Term 2 Lecture 4: Cardiac Output And Control Flashcards
Cardiac output (CO)
CO = heart rate X stroke volume
It is the vol of blood pumped by each ventricle per minute (not total amount pumped by heart)
During any period of time the vol of blood flowing into pulmonary circulation= vol flowing into systemic circulation therefore CO of each ventricle is normally the same (although beat to beat basic minor variations occur)
Determinants of cardiac output
CO=HR x stroke vol.
HR= BPM
Stroke vol. = Vol of blood pumped per beat/ stroke
Average man: 70bpm x 70ml stroke vol
=4900ml/min ~5litres on average
Each half of your heart pumps equivalent of your entire blood vol per min
Equivalent to 2.5 million litres in one year of resting CO
During exercise CO increases to 20-25 litres per min and upto 40litres/min in athletes
Sudden drop in blood pressure
E.g. when getting out of bed
Results in low venous return and therefore decreased stroke vol. Heart rate increases due to sympathetic activity and norm CO is maintained
How do we change HR & SV to increase CO?
HR is determined by Auto NS which innervates the heart
Parasympathetic vagus nerve ( in sacral spinal region and brain stem) to atria SAN/AVN slows things down. Weak effect on ventricles
Cardiac Sympathetic nerve to atria, SAN/AVN and ventricles speeds things up. It has preganglionic neurones and nerves (in thoracic spine and brain) and has a strong effect on the ventricles.
Intrinsic SAN fires 120-130bpm
Under normal conditions at rest: parasympathetic NS inhibits SAN to limit of 70 BPM by prolonging depolarisation - slowing the opening of Na & Ca²+ channels
During exercise:
Sympathetic NS increases firing freq. Shortening depolarisation time. It’s an automatic dynamic process.
So symp and parasymp NS are antagonistic - have opposite impact.
Hormone effects:
Adrenaline (epinephrine) &
Noradrenaline (norephrine) increase HR
Effect of ANS on HR & structures that influence the heart
Effect of parasymp/symp on area
SA node: depolarise to threshold and reduce HR/ depol to thresh increase HR
AV node: decrease excitability increase AV node delay/ increase excite decrease AV delay
Ventricular conduction path: no effect/ increase excitability and conduction in His & Purkinje
Atrial muscle: reduced contractility & weaker contraction / increase & strengthen contractions
Ventricular muscle: no effect/ up contractility & strengthen contractions
Adrenal medulla: no effect/ promotes adrenomedullary secretion of epinephrine
Veins: no effect/ increases venous return & strength of cardiac contraction through Frank-Starling mechanism
2 ways to charge stroke vol.
Determined by extent of venous return and by symp. Activity
Intrinsic - depends on venous return to right atrium, increase in stroke volume increases diastolic volume increasing contraction strength - more blood out
I.e. more blood pumped into heart the more it stretches, greater strength gives greater contraction and greater cardiac output - first described by Frank & Starling: the law of the heart:
The heart normally pumps out during systole the vol of blood returned to it during diastole so increased venous return results in increased stroke vol - the more the muscle is stretched the more it contracts (without ANS influence)
Under normal circumstances the heart operates below optimal end diastole vol (~300ml) and as cardiac output increases ( e.g. during exercise) you move towards optimal by increasing strength of contraction.
Frank and Starling curve explained
Cardiac muscle fibre length is determined by extent of venous filling and is normally less than optimal length (IO equiv to 300ml EDV) for developing max. tension.
Therefore increase in EDV (increase in venous return) by moving cardiac muscle fibre length closer to IO increases the contractile tension of the fibres on the next systole
A stronger contraction squeezes out more blood thus as more blood is returned to the heart and EDV increases the heart automatically pumps out a correspondingly larger stroke vol.
Extrinsic: sympathetic stimulation increases contractility of the heart and thereby increases SV.
End diastolic vol ->stroke vol.->end systolic vol
Norm ( no symp activity)
135ml > 70ml > 65ml
Symp affecting*
135ml>100ml>35ml
Symp+ increased EDV*
175ml>140ml>35ml
- Shifts Frank-Starling curve left
End diastolic vol->stroke vol-> end systolic vol
Norm (no symp activity)
135ml>70ml>65ml
+ Symp*
135>100>35
+Symp+ increased EDV*
175>140>35
*Shifts Frank-Starling curve left
Frank and Starling curve explained (cont.)
Sym activity + adrenaline enhance the hearts contractility
Contractility = strength of contraction at any given EDV
Greater cross-bridge cycling
Frank-Starling curve allows us to work out how healthy/efficient your heart is.
shift left by symp stimulation -For same EDV a larger stroke vol is ejected as a result of increased heart contractility
Shift right observed in heart failure as contractility of heart decreases and symp response to contractility is limited.
Congestive heart failure results in 100% mortality w/out transplant.
The kidneys conserve salt/water expanding blood vol and increasing EDV
Water and salt retention must be reduced to enhance contractility
Baroreceptors and baroreceptor reflex
Getting right amount of blood to the right place at the right time requires actions of blood vessels and heart to be coordinated
If ABP drops a regulatory response kicks in to bring it back to normal
If “ rises “ “ “ regulatory “ “ “ down to normal
Neg. Feedback controls ABP at norm levels
Baroreceptors
Input - arterial baroreceptors: in carotid sinuses at the top of the heart send signals to medulla oblongata which are then passed to the hypothalamus and/or the cerebral cortex before returning to the MO to pass to the parasymp system to produce output in the SAN in right atrium of the heart. Or from MO to spinal cord to output through sympathetic trunk to the veins,arterioles or ventricular myocardium.
Input: venous+ cardiac baroreceptors, arterial chemoreceptors, proprior receptors in muscles/joints and receptors in internal organs to spinal cord and onto MO/cerebral cortex/ back to MO then output either parasymp to SA node or return to spinal cord and onto symp trunk, then veins/arterioles/ ventricular myocardium
Baroreceptors explained
Baroreceptors: sensory non-encapsulated nerve endings located in adventitial layer arteries: aortic arch/ carotid sinuses
Carotid baroreceptors : carotid sinus nerve to glossopharyngeal nerve (IXth cranial nerve) to nucleus tractus solitarius (NTS)
Aortic baroreceptors: aortic depressor nerve to vagus (Xth cranial nerve) to NTS
Baroreceptor properties
Baroreceptors change their function according to the stimuli they receive
They are mechanoreceptors - respond to strength of arterial wall net pressure
Dynamic response: as ABP increases individual baroreceptor fibres fire a burst of AP
Adaptive (static) response - signals rate change pressure, reaches new rate reflecting new pressure (adaptive response)
Fall in ABP - as ABP decreases individual baroreceptors fall silent then renew activity at a slower rate.
Reflex response to baroreceptors unloading is a hemorrhage
In hemorrhage SV, COP (cardiac output pressure), & MAP (mean arterial pressure) decrease
HR and TPR change after reflex responses - autonomic activity.
Decrease in ABP unloading in baroreceptors
Activates baroflex to increase ABP to near initial value
If raised to initial value this shuts off baroreceptor reflex
Lose compensatory response to blood loss and ABP would fall
Lower ABP keeps reflex activated and compensates for lost blood
