cardiac function long Flashcards
cardiac cycle - phase 1
- atrial systole
o p wave is depol of atria which contracts
o atrial pressure increases
• blood through AV valve to ventricle
• 10% of filling
• most filling is passive on venous return before atrial contraction
• 40% in exercise as diastolic filling is shorter
• more in sympathetic nerve activation –atrial kick
• loose atrial kick in af
• increased pressure pump vein and vena cava so get a wave of jvp
• may hear 4th heart sound of ventricle wall vibration from atrial contraction if ventricle stiff from LVH
o backflow stoped by atrial contraction, ‘milking’ effect and inertial effect of venous return
o atrial pressure falls, x descent of jvp
o at end
• max ventricular volume (end diastolic volume EDV)
• LVEDV 120ml, pressure 8-12mmHg
• RVEDP 3-6mmHg
• mitral valve closes as ventricular pressure exceeds atrial at start of ventricular depol and contraction, first heart sound (split as mitral before tricuspid)
cardiac cycle phase 2
- isovolumetric contraction – both valves closed
o anacrotic notch of aortic waveform due to wave against closed valve in contraction
o QRS of ventricular depolarization, myocyte contraction
o Ventricular pressure increases at max slope, volume unchanged
o C wave of jvp from back bulge of tricuspid valve
• meant to be reduced by contraction of papillary muscles attached to cordea tendin attached to valve
o increased pressure in atrium due to backbulge and continuous venous return
cardiac cycle phase 3
- rapid ejection – could be paired with 4, aortic and pulmonic valves open
o ST segment – ventricle depoled and contracting, intraventricular pressure/energy exceeds aorta and pulmonary artery pressure/energy, valves open because of energy gradient
o total energy of blood is pressure energy plus kinetic energy(square of velocity of blood flow)
o ventricular pressure just exceeds outflow tract pressure, this is enough for flow as valve is large with low resistance
o get max vent and aortic/pulmonary artery pressure at end of this
o ventricular pressure decreases and atria fills but pressure drops (ongoing x descent) initially as base of atria pulled down
cardiac cycle phase 4
reduced ejection – could be paired with 3 – aortic and pulmonic vavles still open
o t wave of ventricular repolarization and relaxation – diastole begins
o vent pressure falls below outflow tract pressure but outward flow still happens due to kinetic/intertial flow
o atrial pressure rising – JVP wave starts going up
o ventricular volume reaches lowest
cardiac cycle phase 5
- isovolumetric relaxation
- when energy of blood in ventricles less than energy in outflow tracts, pressure gradient reversal means aortic/pulmonic valves close, 2nd heart sound (audibly split), causes incisura in outflow tract pressure trace
o decline in aortic/pulmonic pressure not abrupt as potential energy in elastic walls and due to vascular resistance
o ventricular volume constant- end systolic volume ESV (50ml)
o EDV-ESV = stroke volume, 60% (70ml)
o Stroke volume/EDV = ejection fraction, >55%
o Atrial pressure rising, get v wave of jvp
cardiac cycle phase 6
- rapid filling – av valve opens – may be coupled with 7
o vent pressure < atrial pressure, av valve opens, vents fill rapidly but relax a bit more so pressure drops before rising and causes diastolic suction which aids filling
o atrial pressure also drops, get y descent of jvp
o S3 normal in kids but pathologic in adults as its from ventricular filling from tense chordae tendineae in ventricular dilation
cardiac cycle phase 7
- reduced filling
o reduced filling as nears completion of diastole, vent pressure rises
o atrial pressure rising as filled from venous
o aortic and pulmonic pressures continue to fall
left atrial pressure wave
o a wave – atrial contraction (phase 1)
o C phase – bulge of mitral in vent systole (phase 2)
o x descent – open aortic valve
o v wave – increasedLA pressure from venous return with AV closed
o y descent – open mitral valve, LV filling
factors that affect LAP - increase
