CVPR Week 2: Cardiac Muscle Physiology II Flashcards
Question
Extrinsic regulation of vascular resistance
- Neural / Hormonal control
Intrinsic regulation of vascular resistance
Regulation by local factors and mechanisms inherent to cells of the vascular wall
Regulation of vascular resistance
Question
Extrinsic regulation of Cardiac output
- Neural/Hormonal control
Intrinsic regulation of Cardiac output
Starling’s Law of the heart
Objectives
How is Heart Rate determined?
HR is determined by pacemaker activity
- Principle control of HR is by the ANS (extrinsic)
How is stroke volume determined?
Both intrinsic (Starling’s Law) and extrinsic (ANS) mechanisms regulate SV
Question
Sympathetic β1 receptors by Norepinephrine to speed up
Sympathetic α1 receptors vascular constriction
M2 by acetylcholine to inhibit adenylate cyclase???
Sympathetic pathway and parasympathetic pathways
What phase of an action potential and what type of action potential is important in determining HR?
Phase 4 of slow-response action potentials in the SA node
How HR is increased?
Ne increases the slope of SA nodal pacemaker potentials to quicken the ‘pace’ resulting in a decreased interval between action potentials thus increasing HR
How HR is decreased?
ACh decreases the slope of the pacemaker potential by hyperpolarizing the SA nodal cells
Identify the effect on HR
Identify the effect on HR
β1 receptor signal transduction mechanism
- NE stimulation of β1 receptor
- Gs-coupled activating Adenylate cyclase creating cAMP and activating PKA
Leads to
- leads to greater Ca2+ influx
- greater CICR from the SR
- greater contraction
- PKa can phosphorylate Ryanodine receptors and can increase sensitivity to Ca2+ so leads to more CICR and therefore greater contraction
Cardiac Muscarininic receptor signal transduction mechanisms
Autonomic tone predominating normal resting individuals
During sympathetic stimulation, not only is contractility increased but cardiac myocytes are receiving action potentials more frequently, so how do cardiomyocytes quickly relax
- PKA phosphorylates PL (Phospho Lambda), which regulates (inhibitory) SERCA pump Ca2+ pump and when phosphorylated by PKA, PL disinhibits SERCA.
- so PKA inhibits PLs inhibition of SERCA
- ACh would have the opposite effect
Parasympathetic effect on contractility
can influence atrial contractility but not really in the ventricles
Effects of NE and ACh on SV
Effects of NE on ventricular myocyte contractility
Effects of ACh on ventricular myocyte contractility
Signal transduction mechanisms associated with β1 receptor and muscarinic receptor stimulation
Summary of autonomic control of the heart: HR regulation
Summary of autonomic control of the heart: Contractility regulation
Starling’s Law of the Heart description
Starling’s Law of the Heart diagram
- ventricular pressure is a function of ventricular end-diastolic volume
- when the volume is really high starling’s law no longer applies and force of contraction is reduced
Thick and thin filament overlap
Starling’s Law of the Heart: Mechanism
Longer fiber lengths ________ spacing between thick and thin filaments.
reduces
Starlings law explanation
greater end diastolic volume stretching the heart = greater stroke volume
Longer fiber lengths increase the affinity of?
Troponin C for Ca2+
Starling Curves altered by stimuli
Starling’s Law of the heart: Physiological significance
Starling’s Law of the heart: Physiological significance diagram
sympathetic venous pressure get increased venous return get increased end-diastolic volume get an increased stroke volume
What mechanisms lead to increased CO?
- ↑ sympathetic activity to the heart increases HR and contractility
- ↑ sympathetic to venous indirectly increase venous constriction and venous return increasing end-diastolic volume (α1 receptors) and thereby increasing cardiac output by starlings law
- parasympathetic is the opposite effect on HR and contractility
Myocardial response to afterload stress
like lifting a heavyweight, increased BP or afterload impairs myocardial performance contraction velocity and cardiac output
What is afterload stress?
the load that cardiac muscle must overcome in order to shorten
Afterload is?
Aortic pressure (MABP)
Myocardial responses to afterload stress results in?
↑ Arterial pressure and decreased myocardial performance
Question
Effects of increasing HR on CO
Decreased SV associated with high HR (tachycardia) can limit?
CO
Decreased SV associated with high HR (tachycardia) can limit? Then what happens with exercise?
so the increased sympathetic tone and venous return helps to mitigate this
Summary of intrinsic mechanisms of cardiac regulation
Summary of physiologic regulation of myocardial performance
Question
Question
Question
chronotropic effects means
time effects in this case HR
Cardiac Function Curve AKA
Starling curve
typical systole time
300 msec
Typical diastole time
500 msec
Cardiac cycle typical time
800 msec
an increase in HR takes time from?
diastole which will decrease cardiac output
Atrial pacing increase reduces
stroke volume
Cardiac output to atrial pacing
Tachycardia can _______ filling time and thereby can reduce _________ and _________.
- stroke volume
- limit cardiac output
What is the principal control mechanism of HR?
Autonomic nervous system (extrinsic)
