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Physiology- CP > Venous Return and Cardiac Output > Flashcards

Venous Return and Cardiac Output Flashcards

1
Q

Which circulation has lower pressure?

A
  • Right heart is lower than leg
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2
Q

What is preload?

A
  • Factors determining ventricular filling
  • Factors determining blood down pulmonary vein through LA into LV considered preload of LV
  • Measured as RAP (right atrial pressue)
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3
Q

What is right atrial pressure?

A
  • Very indirectly used as measure of left ventricular preload
  • Easiest way is to measure jugular venous pressure- cm of blood, measured just above sternal angle
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4
Q

What is left atrial pressure?

A
  • Measure of preload of left ventricle
  • Difficult to measure and ‘pulmonary artery wedge pressure’ may be used instead to estimate
  • Or left ventricular diastolic pressure (LVEDO) is measured directly using arterial catheter passed into LV
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5
Q

What factors contribute to preload?

A
  • Gravity
  • Thoracic pump
  • Muscle pump
  • Co-localisation
  • Venomotor tone
  • Blood volume
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6
Q

Describe how gravity affects preload

A
  • Upright- positive for tissues above heart, negative for below
  • Standing may cause drop in venous return- drop in CO
    • Postural hypotension
  • Supine- venous return increased
    • Increase in blood flow to right heart increases force of contraction and output from right heart
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7
Q

What is the consequence of increased blood flow to right heart lying supine?

A
  • Extra blood pushed into lungs- contribute to orthopnoea (breathlessness lying flat)
  • Lungs may be engorges with blood- stiffer, harder to inflate
  • Obesity–> orthopnoea, overweight abdomen presses on diaphragm
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8
Q

Describe how the thoracic pump affects preload inspiration

A
  • On inspiration, diaphragm flattens, raises ab pressure, thoracic pres falls
  • At same time- blood flows from ab to thorax because mechanism pulling air in, pulls out vena cava and sucks blood into thorax
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9
Q

Describe how the thoracic pump affects preload expiration

A
  • Expiration- dome-shape diaphragm, ab pres falls, blood moves from legs into ab
  • increased thoracic pres, ab tends to fill with blood from legs- used in inspiration
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10
Q

What is the useful feature of the thoracic pump?

A
  • Activity-related

- Venous return increases with increased activity

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11
Q

Describe how the muscle pump affects preload

A
  • Arises due to large veins passing through muscle blocks- particularly in limbs
  • Veins compress when muscle contracts
  • Large veins have valves- only permit blood to move to heart
  • Pump also activity related- increased activity increases venous return
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12
Q

Describe how co-localisation affects preload

A
  • Veins, arteries + nerves tend to run together- ensheathed in tight CT
  • As arteries pulsates- massages vein
  • Valves mean this movement causes blood to move towards heart- so mechanism will function when muscles not that active
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13
Q

Describe how venomotor tone affects preload

A
  • Great veins have some smooth muscle
  • Similar pharmacology to arterioles- NA causes vasoconstriction by acting on α-1 receptors
  • Increase ANS sympathetic outflow to veins–> contraction
  • Large part of circulation-> veins of GI and sup/inf vena cava- contraction increases central venous pres and so right heart preload
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14
Q

Describe how blood volume affects preload

A
  • Great veins- capacitance vessels for blood storage
  • Increased blood vol increases central venous press, and so preload
  • Low blood vol reduces venous press, decreases preload
  • Ability to maintain CO decreases
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15
Q

Describe the relationship between venous return and cardiac output

A
  • Sometimes, increaed VR increases CO, but many factors control CO
  • However, VR always limits CO, if CO increases, must be an increase in VR
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16
Q

What affects cardiac output?

A
  • CO = HR x SC
  • SV acheived by filling ventricle to end diastolic vol and emptying down to a certain vol
  • End diastolic pressure can be used as a measure of preload
  • Heart health can be determined by ejection fraction
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17
Q

How can cardiac output be measured?

A
  • Fick principle-CO in the heart (also alveolar vent in lungs and glomerular filtration in kidneys)
  • Also various imaging systems, Doppler flow measurements
18
Q

How can oxygen uptake be measured?

A
  • Oxygen uptake measured by collecting expired air in ‘Douglas bag’ and measuring oxygen conc.
19
Q

How can pulmonary arterial blood oxygen content be measured?

A
  • Sample of RA obtained by inserting catheter into arm vein and pushing through RA
  • E.g. ant cubital vein, sample collected- mixed venous blood
  • Measure oxygen content
20
Q

How can pulmonary venous oxygen content be measured?

A
  • Measuring oxygen content of blood in any systemic artery
21
Q

How can blood oxygen content be measured?

A
  • Haemoglobin conc and oxygen sat

- 1g of Hb fully saturated binds 1.33ml of oxygen

22
Q

How does the ANS affect heart rate?

A
  • SNS increases, PNS slows
  • Natural inherent rate of SAN= ~100bpm
  • At rest, heart under tonic vagal PNS inhibition
  • HR can increase from 70-100bpm be decreasing PNS activity
  • Increase >100bpm requires increased SNS input
  • Max effective HR is ~180bpm after this- encroachment on rapid ventricular filling time (contraction before proper filling) and SV falls rapidly
23
Q

Describe blood flow through coronary supply

A
  • Blood can only flow through coronary supply when muscle relaxes in diastole
  • When contracted, blood vessels flattened
  • At very high rates- danger of cardiac ischaemia- angina
24
Q

What is the Bainbridge reflex?