o increase venous return/atrial filling
• blood volume increase (overload in CCF)
• posture – increased if supine
• venous tone increase
• decreased intrathoracic pressure (inspiration). Expiration/PPV/PEEP all increase intrathoracic pressure and decrease venous return
• decreased intrapericardial pressure
• muscle pump
o decreased atrial emptying/left ventricular filling
• decreased AV ring size (MStenosis/sclerosis)
• decreased LV compliance (LVF, LVH)
• decreased mitral vavle competence (MR, pap muscle dysfunction, dialated cardiomyopathy, rheumatic heart disease)
• decreased aortic valve competence (AR)
o decreased left ventricular emptying
• decreased contractility, increases LVEDV (lateral AMI, LVF)
• decreased aortic valve size, increases afterload (AStenosis/sclerosis)
• ? decreased IPPV, increases wall tension and afterload
o ? effects of tachycardia
PO 1.45 describe the pressure volume loop
- A – ventricular filling
o ESV 50ml, volume of blood remaining after aortic closes, Pressure ~10mmHg,
o Mitral opens
o Ventricle fills ~70ml along end diastolic pressure volume relationship, gets steep >130ml as ventricle over stretched
o EDPRV slope is elastance (reciprocal of compliance) - B - isovolumetric ventricular contraction (start systole)
o EDV ~120ml
o Mitral closes
o Pressure increases to aortic root pressure ~80mmHg - C – ventricular ejection
o Aortic valve opens
o Stroke volume ~70 ml ejected
o Peak pressure ~120mmHg - D – isovolumetric ventricle relaxation (start of diastole)
o Aortic valve closes ~100mmHg
o Decreased pressure to ~10mmHg with no change in volume
o Mitral valve opens at ~5mmHg
PO 1.45 info got from pressure volume loop
o Stroke volume – b-d, ~70ml
o Ejection fraction – ST/EDV, .55 - .65%
o Peak pressure ~120mmHg
o LVEDV – preload measurement
o Elastance/stiffness – change in p/change in v (inverse of compliance), gradient of a slope so mostly flat at physiological volumes
o Afterload – gradient of LVEDV to Aortic close
o Contractility – gradient of ESPVR
• the max pressure that can be developed by the ventricle at any given volume, as this is the max pressure possible the pressure volume loop can’t cross it
o cardiac work
• in curve is work done by LV
• under line a is diastolic work (work done by blood to streth heart)
• potential work stored in isovolumetric contraction and released as head in diastole is between d and where ESPVR joins EDPRV behind the y axis
- This loop changes in valve disease and heart failure
how are aortic root and radial artery pressure waveforms different
- aortic waveform as previous
o windekessel effect – elastic potential energy stretching the aorta converted to kinetic energy to propel blood in diastole - radial artery waveform
o delay in arrival of impulse
o higher peak pressure due to resonance and reflection (summation of waveforms)
o increased velocity (narrower peak)
o decreased compliance of arterial wall (steeper – loss of windekessel effect)
o diastolic hump from reflection and resonance
o loss of diachrotic/ancrotic notch due to damping of high pressure components
autonomic innervation and effect on heart - diaz table (better cards in neuro humeral)
effect of IPPV on LV output
o Intermittant positive pressure ventilation
• Patient can’t generate negative pressure for air movement so positive pressure to deliver tidal volume in inspiration, expiration is passive
o Inspiration increased ITP
• Initially LVEDV increase, so increase SV and CO
• As raised ITP mobilizes pulmonary reservoir
• Venous return decreases due to raised ITP
• RV outflow decrease due to increased resistence and decreased compliance of pulmonary circuit
• Afterload decreases
• LV outflow decreases due to decreased compliance aortic root so increased afterload
• But increased pressure gradient from thorax to abdo means less resistance
• And raised ITP decreases systolic wall tension (because radius decreases and wall thickness increased as its not stretched by blood) which decreases afterload
• ?? overall effect is decreased CO???
