UNC BIOL252 EXAM 3 STUDY GUIDE

Path of Blood Through The Double Circuit

Vena cava —> Right Atrium —> Right Ventricle —> Pulmonary Trunk (deoxygenated artery) —> Pulmonary Capillaries —> Pulmonary Veins (oxygenated) —> Left Atrium —> Left Ventricle —> Aorta —> Arteries —> Systemic Capillaries —> Veins

• Heart, lungs, heart, body

Aorta

The main artery of the body, supplying oxygenated blood to the circulatory system. In humans it passes over the heart from the left ventricle and runs down in front of the backbone.

Vena cava

very large veins that bring deoxygenated blood to your heart to get oxygen

Right Heart

Received deoxygenated blood from the body and sends it to the lungs

Left Heart

Receives oxygenated blood from the lungs and sends it to the body

Diaphragm

Muscle responsible for quiet breathing and separates the thoracic and abdominal cavities. It flexes during inspiration and relaxes during expiration.

Pericardium

A double-layered membrane that surrounds and protects the heart. The outer layer is fibrous and the inner layer is serous. 

Fibrous pericardium

the tough outer layer that limits the expansion of the heart, anchors it in place, and prevents it from overfilling with blood

Serous pericardium

Produces pericardial fluid and contains the pericardial cavity. This inner layer consists of 2 parts:

1. Parietal layer: lines the inside of the fibrous pericardium

2. Visceral layer: also called the epicardium, covers the heart’s surface

Pericardial cavity

The fluid-filled space between the visceral and parietal pericardia

Pericardial sac

The two outer layers that hold the pericardial cavity and the heart

Myocardium

The innermost muscular layer that makes the heart beat. It is responsible for the contraction of the heart, which pumps blood throughout the body.

Layers of Tissue Surrounding the Heart

1. Fibrous pericardium (outermost)

2. Parietal pericardium (serous)

3. Pericardial cavity

4. Visceral pericardium (serous)

5. Myocardium (innermost)

Intercalated discs

Specialized cardiac muscle junctions that connect individual cardiac muscle cells (cardiomyocytes) to one another: they contain desmosomes and gap junctions

Desmosomes

hold cardiomyocytes together during strong muscle contractions (located inside of intercalated discs)

Gap junctions

allow ions and electrical signals to pass quickly between cells, enabling the heart to contract as one coordinated unit (located in intercalated discs)

Sinoatrial (SA) Node

Establishes the frequency of action potentials through pacemaker cells. It is located in the right atrium near the superior vena cava

Atrioventricular (AV) Node

A cluster of pacemaker cells located posterior and medial to the tricuspid valve. It receives the electrical impulse from the SA node, briefly delays it to allow the ventricles to fill completely, and then passes the signal to the bundle branches and through the Purkinje fibers to trigger ventricular contraction.

Sinus rhythm

A normal heartbeat set by the SA node

Bundle branches

Carry the electrical impulse from the atrioventricular (AV) node down toward the apex of the heart, directing the signal to each ventricle.

• The right bundle branch sends impulses to the right ventricle.

• The left bundle branch sends impulses to the left ventricle.

Purkinje fiber system

The slowest group of pacemaker cells, only depolarize about 20 times per minute. Sometimes called atypical pacemakers because their action potentials rely on different ion channels and they function in a slightly different way.

Pacemaker cells

Specialized cardiac muscle cells found mainly in the SA node that generate their own electrical impulses without external stimulation. These cells set the rhythm of the heartbeat by repeatedly depolarizing and repolarizing, initiating the electrical signals that spread through the heart.

HCN Channels (“Funny Channels”)

Nonspecific cation channels unique to pacemaker cells that open when the cell membrane becomes hyperpolarized (more negative). They allow Na⁺ and K⁺ ions to flow slowly, creating the “funny current” that gradually depolarizes the membrane until it reaches threshold and triggers an action potential

• Hyperpolarizes at -60 mV

• Ca²⁺ voltage-gated channel opens at -40 mV and Na⁺ closes when depolarized

Pacemaker Phsyiology

1. Slow Initial Depolarization Phase: Funny channels open when membrane is hyperpolarized at -60 mV, and Na⁺ enters the cell

2. Full Depolarization Phase: Funny channels close when the cell becomes depolarized. Voltage-gated Ca²⁺ channels open at threshold (-40 mV), Ca²⁺ enters the cell, depolarization occurs

3. Repolarization Phase: Voltage-gated Ca²⁺ channels close at peak depolarization. Voltage-gated K⁺ channels open, K⁺ leaves cell, repolarization occurs. 

