Feb 12 - Cardiac Output and Its Control Flashcards
What is cardiac output (CO)?
It’s the volume of blood pumped by each ventricle per minute. It is determined by two factors: heart rate and stroke volume
What is heart rate?
The number of times the heart beats per minute
The average resting heart rate is 70 beats per minute
What is stroke volume?
The volume of blood that is pumped per beat. The average resting stroke volume is 70 ml of blood per beat
How much is average cardiac output?
CO = HR x SV, therefore it equals approximately 5 L/minute
What is cardiac reserve?
It is the difference between the cardiac output at rest and at its peak (the maximum volume of blood that can be pumped by the heart per minute). During exercise the cardiac output increases to 20-25 L/min
How does the heart increase its output when demands on the body increase?
By increasing heart rate and increasing stroke volume
How does the autonomic nervous system modulate the heart rate
Sympathetic drive increases heart rate, while parasympathetic drive slows it down. In both individuals, both systems are typically active at any given time
What is the situation in which there is no direct autonomic control of the heart rate?
Heart transplant
Describe the SA node below threshold
Below threshold, SA node pacemaker cells high high potassium concentration but low sodium concentration intracellularly; a slow constant influx of sodium leads to progressive depolarization of the cell interior until threshold is hit; meanwhile, there is a low level of potassium leakage via potassium channels
What happens as resting membrane potential passes threshold?
As the resting membrane potential passes threshold, voltage-gated calcium channels open to permit the rapid influx of calcium concentration and the firing of the action potential
What happens as the cell repolarizes?
As the cell repolarizes, calcium is both sequestered internally and pumped out and potassium rapidly exits the cell to restore RMP; the Na/K ATPase restores intracellular sodium and potassium concentrations
How does sympathetic stimulation affect the heart rate?
Norepinephrine, released from sympathetic nerve endings, inactivates the potassium ion channels responsible for the outward leak, resulting in build-up of potassium (and thus positive charge) within the cell; there is also increased inward of the sodium and calcium, adding to this effect
How does sympathetic stimulation affect the AV node?
Sympathetic stimulation also reduces AV node delay, and speeds up the spread of the action potential throughout the specialized conduction pathway
How does sympathetic stimulation affect the force of contraction?
Sympathetic stimulation increases the strength of contraction of the atrial and ventricular cells since calcium influx has increased. Higher intracellular calcium concentration results in more forceful (and more rapid) contraction, i.e. there is an increase in cardiac contractility
How does parasympathetic stimulation affect the SA node?
Acetylcholine released from the parasympathetic nerve endings reduces SA node depolarization. This is achieved by slowing the closure of K ion channels, thereby enhancing K ion permeability, facilitating export of positive charge out of the cell and making the interior more negative (i.e. increasing polarity)
How does parasympathetic stimulation affect the AV node?
It increases AV node delay, and slows the spread of the action potential throughout the specialized conduction pathway
How does parasympathetic stimulation affect contractility?
Parasympathetic stimulation decreases the strength of contraction of the atrial cells by reducing calcium influx and intracellular calcium cycling. It has minimal effect on ventricles
The sympathetic and parasympathetic systems antagonize one another to control heart rate. Explain
The sympathetic nervous system controls the heart rate in emergency situations or when challenged, such as during exercise. The parasympathetic system controls the heart in relaxed situations. The activities of these two systems on the heart are in turn synchronized by the cardiovascular control centre situated in the brain stem.
What would happen if the there was no sympathetic or parasympathetic control of the heart?
In their absence, the heart rate would be around 100 bpm, indicating that at normal resting heart rate (70 bpm), parasympathetic influence prevails
How does epinephrine affect the heart rate?
The hormone epinephrine (adrenalin) is secreted into the blood by the adrenal medulla (in the adrenal glands) upon sympathetic stimulation and has similar actions to norepinephrine: an increase in heart rate and contractility
Mathematically, what is cardiac output?
CO = HR x SV
What determines stroke volume?
Venous return (intrinsic control) Sympathetic nervous system (extrinsic control)
What happens when blood returned to the heart from the venous system increases?
