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Anatomy of the Heart
Coverings:
Pericardium (pericardial sac)
Serous Fluid
Layers:
Epicardium (visceral pericardium)
Myocardium
Endocardium
Chambers:
Right Atrium
Right Ventricle
Left Atrium
Left Ventricle
Valves:
Tricuspid Valve
Biscupid (Mitral) Valve
Pulmonary Semilunar Valve
Aortic Semilunar Valve
Chordae Tendonae & Papillary Muscles
Percadium (pericardial sac)
A tough membrane surrounding the heart
Cavity between the epicardium and the pericardium is filled with lubricating serous fluid
Epicardium (visceral pericardium)
It is the outer layer of the heart
It is the connective tissue attached to the surface of the heart
Myocardium
The middle, and thickest, layer of the heart composed of cardiac cells
It is the contraction of the myocardium that pumps blood through the heart and into the major arteries
Endocardium
The innermost layer of the heart made of simple squamous epithelium
Lines the chambers where the blood circulates and covers the heart valves
Right Atrium
Receives unoxygenated blood via the precava and postcava from the body
Upper heart chamber
Contracts to push blood into the right ventricle
Left Atrium
Receives oxygenated blood from the pulmonary veins
Upper heart chamber
Contracts to push blood into the left ventricle
Right Ventricles
Pumps unoxygenated blood to the lungs
Lower heart chamber
Left ventricle
Pumps oxygenated blood out to the body
Lower heart chamber
Tricuspid Valve
Between right atrium and right ventricle
Bicuspid (mitral) Valve
Between left atrium and left ventricle
Pulmonary Semilunar Valve
Between right ventricle and pulmonary trunk
Aortic Semilunar Valve
Between left ventricle and the aorta
Papillary Muscles
Muscles which aid opening and closing the valves
Chordae Tendonae
Heart strings which connect valves to papillary muscles
Prevent valves from inverting during ventricle contraction
Right Side Heart Blood Flow
Oxygen-poor blood enters the heart from the body → oxygen-poor blood leaves the heart traveling to the lungs
Body →
Pre & Post Vena Cava →
Right Atrium →
Tricuspid Valve →
Right Ventricle →
Pulmonary Semilunar Valve →
Pulmonary arteries →
Lungs
Left Side Heart Blood Flow
Blood is oxygenated → oxygen-rich blood returns to heart from lungs → Oxygen-rich blood leaves the heart traveling to the body
Lungs →
Pulmonary Veins →
Left Atrium →
Bicuspid Valve →
Left Ventricle →
Aortic Semilunar Valve →
Aorta →
Body
Pulmonary Circuit
Transports blood to and from the lungs
Muscle walls on right side of heart are relatively thin because blood is traveling a short distance to the lungs, so not much force is required
Functions to pick up oxygen from the lungs and deliver carbon dioxide to exhaled
Right side of heart → lungs → left side (Gas exchange (O₂ in, CO₂ out)
Systemic Circuit
Transports oxygenated blood to virtually all of the tissues of the body
Muscle walls on left side of heart are much thicker because blood must travel through the entire body, so much more force is required
Returns relatively deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary circuit
Left side of heart → body → right side. (Deliver oxygen/nutrients, remove waste)
Arteries vs. Veins
Arteries
blood vessels that carry blood AWAY from the heart
Veins
blood vessels that carry blood TO the heart
Coronary Arteries vs. Coronary Veins
Coronary Arteries
deliver blood from the aorta to the myocardium
Coronary Veins
drain blood into the right atrium
Cardiac Muscle Cell Characteristics for Coordinated Contraction
Intercalated Discs: Join cardiac cells; contain:
Desmosomes: Prevent cells from separating during contraction.
Gap Junctions: Enable electrical continuity (action potential spread).
Large Mitochondria: 25% cell volume for energy (vs. 2% in skeletal).
Fewer, wider T-tubules: Efficient ion transmission.
Aerobic respiration only: Requires constant oxygen.
Autorhythmic Cells (Pacemakers): Generate spontaneous action potentials.
Autorhythmic (Pacemaker) Cells
Fire spontaneous action potentials that trigger contractions at regular intervals
Cells are self-exciting and establish the fundamental rhythm
Coordinate the contraction of the heart
The autonomic nervous system and endocrine system modify the heart beat
Desmosomes
Mechanical couplings (like rivets) hold cells together, and prevents from separating during contraction
Gap Junctions
Small hollow cylinders (opening) that connect the cytoplasm of two cells and permits the direct transfer of an action potential from one cell to another
They help to synchronize contractions
After an action potential generates at the sinoatrial node, what steps does it take to spread through the rest of the heart?
Sinoatrial (SA) Node fires (70–80 APs/min) → sets sinus rhythm
Signal spreads through atria via internodal pathways.
Arrives at Atrioventricular (AV) Node (~150 ms delay).
Travels down Atrioventricular Bundle (Bundle of His).
Splits into Right & Left Bundle Branches.
Moves through Purkinje Fibers → triggers ventricular contraction (bottom-up).
First step in Cardiac Excitation
Begins at the sinoatrial (sinus) node
A specialized clump of autorhythmic cells
Located in the superior and posterior walls of the right atrium close to the entrance of the pre cava
Generates 70-80 action potentials per minute
Sets the sinus rhythm (normal electrical pattern) of the heart
Second step in Cardiac Excitation
The action potential spreads from the SA node throughout the atria, through specialized internodal pathways, to the atrioventricular (AV) node
AV node is located at base of the right atrium, near the junction of the atria and ventricles
This takes about 150 ms for this occur, during which time the atria begin contracting and blood begins flowing into ventricles
Third step in Cardiac Excitation
The nerve impulse then spreads from the atrioventricular node to atrioventricular bundle (Bundle of His)
What are the steps in Cardiac Action Potential?
