UAlberta Physl 210A Cardiovascular

Cardiovascular System

The heart (cardio) and blood vessels (vascular).

Cardiovascular Functions

Provide oxygen and nutrients and remove waste. It provides a steep concentration gradient within the vicinity of every cell. Maintain optimal blood pressure and blood volume.

Heart

A hollow, muscular organ that that acts like a pump to create pressure to move blood through the body.

Blood Vessels

Tubes that carry blood throughout the body. Blood moves to the lungs to receive oxygen and drop of carbon dioxide and through the GI tract to pick up nutrients.

Blood Flow F

Volume of blood that moves through the system by pressure created by the heart. Measured in L/min. It is not the absolute pressures in the cardiovascular system that determine flow, but the pressure difference between two points.

Bulk Flow

All components of blood flowing together.

Types of Blood Vessels

Arteries, arterioles, capillaries, venules, veins.

"Powerhouse" of the Cardiovascular System

Interface between the capillaries and body cells where most nutrient/oxygen/waste exchange and distribution/action of hormones happens here.

Cardiovascular Organization

Closed circuit system comprised of two loops that join at the heart. Contains the pulmonary and systemic systems.

Pulmonary Curcuit

Involves the lungs. Blood leaves the right side of the heart, travels through the vasculature to the lungs, and returns to the heart on the left side.

Systemic Circuit

Involves body organs. Blood leaves the heart from the left side, travels through the vasculature to the organs, and return to the heart on the right side.

Steps in the Pulmonary Circuit

1. Deoxygenated blood moves from the right atrium to the right ventricle, then through the pulmonary trunk.
2. The pulmonary trunk then divides into two pulmonary arteries that take the deoxygenated blood to the capillaries in the lungs.
3. Blood moves through the lungs while going through gas exchange and becoming oxygenated.
4. Capillaries form venules which turn into 4 pulmonary veins, two for each lung, that carry oxygenated blood to the left atrium.

Steps in the Systemic Circuit

1. Oxygenated blood moves into the aorta from the left ventricle which branches into arteries that travel to the organs. Arteries branch into arterioles which then branch into capillaries.
2. Capillaries facilitate exchange then come together to form venules which come together to form larger veins to bring deoxygenated blood back to the heart.
3. Larger veins from peripheral organs and tissues join together to form the inferior and superior vena cava which collect blood from tissues below and above the heart (respectively).
4. Blood from the vena cava flow into the right atrium.

Parallel Circuit

The cardiovascular system is a parallel circuit meaning, arteries branch to form a parallel circuit and each organ system receives a portion of blood pumped from the left ventricle. This ensures that each organ can receive freshly oxygenated blood and flow can be tailored to each system.

Exceptions to the Parallel Circuit

Portal Systems are connected in series to facilitate their specific functions. Includes the hepatic portal system.

Hemodynamics

The relationship between blood pressure, blood flow, and vascular resistance.

Pressure Gradients (ΔmmHg)

Drives the flow of blood from one region to another, it determines how fast blood will flow in a certain portion of the circulatory system. Blood always flows from high pressure to low pressure. The initial source of high pressure comes from the heart. Ventricular contraction increases aortic pressure over 100mmHg. Venous pressure before entry into the right atrium is almost 0mmHg. This pressure difference drive blood flow from the arteries to the veins.

Hydrostatic Pressure

Pressure exerted by a volume of fluid against a membrane. Blood exerts ___ of vessels.

Vascular Resistance R

How difficult it is for blood to pass through a vessel, determined by viscosity, and vessel length/resistance. Helps determine blood flow.

Blood Flow Formula

Flow(F) = ΔPressure(P) / Resistance(R). Flow is directly proportional to vascular pressure and inversely proportional to vascular resistance.

Viscosity

A liquid's resistance to flowing. Varies with the portions of RBC relative to the amount of plasma (hematocrit) and circulating proteins. Value usually remains the same day-to-day but can change with dehydration, anemia, or protein wasting. It is not a factor when controlling resistance.

Resistance Formula

R=8Ln/[pi]r^4, where L = length, n = viscosity, and r = vessel radius. Inversely proportional to vessel radius to the fourth power. A very small change in radius can create a big change in resistance.

Vessel Length

Remains the same except with growth. It is not a factor when controlling resistance.

Vessel Radius

The most important regulator of vascular resistance. Blood vessels are constantly dilating and constricting, they are dynamic and change according to the bodies needs.