4. Cycle Repeats: Voltage-gated K⁺ channels remain open and depolarization continues. Funny channels will reopen when membrane is hyperpolarized again

How do pacemaker cells increase their pace?

By increasing the membrane’s permeability to Ca²⁺

How do pacemaker cells decrease their pace?

By increasing the membrane’s permeability to K⁺

How could you turn a normal neuron membrane channel into a pacemaker cell?

By adding HCN channels

You engineer a cell that has twice as many Na⁺ funny channels. What effect would this have on the resting membrane potential (RMP)?

It would become more positive as more Na⁺ travels into the cell

Phases of Contractile Cell Action Potential

1. Rapid depolarization: Voltage-gated Na⁺ channels open, Na⁺ enters the cells, membrane depolarizes

2. Initial repolarization: Voltage-gated K⁺ channels open, K⁺ exits the cell, membrane begins repolarizing. Voltage-gated Na⁺ channels inactivate.

3. Plateau Phase: Voltage-gated K⁺ channels remain open and K⁺ exits the cell. Voltage-gated Ca²⁺ channels open and Ca²⁺ enters the cell. Both channels are open at the same time, causing very little change in voltage.

4. Repolarization: Voltage-gated K⁺ channels remain open and K⁺ exits the cell. Voltage-gated Ca²⁺ channels inactivate, causing repolarization to intensify. 

Significance of the Plateau Phase

Ensures the heart has enough time to slowly relax and refill with blood before the next contraction

Influx of Ca²⁺ results in…

1. Release of sarcoplasmic reticulum (SR) Ca²⁺ (calcium-induced calcium release)

2. Binding of Ca²⁺ to troponin

Calcium-induced calcium release

The mechanism where a small calcium influx from outside the cell triggers a larger release of calcium inside the cell, amplifying the signal for heart muscle contraction.

How does calcium return to the extracellular matrix?

P wave

Atrial depolarization // atrial systole

• Pacemaker cells are firing action potentials

• Represents the SA node action potential

QRS complex

Atrial repolarization and ventricular depolarization // ventricle systole

• AV node fires action potentials

T wave

Ventricular repolarization // ventricular diastole

• AV node fires action potentials

Pulmonic Semilunar Valve (pulmonary valve)

Located between the right ventricle and the pulmonary trunk.
It opens when the right ventricle contracts, allowing blood to flow into the pulmonary arteries and toward the lungs. It closes when the ventricle relaxes to prevent backflow of blood into the right ventricle.

AV Tricuspid Valve

Located between the right atrium and right ventricle.
It has three cusps (flaps) and opens to allow blood to flow from the right atrium into the right ventricle during relaxation. It closes during ventricular contraction to prevent backflow into the atrium.

Aortic Semilunar Valve

Located between the left ventricle and the aorta.
It opens when the left ventricle contracts to pump oxygenated blood into the aorta and closes when the ventricle relaxes to prevent blood from flowing back into the heart.

AV Bicuspid Valve (Mitral valve)

Located between the left atrium and left ventricle.
It has two cusps (flaps) and opens to let blood flow from the left atrium into the left ventricle. It closes during ventricular contraction to prevent backflow into the left atrium.

Phases of Blood Flow Through the Cardiac Cycle

1. Ventricular Filling Phase: Ventricles are relaxed (diastole). Change in pressure moves blood to the ventricles.

2. Isovolumetric Contraction Phase: Atria relax (diastole). Ventricles contract (systole). Blood pushes the AV valves closed. Both sets of valves are closed and ventricular volume does not change.

3. Ventricular Ejection Phase: Ventricles continue contracting (systole). Semilunar valved are pushed open, and pressure increase moves blood out of the ventricles. Blood enters the aorta and pulmonary trunk.

4. Isovolumetric Relaxation Phase: Ventricles relax (diastole). Blood pushes semilunar valves closed. Both sets of valves are closes and ventricular volume does not change.

During which phase(s) of the cardiac cycle is no blood moving in the heart?

Isovolumetric contraction and relaxation phases. Prefix “iso” means “same,” so the volume of blood doesn’t change.

During which phase(s) of the cardiac cycle is blood moving from the atria to the ventricles?

Ventricular filling phase

During which phase(s) of the cardiac cycle is blood moving from ventricles to the aorta and pulmonary trunk?

Ventricular ejection phase

During which phase(s) of the cardiac cycle is pressure in the left ventricles greater than the pressure in the aorta?

Ventricular ejection phase

During which phase(s) of the cardiac cycle is pressure in the aorta greater than in the left ventricle?

