18 17-19 temp Flashcards
Cardiac output
Amount of blood pumped out by one ventricle in 1 minute. HRxSV 75x70 =
Stroke volume
Volume of blood pumped out by one ventricle with each beat. (about 70ml)
EDV - ESV = SV
Ejection Fraction
ESV/EDV (i.e. 70/120, 58%)
Factors that influence/regulate HR
- ANS - para ↓HR, symp ↑HR
- Chemicals - Ions (Ca2+/Na+/K+), Hormones (E/NE)
- Other - Age/physical conditioning
Two types of controls that influence SV
- Venous return (intrinsic)
2. Sympathetic stimulation (extrinsic)
Three factors of Stroke volume
Preload (affects EDV),
Contractility and Afterload (both affect ESV)
Length-tension relationship of cardiac muscle
Relationship between length of myofilaments and how much force they can generate.
Frank Starling law - More stretch = more ejection. SV/EDV chart.
Stretching cardiac cells can produce dramatic increases in contractile force because the actin/myosin overlap at an optimal length when stretched.
Preload
An intrinsic control of SV. Venous return and length of diastole are contributors
Stretching cardiac muscle increases contractile force. Venous return is the most important factor in stretching the heart.
…….If venous return ↑, then EDV ↑, then force of contraction ↑, then SV ↑……
How does venous return increase?
- Exercise (causes ↑ in symp activity - and ↑ skeletal muscle and respiratory pumps) Clamps down on blood vessels to return more blood.
- ↓ HR (more time for ventricular filling.)
Contractility
A extrinsic control of SV. ANS/TH contribute
The force of contraction of the myocardium that is influenced by inotropic agents (external factors that affect force of contraction - these are independent of muscle stretch and EDV).
Ca2+ is a key player. More calcium, stronger contraction.
…….Bloodborne E, TH, ect, then ↑ contractility, then ↓ESV, then ↑ stroke volume.
Afterload
ANS is contributor
The pressure that the ventricles must overcome to eject blood.
HTN reduces the ability of the ventricles to eject blood.
Causes ↑ in ESV and ↓ stroke volume.
How is CO maintained if SV declines (loss of blood vol or weakened heart)?
By increasing HR and contractility. Introducing chronotropics to (which either decrease or increase HR.)
How does the ANS regulate the heart?
↑ HR.
-Exercise/fright/anxiety - sympathetic releases norepinephrine at cardiac synapses which ↑ Ca2+/threshold more quickly/SA fires more rapidly
Enhances contractility
-by enhancing Ca2+ movement (enhanced contractility lowers ESV so SV does not decline like if only the HR ↑)
Speeds relaxation - para ↓ HR after stressful situation has passed. (ACh/muscarinic)
How do hormones/ions regulate the heart?
NE/E from adrenal medulla.
TH - in large qty can increase hr.
Ions - electrolyte imbalances are danger to heart.
Effects of ANS on heart + related structures (Para —Symp)
- SA node ↓ HR ↑ HR
- AV Node ↓ HR ↑ HR
- Rest vent conduct sys No effect ↑ HR
- Atrial muscle No effect ↑force of contract
- Ventricular muscle No effect ↑force of contract
- A Medulla No effect ↑ E/N
- Veins No effect vaso-con/dilate
Extrinsic control
Regulation by neural input, circulating hormones, any factor from outside the heart
Factors affecting EDV
Venous return and length of ventricular diastole/fill time
shorter at 180 HR/0.125s than 75 HR/0.5s
Intrinsic control
Factors affecting the heart that originate from the heart.
Intrinsic conduction system, Length/tension relationship of cardiac muscle/Frank Starling law
ANS innervation runs from ? to the heart?
From medulla oblongata.
Cardioaccelatory center sends via Symp Cardiac nerve to SA/AV/Heart muscle/coronary arteries.
Cardioinhibitory center sends impulses down the vagus to the SA/AV.
Factors affecting EDV
Venous return and length of diastole (shorter at 180 HR/0.125s than 75 HR/0.5s)
Inotropic agents
Think contractility.
Ino = fibers
Positive inotropic agents increase Ca2+ (i.e. norepinephrine binds at B1 and by 2nd messenger process opens more Ca2+ channels).
Negative inotropic agents decrease the availability of calcium (i.e., beta blockers, acidosis-excess H+.)
CO factor/Initial stimulus - Exercise. Effect?
Physiological response
↑ Activity of respiratory pump
↑ Activity of muscular pump
↑ Sympathetic venoconstriction
↑ venous return
↑ EDV (preload)
↑ Stroke volume
Result
↑ Cardiac output
CO factor/Initial stimulus - ↓ HR Effect?
Physiological response
↑ venous return
↑ EDV (preload)
↑ Stroke volume
Result
↑ Cardiac output
CO factor/Initial stimulus - Bloodborne (E, TH)
Physiological response
↑ contractility
↓ ESV
↑ stroke volume
Result
↑ cardiac output
CO factor/Initial stimulus - Exercise/fright/anxiety
Physiological response
↑ Symp response/↓Para response
↑ HR
Result
↑Cardiac output
OR… ↑Symp
↑ contractility
↓ ESV
↑ stroke volume
Result
↑ cardiac output
Individual Factors affecting factors that affect SV
Venous rtn/Length of diastole (preload)
ANS/Hormones (contractility)
ANS (Afterload)
Factors that affect filling time
Sym sending blood back faster, Para slowing HR
Chronotropics
Think regulation of HR.
Chrono = time + tropos = change (positive or negative)
ANS,
Hormones,
Age, gender, body temp
How is CO controlled in times of stress vs. resting?
During resting periods, the cardioinhibitory center, venous return largely controls stroke volume. During stress, the cardioaccelatory center takes over activating the sympathetic nervous system and increasing HR (SA node) and stroke volume (by enhancing cardiac muscle contractility which decreases ESV)