The more blood is returned to the heart from the venous system, more blood must be pumped out of the heart. This occurs via an increase in the end-diastolic volume (EDV), which in turn translates into a larger stroke volume (SV)
Why is EDV and SV imporant?
The relationship between the EDV and SV comprises an intrinsic control - it is inherent in the properties of cardiac muscle. This ability of the heart to adjust SV is dependent on the length-tension relationship of cardiac muscle
What is the Frank-Starling Curve? What is the Frank-Starling Law?
Unlike skeletal muscle fibres, cardiac muscle fibre length in the resting state is shorter than the optimal length required for maximal tension development. When stretched, however, cardiac muscle can develop maximal tension. A plot illustrating the relationship between muscle fibre length and muscle tension is called a Frank-Starling Curve; the Frank-Starling law of the heart describes the relationship between EDV and SV
What determines cardiac muscle fibres length?
The major factor determining cardiac muscle fibre length is the amount of blood entering during diastole. The situation is similar to a balloon which, when filled with water, stretches more and becomes larger. Increased filling results in increased stretching of the heart, which results in greater tension development, stronger force of contraction and larger stroke volume
The inherent relationship between venous return and stroke volume has a major benefit - equalization of output between the right and left sides of the heart. Explain
When the right side of the heart receives a large volume of blood, the EDV increases and causes the right ventricle to contract forcefully, propelling blood into the pulmonary circulation. The venous return of this large volume to the left side of the heart increases the EDV and causes the left ventricle to contract forcefully, ejecting blood into the systemic circulation.
What happens if equalization doesn’t occur?
There would be increased damming of blood in the venous system preceding the ventricle with reduced output
How does sympathetic control affect stroke volume?
Sympathetic stimulation is referred to as an extrinsic control of stroke volume - the source of regulation is not inherent to cardiac muscle. Activation of the sympathetic nervous system results in an increase in cardiac contractility (i.e. force of contraction) at any given EDV. This results in an upward shift in the Frank-Starling Curve
How does sympathetic control affect the venous system?
Activation of the sympathetic nervous system also causes constriction of veins, which in turn results in greater return of blood to the heart. This greater return subsequently increases EDV and CO (Frank-Starling mechanism - intrinsic control)
How is cardiac output controlled overall?
Control of cardiac output is thus achieved by a balance between heart rate and stroke volume, and is influenced by both intrinsic and extrinsic factors
How does cardiac output change over time?
Cardiac output reduces with age partly because of a reduction in the release of norepinephrine from nerve terminals of the aged heart
How can pathologies affect cardiac output?
Some pathological conditions may increase the workload of the heart, for example hypertension or a defective valve. The heart has to therefore generate sufficient pressure to overcome the elevated arterial pressure or obstruction caused by the defective valve. The heart becomes larger via hypertrophy of the muscle fibres, enabling it ot maintain a normal stroke volume
What is hypertrophy?
It is a short term compensatory mechanism by which the heart is able to adjust to the increased workload, but sustained workload elevation causes deleterious changes to the heart leading to a state of failure
Why does heart failure occur?
Heart failure occurs when the heart is unable to pump sufficient blood to meet the metabolic demand of organs and tissues. This could be due to damage of the cardiac muscle or sustained workload. The failing heart ejects a lower stroke volume for a given EDV in comparison to a non-failing heart. Thus impaired contractility is the hallmark of heart failure
What are compensatory mechanisms of heart failure?
Elevated sympathetic activity and increased EDV are compensatory measures that recover stroke volume to normal in the initial stages of heart failure
What is the result of heart failure?
Because cardiac output is diminished in the failing heart, the kidneys retain extra salt and water, increasing blood volume and thus elevating EDV. As the disease progresses, the heart is unable to pump a normal stroke volume and progressively less blood is pumped out. This results in backward failure as blood that is unable to enter the heart and blood that cannot be pumped out clog up the venous system. Forward failure soon ensues when the heart cannot pump sufficient blood as a result of progressively diminished stroke volume
