Physiology Flashcards
Why are the baroreceptors important in the baroreflex located in the arterial system?
Not much increase in volume is required to produce a larger change in pressure (less compliance in arterial vessels)
What are the main baroreceptors and where are they located?
Carotid sinus in the internal carotid artery
Aortic baroreceptors in the aortic arch
Describe the carotid sinus
Thin-walled, highly innervated bulbous structure on the internal carotid artery
What changes to the CV system are caused by sympathetic activation?
Increased HR
Decreased SA and (mostly) AV conduction time
Increased contractility
Increased TPR
Increased venous tone (to push blood over to the arteries)
What changes to the CV system are caused by parasympathetic activation?
Decreased HR
Increased SA and (mostly) AV conduction time
What aspects of the CV system does the PNS have no effect on?
TPR (small arteries and arterioles are not innervated by PNS)
How quickly do baroreceptors respond to changes in pressure?
Within 1 cycle
What happens when MAP drops below 60mmHg?
Baroreceptors do not respond to changes in MAP <50-60mmHg and the brain instead receives information about blood flow from other receptors including chemoreceptors
How long does it take for the threshold for baroreceptor firing to reset to new pressure levels?
1-2 days
How is BP maintained in the acute setting?
By the baroreflex
How is BP maintained in the long term?
Predominantly RAAS
Where are the main chemoreceptors located?
Carotid and aortic bodies
When are chemoreceptors stimulated and by what kind of stimuli?
MAP <60mmHg
Respond to low O2, high CO2, low pH
Do men or women have higher BP on average?
Men
What changes occur to BP with age?
Systolic BP rises until and after 60 years
Diastolic BP rises until 60 years then decreases
Pulse pressure therefore increases
What causes the increase in pulse pressure with age?
Decreased large artery compliance
What is the relationship between BP and body size?
Bigger body = higher BP
Describe the diurnal variation of BP
Lower at night by ~20mmHg
Less variability at night
Less sympathetic activity (mostly maintained by RAAS)
How does BP vary between the seasons?
~3mmHg lower in summer compared to winter
Describe the population paradox
More deaths in the people at moderate risk (as there are more of these) than in the people at highest risk (as this is only a small number of people)
What is the formula for relative LV wall thickness?
LV wall thickness/LV chamber size (diameter)
Distinguish between remodelling, concentric hypertrophy, and eccentric hypertrophy
Remodelling: normal LV mass with increased relative wall thickness (heart gets smaller)
Concentric hypertrophy: increased LV mass and relative wall thickness but no increase in chamber size (so wall thickens)
Eccentric hypertrophy: increased LV mass but normal relative wall thickness - increased chamber size
What usually causes concentric hypertrophy?
Pressure overload
What usually causes eccentric hypertrophy?
Volume overload
What changes occur to cardiomyocytes to produce concentric hypertrophy?
More sarcomeres in parallel
What changes occur to cardiomyocytes to produce eccentric hypertrophy?
More sarcomeres in series (myocyte stretching)
What changes to the structure of the cardiac tissue occur with hypertrophy?
Increase myocardial cell size with more mitochondria, myofibrils and SR
Increased fibroendothelial cell numbers
Increased interstitial matrix
What changes occur with decompensation in hypertrophy?
LV dilation
Increased LVEDV
Increased LVESV
Decreased EF
Decreased CO
What clinical signs are seen with LVH?
Forceful apex beat
S3
S4
What causes S3 and S4?
S3 - sound of the blood “sloshing” in the ventricles, heard with volume overload
S4 - blood being forced into a stiff/hypertrophic ventricle
What changes are seen on ECG with LVH?
Tall voltages
T wave inversion
List 3 causes of RVH, giving examples
Congenital
Pulmonary hypertension (e.g. in lung disease, PE, chronic LHF)
Right heart valves (e.g. stenosis/regurgitation)
What does hypertrophic cardiomyopathy increase the risk of?
Ventricular arrhythmias and sudden death
What changes occur in an athlete’s heart?
Eccentric hypertrophy with normal cardiac function (usually regresses)
Can cause enlargement especially of the RV (does not regress, may cause ventricular arrhythmias)
What cardiac changes occur in dehydration?
Decreased CO and BP
How is RVEDP measured?
With a catheter inserted via a vein and placed across the tricuspid valve (measures RAEDP which is equal to JVP and RVEDP)
How is LVEDP measured?
With a catheter inserted via an artery across the aortic valve (measures the LAEDP which is equal to LVEDP)
What type of catheter is used for pressure tracing?
Swan-Ganz
What is PA wedge pressure?
