CARDIOVASCULAR PHYSIOLOGY I - Heart
Chap. 9, 10, 11
I. Introduction
A. General Functions
1. Important transport system
a. If you want to change the composition of any of the fluid compartments then you start at the plasma
2. Important in the immune system
3. Important role in the acid-base balance
B. Components
1. Pump (heart)
2. Vessels (arterioles, capillaries)
3. Blood
C. Divisions: Two complete circuits
1. Pulmonary: Blood is going to the lungs
a. Is a much shorter circuit
b. The right side of the heart
2. Systemic: Blood going to the rest of the body
a. The left side of the heart
3. Both circuits have all the components
II. Heart: Two major components: The contractile portion generates force and decreases the pressure of the cardiac muscle and the conductile portion initiates electrical events and disperses it across the heart muscle (SA node, AV node, the Bundle of His, Purkinje System, and the Bundle Branches) and modifies the cardiac muscle but it unable to contract
A. Microanatomy: The cardiac muscle is branched and striated with dark bands that mark the junctions (boundaries) of the adjacent cardiac muscle fibers called intercalated disks
1. Intercalated disks: Boundaries are areas of low electrical resistance and an action potential is propagated in the cardiac muscle fiber and then is propagated to the adjacent muscle fibers and so on… This is because of the low electrical resistance
2. This is different from skeletal muscle because there is no reason for the cardiac muscle fibers to be privately innervated since it has areas of low electrical resistance
3. Troponin, tropomyosin, actin… Is all pretty much the same
4. Sub-sarcolemma Ca++ stores: Cardiac muscle has sarcoplasmic reticulum to hold Ca++ but also has other storehouse for Ca++ and sub-sarcolemma “pool” and it is underneath the sarcoplasmic reticulum and holds extra Ca++
5. Cardiac muscle has T-tubules and the sarcoplasmic reticulum and also a high density of mitochondria because it needs lots of oxygen (cardiac muscle fibers has the highest metabolic demand of any other tissue in the body)
B. Electrical Events
1. Fast Response
a) Description: Atrial muscle, ventricular muscle, and Purkinje fibers are all contractile fibers
i. Have a resting membrane potential (-95 mv) and is farther from 0 than in the skeletal muscle
ii. 400 milliseconds: longer than action potential in the skeletal muscle
b) Ionic events
i. At 0: What is responsible for the rapid depolarization? Rapid increase in Na+ permeability and causes depolarization
ii. At 3: Repolarization due to decrease in Na+ permeability and an increase in K+ permeability
iii. Depolarization/Repolarization no different than usual action potential
iv. What causes the plateau? Due to an increase in Ca++ permeability from the slow Ca++ channels
v. Because of the influx of Ca++ get the plateau before repolarization; Ca++ coming in to cardiac muscle fiber
vi. See the action potential in atrial, ventricle, and Purkinje fibers and the cardiac muscle fiber absolute refractory is a long period of time so you cannot tetanize cardiac muscle fibers because it has to relax
2. Slow Response
a) Description: Response in the SA node (the pacemaker of the heart) and the AV node (between atrial and ventricle) of depolarization and repolarization
i. At rest it is not nearly as polarized as the fast contractile and barely goes to 0 millivolts before it comes down
ii. No firm resting membrane potential but keeps depolarizing and repolarizing and you cannot call part A a resting membrane potential but a pre-potential
iii. B is depolarization and C is repolarization
b) Ionic events
i. A: Membrane’s permeability to K+ progressively declines and if the membrane is impermeable to K+ then would be at 0 millivolts and when there is progressively less permeability to K+ then line goes up
ii. A little bit of Na+ leakage so the line would go up and finally get a threshold
iii. B: Predominantly due to progressive movement inward of Ca++ through slow Ca++ channels
iv. C: predominantly due to the outward movement of Ca++ and slow Ca++ channels
C. Excitation Coupling: This is only slightly different than in skeletal muscle but uses contractile fibers
1. Get a depolarization on the sarcolemma and T-tubules; When the action potential depolarizes sarcolemma and T-tubules (plateau: Ca++ coming into the cell from the sarcoplasmic reticulum) and causes the release of Ca++ from the sarcoplasmic reticulum and sub-sarcolemma “pools” also (Remember that Ca++ is coming in from extracellular fluid too)
2. Extracellular Ca++ (or trigger Ca++) induces the Ca++ from the pools and the sarcoplasmic reticulum to come in
3. Trigger Ca++ triggers the release of additional Ca++
