Cardiovascular Physiology Flashcards
Cardiac output at rest
75 bpm x 70 mL = 5 L/min
Cardiac output during exercise
150 bpm x 130 mL = 19.5 L/min
Cardiac reserve
Difference between cardiac output at rest and cardiac output during exercise
Cardiac output equation
CO = SV x HR
Stroke volume
Amount of blood pumped with each heartbeat
Venous return
The volume of blood returning to the heart from the vasculature every minute
Describe how hypertrophy can lead to heart failure in terms of cardiac output
Hypertrophy of the heart means the heart has increased in size and become harder to contract
During rest, cardiac output is normal but during exercise cardiac output has decreased therefore the cardiac reserve has decreased
During exercise more blood is required to be pumped around the systemic circuit but with increased size of the heart this is difficult - supply cannot meet demand
Preload
The degree of stretch that the ventricle can undertake
Afterload
The pressure in the major arteries (especially aorta) resisting the blood being pumped from the left ventricle
Contractility
The amount the heart can contract to expel the blood from the ventricle
3 things that regulate stroke volume
Preload
Afterload
Contractility
Describe how stroke volume can be regulated
Preload - larger degree of stretch in the ventricle allows more blood to pool, stroke volume increases
Afterload - high pressures in the systemic arteries are more difficult to overcome, stroke volume decreases
Contractility - larger force of contractility expels more blood from the ventricle, stroke volume increases
Inotropy
Change in stroke volume
Chronotropy
Change in heart rate
Describe Frank-Starlings law of the heart
The more the heart fills with blood during diastole the greater the force of contraction during systole
Preload is directly proportional to end diastolic volume
End diastolic volume
The amount of blood remaining in the ventricle just before systole begins
End systolic volume
The amount of blood remaining in the ventricle at the end of systole
Describe what happens when the conduction system of the heart becomes out of sync
Slightly out of sync: Decreased contractility
Very out of sync: Arrhythmia
3 steps of cardiac muscle contraction
Depolarisation
Plateau
Repolarisation
Describe how an action potential causes ventricular contraction
Autorhythmic cells in the SA node initiate excitation which causes a wave of depolarisation throughout the myocardium as a result of sodium influx when voltage-gated fast sodium channels open
Influx of calcium ions when voltage-gated slow calcium channels open and efflux of potassium when some potassium channels open causes a plateau or maintained depolarisation
The calcium influx ensures that the action potential lasts almost as long as the contraction of the cell which in turn ensures the unidirectional excitation of the myocardium
Repolarisation of the myocardial cells occurs when the voltage dependent calcium channels close and additional voltage-gated potassium channels open
Describe how the different parts of an ECG relate to action potential
P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation
Describe how the sympathetic nervous system sends messages to the heart
Input from sensory receptors or brain centres such as the limbic system or hypothalamus move down into the brainstem to the cardiovascular centre in the medulla oblongata
The nerve moves through the spinal cord into the sympathetic trunk ganglion and to the heart via the cardiac accelerator nerve
Increased rate of spontaneous depolarisation in SA node and AV node increases heart rate
Increased contractility of atria and ventricles stroke volume
Describe how the parasympathetic nervous system sends messages to the heart
Input from sensory receptors or brain centres such as the limbic system or hypothalamus move down into the brainstem to the cardiovascular centre in the medulla oblongata
The nerve bypasses the spinal cord and goes straight to the heart via the vagus nerve
Decreased rate of spontaneous depolarisation in SA node and AV node decreases heart rate
Describe how increased preload can increase cardiac output
Increased end diastolic volume stretches the heart
Preload is increased
Cardiac muscles contract more forcefully with stretching due to Frank-Starlings law of the heart
Stroke volume is increased
Cardiac output is increased due to CO = SV x HR
Describe how increased contractility can increase cardiac output
Positive inotropic agents such as catecholamines, glucagon and thyroid hormones in the blood increase contractility
Positive inotropic agents increase force of contraction at all physiological levels of stretch
Stroke volume is increased
Cardiac output is increased due to CO = SV x HR
Describe how decreased afterload can increase cardiac output
Decreased arterial blood pressure during diastole causes decreased afterload
Semilunar valves open sooner when blood pressure is lower in aorta and pulmonary artery
Stroke volume is increased
Cardiac output is increased due to CO = SV x HR
Describe how the nervous system can affect cardiac output
Cardiovascular centre in medulla oblongata receives input from cerebral cortex, limbic system and receptors
Increased sympathetic stimulation and decreased parasympathetic stimulation leads to increased heart rate
Cardiac output is increased due to CO = SV x HR
Describe how chemicals can affect cardiac output