Constriction

Compression of a vessel that causes narrowing.

Dilation

Stretching of a vessel that causes widening.

Cardiac Anatomy

Powerful, muscular organ about the size of a clenched fist. It is located in the centre of the chest in the thoracic cavity.

Pericardium

Tough fibrous sac that surrounds the heart on top of the epicardium.

Pericardial Fluid

Small amount of lubricating fluid in between the pericardium and epicardium.

Epicardium

Fibrous layer that surrounds the heart under the pericardium and pericardial fluid.

Myocardium

Heart muscles made of cardiomyocytes. They are never at rest.

Apex

Lowest, superficial surface of the heart. The pointy part.

Base

Upper surface where vessels attach.

What are the Chambers of the Heart?

Right atrium, right ventricle, left atrium, left ventricle.

Ventricles

Thick-walled, lower chambers of the heart. They are higher pressure and are responsible for the forward propulsion of blood.

Atria

Thin-walled, upper chambers of the heart. They are lower pressure and receive blood coming back to the heart.

Atrioventricular AV Valves

Passive flaps of fibrous tissue that separate the atria and ventricles. They permit one-way flow; when pressure in the atria is higher, they are pushed open, and when pressure in the ventricles is higher, they are forced close. The right side is a tricuspid valve while the left is bicuspid/mitral.

Chordae Tendineae

Thin bands of fibrous tissue that attach to the valves in the heart and prevent them from inverting.

Prolapse

When the chordae tendineae malfunction, allowing the valves to open in the wrong direction.

Pulmonary Valve

Semi-lunar valve that separates the right ventricle and pulmonary trunk. When ventricular pressure rises, this valve opens to allow blood flow into the pulmonary trunk.

Interatrial Septum

Partition between the right and left atria.

Interventricular Septum

Partition between the right and left ventricles.

Aortic Valve

Semilunar Valve that separates the left ventricle and the aorta. When atrial pressure rises, this valve opens to allow blood flow into the aorta.

Valvular Stenosis

Partial opening of the valves caused by stiffening and crustiness. Creates a high resistance to flow and increased pressure

Jugular Venous Pulse

Escape of blood from the right atrium into the neck veins.

Pulmonary Flow Steps

R atrium->R AV valve->R ventricle->pulmonary valve->pulmonary trunk->pulmonary arteries->pulmonary arterioles->lung capillaries->pulmonary venules->pulmonary veins->L atrium.

Systemic Flow Steps

L atrium->L AV valve->L ventricle->aortic valve->aorta->systemic arteries->systemic arterioles->organ capillaries->systemic venules->systemic veins->vena cava->R atrium.

Cardiomyocytes

Specialized muscle cells connected end-to-end, and arranged in layers. Every cell contracts during a heart beat. Only ~1% of these cells are replaced every year which could pose a problem with disease and acute events.

Autorhythmic Cells

Required for the conducting system to spread spontaneous electrical excitation throughout the heart. Connected to cardiomyocytes by gap junctions.

Parasympathetic Innervation

Fibres travel in the vagus nerve and innervate autorhythmic cells in the atria, and release ACh. They are confined to the autorhythmic system and do not innervate cardiac muscle itself.

Sympathetic Innervation

Fibres come from the thoracic nerves and innervate the entire heart and release NE.

Myocardial Blood Supply

Does not come directly from the chambers because diffusion distance is too great. Coronary arteries branch from the aorta behind the aortic valve cusps and provide blood flow. Coronary arteries also branch into capillaries which supply the myocardium with oxygen and nutrients and remove waste.

Heartbeat Coordination

The heart is essentially two pumps in one; right is the pulmonary and left is the systemic. The atria contract to send blood into the ventricles, ventricles contract, sending blood through the arteries to the pulmonary and systemic circuits, cycles repeats. (ventricles are usually full before the atria contract).

Sinoatrial SA Node

Where initial depolarization begins during a heartbeat. It is the pacemaker that spreads depolarization to the atria then the ventricles. Currents move more rapidly than AV node currents and set the pace.

Atrioventricular AV Node

Node in the base of the right atrium that receives AP from the SA node through nodal pathways.

