t increase in proportion to the hypertrophied muscle mass and subendocardial ischaemia despite normal coronaries.
How much pressure must a true Valsalva manoeuvre generate?
40 mmHg of intrathoracic pressure
Where does the adrenal medulla recieve sympathetic stimulation from?
Directly from a pre-ganglionic nerve fibre.
This releases ACh, which acts on nicotinic receptors to stimulate the adrenal gland to release adrenaline and noradrenaline into the blood stream.
What happens when a person goes from lying supine to standing?
- pooling of blood in dependent capacitance veins in legs due to gravity
- reduces venous return to heart
- immediate fall in SV
- because CO = HR x SV
- both CO and BP fall
What is Class I haemorrhage?
Up to 15% (750ml)
- patient may be anxious
- pulse may be slightly elevated but usually <100 bpm
- BP and pulse pressure normal
What is Class II haemorrhage?
15-30% (750-1500 ml)
- anxiety
- tachycardia
- tachypnoea
- narrowed pulse pressure
- urine OP < 0.5ml/kg/hr
What is Class III haemorrhage?
30-40% (1500-2000ml)
- tachycardia
- tachypnoea
- fall in sys BP
- CNS impairment (drowsiness/confusion)
- urine OP severely compromised
What is Class IV haemorrhage?
>40% ( > 2000ml)
- life-threatening
- urgent fluid resus required
- weak thready pulse
- significantly low sys BP
- anuria
- cold peripheries
- cap refill >5s
- reduced consciousness
What happens when the body suddenly loses 1 litre of blood?
- fall in BP and circulating volume sensed by baroreceptors in the carotid sinus and volureceptors in RA and great veins
- immediately :
- redistribution of CO to preserve flow to core areas
- muscle blood flow decreases
- renal vasoconstriction to minimize fluid loss through urine
- cerebral blood flow is prioritized due to autoregulation, baroreceptor and chemoreceptor reflexes
- catecholamines released by adrenal medulla
- increases HR, cardiac contractility
- vasoconstricts and venoconstricts
- recruitment of effective circulating volume
- venoconstriction mobilizes blood from liver, lungs and muscle beds into circulating volume
- fluid translocated from interstitium into plasma
- reduced renal perfusion pressure = increased renin secretion from JGA, results in ingreased angiotensin II (potent vasoconstrictor) and increased aldosterone (renal retention of Na)
- ADH released from pituitary due to fall in stimulation from atrial stretch receptors -triggers thirst
- also promotes renal H2O conservation in collecting ducts
- also a potent vasoconstrictor at high concentrations
What is the effect on Starling forces in haemorrhage?
Capillary hydrostatic pressure falls in haemorrhage - which generates a Starling forces gradient favouring translocation of fluid from interstitium to plasma.
Up to 0.25 ml/kg/min of fluid can be reabsorbed.
Fluid shifts from intracellular compartment to replenish the interstitium then plasma.
What are the later responses to haemorrhage?
- increased plasma protein synthesis in the liver (takes a few days to restore plasma protein levels)
- increased EPO restores red cell and Hb levels and initially there is a high reticulocyte count because immature RBCs are released into the circulation from bone marrow
What compensatory mechanisms does the body have if you infuse 1 litre of 0.9% saline into a normovolaemic adult?
- Venodilation
- carotid baroreceptors sense an increase in BP - increased firing - inhibits vasopressor centre
- peripheral venodilation decreases venous return and reduces CO - BP normalises
- Fluid redistribution
- increased capillary hydrostatic pressure causes extrusion of fluid into the interstitium
- presence of Na+ (charged) limits distribution of the IV fluids, this type of fluid is limited to ECF (made of intravascular fluid and interstitial fluid)
- ISF 75%, IVF 25%
- 1 litre of 0.9% saline = 750mls ISF and 250mls IVF
- increased BP leads to pressure diuresis and natriuresis
- volureceptors have a threshold of 8-10%, if this is exceeded then ADH is inhibited and diuresis promoted
- osmoreceptors may be stimulated, change of 1-2% is required for threshold to be exceeded, so if osmolality falls - ADH is inhibited to promote diuresis and normalisation of serum osmolality
How will 1 litre of 5% glucose be distributed in the normovolaemic adult?
