55 terms

Davis: Anatomy and Physiology, the Heart Part 2

Physiology of the Heart: cardiac cycle, conduction systems, heart rate,
maintains steady and regular rhythm which is a steady cycle of contraction and relaxation.
a. Occurs from birth to death
b. Average Heart Rate (HR) of healthy adult is 75BPM
c. Women usually 72-80BPM at rest
d. Men usually 62-72BMP at rest
e. Metabolic rate, heart size, physical exercise affect HR
f. Humans (Vertebrates) contain a Myogenic Pulse
Myogenic Pulse
the ability for the heart to create its own electrical impulse.
Pacemaker of the Heart
path of tissue that generates electrical impulse that is independent from the rest of the body's NS.
a. Receives sympathetic innervation by Cardiac Nerves that originate in the cervical ganglia
b. Receives Parasympathetic innervation by the Vagus Nerve (CN-X) which sends branches to the Pacemaker to slow down pulse rate constantly.
c. Electrocardiogram (ECG or EKG) measures heart rate
d. It is autorhythmic (self-stimulating) eventhough the brain can tell the heart to heat harder or slower.
Cardiac Cycle
controls routes and timing of electrical conduction
i. Beats in sequence, whole heart does not beat at the same time.
ii. Regulates flow of electricity in correct order, order of circulation
iii. Sinoatrial Node
v. Atrioventricular Node: (AV Node) forks to
vi. Atriovenricular Bundles split into
vii. Purkinje Fibers that attach to some
viii. Cardiocytes:
Sinoatrial Node (SA Node)
(SA Node) pacemaker of heart, small path of modified myocytes found in rt. Atrium, near the opening of Vena Cava
1. produces an regular electrical stimulus, a constant AP to allow blood to move through the system
2. sends signals to rt and left atrium
3. Produces regular electrical stimulus
4. Travels to rt atrium then to left atrium
Atrioventricular Node (AV Node)
located near right AV valve and found at inferior end of atrioventricular septum
1. Functions
a. Transfers signal from atria (of SA node) to ventricles
b. Slightly delays the signal to give time for ventricles to fill up
c. Transfers signal from atria (of SA node) to ventricles
d. Slightly delays the signal to give time for ventricles to fill up
2. Gateway to allow the heart to get electrical impulse from top to bottom because of non-conductive fibrous skeleton
Atrioventricular Bundles (Bundle of His)
found in the ventricles where the AV node forks and distributes to Rt and Left Ventricles.
a. Right bundles go to rt. Atrium
b. Left bundles go to left atrium, purkinje fibers are more elaborate in order to produce a more forceful charge.
Purkinje Fibers
small nerves that distribute electrical signals to myocytes/Cardiocytes of ventricles. Extends from Bundle of His.
cells of the heart
1. Mono-nucleated
2. Thick
3. Y-shaped
4. Joined to others end to end
5. Can directly stimulate to each other by intercalated disks
a. contains Gap Junctions: provide a place for an electrical signal to cause a contraction
6. Cells contract in a wrapped sequence
7. Contains much more mitochondria and is much larger - for its need to be constantly working
8. runs on aerobic respiration
9. Fuel Use:
a. 60%-Fatty Acids
b. 35%- Glucose
c. 5%- proteins and other molecules
10. Contains many Myoglobins: storage for O2
11. Contractions are usually long and slow, and will not experience swift twitch
a. Absolute Refractory Period is 200-250 msec.
b. Prevents summation of tetani
c. Provides sustained pressure to squeeze blood out of ventricles.
12. Highly resistant to tetanus
13. Requires a lot of O2, energy, and nutrients to keep the cells running - "expensive"
14. Non-mitotic
15. Damage will be healed by fibrosis (scar tissue)
16. Contains a small amt. of Satellite Cells: stem cells that decrease as age increases
Ectopic Focus
any part of the heart other than the SA node that fires an electrical impulse.