Path of Electrical Excitation

1. SA node depolarizes and generates and AP that spreads through gap junctions to depolarize cardiac muscle. Depolarization spreads through the atria muscle first and it so fast that it supports the simultaneous contraction of the right and left sides.
2. The AV node conducts AP quite slowly in order to allow atrial contraction to complete, and the ventricles to be filled before they contract themselves.
3. After the AV node is excited, the AP moves along the Atrioventricular bundles (Bundle of His) which electrically connect the atria and the ventricles. AV bindles are located in the interventricular septum.
4. AP travels along the right and left branches of the Bundle of His before reaching an extensive branching network of Purkinje fibres located within each ventricular wall.
5. The Purkinje fibres rapidly conduct AP to ventricular myocytes, have a large diameter and low resistance to gap junctions. Their anatomy and pattern of distribution causes simultaneous depolarization of all left and right ventricular cells. It also permits coordinated contraction that begins at the apex, spreading upwards.

Purkinji Fibres

Specialized electrical conducting fibres in the heart that rapidly conduct the AP to ventricular myocytes.

Bundles of His (AV Bundle)

Continuation of the specialized tissue of the AV node, that transmit the electrical impulse from the AV node to the Purkinje fibres of the ventricles.

Ventricular Myocyte AP

Kind of in the shape of a rectangle.
-Starting at the resting state, the membrane is more permeable to K+, so the resting membrane potential is closer to the eq potential for K+ (-90mV) than Na+ (+60mV).
-When the cell becomes depolarized, voltage gated Na+ channels open and Na+ rushes into the cell (Na+ conductance increases). Depolarization stimulates the opening of more Na+ channels (+ feedback).
-Sodium channels are inactivated quickly and there is partial repolarization with the opening of transient K+ channels which lets a little bit of K+ out of the cell.
-Membrane remains depolarized and there is a plateau at 0mV as K+ permeability decreases. There is a large increase in Ca2+ permeability that also maintains this depolarization (calcium conductance increases). The opening of voltage gated Ca2+ channels, Ca2+ flows into the cell. These channels also open slowly and so are called L-Type Ca2+ channels.
-Once the L-type Ca2+ channels deactivate, another K+ channel opens, allowing K+ to leave the cell, and contributes to the repolarization.

Nodal Cell AP.

Looks more like a wave with a gradual increase before a spike that drops and begins to rise again.
-The SA node has unstable resting membrane potential. Slow gradual increase (depolarization), also called the pacemaker potential.
-At the threshold is when AP is triggered. When the AP is triggered, there are 3 main ion channel mechanisms associated with the pacemaker potential:
1. Slow decrease in K+ permeability
2. Funny Na+ channels
3. T-type Ca2+ channels.
-When the nodal cell is brought to threshold, an AP is triggered, and depolarization mediated by Ca2+ into the cell via L-Types Ca2+ channels. They facilitate slower rate of depolarization compared to the voltage gated Na+ channels with the ventricular myocyte AP.
-The L-Type calcium channels eventually become inactivated and close, reducing calcium conductance. K+ channels open and K+ leaves the cell, repolarizing it, and returns the cell to negative potentials (Cycle repeats).

K+ Channels

Channels that progressively close after repolarization upon reaching negative potential.

Special (Funny) F-Type Channels

Channels that mainly carry Na+. They open at negative potentials, allowing Na+ to move into the cell and cause depolarization.

Transient T-Type Channels

Channels that carry Ca2+ into the cell to give a depolarizing boost to bring membrane potential to threshold.

L-Type Channels

Channels that also allow Ca2+ into the cell. They slowly facilitate the entry of Ca2+

Automaticity

The ability of the heart to generate and conduct electrical impulses on its own.

Heart Rate

A measure of cardiac activity usually expressed as the number of beats per minute. Normal HR is 72bpm. The slope of the pacemaker potential, how fast it reaches threshold, determines how fast the next AP is triggered, and determines heart rate.

Intrinsic Firing Rate

The normal firing rate for the rhythm of a certain pacemaker; 100bpm.

AV Conductive Disorder

When the SA node is working, but the AV node is no longer conduction depolarization, inhibiting the depolarization to reach the ventricles. Autorhythmic cells of the bundle of His and Purkinje fibres can initiate excitation and follow their own rate and become the pacemaker, but much slower (25-40) and not in synch with atrial contraction and my requires an artificial pacemaker.

Electrocardiogram ECG

Reflects the electrical events of the heart where currents are conducted in body fluid and detected at the skin. It does not tell us about contractions or valve failures.