The glucose is taken up by the cells and metabolized. The remainder is free water which distributes across all fluid compartments.
ICF - 66%
ECF - 33% (ISF 75% + IVF 25%)
Therefore, 660mls intracellular fluid.
340mls ECF = 255mls ISF, 85mls IVF.
This is such a small volume that the volureceptor threshold is probably not triggered to inhibit ADH, but the osmolality is probably reduced and so osmoreceptor threshold is likely exceeded.
What effects does the Valsalva manoeuvre lead to on the CVS system?
Defining feature - increased intrathoracic pressure. Can be achieved by expiration against a closed glottis.
What is Phase I of the valsalva manoeuvre?
- BP slight rise, HR steady
- squeezes intrapulmonary vessels
- returns more blood to LA
- increased preload results in increased SV
- direct transmission of intra-thoracic pressure onto aorta
What is Phase II of the valsalva manoeuvre?
- BP falls, HR rises
- impaired blood return to thorax
- reduces CO and BP
- baroreceptors sense reduced BP
- sympathetic compensation increases HR and peripheral vasoconstriction
What is Phase III of the valsalva manoeuvre?
- slight fall in BP, HR still rising
- release of strain leads to loss of squeeze on intrapulmonary vessels
- calibre of intra pulmonary vessels increases
- this temporarily reduces return of blood to heart, BP falls
- too brief an interval for HR changes
What is Phase IV of the valsalva manoevre?
- BP overshoots, HR slows
- venous return to LA normalises
- CO now delivered to highly constricted peripheral circulation
- overshoot of BP sensed by carotid baroreceptors
- reflex vagal slowing of HR
What is the valsalva ratio?
A ratio of > 1.5 indicates competent functioning of the autonomic cardiac control.
What is the effect of age on the Valsalva ratio?
Blunts the baroreceptor response so reduced Valsalva ratio.
Where are the baroreceptors located?
- carotid sinus (an enlargement of the internal carotid just above the carotid bifurcation)
- aorta
- heart
What is the afferent neuronal pathway from the carotid sinus baroreceptors to the vasomotor centre?
Via the Nerve of Nering, a branch of the glossopharyngeal nerve.
Baroreceptors from the aorta and heart project via the Vagus nerve.
What are pre-ganglionic fibres in the sympathetic NS like?
Typically short and myelinated.
They’re B fibres (in the Erlanger and Gasser classification system). Other nerve fibre types in this classification are: Aα, Aβ, Aγ, Aδ, and C fibres.
What neurotransmitter does synaptic transmission between pre- and post-ganglionic sympathetic fibres use?
Both the sympathetic and parasympathetic use ACh between pre and post ganglionic fibres which acts on nicotinic receptors.
Where do the majority of pre-ganglionic sympathetic fibres synapse?
On post ganglionic fibres in the paravertebral chain.
This means pre-ganglionic sympathetic fibres are typically short, ganglia are located far away from the target organ and the post-ganglionic fibres are long structures.
The reverse is true in the parasympathetic system where pre-ganglionic fibres are long and the ganglia are found close to or within the walls of the target organ.
What is the neurotransmitter used in the majority of blood vessels?
The majority of blood vessels receive noradrenergic stimulation from post-ganglionic sympathetic fibres.
But blood vessels in skeletal muscle have post-ganglionic sympathetic cholinergic transmission (onto muscarinic receptors) and some renal vessels have dopaminergic transmission (D1 receptors).
How does alpha blockade affect the Valsalva manoeuvre?
- alpha blockade prevents vasoconstriction during the body’s attempt to restore CO in phase II
- therefore there is an exaggerated increase in HR
- when strain is released and venous return restored, the elevated HR increases CO and overshoots the BP in phase IV
Where are volureceptors located?
The right atrium and great veins
Where are baroreceptors located?
The carotid sinus
What is the volureceptor threshold for stimulation?
8-10% (400-500mls)
