Cardiovascular Physiology 4 Flashcards
What are the factors influencing contractility in cardiac muscle ?
How effectively the heart pumps depends on 3 factors- preload, heart rate, and contractility
Force of contraction depends on 2 factors
-length of the muscle fibers at the start of contraction (Frank Starling law)
-Contractility which is the intrinsic ability of cardiac muscle to contract at a given fiber length (depends on sympathetic and parasympathetic stimulation)
Briefly describe cardiac muscle length-tension relationship
Increased stretch (filling/EDV) causes an increase in sarcomere length to produce an increase force/tension production. ‘Frank Starling Mechanism’.
As muscles is stretched, more tension is generated
Cardiac muscle is much more stiff than skeletal muscle, and held by tendons, so not held at optimum overlap
Physiological range for cardiac muscle 8s between 80 and 100 percent (at 80% length there is 20% length, skeletal the relationship is closer to 1 to 1)
Explain the length tension relationship of of cardiac muscle length( frank starling mechanism)
- skeketal muscles resting length is the optimal length & at which it develops maximum tension
- Resting length of cardiac muscle is optimal
- Increased length to optimal will increase contractile tension
- for cardiac muscle the major determinant of fiber length is EDV
- the higher the EDV, the higher the stretch and the higher the force of contraction and SV
- This intrinsic relationship between SV and EDV is called the Frank Starling law of the heart(more you stretch, the more you pump
Why is it called Frank Starling law law?
Named after two physiologist who found this law
Increased EDV(volume coming in) produces more stretch in the myocardium. This is refferred to as ‘preload’. Under ‘normal ‘ conditions the greater the stretch/ preload the greater the SV. (can also be a function of diastolic pressure)
What is the stretch in starling graph?
Indicated by ventricular end-diastolic volume (mL)
Descending limb of length tension doesn’t exist in normal heart(starling graph) (this due to no effective pump occurring)
That is when within physiological limits muscle doesn’t get stretched beyond the optimal length to a point that contractile strength diminishes with further stretching
How does sympathetic nerve stimulation affect contractility?
Under sympathetic NS influences same EDV/preload we have a greater SV
More norepinephrine causes more tension for the same volume
Contractility increases under sympathetic nerve stimulation
What does the workload of the heart depend in?
Preload
After load
What are the loading conditions of preload?
- Equal to the amount of myocardial stretch before ventricular contraction
- Is a function of Left Ventricular EDV/ Left Ventricular EDP
- Can also be changed independently of EDV/EDP via changes in myocardial compliance
What are the loading conditions of the cardiac cycle?
- Is primarily a function of aortic pressure (this is about 80mmHg)
- Equal to the forces the myocardium overcomes to eject a given amount of blood
- Can also be altered through changes in ventricular radius, and resistance of valves
Explain the pressure volume curve of the cardiac cycle
A—> B: Ventricle relaxed AV valve open and being filled from atria till EDV-end diastolic volume135 mL
B—>C: at point B, ventricle pressure rises to about 80 mmHg (first heart sound at point B. Ventricles contract (force related to EDV); mitral and aortic valve shut: isovolumetric contraction
C—> D: Aortic valve opens, ventricular volume decreases (SV) leaving ESV in ventricle; ventricles starts to relax. At point D all four valves are now closed(second sound)
D—> E: Aortic valve closes. Isovolumetric relaxation. Ventricular pressure< Atrial pressure AV valve open
What happens when preload is increased?
You will pump more blood, increasing stroke volume, provided other constants are kept constant
What happens in changes in afterloqd?
Increase in after load, causes there is a EDV decreases SV ( under normal conditions )
If we don’t control hypertension, we won’t pump effectively
What are the effects of inotropic drugs?
Inotropic drugs change contractility
Positive inotropic drugs are used to increases stroke volume at the same EDV compared to normal
Negative inotropism decrease stroke volume at same EDV compared to normal (like calcium blockers) so residual volume increases
Describe cardiac performance
-Cardiac performance can be assessed by measuring cardiac output
-Cardiac output is measured over a period of time, which is one minute
CO= SV*HR (heart rate)
- Stroke volume(SV) is the amount of blood ejected from the ventricle per contraction and depends on the force generated during contraction
- Stroke volume= EDV- ESV
- ejection fraction used to measure pump efficiency
- EF(%)= SV/EDV
In average adult CO is 5 L/min
What are the effects of the autonomic nervous system of the heart?
Sympathetic nerve- increases heart rate, speed of conduction, force of contraction-contractility, and excitability
Parasympathetic nerve- decreases heart rate (innervates only the SA node and the AV node
Explain parasympathetic regulation of heart rate
Acetylcholine acts on Muscuranic receptors reduces excitability of pacemaker cells primarily in SA node via:
-Increased K+ conductance (Ik+) hyperpolarizes
-Decreased Ca2+ conductance (ICa2+) slower rate of depolarization
(Acetylcholine also acts at AV node to reduce Ca2+ conductance (ICa2+). This effect reduces conduction velocity
Explain sympathetic regulation of heart rate
- Catecholamines act on B1 receptors on pacemakers in SA node to increase rate, excitability & conduction velocity via:
- Increased conductance of IF channels & ICa2+ channels depolarizes membrane potential & increase rate of depolarization of pacemaker potential
- Imcreased rate of depolarization also increases conduction velocity
Hyper excitable, step AP
Explain sympathetic regulation of contractility of cardiac cells
- Action potential enters from adjacent cell
- Voltage-gated Ca2+ channels open. Ca2+ enters cell
- Ca2+ induces Ca2+ release through ryanodine receptor-channels
- Local release causes Ca2+ spark
- Summed Ca2+ sparks create a Ca2+ signal
- Ca2+ ions bind to troponin to initiate contraction
- Relaxation occurs when Ca2+ unwinds from troponin
- Ca2+ is pumped back into the sarcoplasmic reticulum for storage
- Ca2+ is exchanged with Na+
- Na+ gradient is maintained by the Na+-K+-ATPase
Activation of B1 receptors on cardiac myocytes produces increased Ca2+ influx via L- type Ca2+ channels
How does sympathetic regulation pose a problem ?
Sympathetic regulation of contractility primarily involves increased Ca2+ influx
-There’s a problem … how to increase heart rate and contractility at the same time
Don’t want to increase action potential in the plateau phase of the curve as it will prolong the refractory period
Heart overcomes this by increasing sarcoplasmic reticular activity
More calcium is taken up quickly, which also shortens duration of action potential and increases heart rate, solv8ng the problem and gives more forceful contraction
Contrast the effects of the autonomic nervous system on the heart
Sympathetic- increase heart rate, increase speed of conduction, increased force of contraction and increased excitability
Parasympathetic- decreases heart rate
What does chronotropic mean?
Increasing heart rate
What does dromotropic mean?
Speed of conduction
What does inotropic mean?
Force of contraction
What does bathrotropic mean?
Excitability