ECG Parts

-P wave: atrial depolarization characterized by a small bump in the line.
-QRS Complex: ventricular depolarization characterized by sharp, small dip (Q), large spike (R), and the sharp fall and dip (S).
-T: ventricular repolarization characterized by another small bump.

Partial AP Block

AV node damage where only some atrial impulses are transmitted to the ventricles. PQRST P PQRST P PQRST.

Complete AP Block

There is no synchrony between atrial and ventricular electrical trace. The ventricle is driven by slow Bundle of His impulses. P PQRST P P QRSP T.

Excitation-Contraction Coupling

AP in cardiac contractile cells->travels down T-tubules->Sm amount of Ca2+ enters from the EFC which triggers a large Ca2+ from the sarcoplasmic reticulum->Increase in cytosolic Ca2+->Troponin-Tropomyosin complex in thin filaments are pulled aside->cross-bridge cycling between thick and thin filaments->thin filaments slide along thick filaments->contraction.
-The amount of Ca2+ in cytosol also determines strength of muscle contractions.

-More calcium released from SR, increased strength of contraction.

-The contraction ends when Ca2+ is actively pumped out of the cells or back into the sarcoplasmic reticulum.
-There is no summation in the contraction of cardiac muscles. This preserves the heart's function as a pump as it requires relaxation to refill.
-Long refractory period prevents multiple re-excitement of cardiac muscle cells during ongoing contraction.
-The refractory period follows AP and is linked to inactivation of Na+ channels.

Cardiac Cycle

A complete heartbeat consisting of contraction and relaxation of both atria and both ventricles.

Phases of the Cardiac Cycle

Systole and diastole.

Systole

Ventricles contract and eject blood. 72bmp, lasts for 0.3sec.

Diastole

Ventricles relax and refill with blood. More time is spent here. Lasts for 0.5sec.

Isovolumetric Ventricular Contraction

Early phase of systole when atrioventricular and aortic valves are closed and ventricular blood volume remains constant. Pressure increases until it exceeds pulmonary trunk and aortic pressure.

Ventricular Ejection

After isovolumetric ventricular contraction when blood is ejected into the vessels.

Stroke Volume

The amount of blood that is ejected during ventricular ejection.

Factors that Control Stroke Volume

End-diastolic volume (preload), sympathetic tone to the ventricles, and cardiac work against arterial pressure (after-load).

Isovolumetric Ventricular Relaxation

Early phase of diastole when AV, aortic, and pulmonary valves are closed and ventricular blood volume remains constant.

Ventricular Filling

When enough blood has entered the atria, it flows from the atria to fill the ventricles mostly before the atria contract. This ends with atrial contraction and the excitation will spread and trigger ventricular contraction to start the cycle over.

Filling/Pumping Steps (Left)

Mid/Late Diastole
1. Left atrium and ventricles are both relaxed. Atrial pressure is a little higher than ventricular pressure because blood is entering.
2. AV valve is held open by this pressure difference, and blood entering the atrium from pulmonary veins continues to the ventricle.
3. Aortic valve is closed because the aortic pressure is higher than the ventricular pressure.
4. Aortic pressure is slowly decreasing because blood is moving out of the arteries and through the vascular system.
5. Ventricular pressure is slowly increasing because blood entering the relaxed ventricle from the atrium.
6.SA node discharges and the atria depolarize, P-wave.
7. Contraction of the atrium causes an increase in atrial pressure.
8. Increased atrial pressure forces a small volume of blood into the ventricle, aka atrial kick.
9. The amount of blood in the ventricle at this time is called the end-diastolic volume
Systole
10. Depolarization from the AV node passes into and throughout the ventricular tissue-as signified by the QRS complex. This triggers ventricular contraction.
11. As the ventricle contracts, ventricular pressure increases rapidly, and pressure exceeds atrial pressure.
12. Change in pressure gradient forces the AV valve to close and prevent backflow.
13. Aortic pressure still exceeds ventricular pressure and the aortic valve remains closed, inhibiting the emptying if the ventricle. All valves are closed, and backward bulging of the closed AV valve can cause a small upward deflection in the atrial pressure wave.
14. Brief phase when the rapidly increasing ventricular pressure exceeds aortic pressure.
15. Pressure gradient now forces the aortic valve open and ventricular ejection begins.
16. Ejection is rapid at first and slows.
17. Blood remaining in the ventricle after ejection is called the end-systolic volume.
18. As blood flows into the aorta, aortic and ventricular pressure increase. Throughout ejection, very small pressure differences exist between the ventricle and aorta because the open aortic valve offer little resistance.
19. Peak ventricular
and aortic pressures are reached before the end of ventricular ejection because of the strength of ventricular contraction diminished during the last part of systole.
20. Force reduction is demonstrated by the reduced rate of blood ejection during the last part of systole.
21. Volume and pressure in the aorta decrease as the rate of blood ejection from ventricles becomes slower than the rate at which blood drains from the arteries into tissue.
Early Diastole (bulk of ventricular filling)
22. Ventricular repolarization, T-wave.
23. As ventricles relax, pressure decreases below aortic pressure. This pressure gradient forces the aortic valve to close. The combination of the aorta's elastic recoil and blood rebounding against the valve causes a rebound of aortic pressure called the dicrotic notch.
24. AV valve remains closed because ventricular pressure is still higher than atrial. All valves are closed again.
25. Phase ends as decreasing ventricular pressure decreases below atrial pressure.
26. Change in pressure gradient results in the opening of the AV valve.
27. Venous blood that had accumulated in the atrium since the AV valve closed flows rapidly into the ventricles.
28. Rate of flow in enhanced during initial filling phase by a rapid decrease in ventricular pressure because the ventricles previous contraction compressed the elastic elements of the chamber so that the ventricle tends to recoil outward once systole is over. This expansion lowers ventricular pressure more rapidly and may even create negative pressure. Some energy is stored within the myocardium during contraction and released during relaxation.

