Venous Return and Cardiac Output Flashcards
1
Q
Which circulation has lower pressure?
A
- Right heart is lower than leg
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)
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
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
5
Q
What factors contribute to preload?
A
- Gravity
- Thoracic pump
- Muscle pump
- Co-localisation
- Venomotor tone
- Blood volume
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
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
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
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
10
Q
What is the useful feature of the thoracic pump?
A
- Activity-related
- Venous return increases with increased activity
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
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
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
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
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
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
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
