Flashcards in Chapter 5 - Regulation Of The Heart Deck (36):
The quantity of blood pumped by the heart each minute.
Cardiac output is the product of heart rate and stroke volume; that is,
CO = HR × SV
Considerations of the control of cardiac activity.
i. regulation of pacemaker activity
ii. regulation of myocardial contraction
Factors affecting SA Node discharge frequency
i. Local factors e.g. temperature, tissue stretch
ii. *****Autonomic Nervous System*****
iii. Humoral factors e.g. Drugs, hormones...
iv. Intrinsic mechanisms
SA Node firing rate
AV Node firing rate
Purkinje fibre firing rate
Resting heart rate in :
1. Typical Adult
2. Trained Athlete
Why is resting heart rate 70 bpm although SA Node sets the rhythm between 90 - 120 bpm?
Because a rest vagal/parasympathetic tone dominates and as such slows the resting rate to about 70bpm
Autonomic Nervous System
In the heart there is always some sort of balance between the two divisions of the ANS. increased heart rate is produced by a diminution of parasympathetic activity and a concomitant increase in sympathetic activity; deceleration is usually achieved by the opposite mechanisms.
Intrinsic Heart Rate
Also known as the *true* heart rate is, the rate that prevails after complete autonomic blockade.
~100bpm in young adults
originate in the medulla oblongata, in cells that lie in the dorsal motor nucleus of the vagus or in the nucleus ambiguus.
Parasympathetic only goes to nodes ****NOT MUSCLE****
Right Vagus - SA Node mainly
Left Vagus - AV Node mainly
Ach is neurotransmitter
Muscarinic, M2 Receptor
Short latency because no need for 2nd messenger, Ach opens K+ channels
Rapid decay because nodes are rich in cholinesterase
originate in the i mediolateral columns of the upper five or six thoracic and lower one or two cervical segments of the spinal cord.
Sympathetic innervates myocardium, vasculature and nodes
Norepinephrine is the neurotransmitter
B1 receptor - Nodes, myocardium
B2 receptor - Blood vessels
Both receptors are Gs, GPCRs.
Longer latency since cAMP build up needed
Influences of higher centers
Cerebral cortex can slow down or speed up rate
Thalamus can cause tachycardia
Hypothalamus can go both ways
Medulla Oblongata can go both ways as well
Pressure receptors mainly in Aortic Arch and Carotid Sinus
Detect blood pressure changes
Increase in arterial pressure causes slowing of heart rate and vice versa
Most prominent between 70 and 160 mmHg
Both atria have receptors that influence heart rate. They are located principally in the venoatrial junctions—in the right atrium at its junctions with the venae cavae and in the left atrium at its junctions with the pulmonary veins.
infusions of blood or saline accelerate the heart rate. This increase in heart rate occurs whether arterial blood pressure rise or nah. Tachycardia is observed whenever central venous pressure rises sufficiently to distend the right side of the heart, and the effect is abolished by bilateral transection of the vagi.
Chemical receptors located in the carotid bodies
Caused by phases of respiration
Rate increases during inspiration
Rate decreases during expiration
Chemoreceptors activation increases the heart rate although this change is secondary to respiratory changes
Just as the heart can initiate its own beat in the absence of any nervous or hormonal control, the myocardium can adapt to changing hemodynamic conditions by mechanisms that are intrinsic to cardiac muscle.
i. Starling’s law of the heart
ii. Changes in Heart Rate
Starling’s law of the heart
Increases in preload increase cardiac output and conversely
Increases in afterload decrease cardiac output and vice versa
The ventricular filling pressure just before ventricular contraction constitutes the preload for the myocardial fibers in the ventricular wall
The resistance the ventricle had to pump against which is the aortic/pulmonary pressure; this pressure constitutes the afterload for left ventricular ejection
Changes in heart rate
Affect contractile force
1. progressive increase in developed force induced by a change in contraction frequency is known as the staircase, or Treppe, phenomenon.
2. Postextrasystolic potentiation
Mechanism Of Treppe
The initial progressive rise in developed force when the interval between beats is suddenly decreased is achieved by a gradual increase in intracellular Ca ++ content.Two mechanisms contribute to the rise in Ca ++ content:
1. an increase in the number of depolarizations per minute
2. an increase in the inward Ca ++ current per depolarization.
Silly little child.
Cardiac muscle doesn't undergo tetanus contractions.
Mechanism Of Tetany
Got you again. Man, you're gullible
Nervous factors. Sympathetic mechanism
Stimulation results in release of norepinephrine.
Binds to B1 receptors>activates adenyl cyclase>increases cAMP>activates Protein kinase A.
Protein Kinase A then phosphorylates a whole host of proteins including,
1. Phospholamban - Increases activity of SERCA pump to hasten relaxation
2. Troponin I - reduces Ca++ sensitivity thereby accelerating relaxation
3. Ca++ channels - increases Ca++ influx during action potential
Nervous factors: Parasympathetic mechanism
Stimulation results in release of acetylcholine.
Binds to M2 receptors>deactivates adenyl cyclase>decreases cAMP>Inactivates Protein kinase A.
Also released Ach suppresses norepinephrine release
Hormones regulate cardiac performance. Which ones?
1. Adrenomedullary hormones
2. Adrenocortical hormones
3. Thyroid hormones
Although cardiovascular effects of circulating catecholamines are minimal at rest. They have significant dromotropic, ionotropic and chronotropic effects during moderate to heavy exercise
Adrenocortical hormones enhance water retention thereby increasing blood volume hence stroke volume and cardiac output