Catheter wedged into pulmonary artery
Measures pulmonary venous pressure (which is equal to LAP and LVEDP)
How can one catheter be used to measure all the cardiac pressures?
Place catheter across tricuspid valve, measure R cardiac pressures
Measure PA wedge pressure
Provides a measure of preload for RV and LV
Why doesn’t increased arterial pressure cause oedema?
Because the arterial pressure is “knocked off” by the arteriole before blood enters the capillaries
What are the 4 causes of oedema?
Increased hydrostatic (venous) pressure
Decreased oncotic pressure
Blocked lymphatics
Increased capillary permeability
What kind of oedema is caused by increased RVEDP? By increased LVEDP?
Increased RVEDP causes peripheral oedema
Increased LVEDP causes pulmonary oedema
Describe the process whereby cardiac failure causes pulmonary congestion
Decreased contractility (due to a reduction in sensitivity to sympathetic drive, caused by downregulation and impaired coupling of B1-adrenoceptors) causes a drop in CO
In an attempt to sustain CO, the ventricles fill more (increased LVEDP) - also due to fluid retention
This increases PVP above threshold (~20-30mmHg) and causes fluid to leak out of the pulmonary capillaries
What are the 3 main causes of cardiac failure?
Loss of myocardial muscle (e.g. IHD, cardiomyopathy)
Pressure overload (e.g. stenosis, hypertension)
Volume overload (e.g. regurgitation, shunts including septal defects)
List 4 symptoms of LHF
SOB
Fatigue
Tachycardia
Lung crepitations (pulmonary oedema)
What adaptations occur in cardiac failure?
Activation of RAAS due to decreased renal blood flow: causes fluid and Na+ retention with K+ loss, as well as vasoconstriction
SNS activation: causes increased contractility and vasoconstriction, can cause ventricular arrhythmias and have a direct toxic effect on the myocardium
What is the purpose of fluid retention in cardiac failure? What complications does it cause?
To sustain CO by increasing LVEDP
Increased LVEDP causes pulmonary congestion, and the fluid retention also causes increased RVEDP which causes peripheral oedema and liver congestion
What are the 3 main causes of RHF?
Global heart disease
Specific RH disease
LHF
List 5 specific RH diseases which can cause RHF
RV cardiomyopathy
Right-sided valves, shunts
Pericardial disease
Pulmonary hypertension (arterial; caused by cor pulmonale or PE)
How does LHF cause RHF?
LHF causes pulmonary congestion (via pulmonary venous hypertension)
Pulmonary congestion causes chronic hypoxia of the lungs
Lungs respond via release of endothelin and angiopoietin to produce pulmonary vasoconstriction
Widespread pulmonary vasoconstriction causes pulmonary arterial hypertension
Sustained PA hypertension causes RHF
What is diastolic HF?
Normal systolic function but reduced LV compliance (due to scar from infarct or chronic hypertension/hypertrophy) causes increased LVEDP and therefore PVP (causes pulmonary congestion)
Why is the pressure gradient across the valve increased in aortic stenosis?
Because the LV needs to achieve higher pressures to push open the valve and empty into the aorta (normally it just needs to equal the pressure in the aorta, so emptying occurs once the gradient reaches 0, but in severe stenosis the gradient can be as high as 50mmHg)
This means that if MAP is measured as 120/80, the pressure in the ventricle is actually 170/80
What type of valve dysfunction causes pressure overload?
Stenosis
What type of valve dysfunction causes volume overload?
Regurgitation/incompetence
What causes aortic stenosis?
Fibrosis/calcification (common in ageing)
What is the LV response to aortic stenosis?
Pressure overload causes concentric hypertrophy
Less compliant LV walls require increased atrial contraction to produce adequate LV filling
Changes reverse after surgery
What are some possible causes of aortic regurgitation? Give examples of each
Damaged leaflets (e.g. endocarditis, RHD)
Dilated leaflets (e.g. Marfan’s syndrome, aortic dissection)
What cardiac pathologies can be caused by RHD?
Aortic regurgitation
Mitral regurgitation
Mitral stenosis (most characteristic)
What is the LV response to AR?
Part of each SV leaks back into LV during diastole
To compensate, LV pumps an increased SV and EF (this requires an increased EDV)
End systolic volume is normal (the same amount of blood is left over in the heart but more is ejected, to compensate for the amount that will leak back during diastole)
Pulse pressure is increased
What causes the increased pulse pressure in AR?
“Bounding” and “collapsing” pulse, due to increased EF entering the aorta (causing an increased systolic pressure), and then reduced aortic diastolic pressure following the leaking of blood back into the LV
What findings will be present in AR on auscultation?