4. In the skeletal muscle the sarcoplasmic reticulum releases just enough Ca++ for the troponin binding sites and have the maximum affect possible and don’t stimulate more since already achieved maximum affect but in cardiac muscle, if you have extra Ca++ for contracting myosin
5. Ca++ can increase by an increased amount of intracellular Ca++ and to keep Ca++ channels open longer you need more trigger Ca++ and this would cause the heart to contract more forcefully
D. Effect of Autonomic N. System
1. The parasympathetic nervous system response when stimulated by M2 receptors and these receptors are around the AV node and decreases heart rate
2. Do something to the A slope to affect heart rate and M2 receptors should decrease the slope
3. A progressive decline in the K+ permeability affects the line so you want a decrease in the rate at which the K+ permeability progressively declines; M2 receptors decrease the rate of K+ so heart rate decreases
4. Sympathetic stimulation increases heart rate and affects pre-potential and there is norepinephrine and epinephrine with beta-1 receptors increases heart rate and the force of contraction
5. Heart rate in the pacemaker tissue, SA node, so if you change the slope of the A line to an increase or you increase the rate at which K+ permeability progressively declines
6. The force of contraction of cardiac muscle fibers is so fast that you leave the Ca++ channels open and wider so more Ca++ coming in (trigger Ca++) and there is more free Ca++ from the sarcoplasmic reticulum and the sub-sarcolemma pools so the heart contracts more forcefully
E. Gross Morphology
1. Pericardial Sac: The heart is contained within this and it holds the heart in place
a. There is two layers: A tough layer called the fibrous pericardium and it anchors the heart and keeps it from over extending; The inner layer is called the serous pericardium and is very thin
b. Pericarditis: An inflammation of the pericardium
2. Heart Wall: There are three layers
a. Epicardium: On the outside and is continuous with the serous pericardium and the space between them is called the pericardial cavity and is filled with pericardial fluid since you want the heart lubricated because it’s contracting all the time
b. Myocardium: Ventral and atrial muscle fibers and is the bulk of the heart
c. Endocardium: Part of the heart that comes in contact with the blood and lines inside of the heart and valves; Its role is in regulating cardiac function and is an important component of the anatomy of the heart
3. Chambers
a. The heart is not heart shaped and the atria hang out on the side; The ventricles are more heart shaped and the left is the right and right is the left
b. Blood is coming from the systemic circulation into the right atria and goes through the tricuspid valve into the right ventricle and then through the pulmonary semilunar to the lungs and then to the pulmonary vein to the left atrium and bicuspid valve (mitral) to the left ventricle and through the aorta
c. Need a lot more cardiac muscle to pump blood through the systemic circulation then through the systemic circulation
d. The heart consists of two functional syncitium:
i. Contractile: Two atriums: Left and right and are interconnected electrically so the action potential propagates to both
ii. Ventricles: Action potential in the ventricles and spreads through all the ventricles
4. Conductile System
III. Mechanical Events of Heart: SA node in the right atrium and the AV node is in the right ventricle and leads to the Bundle of His and the left and right bundle branch which leads to the Purkinje fibers
A. Frequency by which depolarize and Velocity of Conduction
1. The heart rate is dictated by the rate of the most frequent depolarized structure
2. You don’t want the atria and the ventricles to contract simultaneously but they can relax simultaneously
3. If you don’t want the mechanical events to occur at the same time then don’t let the electrical events occur at same time
4. You don’t want the ventricles to contract during atria depolarization
5. The action potential goes to the AV node and the Bundle of His but there is not much velocity so the action potential is delayed and then the action potential is in the bundle branches of ventricles
6. Want all the fibers in the ventricles to contract at the same time so you want depolarization at the same time
B. Atrial contraction: Systole
1. Atrial relaxation: Diastole
2. Ventricular contraction: Systole
3. Ventricular Relaxation: Diastole
4. Atrial and ventricular systole don’t happen at the same time but atrial and ventricular diastole can happen at the same time
C. End systolic volume, end diastolic volume, stroke volume, ejection fraction.
1. The below picture represents 1 cardiac cycle; The outside area of the picture represents ventricular events and the inside area represents atrial events.
