Lecture 30: Heart Control Flashcards
Cardiac output (Q) averages
- At rest: 4-6 L/min in average adult
- Strenuous exercise: 15+ L/min
- Increases occur with minimal changes in blood pressure
Cardiac output is determined by 2 parameters
- Stroke volume
- Heart rate
- Both intrinsic and extrinsic mechanisms can alter parameters
Normal adult heart rate
- About 70 beats/min
- Much higher in children
- Sleep decreases heart rate by 10-20 beats/min
- Anxiety, activity and exercise increase it
Heart rates of well-trained athletes
- Lower resting heart rates
- About 50 beats/min
- Resting cardiac outputs are the same for sedentary and well-trained athletes
Intrinsic factors altering heart control
- Relatively minor importance, evokes subtle effects
- Atrial stretch (distension)
- Temperature
- Ionic Changes
Atrial stretch or distension (intrinsic)
- Stretch of SA node pacemaker cells
- Increase excitability
- Increases HR by 15%
Temperature (intrinsic)
- Increase in temperature increases HR by increasing ionic permeabilities
Ionic changes (intrinsic)
- Alterations in electrolyte balance
- Particularly K+ and Ca2+
- Effects excitability of pacemaker cells
- High Ca2+o or high K+o decreases HR
Extrinsic control of the heart
- Neurohormones
- Sympathetics
- PNS
- Bainbridge reflex
- Baroreceptor reflex
- Higher center control
- Respiratory
- Chemoreceptors
Sympathetics (extrinsic)
- Accelerate
- Norepinephrine effects on SA node
PNS (extrinsic)
- Decelerate
- Acetylcholine effects on SA node
Bainbridge reflex
- Stretch of atrial receptors in veno-atrial junctions of left and right heart
- Sensory impulses via vagus to cardiovascular center
- Increase sympathetic and decrease parasympathetic output to heart
- Therefore, an increase in HR
Bainbridge reflex stretching
- Accounts for 50-60% of stretch effect (along with SA nodal stretch effect)
Baroreceptor reflex relationship
- Inverse relationship between blood pressure and heart rate
In hypotension, such as that induced by hemorrhage, in response to the loss of a moderate amount of blood,
- Vagal tone diminishes
- Sympathetic activity increases
- Vagal activity ceases after BP declines to 20-30 mmHg below normal level
- Further acceleration of heart in response to declines in BP is mediated exclusively by increases in sympathetics
Higher center control (extrinsic)
- Cerebral cortex, hypothalamus, thalamus
- First two play roles in HR changes seen in excitement, anxiety
- Hypothalamic responses seen with temperature changes
Cortical and diencephalic centers
- Initiate cardiovascular reactions that occur during excitement, anxiety, and other emotional states
- Also during certain febrile disease states
Respiratory (extrinsic)
- Increase HR during inspiration
- Decrease HR during expiration
- Changes more pronounced in children
- Mediated via stretch receptors in lungs, via changes in venous return (i.e. Bainbridge reflex and baroreceptor reflex)
Chemoreceptors (extrinsic)
- Stimulation of receptors produces slight effects on HR
- Primary reflex effect of carotid chemoreceptor stimulation on SA node is inhibitory
- Secondary effects via changes in pulmonary ventilation (small increase, small increased HR; large increase, marked increased HR)
Hormones (extrinsic)
- Epinephrine (like sympathetic norepinephrine) produces a positive chronotropy
- Atrial natriuretic peptide (ANP), produced by atrial cells when stretched, affects blood volume, but probably has no effect on heart rate
Stretch effect (intrinsic control of SV)
- Starling’s Law of Heart (heterometric autoregulation)
- In simple terms cardiac output matches venous return
Increased venous return in Starling effect leads to an increase in
- EDV
- Stretch of ventricular fibers (increased sarcomere length)
- Force of contraction
- SV
Stretch effect is measured in
- Heart lung preparation
- Family of ventricular function curves are used as other parameters are changed
- These other parameters are related to changes in contractility (inotropism)
Changes in contractility
- Inherent changes due to alteration of Cai, Ki, other ions
Homeometric autoregulation
- Pressure induced (Anrep effect)
- Increase in afterload
- Decrease in SV
- Seen only at blood pressures above 160 mmHg
Rate induced changes
- Treppe/staircase
- After period of rest
- Ventricle responds to repetitive stimulation by increase in force of contraction
Alteration of blood gases
- Decreased Po2
- Increased Pco2
- Decreased pH
- Last two probably via decrease in pHi (since acidosis of cardiac muscle depresses contractility)
Inhibitory interactions between vago-sympathetic divisions
- Direct and indirect vagal effects via sympathetic inhibition
Increase in cyclic GMP causes
- Decrease SV (direct)
Decrease in cyclic AMP causes
- Decrease SV (indirect)
Increase in cyclic GMP due to
- Increased breakdown of cyclic AMP
Presynaptic inhibition of sympathetic terminals by vagal terminals effects
- ACh from vagal terminals inhibits sympathetic NE release
Presynaptic inhibition of parasympathetic terminals by sympathetic terminals effects
- NPY from sympathetic terminals inhibits vagal ACh release