Decrescendo diastolic murmur (murmur replaces 2nd heart sound; due to the leaking of blood back across the valve in diastole)
What are the symptoms of AR?
Asymptomatic if mild or moderate
Severe will cause acute pulmonary oedema (due to increased LVEDP and LAP) and cardiogenic shock
What changes occur with decompensation in prolonged severe AR?
LV diastolic volume increases markedly (increased LVEDP)
LV function decreases (and therefore EF and contraction)
LV systolic volume increases (due to reduced EF)
These are IRREVERSIBLE changes
List 7 possible causes of MR
Myxomatous degeneration (causes prolapse)
Ruptured chordae tendinae (flail leaflet)
Infective endocarditis
Myocardial infarct leading to rupture of a papillary muscle
RHD
Collagen vascular disease
Cardiomyopathy
How does cardiomyopathy cause MR?
Change in ventricular shape causes change in the geometry of the valve leaflets
What cardiac changes occur with MR?
Portion of SV ejected into LA (increased LAV, LAP)
LV must pump greater SV to maintain CO, which requires a greater EDV and therefore EF
ESV is normal
What LV changes occur with decompensation in prolonged severe MR?
LV diastolic volume increases markedly (increased LVEDP)
LV function decreases (and therefore EF and contraction)
LV systolic volume increases (due to reduced EF)
These are IRREVERSIBLE changes
What LA changes occur in MR and what are some possible sequelae of these?
LAP and LAV increase (risk of AF)
AF can cause thrombus production and embolism (esp to brain or kidney)
Increased PVP causes pulmonary congestion, oedema and hypoxia
Hypoxia leads to widespread vasoconstriction, causing increase PAP (pulmonary hypertension) - this may cause RHF
Define cardiac failure
CO < body needs (usually systolic failure due to loss of contractility)
What cardiac changes occur with MS?
Pressure gradient across the mitral valve
Reduced filling of LV Increased LAP and LAV
What LA changes occur in MS and what are some possible sequelae of these?
As in MR:
LAP and LAV increase (risk of AF) AF can cause thrombus production and embolism (esp to brain or kidney)
Increased PVP causes pulmonary congestion, oedema and hypoxia
Hypoxia leads to widespread vasoconstriction, causing increase PAP (pulmonary hypertension) - this may cause RHF)
What in MS serves as a trigger for intervention?
Development of symptoms (including pulmonary hypertension)
What interventions are used to treat MS?
Valvotomy (surgical or balloon dilatation
Valve replacement
What compensatory changes occur in AS, AR, MR and MS, respectively?
AS: LV concentric hypertrophy
AR and MR: LV eccentric hypertrophy/dilation
MS: LA dilation and increased pressure
Draw and describe the SA node pacemaker potential
Phase 4: unstable membrane potential (~-60mV to +20mV), spontaneous depolarisation, Na+ and Ca2+ in
Phase 0: depolarisation, Ca2+ in
Phase 3: repolarisation, K+ out
Draw and describe the ventricular AP
Phase 0: depolarisation, Na+ in
Phase 1: rapid repolarisation, K+ out
Phase 2: plateau, Ca2+ in, K+ out
Phase 3: repolariation, K+ out
Phase 4: RMP (~-90mV)
How does the PNS cause bradycardia?
ACh acts on M2 receptors; signalling cascade decreases cAMP
Decreased cAMP leads to K+ channel opening
K+ efflux slows Na+ and Ca+ influx
Slowed phase 4 and therefore rate of conduction
How does the SNS cause tachycardia?
NA and adrenaline act on B1-adrenoceptors; signalling cascades increases cAMP
Increased cAMP leads to Ca2+ channel opening
Increased Ca2+ influx increases the slope of phase 4 depolarisation to increase rate of firing in the SA node, and speed of conduction in the AV node
Also increases contraction in myocardial cells
List 4 symptoms of dysrhythmia
SOB
Fainting
Fatigue
Chest pain
What 3 factors (other than ANS innervation) can alter cardiac rate and rhythm, and potentially cause dysrhythmias?
Ionic balance (Na+, Ca2+, K+)
Myocardial integrity (compromised by ischaemia, infarct or fibrosis)
Drugs
What are the 3 main mechanisms underlying dysrhythmias?
Altered impulse formation
Altered impulse conduction
Triggered activity (early or late after-depolarisations)
Give 2 examples of mechanisms underlying altered impulse formation
Automaticity of pacemaker cells
Abnormal generation of APs at sites other than the SA node
Give 2 examples of mechanisms underlying altered impulse conduction
Conduction block (ventricles adopt own slower rate)
Re-entry (extra beats increase rate)
Formula for CO
CO = HR x SV
Formula for MAP
MAP = CO x TPR