a. 72 bmp and a complete cycle occurs in 8/10 of a second
2. #1 in the above picture represents the atrial-ventricle valves open; The heart fills with blood and the ventricles fill up 70%
3. #2: The atrium’s going into systole and nothing happens to the AV valve, they stay open; The atria contracts and adds 30% to the ventricles so that they now contain 120-130 ml of blood
a. End Diastolic Volume: 120-130 ml of blood at the end of ventricular diastole
4. #3: Ventricular Systole: Blood is going out of the aorta and the pulmonary artery but not back to the atria; So the AV valves close and you can hear the valves close and this is called the 1st heart sound
a. The semilunar valves open after a period of time and the heart contracts with the valves closed in order to compress the liquid and this makes the pressure increase; When the semilunar valves open the blood is ejected out of the ventricles but only a fraction of the end diastolic volume is ejected, about 70-90 ml and this is called Stroke Volume
5. #4: End Systolic Volume: Amount of blood left after the stroke volume is ejected
a. Stroke volume is less than end diastolic volume
b. Ejection fraction= (Stroke Volume)/(End Diastolic Volume)
c. If you’re under sympathetic duress stroke volume would increase and end systolic volume is decreased
IV. Electrical events (EKG)
A. William Einthoven described electrical events of the heart, EKG, and it did one thing: it compared on the surface of the body whether it was electrically negative or positive
1. If the right leg is positive and the left arm is negative then a machine would record upward deflections
2. EKG’s measure the electrical events on the surface of the body and is called P, Q, R, S, T which were seen during each cycle of the heart
a. P Waves represent atrial depolarization
b. QRS Complex represents ventricular depolarization
c. T Waves represent ventricular repolarization
3. What about atrial repolarization? It occurs at the same time as the QRS complex so you cannot see it because the QRS complex has a greater magnitude and obliterates it
4. The P wave is an upward deflection in terms of the right arm in respect to the left leg
B. Two Atria prior to depolarization:
1. As a negative charge spreads across all the atria the pen goes back to the baseline
C. QRS Complex: Not going to worry about the Q or S (ventricles), just the R spike which is a major electrical event
1. The T Wave is an upward pen deflection and so repolarizes from the apex to the base
V. Abnormal Electrical Events
A. Abnormal rhythmicity of pacemaker
1. Tachycardia: Heart rate is too high at rest and is greater than 100 bmp
a. The rhythm is normal it’s just too fast
b. Caused by an increase in temperature, anxiety, or increased sympathetic affect
c. Pathological Reason: Heart muscle is weakened and it cannot contract forcefully so it beats more frequently
2. Bradycardia:
a. It is due to atherosclerosis plaques and if the receptors are stimulated then slows the heart down so plaques affect heart rate
B. Abnormal rhythmicity resulting from blocks
1. A-V blocks: Most common
a. Causes: Due to ischemia; Scar
tissue after inflammation and causes scarring in the heart and the impulse is
blocked from the atria to the ventricles
b. Types: Degrees:
i. 1st Degree: Heart block, pattern’s normal but the P, R interval is lengthened (too much time between the atria and ventricular depolarization); Blockage at the AV node
ii. 2nd Degree: All QRS complexes are proceeded by P waves but not all the P waves are followed by QRS complexes; Depolarization wave is being blocked at the AV node (long time) and there is another P wave before QRS complex (expressed as an integer)
iii. 3rd Degree: Complete heart block and complete dissociation between atrial and ventricular events and is not expressed as an integer
C. Abnormal pathway of impulse transmission
1. Generalizations
2. Circus Movement: Heart has to have electrical events to proceed across it in
order and the heart doesn’t self initiate because of absolute refractory but
you can get reentry
a. The electrical event enters where it’s not supposed to and you get a bizarre electrical event called circus movement
b. Reasons: If the conduction pathway is longer you can get circus movement (enlarged heart)
c. It is not absolute refractory when you get back so it is depolarized again
d. There are blockages in conduction systems so it takes longer and get circus movement
e. Drugs decrease refractory time and lead to circus movement
i. If it starts depolarizing and it will start contracting and make circus movement
3. Re-entry (Fibrillation): Bizarre circus movement in the heart and the EKG is wild
a. There are little clusters of muscle fibers all doing their own thing (contracting unorderly)
b. Anarchy in ventricular muscle fibers because not controlled by SA node and is life threatening
c. Paddles on chest that apply electrical stimulation because can depolarize excitable tissue
d. Try to depolarize everything so that the SA node will pick up normal rhythm and a “sinus” rhythm
4. Atrial Fibrillation: Ventricles fill without atria but the blood doesn’t go out of the atria and can get blood clots