o Expiration, decreased ITP
• Initially LVEDV decrease, so decrease SV and CO
• As low ITP decreases pulmonary vascular resistance so increases pulmonary blood volume
• Then increased veous return, decreased RV afterload (due to decreased resistance), so increased LA return, increased LVEDV, SV and CO
o Baroreceptor reflex fights this:
• Low MAP means less firing barorecetpors of carotid sinus, so increased sympathetic activity to increase HR, contractility and vasovenoconstriction to maintain MAP
o PEEP and hypovoleamia exacerbate this effect
• Maintains low VR, adds to pulm vascualar resistance, loose your MAP
pressures in the heart
Po1.45 factors that determine cardiac output
- Heart rate and stroke volume
- aim of heart is to give energy to blood to get BP to adequately perfuse organs
o CO (L/min)= SV(mL/beat) x HR (beat/min)
normal 5-6L/min
o Cardiac index = CO/BSA in square meters normalizes CO to different sized ppl
normal 2.6-4.2 L/min/meters squared
o BSA = square root of hight (cm) x (weight(kg)/3600)
- HR can increase 100-200% (symp and para on SAN), CO only by 50%
- Increasing HR decreases SV as ventricular filling time decreases
o But in exercise mechanisms act to incrase the stroke volume (chap 9)
o If these fail get heart failure and limited exercise capcity
PO 1.45 factors that determine CO - stroke volume
- SV = EDV – ESV , normally 120ml- 50ml = 70ml
- EDV and ESV regulated by preload, afterload and contractility. EDV and ESV interdependent so if change one you change the other
PO 1.45 factors that determine CO preload
preload determines SV determins CO
o Depends on venous return and stretch of fibres - amount of blood at end of passive filling and atrial contraction (EDV)
o Stretching of myocyte before contraction so related to sarcomere length at end of diastole
• Depends on interplay between EDP, EDV and compliance (see compliance card)
o Measured indirectly by EDV and P in acute changes, this doesn’t work chronically as compliance affected (heart failure)
Affected by:
• Venous pressure, afftected by:
- Venous compliance decreased by sympathetic activation as smooth muscle contracts, this increases venous pressure
- Venous blood volume influenced by:
- Total blood volume – regulated by kidneys
- Venrous return – depends on gravity, mechanical pumping of skeletal muscles, resp activity
- Ventricular compliance
- HR inverse due to influence on filling time
- Atrial contraction minimal effect except in high HR where symp activation enhances it to 40%
- Increased inflow resistance in Tricuspid stenosis
- Increased outflow resistance in Pulm stenosis or pulm hypertension
- Ventricular failure because inotropy less and can’t eject as much so its left over
- NOTE above works for left ventricle but venous pressure is pulmonary pressure, inflow resis is mitral, outflow resis is aortic valve and pressure. Resp activity also influences
PO 1.45 factors that determine CO preload, compliance
o Compliance = change in volume / change in pressure
• Determined by tissue of vent wall and state of relaxation
• Ventricular hypertrophy, thick, decreased compliance
• Diastolic failure, decreased compliance
• Dilated heart moves curve to the right (image 29 ? means more compliant, ? cardiomyopathy)
o Reciprocal of compliance is stiffness/elastance, pressure plotted against volume
• Compliance decreases (so stiffness increases) with increasing pressure or volume image 29 where stiffness is slope of tangent at any point
• Less compliant means less volume for given pressure or more pressure for same volume
PO 1.45 factors that determine CO preload, frank starling mechanism
- Relates sarcomere length/preload (or index – LVEDV/LVEDP) to force of contraction generated (or index – SV)
- Intrinsic property of the heart - Increasing venous return and ventricular preload increases stroke volume
- The relationship holds to a point which corresponds to sarcomere length 2.2 microm (beyond this decreased force of contraction)
- Curve changes with afterload and iontropic state of heart
- Increased venous return -> increased LVEDV and LVEDP and therefore increased preload -> increased SV along the frank starling curve defined by the afterload and ionotropy
- Ensures that output of ventricles is matched so blood volume doesn’t shift between circulations
- Increased volume stretches myocytes and increases force generated
PO 1.45 factors that determine CO preload effect on LV pressure volume loop
- Increased venous return increases ventricular filling along its passive filling curve (EDPVR line), this increases EDV
- If get contraction at this increased preload and aortic pressure (afterload) is constant get u empty to the same ESV so SV larger (PV loop increases in width)
- In reality increased SV causes increased aortic blood pressure so u get a small increase in ESV but net effect is still an increase in SV
- Increased area demonstrates increased ventricular stroke work
PO 1.45 factors that determine CO preload on length tension relationship
- Increased initial length (preload) leads to increased active tension (force) when the muscle contracts isometrically. As the duration of contraction and time to peak tension remain unchanged the rate of tension development increases with increase preload (has to get to a higher value quicker) image 32
- Can represent as tension against length image 33. This shows as preload increase can increase active tension up to limit, max active tension is with sarcomere 2.2microns
- In reality muscles isotonically contract (get shorter from preload length), it shortens to the same minimal length despite preload (higher velocity for increased preload) so image 32 is inverted. Therefore increased EDV (preload) increases SV without changing ESV (cos muscle always contracts to minimal length)