Catecholamines or thyroid hormones in the blood increase heart rate
Cardiac output is increased due to CO = SV x HR
How to calculate mean arterial pressure
Diastole + 1/3 systole = MAP
Hypertension blood pressure
140/90
Normal blood pressure
120/80
Blood volume in the systemic capillaries
7%
Describe how blood pressure affects gas exchange
Increased blood pressure means more blood is coming into the capillaries and more gas is available for exchange
Increased BP = increased exchange
Stable BP = stable gas exchange in capillary beds
Describe how blood pressure varies throughout the cardiovascular system
In the aorta and arteries, systolic blood pressure and diastolic blood pressure are very different
In the arterioles the blood pressure drops and gets more stable. There is still some difference between diastolic and systolic because of the arterioles ability to adjust diameter
Capillaries have lower blood pressure
Venules, veins and vena cavae have very low blood pressure with almost no fluctuation
Starlings law of the capillaries
(BHP + IFHP) - (BCOP + IFOP) = NFP
Blood hydrostatic pressure + interstitial fluid hydrostatic pressure - blood colloid osmotic pressure + interstitial fluid osmotic pressure = net filtration pressure
Describe how capillary flow works
Lymphatic fluid from lymphatic capillary returns to the blood plasma
The blood flows from arterioles into the arterial end of the capillary where blood hydrostatic pressure and interstitial fluid osmotic pressure are pushing into the interstitial fluid. These are pressures promoting filtration. This is balanced somewhat by blood colloid osmotic pressure pushing into the capillary.
The blood continues to flow through the capillary to the venous end where blood hydrostatic pressure continues to push out of the capillary but interstitial fluid hydrostatic pressure and blood colloid osmotic pressure are now pushing into the capillary. These are pressures promoting reabsorption.
Leftover blood not filtrated or reabsorbed flows from the capillary into a venule to continue into veins and back to the heart.
Describe why circuits are arranged in parallel
To distribute even pressure among organs
Poiseuilles law of the heart
R ∝ Ln
Vessel resistance is directly proportional to the length of the vessel and the viscosity of the blood
R is inversely proportional to r^4
Describe the relationship between blood flow velocity and total-cross sectional area of vessels
The larger the total cross-sectional area of a blood vessel the slower blood will move through it
e.g. capillaries have the largest cross-sectional area of any blood vessels therefore blood moves the most slowly through them
How to calculate blood pressure
BP = CO x TPR
Factors influencing blood pressure
Increased heart rate
Increased contractility
Vasoconstriction and vasodilation
Blood volume increase or decrease
Factors influencing TPR
Blood vessel radius
Blood viscosity
Blood vessel length
Describe how norepinephrine affects blood pressure
Norepinephrine is released by stimulation of the sympathetic nervous system
Norepinephrine increases heart rate and contractility
Increased blood pressure
Describe how Angiotensin II affects blood pressure
Angiotensin II (and ADH) is a potent vasoconstrictor Vasoconstriction increases total peripheral resistance which increases blood pressure
Describe how nitric oxide affects blood pressure
NO (and ANP and epinephrine in some cases) is a potent vasodilator
Vasodilation decreases total peripheral resistance which decreases blood pressure
Describe how aldosterone affects blood pressure
Aldosterone (and ADH) retain water from being excreted by the kidneys, increasing blood volume and increasing blood pressure
Describe how ANP affects blood pressure
Atrial Natriuretic Peptide promotes water excretion through urine via the kidneys, decreasing blood volume and increasing blood pressure
Describe where the baroreceptors are found
Carotid sinus and arch of aorta
4 things that increase venous return
Vasoconstriction
Respiratory pump
Skeletal muscle pump
Increased blood volume
Describe how increased venous return could affect mean arterial blood pressure
Increased venous return increases stroke volume
Increased stroke volume increases cardiac output
Increased cardiac output increases MAP
MAP = CO x TPR
Describe how the body acts to restore homeostasis during hypovolemic shock
Hypovolemic shock occurs when you lose more than 20% of your blood supply
Massive decrease in blood pressure means baroreceptors in carotid sinus and aortic arch fire less in response to decreased stretch
Decreased rate of nerve impulses from the baroreceptors signals the cardiovascular centre in the medulla oblongata to increase sympathetic stimulation and hormones from adrenal medulla
Decreased rate of nerve impulses from baroreceptors also signals the hypothalamus to synthesis ADH and the posterior pituitary to release the ADH
The ADH acts on the kidneys to conserve salt and water, rate of urine production decreases which increases blood volume
ADH also acts on blood vessels to constrict them to increase total vascular resistance
Sympathetic stimulation acts on the heart to increase heart rate and contractility which increases cardiac output
The three results:
Increase in blood volume
Increase in vascular resistance
Increase in cardiac output
All act together to increase blood pressure and restore homeostasis