D. Ectopic foci: Small area of the heart becomes hyperexcitable and depolarizes more frequently than the SA node and becomes its own pacemaker
1. P.A.C.'s:
Premature Atrial Contractions
2. P.V.C.'s: Premature Ventricular Contractions:
Induced stress, caffeine, lack of sleep but indicative of cardiological
myoischemia
VI. Regulation of Cardiac Output
A. Factors influencing: Cardiac Output (C.O) is the amount of blood the heart pumps in a minute (average male = 5000ml/min at rest but is much greater than this during exercise)
1. Two variable: CO=(H.R.)(S.V.) Heart rate (is the number of times the heart beats per minute) and stroke volume (which equals how much the heart ejects every time if beats or the amount of blood the heart pumps each time the ventricles contract)
2. Cardiac Output Max
-Cardiac Output Rest
Cardiac Reserve
3. Cardiac Output at rest is very different then when running
B. Intrinsic mechanisms exist only in the heart and involve stretching the atria or the ventricles
1. Hemometric: The atria are stretched and make the SA node more irritable and make it depolarize more frequently
a. If the SA node depolarizes more frequently then this increases heart rate
2. Heterometric -- Starling's Law – Preload
a. If you increase the stretch of the ventricles then you increase the force of contraction
b. If you increase the filling of the heart then you stretch the ventricles and this would increase the force of contraction and increase the stroke volume and increase the cardiac output and according to Starling’s Law you would increase the stroke volume
3. What causes the ventricles or atria to stretch? An increase in end diastolic volume or increase in preload
C. Extrinsic: Nervous System
1. Parasympathetic
a. Innervation: The left and right vagus nerve
i. The left vagus nerve innervates the AV node and the atrial muscle fibers
ii. The right vagus nerve innervates the SA node and the atrial muscle fibers
iii. The cause a decrease in heart rate by decreasing the rate of K+ permeability decline and decreasing stroke volume
b. Effect and ionic explanation
2. Sympathetic
a. Innervation: From the thoracic spinal nerves
i. Increases the rate of K+ permeability declines and increase the heart rate
b. Effect and ionic explanation: Sympathetic nervous system increases the availability of intracellular Ca++ by increasing the amount of trigger Ca++ and this increases the interaction of actin and myosin and increase heart rate and stroke volume so increases the cardiac output
D. Effect of Afterload
1. Look at arteriole diastlolic pressure: The left ventricle contracts and the semilunar valve opens and blood goes into the aorta; The pressure in the aorta (diastolic pressure) is not 0 during afterload
2. The greater the afterload (diastolic pressure), the less the stroke volume
3. Afterload has an inhibitory affect
E. Summary (See Figure 2)
VII. Congestive Heart Failure: There is some deficiency in the myocardium (degenerative) and it causes the heart to not eject blood efficiently
A. Etiology: There is an increase in end diastolic volume and the heart doesn’t efficiently empty and you get an increase in ventricular pressure
1. The pressure backs up and increases the left atrial pressure and pulmonary pressure and capillary pressure and you eventually get pulmonary edema and have a problem with respiration and get systemic edema
a. There is considerable mortality
B. Treatment
1. Diuretics: There help move
fluid and decrease edema
2. Cardiac glycosides: Inhibits the mechanism that dumps free Ca++ from the
cell into the interstitial fluid; The trigger Ca++ comes into the heart and
some is pumped back out but if it is not then you get an increase or
accumulation of Ca++ and the result is a more forcible contraction and an
increase in stroke volume which helps to rectify the problem of pulmonary edema
a. digoxin (Lanoxin)
VIII. Coronary Blood Flow
A. Normal Physiology: The heart is supplied with blood and the myocardium is supplied with branches from the left and right coronary arteries which come off the aorta beyone the left ventricle
1. Coronary blood flow and coronary artery flow is greater during the diastole than during the systole
2. There is greater flow during diastole because blood has greater access to the heart during this period due to two reasons:
a. During systole the semilunar valves are open and block the entry of the coronary arteries but during diastole the semilunar valves are closed so there is more access to the coronary arteries
b. When the heart contracts during systole it compresses the coronary arteries and increases the resistance and decreases the flow into the coronary arteries
3. Blood flow to the heart is important because the heart has a tremendous demand for oxygen and consumes more oxygen per gram than any other tissue in the body so when blood flows through the heart 75% of the oxygen in the blood is removed at rest
a. Increased heart rate when there is a demand for more oxygen
b. Must have coronary arteries with a sufficient diameter
c. If the demand is not met then you get myocardial ischemia which is a reduced blood flow to the heart or the blood flow to the heart is less than the demand of the heart for oxygen
