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Functions of the circulatory system
Brings oxygen, nutrients, and hormones to cells
Fights infections
Regulates body temperature
Facts about the heart
Made of cardiac muscle
Average of 65-85 bpm (beats per min)
Chambers of the heart
4 chambers: Left and right atriums, left and right ventricles
Right side (in anatomical position): Pumps deoxygenated blood to the lungs
Left side (in anatomical position: Pumps oxygenated blood to the body
Valves of the heart
4 valves:
Atrioventricular (AV):
Tricuspid
Bicuspid (mitral)
Semilunar:
Pulmonary
Aortic
Tricuspid valve
The valve that separates the right atrium from the right ventricle
Bicuspid valve
The valve that separates the left atrium from the left ventricle
AKA “mitral valve”
Pulmonary valve
The valve that separates the right ventricle from the pulmonary artery leaving the heart
Aortic valve
The valve that separates the left ventricle from the aorta leaving the heart
Main blood vessels of the heart
2 veins:
Superior and inferior vena cavas
2 arteries:
Pulmonary artery
Aorta
Superior and inferior vena cavas
The veins of the heart that brings deoxygenated blood back to the heart through the right atrium
Pulmonary artery
The artery that takes deoxygenated blood away from the right ventricle in the heart and moves it to the lungs
Aorta
The artery that takes oxygenated blood away from the left ventricle in the heart and distributes it throughout the body
Interventricular septum
The muscular wall in the heart separating the left and right ventricles
Chordae tendineae
Thin, fibrous strands of connective tissue that anchor the AV valves’ leaflets to papillary muscles within the ventricles
AKA “heartstrings”
Papillary muscles
Specialized, pillar-like muscles in the ventricles that prevent AV valves prolapse and regurgitation during systole
Blood flow through the heart (deoxygenated)
Deoxygenated blood enters the right atrium via the superior and inferior vena cavas and coronary sinuses
The right atrium contracts, forcing blood through the tricuspid valve and into the right ventricle
The right ventricle contracts, forcing blood through the pulmonary valve and into the pulmonary trunk and arteries
The pulmonary arteries carry blood to the lungs, where it can ride itself of excess carbon dioxide and pick up a new supply for oxygen
Blood flow through the heart (oxygenated)
Freshly-oxygenated blood returns back to the heart in the left atrium through the pulmonary veins
The left atrium contracts, forcing blood through the bicuspid (mitral) valve into the left ventricle
The left ventricle contracts, forcing blood through the aortic valve and into the aorta for distribution throughout the body
Heartbeat/cardiac cycle
Atria systole
Atria diastole
Ventricular systole
Ventricular diastole
Actions of the heart
Atria contracts (atria systole) while ventricle relaxes (ventricular diastole)
Ventricle (ventricular systole) contracts while atria relaxes (atria diastole)
Then, the atria and ventricles both relax for a brief period
Atria systole
Contraction of atria
Atria diastole
Relaxation of atria
Ventricular systole
Contraction of ventricle
Ventricular diastole
Relaxation of ventricle
Sounds of the heart
Due to vibrations in heart tissues as the valves close
Can be described as “lub-dub” sounds
“Lub” → Ventricular systole
“Dub” → Atrioventricular (tricuspid and bicuspid) valves closing
Heart murmur
An abnormal heart sound due to valve damage
Caused by valve stenosis or valve prolapse
Valve stenosis
A serious, progressive heart condition where the aortic valve narrows, restricting blood flow from the hear to the body
It causes the heart to work harder, leading to thickened heart muscle, potential heart failure, and death if untreated
Valve prolapse
A heart condition where the bicuspid (mitral) valve’s flaps (leaflets) are too stretchy, causing them to bulge or flop back into the left atrium during contraction, often resulting in leakage (regurgitation)
Blood supply to the heart
The first branches off of the aorta (which carries freshly oxygenated blood) are the left and right coronary arteries that feed the heart muscle itself
Branches of the coronary arteries feed many capillaries of the myocardium
Blood flows best during the relaxation periods of the heart because contraction squeezes the blood vessels closed
Heart attack
The death of cardiac muscle cells, caused by plaque dislodges blocking a coronary artery
Blocking of coronary artery results in cardiac muscle cells starved for oxygen, resulting in death
After, scar tissue forms where cardiac muscle cells die, reducing function of the heart
Severity of this disorder depends on the size and area supplied by the artery
Risk factors: Smoking, high blood pressure (bp), high LDL cholesterol, diabetes
AKA “myocardial infarction (MI)”
Atherosclerosis
Plaque buildup that clogs arteries, reducing or even stopping bloodflow
These plaques can break off, causing a heart attack or stroke
Risk factors: Smoking, high blood pressure (bp), high LDL cholesterol, diabetes
AKA “coronary artery disease”
Stroke
A blood vessel in the brain is blocked (by dislodged plaque, or bursts, starving the cells of oxygen)
