Lecture 12 - Regulation of Cardiac Output Flashcards
Describe the speed and duration of the ANS effects on HR.
- Sympathetic: slow and last longer because the NTs must go through a slow reuptake mechanism
- Parasympathetic: fast onset and short because of the abundance of cholinesterase in synapses that can remove ACh quickly
Other name for sympathetic effects on the heart?
Beta-adrenergic effects
What compounds block beta-adrenergic effects on the heart? Resulting effect?
Beta-blockers = slight HR reduction because at rest the sympathetic effect on the heart is minimal
What compound blocks parasympathetic activation of the heart? Resulting affect?
Atropine = large increase in HR because at rest the parasympathetic effect on the heart is significant
Through what mechanism is ANS regulation of the CV system established? Example?
Reciprocal changes in sympathetic and parasympathetic NS activity
E.g. during exercise, you are increasing sympathetic activity and decreasing parasympathetic activity
Describe the regulation of BP via arterial baroreceptor reflex. Purpose?
Baroreceptors in the aortic arch and carotid sinus which monitor BP by detecting stretch and then trigger ANS activity adjustment
Purpose: keep arterial pressure constant to provide adequate perfusion to tissues
Describe the steps of the mechanisms of the regulation of BP via arterial baroreceptor reflex.
- Increase in BP
- Baroreceptors in aortic arch/carotid sinus are stretched
- Afferent sensory signals sent to medullary cardiovascular center
- Reciprocal adjustment of ANS by the medulla to decrease HR = increase in parasympathetic activity and decrease in sympathetic activity
5a. Increased para => decreased HR
5b. Decreased sympa => decreased venomotor tone => increased venous volume => decreased EDV + decreased contractility => decreased SV + decreased HR => decreased CO + decreased TPR - Decreased arterial pressure
More NE or EPI released by sympathetic NS onto the heart?
NE
How does standing up affect BP?
Decrease in BP
What is the carotid sinus?
Dilated area at the base of the internal carotid artery just superior to the bifurcation of the internal carotid and external carotid
What is venomotor tone?
The degree of tension in the muscle coat of a vein that determines the shape of the vein
What is the bainbridge reflex?
Sudden IV infusion => increased RA pressure => stimulation of RA low pressure baroreceptors aka cardiopulmonary baroreceptors => bainbridge CNS reflex to increase HR to redistribute BV
What does the response to a physiological challenge depend on? E.g.?
Initial physiological state
- IV to patient who has a slow heart rate because normal BV (has NOT suffered a hemorrhage) => bainbridge reflex to increase arterial pressure until the baroreceptor reflex kicks in
- IV to patient who has a fast heart rate because dcreased BV (e.g. has suffered a hemorrhage) => instead baroreceptor reflex to decrease arterial pressure
Other name for baroreceptors?
Stretch receptors
Describe the regulation of the HR via peripheral chemoreceptors.
Chemoreceptors in aortic arch and carotid sinus that detect the quality of the arterial blood: PO2, PCO2, pH levels
Other name for peripheral chemoreceptors in aortic arch and carotid sinus?
Aortic and carotid bodies
How do PCO2, PO2, and pH levels vary in aortic and carotid bodies in a healthy normal individual? What does this mean for the peripheral chemoreceptor regulation of the heart?
They do not! Changes indicate a problem
Peripheral chemoreceptor regulation of the heart is an emergency system
Describe the mechanisms of the regulation of HR via arterial aka peripheral chemoreceptor reflex.
High PCO2/Low CO2/Low pH:
- Primary effect: chemoreceptors send signals to the medullary CV center to decrease HR to redirect blood flow to the brain (survival mode)
- Secondary effect: due to chemoreceptors sending a signal to the lungs and causing hypocapnia and increased lung stretch => inhibition of the medullary CV center to stop it from decreasing HR and make it go back to normal (bradycardia is transient if respiration is successfully increased)
Other name for medullary cardiovascular center?
Medullary vagal center
What is hypocapnia?
State of reduced carbon dioxide in the blood resulting from deep or rapid breathing, aka hyperventilation
Normal PO2?
95-100 mmHg
Normal PCO2?
40 mmHg
Normal pH?
7.4
How does respiration affect HR? What is this called in children?
