Lecture 14: Cardiac Output Flashcards
Cardiac output
Volume of blood each ventricle pumps per unit time
CO = HR * Stroke Volume
HR control
Parasymp. + symp. to SA node (chronotropic)
Symp. to entire conducting system, parasymp. to atria/AV node conducting (dromotropic)
Parasympathetic stimulation of SA node
Lowers heart rate by decreasing F-type Na+ channel permeability, increasing K+ permeability - pacemaker potential starts lower, rises slower
Sympathetic stimulation of SA node
Increases HR by increasing F-type Na+ channel permeability - pacemaker potential reaches threshold faster
Heart adrenergic receptors
Epi from adrenals (increases HR) and NE from ANS neurons interact with the same β adrenergic receptors to change HR
Stroke volume control
SV is most important variable influencing CO - more force = more emptying
3 main factors for contractility:
1. Change in EDV (preload)
2. Change in symp. input magnitude to ventricles
3. Change in arterial pressure (afterload)
Frank-Starling mechanism of the heart
Length-tension relation for cardiac muscle; more diastolic filling -> more forceful contraction. Thus increased venous return -> increased CO due to more EDV increasing SV
Why does more cardiac stretch increase contractile force?
- Change in thick/thin filament overlap (more stretch -> more overlap)
- Decreased spacing between thick/thin filaments
- Increased sensitivity of troponin for Ca++ binding
- Increased Ca++ release from SR
ANS innervation of the ventricles
Only sympathetic nerves are distributed to the entire myocardium; NE to β-receptors increases ventricular contractility at any EDV (inotropic effect)
How does sympathetic stimulation affect cardiac contraction/relaxation speed?
Sympathetic stimulation increases speed of contraction and relaxation. Almost no parasympathetic stim. of ventricles
Adrenergic GPCR cascade
Adrenergic symp. activation triggers a G-protein coupled cascade -> cAMP production -> PKA activation
How does PKA activation increase cardiac contractility?
PKA phosphorylates several proteins to increase contractility
-L-type Ca++ channels more active
-RyRs more active
-Phospholamban less active (doesn’t close SERCA) (lusitropic)
-Decreased Ca++ affinity for TnC (lusitropic)
-Thick-f proteins assoc. w/ X-bridges
-Titin less stiff (easier filling)
Overall net effect of PKA activity on contractile cardiomyocytes
Increased contractility due to:
1. Faster and greater Ca++ release
2. Faster Ca++ return
3. Accelerated X-bridge activation and cycling
Preload
EDV; amount the heart gets filled
Afterload
Arterial pressure; defines how hard the heart has to work to open valve and pump blood. Increased arterial P -> more vent P needed to start ejection -> longer latent period, slower ejection velocity
Factors influencing CO
Primary: SV, HR
Secondary (SV): preload, afterload, contractility
Why is Frank-Starling important for the CVS in series?
Length-tension maintains equal systemic/pulm. flow; more filling leads to more ejection
How does an increase in cardiac contractility affect the Frank-Starling curve?
Increased contractility shifts the F-S curve upwards; i.e. more SV at a given EDV
Law of Laplace
Wall stress σ = Pr / 2h where h = wall thickness
How does the Law of Laplace affect the heart?
Increased radius increases wall stress i.e. more filling stresses the heart more. This is compensated by increasing the wall thickness, i.e. cardiac hypertrophy
Fick’s method for measuring CO
CO = vO2 / C_a - C_v where vO2 = O2 inspired by body, C_a = [O2] leaving lung, C_v = [O2] entering lung
Indicator dilution for measuring CO
Injection of dye to the heart; measuring concentration tells us flow aka vol. / time (V1C1 = V2C2)
Thermodilution for measuring CO
Swan-Ganz catheter injects cold saline and a temperature detector measures how long it takes for the colder fluid to flow through
Echocardiography
Mapping heart transthoracically with sound; allows us to measure ESV and EDV.