Premature Ventricular Contractions (PVC)
aka extrasystole
a. Extra contraction
b. Not as forceful as normal rhythm
c. Usually originates from AV node - causing a Nodal Rhythm
i. Cardiocytes can generate their own pulse but it's even slower (20-40BPM)
Nodal Rhythm
which produces a slower pulse (40-50BPM) that is not enough to maintain function
contraction of the heart
relaxation of the heart
Sinus Rhythm
SA Node contains no stable electrical charge
a. Usually beats at 100bpm but Vagus Nerve will slow the heart to 75bpm
b. Runs on Pacemaker Potential:
Pacemaker Potential
i. At -60mv charge begins to increase
ii. When it is reached to -40mv, stimulates gated ion channels to open and Ca2+ rushes into cardiocytes causing an increase of electrical charge (depolarization)
iii. When the membrane potential reaches >0mv, Pacemaker Potential becomes +, stimulates other channels to open rushing K+ out of cardiocytes (repolarization), charge will reach to -60mv again.
iv. It takes .8sec for 1 AP to occur causing a contraction
v. About the same time that an AP is produced Rt. Atrium will contract.
vi. After 50msec, the SA node will send an electrical signal to the AV node which will delay the AP by .100msec.
vii. The AP will travel to the AV branches, Purkinje Fibers
viii. Ventricles will depolarize after 200msec.
ix. Both ventricles will contract almost simultaneously.
Cardiac Cycle
1 complete contraction and relaxation of all 4 heart chambers
i. Propels blood through circuits
ii. Short term changes to BP
iii. Forms heart sounds as blood pumps
Sounds of the Heart
1. S1- "Lubb" - long sound
2. S2 - "Dubb"- short sharp sound
3. S3 - galloping effect on sound due to extra-systole, common in children
4 Phases of the Cardiac Cycle
All chambers of the heart are in diastole
1. Ventricular Filling:
2. Isometric Contraction:
3. Ventricular Ejection:
4. Isometric Relaxation
Ventricular Filling
ventricles fill with blood
a. Ventricles are in diastole and expand due to elastic re-coil
b. Internal ventricle pressure decreases
c. Pressure gradient occurs as the atrial pressure increases and ventricular pressure decreases.
d. AV valves will open and blood will fill into ventricles.
i. Rapid Ventricle Filling will occur initially
ii. Diastasis: flow tapers off
iii. Atrial Systole: will depolarize and contract to squeeze the rest out.
1. occurs for about 0.1sec
e. Rt. Atrium will contract slightly before left atrium
f. As Atrium empties, Atrial Pressure increases
g. End Diastolic Volume (EDV) - approx. 130 mL in ventricles (same for both ventricles)
Isometric Contraction
a. Ventricles begin to systole
i. Occurs for about 0.3sec
b. In the meantime, Atria will repolarize and stay in diastole for rest of cardiac cycle
c. AV node will send signal to ventricles, depolarization and systole occurs
d. Internal ventricular pressure increases - which pushes blood upward causing AV valves to close (Backflow mechanism); causing S1 sound
e. No blood releases until the pressure in ventricle > arterial pressure
Ventricular Ejection
a. Once ventricle pressure>arterial pressure
i. Left ventricle>100mHg (aortic pressure)
ii. Right Ventricle >25mmHg (pulmonary pressure)
b. Semilunar valves open and blood rushes into arteries
c. Rapid Ejection: initial rapid flow of blood
d. Reduced Ejection: as pressure decreases blood flow slows down to match arterial pressure
e. occurs between 200-250 msec. = Cardiac AP
f. Ventricles do not eject all blood
i. Ejection Fraction: 54% in normal person, and as much as 94% in active person
ii. Stroke Volume (SV):
g. End Systolic Volume (ESV):
Isometric Relaxation
a. Ventricles are in diastole and are not expanded therefore no blood flow
b. Semilunar valves will prevent any backflow that usually occurs when the ventricles are in diastole
i. S2 sound occurs- blood rebounding off of semilunar valve
ii. Quiescent Period:
d. then ventricular filling may begin again
5. Full cardiac cycle occurs for a total of 0.8sec /60sec. = 75bpm
Stroke Volume
amount of blood that is ejected from the ventricles, approx. 70mL in textbook case
End Systolic Volume
amount of blood left in ventricle after systole (both ventricles)
i. Usually about 60mL
ii. EVS= EDV-SV (60mL = 130mL-70mL)
Quiescent Period
entire heart in diastole
c. ventricle pressure drops below arterial pressure
i. occurs for about 0.4sec.
Effects of ESV
1. Pressure in arteries affect volume ejection
2. Volumetric pressure needs to be the same in both circuits to prevent backflow and buildup
3. Fluid will usually accumulate in the circuit that doesn't work
4. There is a disruption to homeostasis
Congestive Heart Failure
one side works harder than the other.
i. Caused by weakened heart muscle from heart disease, injury, infection, etc.
1. Valvular insufficiencies
2. Chronic Hypertension
3. Congenital Deficiencies
a. Dropsy
3. Aneurisms
4. Kidney failure
5. Heart failure - leads to stroke
iv. Progressive condition where one side will affect the other
v. Irreversible
vi. Management can be done but there is no cure.