• Can replace image tension with pressure and length with volume - see card 24
PO 1.45 factors that determine CO preload and how it increases force
3 theories of length dependant activation:
• sensitizes trop C to calcium so don’t need increased Ca++ to Increase Ca++ binding and force
• Stretching alters calcium homeostasis so more available to bind
• Stretching decreases diameter so actin and myosin closer together facilitating interactions
• Length dependant activation of myofilaments means that maybe the frank starling mechanism increases inotropy
PO 1.45 factors that determine CO preload on length tension relationship seond image where u replace length tension with ventricular pressure and volume
PO 1.45 factors that control cardiac output afterload
o Load against which heart must contract against to eject blood/forces that oppose LV ejection
o Increased afterload increases ESV (decreases SV)
o factors that influence it:
• aortic pressure is large component
• wall stress image 34 La places law
- So afterload increase with increased intraventricular pressures in systole as well as will ventricular dilation (increased radius)
- After load decreased with ventricular hypertrophy – happens to offset increased wall stress caused by increased aortic pressure (AS or vent dilation)
- Wall stress is the tension that muscle fibres have to generate to shorten against the intraventricular pressure
• Systemic vascular resistance also major contributor
- Define
- Role in determining afterload
- Factors which alter
- Sympathetic NS, vasoconstrict, increase SVR
- Local tissue autoregulation
- Law of LaPlace and Hagen –Poiseuille equation
- Left ventricular outflow tract resistance
- Aortic valve
- aortic compliance
- intrathoracic pressure changes
- if ITP > aortic pressure it determines outflow (starling resistor mechanism)
- ?IPPV reduces afterload as it decreases transmural pressure
- Blood viscosity
- Arterial impedance
PO 1.45 factors that control cardiac output afterload, its affect on frank starling
change in afterload causes change in preload and stroke volume
PO 1.45 factors that control cardiac output afterload, its affect on force velocity relationship
- The greater the afterload the slower the velocity of shortening until its so great that contraction becomes isometric (muscle can’t shorten) image 34
- Increasing preload shifts this curve to the right as if increase preload u get a greater velocity of shortening at a given afterload image 35
- So increase in preload helps to offset reduction in velocity that happens due to increased afterload
PO 1.45 factors that control cardiac output afterload, its affect on pressure volume loop
- This loop shows how after and pre load are interdependent (as per frank starling image)
- Increased after load means decreased ejection velocity (force velocity relationship) and SV so greater ESV. This adds to the venous return so EDV is greater BUT ESV increase by more than EDV after a few beats so still get decreased SV overall, its just that frank starling partially compensates for decreased SV from high afterload because EDV increases a bit
PO 1.45 factors that determine CO, inotropy, effect on length tension
- Inotropes can increase the active tension at any initial preload length
- This is cos ionotropy acts independent of changes in sarcomere length, eg norad on B1 adrenoceptors increasing Ca+ entry into cell
PO 1.45 factors that determine CO, inotropy, effect on force velocity
• Shifts curve up and to the right so get increased velocity at any given afterload, this time u CAN increase V max as the muscle has more intrinsic cabability to increase force despite load
PO 1.45 factors that determine CO, inotropy, effect on pressure volume
- Increased ejection velocity and stroke volume and so decreased ESV and therefore decreased EDV but to a lesser degree
- Increased slope of end systolic pressure volume relationship because vent can generate increased pressure at any given volume
PO 1.45 factors that determine CO, inotropy, effect on frank starling
- To the left and up so decreased preload and increased stroke volume imag 31
- Increasing ionotropy increases efection fraction as bigger SV and smaller EDV. Decreased iontropy causes opposite – eg heart failure, increased preload and fall in stroke volume
- Helps maintain stroke volume at high heart rates – exercise
PO 1.45 factors that determine CO, inotropy, factors that influence it
- Autonomic nerves
- Sympathetic – norepinephrine to B1 adrenoceptors on myocytes
- Parasympathetic – acetylcholine to M2 muscarinic on atrial myocytes more than ventricular
- Anrep effect – abrupt increase in afterload causes modest increase in inotropy
- Bowditch effect/treppe/frequency-dependent activation – increased heart rate causes increased inotropy bacue Na+/K+ pump can’t keep up with increased Na+ so get raised intracellular Ca+ because of Na+/Ca+ exchanger
- Loss of intrinsic inotropy in systolic failure from
- Cardiomyopathy
- Ischemia
- Valve disease
- Arrhythmia
- Drugs to increase inotropy in heart failure
- Digoxin – inhibits Na-K+ ATPase
- Dopamine, dobutamine, epinephrine, isoproterenol - B-adrenoceptor agonists
• Milrinone – phosphodiesterase inhibitors
PO 1.45 factors that determine CO, inotropy, mechanisms
- Anything that works as length independent activation – alters myosin ATPase activity for a given length
- Increased Ca++ influx via Ltype Ca+ chaneel
- Increased Ca++ release by sarcoplasmic reticulum
- Sensitizing troponin C to Ca++
- B1 adrenoceptor activation does all 3
- Cardiac glycosides like digoxin
- Inhibit Na+/K+ ATPase, increased intracellular Ca+, increased, inotropy
