Lecture 13: Regulation Of Cardiac Output Flashcards
How is cardiac output regulated?
Cardiac output is regulated by changing heart rate and or stroke volume
What is cardiac output. How do you calculate it?
Cardiac output = amount of blood pumped by each ventricle each minute
Cardiac output = HR X SV
Intrinsic vs extrinsic regulation of cardiac output
Intrinsic control = regulation of an organ by factors arising within that organ (autoregulation)
Extrinsic control = regulation of an organ by factors arising outside of that organ (neural of hormonal)
Regulation of heart rate
Sa node
Neuronal and hormonal
HR is determined by SA node which depolarises spontaneously
-HR is subject to both neuronal and hormonal regulation
Note: autonomic nerves modulate heart rate but don’t cause the heart beat
Neuronal control of hear rate
SA node is innervated by both sympathetic and parasympathetic nerves
-at rest, parasympathetic activity dominates
-intrinsic SA node firing rate + 100BPM
-normal resting HR = 75 BPM
Effects are mediated by adrenergic and cholinergic receptors on SA node
Autonomic innervation to the heart
Vagus nerve and cardiac nerve
Describe the parasympathetic effects on SA node firing
Parasympathetic nerve firing decreases HR and CO
Parasympathetic nerve firing (vagus) –> muscarinic cholinergic receptors –> opens K+ channels–> K+ efflux–> hyperpolarizes SA node cell –> decreases HR and CO
So it takes longer for the cells to reach its action potential level?
Sympathetic effects on SA node firing
Sympathetic nerve firing increases HR and CO
Sympathetic nerve firing –> adrenergic receptors –> open Na+ and Ca2+ channels –> Na+ and Ca2+ influx –> rate of depolarisation increases –> increases HR and CO
Hormonal control of heart rate
Adrenaline released from the adrenal medulla in response to sympathetic NS activation
-acts in adrenergic receptors –> increased HR
(Mimics sympathetic nerve action)
Regulation of stroke volume. What is it regulated by?
End diastolic volume (volume of blood in the heart before contraction starts)
Strength of ventricular contraction
After load (pressure ventricles have to work against to pump blood out)
Who does end diastolic volume affect stroke volume? The starling effect
- Force of contraction is related to amount of blood in ventricle.
- Intrinsic mechanism to match the amount of blood expelled to the amount of blood received, prevents blood pooling
- means that heart can match the output of the 2 ventricles, moment to moment, in the absence of external regulation.
Ie ⬆EDV ➡ ⬆ventricular contraction➡ ⬆stroke volume ➡ ⬆CO ➡ ⬇EDV etc
Cellular mechanisms:
⬆ EDV ➡stretching of heart muscle ➡more overlap between myosin heads and actin filaments ➡ more cross bridge formation ➡ stronger contraction
Explain how venous return effects end diastolic volume (EDV)
-its a major determinant of EDV
-increased venous return ➡ increased cardiac output
Venous return is determined by:
-skeletal muscle pump
-respiratory pump
-venoconstriction
-blood volume
How does skeletal muscle pump effect venous return?
- thickening if skeletal muscles during conaction increases pressure in veins
- venous valves ensure blood moves towards heart and does not flow back during relaxation
- contraction ➡ increased venous return ➡ increased CO
Respiratory pump and venous return
Inhalation decreases the ossified in the thorax, in cases venous return and increases cardiac output
Diaphragm drops during inhalation ➡reduced pressure around the heart➡ large veins distend ➡ blood drawn u towards the heart ➡ increased venous return
Venoconstriction and venous return
About 60% of blood is stored in the veins at rest
Sympathetic NS activation ➡ venous smooth muscle contraction ➡ venoconstriction ➡ blood forced towards heart ➡ venous return increases
Venous valves ensure blood moves towards the heart and does not flow backwards during inhalation
Venoconstriction ➡ increased venous return ➡ increased CO
Blood volume and venous return
Blood volume changes due to bleeding, dehydration
Decreased blood volume➡ decreased venous pressure ➡ decreased venous return ➡ decreased EDP and EDV ➡ decreased stroke volume ➡ decreased cardiac output
Regulation of blood volume relies on the renal system. Thus the renal system effects cardiac output and blood volume
Ventricular contractility and stroke volume
It is the contractile strength at a given EDV
- increased ventricular contractility ➡ increased stroke volume
- contractility is modulated by the sympathetic NS and hormones, especially adrenaline
Autonomic innervation of myocardial cells
Myocardial cells mostly innervated by sympathetic NS
Parasympathetic innervation insignificant
Sympathetic control of ventricular contractility
Sympathetic actions on myocardial cells
Sympathetic activity or circulating adrenaline
1) increases contraction strength
2) increased rate of contraction
3) increased rate of relaxation
Actions:
- noradrenaline/ adrenaline bonds to myocardial adrenergic receptors
- good example of divergent action of metabotropic receptors
B1adrenergic receptor ➡ G protein ➡ protein kinase ➡
-⬆ ca2+ release from SR
⬆Ca2+ entry from ECF
⬆Myosin ATPase activity (the above increase strength and speed of contraction)
⬆ Ca2+ reputable to SR (increases speed of relaxation
How does afterload effect stroke volume
Afterload= pressure in the aorta during ventricular ejection (unfiltered arrows)
- generally, afterload increases with increasing mean arterial pressure
- the heart must fight against the afterload to eject blood
- increased afterload ➡ reduced stroke volume
What is congestive heart failure?
A change in cardiac muscle (eg scar tissue from heart attack)
- as volume of blood in heart increases, amount of blood ejected from the heart does not increase enough to match it
- can leads to pulmonary edema
Cardiac hypertrophy
Increase in mass (and strength) of heart muscle
1. Physiological hypertrophy
-proportional change in cavity size and wall thickness eg endurance training. Has normal diastolic ventricular compliance.
2. Eccentric hypertrophy: big cavity thin walls
-response to volume overload
Eg renal disease, valve dysfunction
-increased diastolic ventricular compliance
3. Concentric hypertrophy
-reduced cavities, thick walls
-response to pressure overload (⬆ afterload)
-eg hypertension, weight lifting
-reduced diastolic ventricular compliance