Right CHF
accumulation of blood in pulmonary circuits causes pulmonary hypertension , edema, and suffocation
Left CHF
build-up in systemic circuits
1. Hypertension
2. Systemic Edema - fluid build-up
enlarged liver, swelling of fingers, ankles, and feet, distension of jugular vein, and build-up of fluid in abdominal cavity.
Cardiac Output
amount of blood ejected by each ventricle in 1 minute
i. =75mL*75BPM
ii. = 5,250mL/min - resting CO
b. 4-6L of blood in each complete cycle
c. Max CO = 21mL in healthy adult, and 35mL in Olympic trained athlete
d. Heart contains a Cardiac Reserve
i. The closer the cardiac reserve is to CO the less apt a person is for physical activity
ii. Large CR is better equipped for exercise
Cardiac Reserve
max CO - Rest CO
- increased HR > 100BPM
- causes Hypertension, enlarging of the heart muscle which decrease SV, anxiety, heart diseases, fever, response to significant blood loss, heart muscle damage.
- decrease HR< 60BPM
i. Hypothermia, depressant drugs - alcohol, damage to nodes - cardial conduction.
ii. Usually an indicator of good health
Positive Chronotropic Agents
agents that cause an ↑ HR
Negative Chronotropic Agents
agents that cause a ↓ HR
ie) Vagus Nerve
Cardiac Center of the Brain
1. Located in the amygdala oblongata
2. Allows the heart's rate reach up to 200 BPM max
3. Max CO is 160-180BPM
4. Ability to stimulate sinus rhythm to slow down, lowest CO = 20BPM
5. Responds to sensory or emotional stimuli which is how HR can increase or decrease
a. Ie) hormonal fluctuations, electrolyte levels, external and internal chemical stimulation
Effects of Stroke Volume on CO
1. Preload
2. Contractability
3. Afterload
muscular tension in ventricular myocardium prior to contraction
a. Higher Preload = Higher SV
i. Frank-Sterling Law of Heart: SV proportionally related to EDV
Heart Contraction
a. Increased Contraction = increased SV
b. caused by Positive Inotropic Agent and Negative Inotropic Agent
Positive Inotropic Agents
causes an increase in contraction
1. ie) Glucagon, elevated Ca2+ levels, epinephrine or norepinephrine, Toxin - Digitalis
Negative Inotropic Agents
causes a decrease in contractibility and causes a decrease of SV
1. ie) Vagus Nerve, excess K+ - Hyperkalemia, drugs, enlarging of the heart
BP in Great Arteries
a. Arterial Pressure increases than SV decreases
b. Arterial Pressure decreases than SV increases
c. Causes of increased pressure in Arteries
i. Atherosclerosis:
ii. Scarification in Lungs
hardening of arteries will increase BP and decrease SV
Scarification of Lungs
cause pulmonary circuit to work harder
1. Causes: Chronic Bronchitis, Black Lung Disease, and Brown Lung Disease
inconsistent Heart beat
i. Usually transient events
ii. Persistent Arrhythmia
1. Cause by insufficiencies of K+ and Ca2+
2. Excess Hypercalcemia or Hyperkalemia
Heart Block
caused with no outside stimulus
a. Disruption in cardiac conduction system
i. To nodes and bundle branches
ii. Types : Bundle Branch Blockage and Total Heart Block:
Bundle Branch Blockage
pathologic degeneration of some portion of the bundle branches
1. Causes: physical damage, bacteria or viral infections, obesity, genetics
Total Heart Block
heart block in AV node
a. no signal from atria to ventricles
b. ventricles develop ectopic foci
Common Arrhythmias
1.Ventricular Fibrillation
2. Arterial flutter
3. PVCs - skips a beat
Ventricular Fibrillation
signals arrive at ventricles creating an uncoordinated pulse
a. Due to: Total Heart Block, Myocardial Infarction, inability to generate strong impulse, ischemia, and immediate death.
Aterial flutter
ectopic focus in atria, beats spontaneously
a. Cause atrial pulse to be 200-400BPM
b. Caused by fear or emotional shock
powerful electrical shock to heart causing it to depolarize and reset so SA Node and AV Node may pick up a normal pulse (assuming it has not been damaged)
Artificial Pacemaker
is used to replace electrical impulse created by SA Node which keeps the conduction system going.
a. Downfall: it requires a battery to run it which means it needs to be replaced.