A
  • HR increases when RAP increases- hence HR increases on inspiration and falls on expiration (sinus arrhythmia)
25
Q

What parts of the heart does the PNS innervate?

A
  • SAN and AVN
26
Q

What parts of the heart does the SNS innervate?

A
  • Nodes and heart muscle

- Changes rate and ventricle contractile strength, therefor SV

27
Q

Describe the role of stroke volume

A
  • SV can be increased by filling ventricle more or by emptying it more
  • Effect of increasing ventricular filling (i.e. stretching ventricle) investigated by Starling– starling resistor
28
Q

What did Starling’s experiments involved?

A
  • Isolated heart lung preparation in dogs
  • Replaced systemic circulation with artificial ‘Starling Resistor’
  • Vary peripheral resistance
  • Vary preload (RAP) by raising or lowering reservoir connected to RA
29
Q

Briefly describe Starling’s first experiment

A
  • Heart filling and emptying
  • Half way through, lifts venous reservoir, increases RH preload
  • Ventricles fill more due to blood flow to ventricle at higher press.
  • Increased RAP increases end diastolic vol
  • Next time heart beats, empties down to same end systolic vol as before- CO increased, heart does more work and end diastolic volume increased
30
Q

Briefly describe Starling’s second experiment

A
  • Increased resistance, raises arterial blood press
  • Heart tries to empy, can’t do as much as before
  • So, after a heartbeat, ventricles stretched to greater end diastolic volume
  • Heart maintains same SV, CO maintained- done when afterload greater
  • Heart doing more work when end diastolic vol increased
31
Q

What is Starling’s law of the heart?

A
  • Work done by heart in systole related to resting (end diastolic) length of ventricular muscle fibres
  • Stretch muscle fibres during period heart is filling- next time they contract- more forcefully
32
Q

What is the molecular basis of starling’s law?

A
  • Increased force of contraction from actin and myosin strands drawn closer together (compensation)
  • If fibre stretched too much, cross bridge formation reduced due to reduced overlap of actin and myosin fibrils, force of contraction diminished (decompensation)
  • Heart with grossly increased EDV contracts poor;y
33
Q

What is the role of Starling’s Law?

A
  • Implies increase in venous return causes increase in CO
  • Early in exercise
  • Main role of law is to ensure ventricular balance
  • If you fill heart more- empties to same amount as it did before
34
Q

Describe contractility

A
  • SNS stimulation, or positive inotrope increases
  • Increase in force not resulting from muscle stretch in diastole (not Starling’s) permits ventricle to contract to a smaller ESV
35
Q

How is contractility expressed on a Starling curve?

A
  • Increased and decrease preload- up and down starling curve
  • Increase and decrease intracellular Ca- switch between starling curves
  • Flat part of curve- changes in preload no longer increase force of contraction or amount of work done as a result of Starling mechanism
36
Q

What is ventricular failure?

A
  • Inability of heart to pump as hard as it should
  • Can result in ischaemia, acidosis or death of muscle fibres
  • If in LV- ventricular balance disturbed- RV continues to pump into lungs, not cleared effectively by LV
  • Press in pulmonary artery, capillaries, vein increase- LV preload increases
  • LV stretched more
37
Q

Describe the expression of ventricular failure on Starling’s curves

A
  • Failure of LV to clear blood from pulmonary circulation results in dropping to a different starling curve
  • LV preload increasing results in movement up its new lower curve and eventually ventricular balance restored
  • But price - pulmonary congestion, possible breathlessness and pulmonary oedema
38
Q

What is Heart Failure?

A
  • Inability to maintain normal CO at normal preload
  • LH failure- raised pulmonary BP and thus dyspnoea (stiff lungs), maybe pul. oedema
  • Increased RH after load- may cause RH failure- vasoconstriction due to hypoxia
39
Q

Describe the sequence of events that lead to congestive heart failure

A
  • Fall in CO and kidney perfusion, retain water, increased blood vol–> congestive heart failure (compensation)
  • Increased central venous press –> peripheral cap pres increases –> peripheral oedema- gravity- ankles
  • Combined L and R HF = congestive heart failure
40
Q

Describe left heart failure

A
  • Often suffer from orthopnoea
  • Increased venous return, increases RH preload,
  • RH output and pulmonary BP rise since LH insufficient at increasing output
  • In severe cases- paroxysmal nocturnal dyspnoea- wakes with severe breathlessness and coughing up fluid
  • Nocturnal asthma attacks may be mistaken for PND caused by HF
41
Q

What happens in exercise?

A
  • Increased venous return with isotonic exercise
  • Cardiac filling increased- sends heart up Starling curve
  • Cardiac contractility increased by SNS- new higher curve and less blood left in ventricle at end of systole
  • HR increases
  • Mac CO- 25L/min in healthy young adult in male
  • Most factors contributing to exercise are anticipatory
  • SV can increase considerably

Physiology- CP (19 decks)

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