L20. Control of the Heart Flashcards
(20 cards)
Cardiac output changed by controls?
CO = HR x SV (ml/min)
- Chronotropic refers to heart rate
- Inotropic refers to the force of contraction
Intrinsic control of stroke volume?
- SV is the difference between the end diastolic volume (EDV) and the end systolic volume (ESV)
- SV = EDV - ESV
- With every beat the heart pumps about 60% of the blood in its chambers (65-70mL)
- SV is determined by the preload, afterload and contractility of the heart
Preload (Intrinsic)?
Preload determines the initial (pre-contraction) muscle fibre length
- For the left ventricle (LV) this is related to the end diastolic volume (LVEDV) and to the end diastolic pressure (LVEDP); when LVEDV and LVEDP increase, preload increases
- LVEDV/P will be used as the index of preload of the left ventricle
Frank-Starling mechanism?
The responses to changes in preload: “if LVEDV increases, the left ventricle responds by doing more work”
- Usually, the extra work done by the left ventricle produces a larger stroke volume
- “More fill –> more empty”
Afterload (Intrinsic)?
Afterload is the tension the fibres must generate before they can shorten
Afterload is the pressure that the ventricles must overcome to force open the aortic and pulmonary valves
- Anything that increases systemic or pulmonary arterial pressure can increase afterload e.g. hypertension
- Mean aortic (or mean arterial) pressure will be used as the index of afterload of the left ventricle
Extrinsic control of contractility?
Catecholamines released from the adrenal medulla, and from sympathetic nerves in the heart, can alter ventricular function without a change in LVEDV
- Improve contractility
- “More effective pump”
Causes contraction and relaxation to occur more quickly
Increased ejection fraction?
One way to quantify contractility is through the ejection fraction (EF), defined as the ratio of stroke volume (SV) to end diastolic volume (EDV):
EF = SV/EDV
- Expressed as a percentage, the ejection fraction normally averages between 50 and 75 percent under resting conditions (e.g. if SV = 70ml and EDV = 130ml; EF = 54%)
- Increased contractility (SV increases) causes an increased ejection fraction
Inotropic effects on cardiac muscle?
Increase activity of sympathetic nerves to heart (increases contractility),
Increase EDV,
Increase plasma epinephrine (increases contractility)
= All adding up to an increase in stroke volume
Controlling heart rate intrinsically?
Intrinsic mechanisms play a very limited role on heart rate
- Increases in right atrial pressure have a small direct effect on the frequency of action potential generation by the SA node
- An increase in core temperature increases heart rate ~ 10 beats min-1 degrees-1
Controlling heart rate extrinsically?
Extrinsic mechanisms (nervous and endocrine) are major controls of heart rate
- These operate in a tonic manner; that is they are active most of the time, and they control the cardiovascular system by an alteration in the level or degree of their control, rather than by simply switching on and off
Nervous changes to the heart?
Effect of sympathetic and parasympathetic nerve stimulation on heart rate:
- An increase in parasympathetic nervous activity (Vagus nerve) to the SA node reduces HR (110bpm to 70bpm)
- Increases in sympathetic nervous activity increase in the frequency of AP generation in the SA node i.e. increases HR (110bpm to 170+bpm)
- These two branches of the autonomic nervous system act reciprocally
- Agents that alter heart rate are said to have a chronotropic effect
- The chronotropic effects of the parasympathetic and sympathetic nervous systems are brought about primarily by alterations to the slope of the slow diastolic pacemaker potential, through changes in the permeability of the SA nodal cell membrane to K+, Na+ and Ca2+
Sympathetic nervous effects on the heart?
- Increase in conduction velocity
- Greater synchrony of both atrial and ventricular contractions
- Reduction in the duration of the plateau phase of the myocardial action potential and in the duration of systole
Overall, when sympathetic activity increases we get:
- Increase in heart rate
- Increase in conduction velocity
- Reduction in the duration of diastole and a smaller reduction in the duration of systole
- Better synchronisation of contractions
- Elevated contractility (SV is maintained despite HR increase)
Increase in HR, increase in SV –> Increase in CO
Cardiac work?
The work the heart has to do - and hence the metabolic cost (O2 demand) is determined by tension development in the cardiac muscle
- Described by Law of Laplace:
The muscle tension (T) that must be generated to develop a given ventricular pressure (P) depends upon the radius of the ventricle (r) and the thickness of the ventricle wall (u)
Cardiac work equation?
Tension = transmural pressure x radius / 2x wall thickness
T = P x r / 2 x u
Thus:
T is proportional to P
T is proportional to r
T is proportional to 1/u
- Metabolic cost of running the heart is related more to tension development than muscle shortening
- For a constant afterload (mean arterial blood pressure), the tension that has to be generated by the ventricular muscle increases as the radius (LVEDV) increases
- Or, for a constant radius, the tension that has to be generated by the ventricular muscle increases as the afterload increases
Acute heart failure (preload)?
- The left ventricle is unable to contract effectively at a normal LVEDV
- It fills more - larger LVEDV - in order to generate a normal stroke volume (Starling’s law of the heart - an intrinsic response)
- By continuously operating at this larger volume (larger radius), the ventricle will have to generate more tension; in addition, the dilated ventricle will have a thinner wall (smaller u) - which compounds the problem
Arterial hypertension (afterload)?
- The ventricle has to generate a higher pressure than normal
- This requires greater tension development
- Hypertrophy of the ventricular wall leads to an increase in wall thickness, bringing wall tension development back towards normal
- The larger mass of heart muscle will require more oxygen (and coronary blood flow reduced to thick muscle)
The force production of a cardiomyocyte increases at longer lengths due to:
i. Increased concentrations of Ca2+
ii. Increase in number and strength of cross bridges
iii. Increase in the Ca2+ sensitivity of the myofilaments
A. All of the above are correct
B. Only i is correct
C. Only ii is correct
D. Only ii + iii are correct
D
What does chronotropic refer to?
Heart rate
What does inotropic refer to?
Stroke volume
Define contractility?
Ability of muscles, particularly heart muscle (myocardium), to shorten and generate force