Pulmonary Circulation Pressures

The same steps of pumping and filling occur on the right side of the heart but at a much lower pressure. This lower pressure is because the right ventricular wall is less muscular. While systemic arterial pressures are ~120mmHg and pulmonary arterial pressures are ~25mmHg, the stroke volume from each side is the same.

Heart Sounds

Low pitch "lub" which corresponds to the closure of AV valves and the start of systole. Loud "dub" which corresponds to the closure of the pulmonary and aortic valves at the onset of diastole.

Murmurs

Abnormal heart sounds which can be the sign of heart disease and can lead to loud and turbulent blood flow.

Systolic Murmur

Murmur caused by a stenotic pulomonary or aortic valve, insufficient AV valve function, or a hole in the ventricular system.

Disatolic Murmur

Murmur caused by a stenotic AV valve or an insufficient pulmonary or aortic valve.

Cardiac Output CO

The volume of blood pumped from either ventricle per unit of time (L/min). The output passing into the systemic and pulmonary circuits is the same.

Cardiac Output Equation

CO = HR x SV. CO is directly proportional to both heart rate and stroke volume.

Total Blood Volume

5.5L

Normal Cardiac Output

5L/min. Essentially our entire blood volume is circulated every minute.

Cardiac Output During Exercise

Heart is pumping more so it is being circulated faster; up to 35L/min.

What Can Vary the Heart Rate?

Absence of neurohormonal control (nerves and hormones) can get heart rate to 100bpm which is the intrinsic firing rate of the SA node, epinephrine binding to B-adrenergic receptors in the SA (speeds), body temp, electrolytes, adenosine from caridomyoytes, and ESPECIALLY cardiac para/sympathetic nerves.

Sympathetic Effect

Increased slope of pacemaker potential, increased F-Type channel permeability, faster depolarization, rapid rise to threshold, heart rate speeds up. They innervate the entire cardiac conduction system which speeds up the conduction of impulses.

Parasympathetic Effect

Decreased slope of pacemaker potential due to a reduced permeability to Na+, slower depolarization, slower rise to threshold, heart rate is slower. They innervate the AV node and decrease the rate of electrical conduction through the atria and AV node which slows heart rate.

End-Diastolic Volume and Ventricular Contraction

Relationship is called the Frank-Starling Relationship. Increased filling of the ventricles will stretch the cardiac muscle and create optimal contact between actin and myosin. This increased cross-bridge formation increases sensitivity of troponin for Ca2+, there is an increased release of ca2+ from the SR. The key is increased venous return to the heart to fill the ventricles and increase end-diastolic volume and increased force of ventricular contraction due to increased end-diastolic volume has NOTHING to do with contractility of cardiac muscle.

Ejection Fraction EF

Measurement of the percentage of blood leaving your heart every time it contracts. At rest, EF = 50-75%.

Ejection Fraction Equation

EJ = SV / End-Diastolic Vol. Ej is directly proportional to stroke volume but inversely proportional to end-diastolic volume.