- During inspiration, there is negative thoracic pressure (decrease in pressure) and positive abdominal pressure to bring in the air => increase in venous blood return => increase in RA pressure and stretch => bainbridge reflex => increase in HR
- During expiration, lung stretch receptors and arterial baroreceptors play a role in lowering the HR back
In children, this is called respiratory sinus arrhythmia = normal HR variation with respiration
How can hormones affect HR?
EPI and TH raise HR
How can temperature affect HR?
High temperatures cause a direct increase in SA nodal HR
What are the limitations of HR increasing the CO?
If you electrically stimulate the heart of a patient and keep everything else constant:
CO will increase with HR pretty proportionally to a certain point = past diastasis (around 100 bpm) and into rapid passive filling
Past this point, CO will decrease because the ventricles do not have as much time to fill
How did Frank-Starling figure out the Frank-Starling mechanism?
Experiments on dog hearts to investigate the effects of preload on SV by varying it using a venous reservoir to decrease/increase venous pressure and ventricular filling
What is preload? What are 2 measures of it?
The degree of filling of the ventricle before contraction:
- EDV in an intact CV system
- Initial sarcomere length
Describe the Frank-Starling mechanism.
Higher preload => higher filling => more optimal sarcomere length for subsequent contraction => greater SV and greater force of contraction (NOT a change in contractility)
What does a change in heart contractility refer to?
Refers to inotropic effects on the heart which increase its inherent strength
What is the difference between force of contraction and contractility?
- Force of contraction = power exerted by the heart during contraction
- Contractility = intrinsic ability of the myocardium to contract and create force (its “strength”) INDEPENDENT OF PRELOAD AND AFTERLOAD
What is force of contraction dependent on?
- Preload
- Afterload
- Underlying contractility
What is afterload? What is it loosely synonymous with?
Pressure against which the heart contracts (the force that the ventricle must pumo against) = arterial or ventricular pressure during contraction
Synonymous to force of contraction
In what activity does the Frank-Starling mechanism play an important role?
During exercise to increase CO
What is the driving gradient/force for blood flow in the CV system? How is this gradient increased?
The difference between end diastolic pressure and systolic pressure:
- Increased EDV causes small increase in EDP
- Increased EDV causes a MARKEDLY higher systolic pressure
=> therefore as EDV increases, the gap between these 2 gets bigger and bigger
What is the Treppe effect? In what conditions is this true?
Increase HR => decreased time between myocyte contraction => decreased calcium sequestration intracellularly => increase in free calcium levels in the cardiac myocytes => increased contractility => increased force of contraction building up over several beats (staircase)
WITH PRELOAD AND AFTERLOAD HELD CONSTANT
What is another name for the Treppe effect?
Staircase phenomenon
What factors increase heart contractility?
- NE
- Dopamine
- Aerobic exercise aka conditioning
- Digitalis
What factors decrease heart contractility?
- Infarction
- Ischemia
- Heart failure
What is stroke work?
SV x systolic pressure
To what receptors do NE and EPI secretion by the sympathetic NS bind to on the heart?
Beta 1 adrenergic receptors
Does the parasympathetic NS affect contractility?
Barely because the ventricular myocardium lacks PNS innervation
What does the slope of the Frank-Starling mechanism (of end diastolic pressure vs stroke volume) represent?
It’s a measure of contractility
Where is the PNS innervation in the heart?
Pacemakers and atria
How will myocardial infarction affect the sympathetic innervation of the heart?
MI => contractility is reduced => inadequate cardiac output => SNS activity increased
What is mean circulatory pressure affected by?
- BV
2. Venous tone
Through what 2 mechanisms is the heart’s contractility increased by conditioning?
- Hypertrophy
2. Increased intracellular Ca++ baseline
What are all of the effects of a fall in systemic TPR IF CO is maintained constant?
Lower systemic arterial pressure => HIGHER CENTRAL VENOUS PRESSURE => higher venous return => increased preload on the RV (higher RVEDP) to maintain CO constant
Why does exercise keep MAP constant but increases pulse pressure?
Increase in systolic due to sympathetic effects but decrease in TPR causes a decrease in diastolic: overall MAP is the same, but pulse pressure is higher
How does increasing the heart rate affect the time spent in systole and diastole?
Both decrease, but time in diastole decreases more
How will a person with aortic stenosis react to exercise?
Syncope because TPR decreases but no way of increasing CO enough to compensate so huge drop in pressure
Role of stellate ganglion?
Site of SNS stimulation of the heart
Is contractility dependent on preload and afterload?
NOPE