Symptoms: Numbness, vision changes, speech changes, confusion
Risk factors: Smoking, high blood pressure (bp), high LDL cholesterol, diabetes
Cardiac conduction system
Specialized cardiac muscle tissue conducts impulses throughout the myocardium and compromises this system
Sinoatrial (SA) node fires
Excitation spreads through atrial myocardium
Atrioventricular (AV) node fires
Excitation spreads down AV bundle
Purkinje fibers distribute excitation through ventricular myocardium
Pacemaker physiology
Each depolarization of the SA node sets off one heartbeat
At rest: Fires every 0.8 second or 75 bpm
SA node is the system’s pacemaker
SA node does not have a stable resting membrane potential
Starts at -60 mV and drifts upward from a slow inflow of Na+
When it reaches threshold of -40 mV, voltage-gated fast Ca2+ and Na+ channels open
Faster depolarization occurs peaking at 0 mV
K+ channels then open and K+ leaves the cell, causing repolarization
Once K+ channels close, pacemaker potential starts over
Electrocardiogram (ECG/EKG)
A recording of electrical changes that occur during a cardiac cycle
P wave
The first recorded wave of electrical changes in an ECG/EKG, which corresponds to the depolarization of the atria which leads to the contraction of the atria
QRS complex
In an ECG/EKG, this recorded complex corresponds to the depolarization of the ventricles, leading to the contraction of the ventricles and hides the repolarization of the atria
T wave
The last major recorded wave in an ECG/EKG that ends the pattern, which corresponds to ventricular repolarization and relaxation
What an ECG/EKG tells us
The intervals between the waves and the size of the waves give information about the heart’s ability to conduct impulses
Arrhythmia
An abnormal heart rhythm, with irregular or skipped heartbeats
Cause: Normally, the heart uses electrical signals created in the SA node in the right atria to begin a heartbeat. However, irregular firing of the SA node causes abnormal rhythm. The atrial form of this condition are less dangerous than the ventricular form of this condition.
Risk factors: Generally random, but factors are stimulants (ex. caffeine), fevers, stress, or genetic disorders
Tachycardia
A resting heart rate of 100+ bpm
Brachycardia
A resting heart rate of less than 60 bpm
Blood vessels
Carries blood to cells, lined with smooth muscle tissue and epithelium, simplest and most common route
Heart → arteries → arterioles → capillaries → venules → veins
Arteries
Carries oxygenated blood away from the heart to the rest of the body
Has strong, thick, elastic walls adapted for high pressure that becomes smaller as they divide and give rise to arterioles
Walls of arterioles get thinner as they approach capillaries
To regulate blood flow and pressure: Capable of vasoconstriction as directed by sympathetic impulses, and capable of vasodilation as directed by parasympathetic impulses
Aneurysm
A weak point in an artery or the heart wall
Forms a thin-walled, bulging sac that pulsates with each heartbeat and may rupture
Dissecting aneurysm: Blood accumulates between the tunics of the artery and separates them
Most common sites: Abominal aorta, renal arteries, and arterial circle at the base of the brain
Can cause pain by putting pressure on other structures
Can rupture, causing a hemorrhage
Results from congenital weakness of the blood vessels or result of trauma or bacterial infections (ex. syphilis)
Most common cause is atherosclerosis and hypertension (high blood pressure)
Capillaries
The smallest of the blood vessels (some have diameters as small as one red blood cell) that branch off arterioles, taking blood to cells where nutrients and gases are exchanged
Their permeability varies from one tissue to another: Generally more permeability in the liver, intestines, and certain glands, while less permeability in muscle
Areas with a great deal of metabolic activity have higher densities of these blood vessels
Precapillary sphincters: Regulates the amount of blood entering a capillary bed, controlled by oxygen concentration in the area
If blood is needed elsewhere in the body, the capillary beds in less important areas are shut down
Hydrostatic pressure
Drives the passage of fluids and very small molecules out of the capillary at the arteriole end by diffusion
Osmotic pressure
At the venule end, osmosis causes much of the tissue fluid to return to the bloodstream
Venules
Leading from capillaries, merge to form veins that return deoxygenated blood to the heart
Veins
Carries deoxygenated blood towards the heart
Have the same 3 layers as arteries have, except that the muscle layer is thinner, and have a flap-like valve inside to prevent backflow of blood
The lumen of the vein is larger than an artery’s
Don’t carry high-pressure blood
Also functions as blood reservoirs
Greater capacity for blood containment than arteries
Thinner walls, flaccid, less muscular and elastic tissue
Collapses when empty, expands easily
Has steady blood flow
Merges to form larger veins
Subjected to relatively low blood pressure
Remains 10 mm Hg with little fluctuation
Varicose veins
Blood pools in the lower legs in people who stand for long periods of time, as it stretches the veins