Ventricular filling phase, isovolumetric contraction phase, isovolumetric relaxation phase

S₁ Heart Sound

Heard as the AV valves close (tricuspid and bicuspid valves)

S₂ Heart Sounds

Heard as the SL valves close (pulmonary and aortic valves)

Stroke Volume (SV)

The amount of blood pumped by the left ventricle in one heartbeat

• Calculation: SV = EDV - ESV

End-Diastolic volume (EDV)

Amount of blood in the left ventricle after it has filled. Affected by 2 variables:

1. The length of time the ventricle spends in diastole

2. The amount of blood returning to the right atrium from the systemic circuit

End-Systolic volume (ESV)

amount of blood in the left ventricle at the end of a contraction

Cardiac Output (CO)

The amount of blood pumped out of the heart per minute. It is the same for both sides of the heart. 

• Calculation: CO = HR x SV

Each side of the heart has the same…

Stroke volume, heart rate, and cardiac output

Factors the Influence Stroke Volume

1. Preload

2. Afterload

3. Contractility

Preload

Refers to the degree to which the sarcomeres in the ventricular cells are stretched before they contract. When venous pressure rises, and more blood flows into the ventricle, the ventricular wall is stretched. Enhances contractility and stroke volume.

Frank-Starling Law

The greater the end-diastolic volume (EDV), the greater the stroke volume (SV)

Situations that Increase Preload

1. Exercise: muscle contractions push more blood back to the heart, increasing venous return

2. Increased blood volume: conditions like excessive IV fluid administration or kidney disease lead to higher blood volume, increasing venous return

3. Lying down: Gravity no longer pulls blood down into the lower extremities, so more blood returns to the heart

Afterload

The blood pressure in the aorta and the pulmonary trunk that resists the ejection of blood from the ventricles during systole. It opposes ventricular ejection and reduces the stroke volume.

• High afterload causes a weak heart and low contractility

Situations that Increase Afterload

1. Hypertension: Increased arterial pressure makes it harder for the heart to eject blood

2. Aortic Stenosis: A narrowed aortic valve increases resistance, requiring more forceful contractions

3. Vasoconstriction: Conditions like stress or cold exposure can cause blood vessels to narrow, increasing resistance to blood flow 

Contractility

The intrinsic strength of the cardiac muscle contraction, independent of preload and afterload

Inotropic agents

Affects contractility

• Norepinephrine increases contractility

• Acetylcholine decreases contractility (small effect)

Chronotropic agents

Affects heart rate

• Sympathetic NS (NE) = positive agent, regulated by cardiac nerves

• Thyroid Hormones E & T₃ = positive agents

• Parasympathetic NS (ACh) = negative agent, regulated by CN X, perform action on pacemaker cells

Baroreceptors

Provide information on blood pressure and respond to changes in blood pressure. Contained in carotid sinuses.

Chemoreceptors

Respond to changes in blood chemistry. Contained in carotid and aortic bodies.

In cases of hypotension, baroreceptors would tell the cardiac centers to stimulate the heart with the _____ nervous system. Heart rate would _____, and the CO would _____, returning BP to normal. 

Sympathetic, increase, increase

In cases of hypertension, baroreceptors would tell the cardiac centers to stimulate the heart with the _____ nervous system. Heart rate would _____, and the CO would _____, returning BP to normal. 

Parasympathetic, decrease, decrease

Structure of Blood Vessels

1. Tunica intima

2. Tunica media

3. Tunica externa

Echocardiogram (ECG)

A graphic depiction of the electrical activity occurring in all cardiac muscle cells over a period of time. They can only show electrical changes that occur in contractile cells, so it appears flat when the pacemaker cells have their action potentials.

R-R Interval

entire duration of a cardiac action potential, determines heart rate

P-R interval

duration of atrial depolarization and AV node delay

Q-T interval

entire duration of ventricular action potential

S-T segment

ventricular plateau phase

Diastole

a period of relaxation

Systole

a period of contraction

Arteries

The distribution system of the vasculature: they travel away from the heart, branching into vessels of progressively smaller diameter.

• Pulmonary circuit: transport deoxygenated blood

• Systemic circuit: transport oxygenated blood

Capillaries

The exchange system of the vasculature: they are vessels of very small diameter that form branching networks called capillary beds. Gases, nutrients, wastes, and other substances are quickly exchanged between cells and the blood through the walls of these vessels.

• Contain only tunica intima

• Has porous intercellular connections and fenestrations

Veins

The collective system of the vasculature: they drain blood from capillary beds and return it to the heart. These vessels become progressively larger as they get closer to the heart.