Initiation
Depolarization
Plateu Phase
Repolarization
Refractory Period
Initiation
An action potential is generated by the sinoatrial node & travels down the conduction system
Action potential spreads to the working muscle fibers
Summary:
SA Node triggers AP, spreads through conduction system
Depolarization
Resting membrane potential is -80 mV for cells in the atria and -90mV for cells in the ventricles
Voltage-gated fast sodium Na+ channels open
Results a rapid depolarization to approximately +30mV
Within a few milliseconds the fast sodium Na+ channels close
Summary:
Na⁺ channels open → rapid influx → membrane potential spikes to +30mV.
Plateau Phase
Voltage-gated slow calcium Ca+ channels open in the cell membrane & sarcoplasmic reticulum
Calcium Ca2+ flows into the cell’s cytoplasm and uncovers the myosin binding sites on actin
As Calcium Ca2+ enters, some potassium K+ channels open and potassium K+ leaves the cell
A small potassium K+ out flow now balances calcium Ca+ inflow & the membrane potential plateaus
The relatively long plate
Summary:
Ca²⁺ channels open → Ca²⁺ enters → K⁺ starts to leave → charge stabilizes
Repolarization
Voltage- gated potassium K+ channels open and potassium K+ flows rapidly out of the cell
At the same time calcium Ca2+ channels close
Potassium K+ leaving the cell restores the resting membrane potential
This last approximately 75 ms
Summary:
Ca²⁺ channels close, K⁺ exits quickly → restores resting potential
Refractory Period
The absolute refractory period for cardiac is approximately 200 ms
The relative refractory period last approximately 50 ms
This extended period is critical, since the heart must fully contract to pump effectively
Without extended refractory periods, premature contractions would occur and the heart would not be able to fill or effectively pump the blood
Summary:
Absolute: 200ms, Relative: 50ms → prevents early contractions → allows refilling.
Relaxation Period
Diastole
End of a heartbeat when the ventricles start to relax, atria are starting to contract
As ventricles relax, pressure lessens & blood back flows from the pulmonary trunk & aorta
Aortic & pulmonary semilunar valves close to prevent backflow of blood into the heart
Ventricles continue to relax & pressure continues to drop
When pressure in the ventricles drop below the atrial pressure, the atrioventricular valves open & ventricles begin to fill
Summary:
Atria contract → ventricles fill.
AV valves open, semilunar valves closed.
Ventricular Contraction
Systole
Near the end of atrial systole, the AP from the atrioventricular node causes depolarization in the ventricles
Begins form the bottom up
Blood is pushed against the atrioventricular valves closing them
For about 50 milliseconds, all the heart valves are closed
Muscles continue to contract increasing the blood pressure inside the ventricles
Semilunar valves open when the blood pressure in ventricles exceeds the blood pressure in the pulmonary trunk & aortic arch
Blood is pushed out of the heart & continues until the ventricles start to relax
Summary:
Ventricles contract from base upward.
AV valves close, semilunar valves open.
Blood ejected into pulmonary trunk & aorta.
Cardiac Output
Total amount of blood moved among a period of time, depends upon heart rate & stroke volume
Will initially stabilize with the increasing heart rate & compenstates for decreasing stroke volume
At very high rates, the output will decrease as increasing heart rate is no longer able to compensate for the decreasing stroke volume
Stroke Volume
how much blood is actually pumped
Initially, physiological conditions that cause heart rate to increase also triggers an increase in stroke volume
As heart rate rises, less time is spent in diastole & so there is less time for the ventricles to fill
Stroke volume initially remains high, but as heart rate increases stroke volume gradually decreases due to decreased filing time
Factors that Affect Heart Rate
Hormones (Epinephrine, norepinephrine, & thyroid hormone)
Calcium ions
Caffeine
Nicotine
Age
Gender
Physical condition
Bodhy Temperature
Hormones
Epinephrine, norepinephrine, & thyroid hormone)
These hormones increase cardiac rate & contractility
↑ HR & contractility (via sympathetic nerves).
Calcium Ions
as ion levels increases, so do heart rate & contractility
↑ HR and contraction strength
Caffeine
works by increasing the rates of depolarization at the SA node
↑ HR by increasing SA node depolarization and sympathetic activity
Nicotine
stimulates the activity of the sympathetic neurons that deliver impulses to the heart
↑ HR by increasing SA node depolarization and sympathetic activity
Age
Heart rate increases w/ age
The ability to generate maximum heart rates decreases w/ age
↑ HR in infants, ↓ max HR as age increases.
Gender
Average adult male heart rate is between 70-72 bpm
Average adult female is between 78-82 bpm
Difference is largely due to size of the heart
Females heart is smaller than males
Females: slightly higher resting HR due to smaller heart size.
Physical Condition (health)
The heart is like a muscle, it becomes stronger as a result of exercise
Resting heart rate of those in good physical condition is slower, because less effort is needed to pump blood
↓ Resting HR; more efficient stroke volume.
Body Temperature
Increased body temp increases heart rate
Decreased body temp decreases heart rate
↑ temp = ↑ HR; ↓ temp = ↓ HR.
Chemical recations that decrease Heart Rate
Thyroid Hormones (lower than average)
Estrogen (higher than average)
Alcohol (don't mix w/ medications, which both slow down heart rate)