Cusps of the valves pull apart in enlarged superficial veins further weakening vessels
Blood backflows and further distends the vessels, causing their walls to become weak and develop into these type of veins
Hereditary weakness, obesity, and pregnancy also promote problems
Hemorrhoids: Varicose veins of the anal canal
Treatment for varicose veins
Sclerotherapy
Laser surgery
Sclerotherapy for varicose veins
Procedure where the doctor injects the veins with a solution that scars and closes the veins, causing the blood to reroute through healthier veins
Vein ligation/striping
Laser surgery for varicose veins
Procedure that sends strong bursts of light into the vein that make the vein slowly fade and disappear, often less effective than sclerotherapy, but no incisions or needles are used
Blood pressure
A measure of the force exerted by the blood on the wall of the arteries using a sphygmomanometer
Pressure decreases as distance from the left ventricle increases
Rise with age: Arteries are less distensible and absorb less systolic force
Determined by cardiac output, blood volume, peripheral resistance, and blood viscosity
Systolic pressure/diastolic pressure (ex. 120/80)
Systolic pressure
The result of the contraction of the ventricles (normal is 110-140)
Diastolic pressure
The relaxation of the ventricles (normal is 70-90)
Hypertension
High blood pressure with diastolic pressure over 90
Chronic if resting blood pressure is greater than 140/90
Consequences: Atherosclerosis, and can weaken small arteries and cause aneurysms
Why it’s dangerous: Excessive pressure can cause arteries to thicken, blood vessels to weaken and rupture, leading to heart failure, stroke, kidney failure, and loss of sight when vessels in eye burst
Risk factors: Genetics, obesity, limited physical activity, smoking, alcohol consumption, certain medications
Hypotension
Chronic low resting blood pressure caused by blood loss, dehydration, and/or anemia
Cardiac output
Stroke volume x heart rate
Stroke volume: The amount of blood discharged from the ventricles with a contraction (about 70 mL)
Heart rate: Bpm (average is 72 bpm)
Blood volume
The sum of the formed elements and plasma volume in vascular system
Varies with age, body size, gender, and dehydration
Normally, blood pressure is directly proportional to the volume of blood within the cardiovascular system
Peripheral resistance
The opposition to flow that blood encounters in vessels away from the heart
Vessel radius: The most powerful influence over flow
Vasoconstriction: Increases resistance, increases blood pressure
Vasodilation: By relaxation of smooth muscle, decreases resistance, decreases blood pressure
Blood viscosity
Greater the viscosity, greater the resistance to flow
Increase in blood cells and plasma
Dehydration also increases viscosity
Control of blood pressure
Blood pressure is determined by cardiac output times peripheral resistance; BP = CO (heart rate X stroke volume) x PR
The body maintains normal BP by adjusting cardiac output and peripheral resistance
Frank-Starling law of the heart: The relationship between fiber length and force of contraction
As blood enters the heart, the walls are stretched, giving a stronger contraction
Stronger contraction increases stroke volume and therefore increase cardiac output as well
Baroreceptors sense change in BP
The volume of blood that enters the right atrium is normally equal to the volume leaving the left ventricle
If arterial pressure increases, the cardiac center of the medulla oblongata sends parasympathetic impulses to slow the heart rate (cardioinhibitory reflex)
If arterial pressure drops, the medulla oblongata sends sympathetic impulses to increase heart rate to adjust blood pressure (cardioaccelerator reflex)
Other factors (ex. emotional upset, exercise, rise in temperature) can result in increased cardiac output and BP
Peripheral resistance also controls BP
Sympathetic nerves change the diameter of arterioles in response to BP changes
Vasodilation decreases PR and BP, while vasoconstriction increases PR and BP
The vasomotor center of the medulla oblongata can adjust the sympathetic impulses to smooth muscles in arteriole walls, adjusting BP
Certain chemicals can also affect PR by affecting precapillary sphincters and smooth muscle of arteriole walls
Increased CO2, decreased O2, and decreased pH causes vasodilation into tissues with high metabolic needs
Epinephrine and norepinephrine cause vasoconstriction
Hormonal control of blood pressure
Hormones influence blood pressure through vasoactive effects and regulating water balance
Angiotensin II: Potent vasoconstrictor that raises BP, promotes Na+ and water retention by kidneys, and increases blood volume and pressure
Atrial natriuretic peptide: Increases urinary sodium excretion, reducing blood volume and promotes vasodilation, lowering BP
Antidiuretic (ADH) hormone: Pathologically high concentrations that are also vasoconstrictors that promotes water retention and raises BP
Epinephrine and norepinephrine: Most blood vessels bind to α-adrenergic receptors causing vasoconstriction, while skeletal and cardiac muscles bind to β-adrenergic receptors causing vasodilation