d. If ischemia becomes more severe it results in a heart attack
B. Pathophysiology: What causes myocardial ischemia?
1. Vascular spasm: Spastic contractions of arterioles which are serious but short lived and the person can survive
a. NO: endothelial relaxing factor and keeps the arterioles from having vascular spasms
2. Coronary atherosclerosis: The progressive degeneration of the arteriole wall and leads to a decrease in blood flow
a. Mechanism: There is an accumulation of lipids (rich in cholesterol) which are deposited in the endothelium lining the blood vessels and can lead to a fatty streak in the arteries and the smooth muscle cells in the arteriole wall migrate to the muscle layer
i. Muscle cells form an atheroma (a noncancerous growth) and plaque which lines the arterioles and coronary arteries
ii. 75% of college men have fatty streaks in arteries
b. Risk Factors: High blood
pressure, cholesterol, diabetes, genetics, cigarette smoking, or lack of
exercise
c. Ischemia – angina: Visceral pain; Occurs when the heart’s demand for oxygen
is greater than can be supplied and can result in myocardial ischemia
i. Can have ischemia without ever having angina
d. Infarction
3. Thromboembolism: A consequence of artherosclerosis
a. A piece of plaque breaks off and you get some bleeding which clots and the clot then breaks off and flows downstream to smaller vessels which can block the blood flow and causes a heart attack
C. Pharmacology
1. Nitrates
a. Nitroglycerine (Nitrostat, Transder-Nitro): Donate NO which causes vasodilation and ultimately decreases preload and afterload and decreases the work of the heart
i. These are administered in the form of a patch or placed under the tongue; You don’t swallow because the liver “chews” up the product so it’s more efficient when dissolved before it reaches the liver
b. Isordil: Vasodilation and is similar to nitrates and decreases the resistance and afterload and preload
2. B-blockers: Vasodilate coronary arteries and decreases demand and increases supply
3. Ca++ Channel Blockers:
a. Mode of action: Relieves the
symptoms of angina by blocking the slow Ca++ channels and then decreases heart
rate, decreases the amount of trigger Ca++ so decreases the force of
contraction and decreases the demand for oxygen
b. (Isoptin)(Calan)
c. (Procardia)(Adalat)
d. (Cardizem)
e. (Norvas)
IX. Valvular Diseases & Murmurs: Abnormal heart sound and is generally associated with cardiac disease; Can have a dysfunction murmur (without disease)
A. Examples
1. Regurgitations (insufficiency, incompetency): Hear an abnormal sound because the valve is
not closing properly and a whistle sound results
2. Stenosis: Murmur occurs when the valve doesn’t
open completely and the blood moves at a greater velocity and makes a swishing
sound
3. Mitral Valve Prolapse: Flaps of the valve extend back into the right atria when the left ventricle contracts and this causes leaking and is common in 5% of the population and is asymptomatic
B. Diagnosis
C. Causes
1. Rheumatic fever
2. Prolapse
X. Work of Heart: A function of potential energy (the development of high pressure, from high pressure to low pressure) and kinetic energy (movement of blood)
A. The work involved in potential energy is greatest
1. PE = (blood pressure) (velocity)
B. The factors that are important are potential energy and blood pressure
C. Harder work makes the heart bigger (muscle increases in size)
1. As the muscle gets bigger the vascularation can’t keep up and this can cause circus movement and as the heart gets bigger there is a danger in hypertension arrhythmias
2. In athletes the heart gets bigger but the vascularation keeps ups with the growth of the heart and the heart doesn’t get nearly as large as in chronic hypertension