• Pulmonary circuit: transport oxygenated blood

• Systemic circuit: transport deoxygenated blood

Tunica intima

The innermost layer of tissue composed of ENDOTHELIUM: consists of a sheet of simple endothelium and its basal lamina.

Endocardium

The inner lining of the heart, which is also composed of endothelium

Tunica media

The middle layer of the blood vessel wall. The smooth muscle cells control the diameter of the blood vessel and so the amount of blood flow to the organs. It has 2 layers:

1. A layer of smooth muscle cells arranged in a circular manner around the lumen

2. A layer of elastic filaments called external elastic lamina

Tunica externa

The outermost layer of tissue composed of dense irregular collagenous connective tissue that supports the blood vessel and prevents it from overstretching.

Vaso Vasora

“vessels to the vessels” —> tiny vessels supplying the tunica media and tunica externa. They supply O₂ and nutrients to the outer layers of larger blood vessels, whose cells are too far away from the lumen to receive O₂ and nutrients by diffusion alone.

Elastic arteries

High blood pressure vessels closest to the heart. They have the largest diameter and have very extensive elastic lamina.

• Ex. Aorta

Muscular arteries

Have extremely thick tunica media, and are responsible for controlling blood flow to organs and consist of smooth muscle. Major site of vasodilation and vasoconstriction. They make up the smaller branches of the aorta.

• Ex. renal artery

Aterioles

Thin-walled (1 layer of endothelial cells) vessels that contain smooth muscle and control blood flow to tissues. They are also major sites of vasodilation and vasoconstriction, and exchange materials.

Fenestrations

Holes in the plasma membrane allowing easy movement of materials through

Venules

The smallest veins which drain blood from capillary beds. Consists of thin walls and little smooth muscle. Some exchange continues here, and there is little tunica media/externa

Venous and Arterial Anastomoses

Connection between two veins or two arteries allowing blood to reroute in case of a blockage

Ateriovenous anastomosis (shunt)

A direct connection between an artery and a vein, bypassing capillaries to regulate blood flow as in thermoregulation

Factors that Influence Blood Pressure

1. Cardiac output (CO): blood flow into the vessels

2. Blood volume: total volume of the circulatory system

3. Resistance: prevention of flow

4. Compliance: stretchiness of vessels

Factors Determining Peripheral Resistance

1. Vessel radius (smaller radius = more resistance)

2. Blood viscosity (higher viscosity = more resistance)

3. Blood vessel length (longer length = more resistance)

4. Obstructions in vessels

Mean arterial pressure (MAP)

diastolic pressure + 1/3(systolic pressure - diastolic pressure)

Which two values account for the pressure change that drives blood flow?

Cardiac output and peripheral resistance

How does venous blood get into the heart?

1. Venous valves that dictate one direction of flow

2. The muscular pump

3. The respiratory pump

4. Venoconstriction (smooth muscles in vein walls)

Baroreceptor reflex

When MAP is low, the sympathetic neurons increase heart rate and contractility, which increases cardiac output, leading to increased MAP. Sympathetic neurons also cause vasoconstriction of arterioles, which increases peripheral resistance, leading to increased MAP and BP.

When MAP is high, parasympathetic neurons decrease the heart rate and contractility, which decreases cardiac output, leading to decreased MAP. Sympathetic neurons are inhibited, but there is no parasympathetic innervation to blood vessels. If there is no sympathetic stimulation, the vessels naturally dilate.

Chemoreceptors

Located around the great vessels (the aorta and carotid arteries), and also in the medulla. The carotid bodies sense changes in the blood’s gasses and accompanying pH changes. Low O₂/high CO₂ result in sympathetic activation of the heart and blood vessels that lead to increased MAP.

ADH

Stimulated by high Na⁺ levels. Response is thirst, water retention, and vasoconstriction.

Aldosterone

Stimulated by low Na⁺ levels. Response is Na+ retention.

Angiotensin-II

Powerful hormone stimulated by low blood volume. The response is thirst, Na⁺ retention, and vasoconstriction.

1. Promotes vasoconstriction of efferent arterioles (keeps kidneys working properly with low BP)

2. Promotes vasoconstriction of systemic blood vessels (arterioles have receptors for this hormone)

3. Promotes reabsorption of Na⁺ and Cl^- from the proximal tubule (region of kidney that gets H₂O back into circulation) and H₂O follows

4. Promotes aldosterone release, leading to increase Na⁺ and H₂O reabsorption

5. Stimulates thirst center in hypothalamus, which may increase fluid intake.

ANP

Hormone stimulated by high blood volume. Response is Na⁺ and H₂O excretion and vasodilation.