BSCI202 Exam 2

Location of the heart

Location of the heart

Mediastinum

- superior surface of the diaphragm

- anterior to vertebral column

- posterior to sternum

Arteries

Carry blood away from the heart. They have thick walls and small lumens.

Veins

Carry blood towards the heart. They have thin walls and large, lumens; they having a lower pressure than arteries.

Four chambers of the heart

Left/Right Atrium

Left/Right Ventricle

Coronary circulation

Circulation of blood in the blood vessels of the heart (myocardium).

Coronary arteries deliver oxygen-rich blood to the myocardium.

Coronary veins remove deoxygenated blood from the heart.

Coronary circulation ≠ blood in chambers

Pulmonary circuit

Receives oxygen-poor blood from the tissues. Right side pumps blood to lungs to get rid of CO2 and pick up O2.

Right atrium—> tricuspid valve—> right ventricle—> pulmonary semilunar valve—> pulmonary trunk—> pulmonary arteries—>lungs—> pulmonary veins—> left atrium

Systematic circuit

Receives oxygenated blood from lungs. The left side pumps blood to the body tissues.

Left atrium—> mitral/bicuspid valve—> left ventricle—> aortic semilunar valve—> aorta —>systemic circulation

Asymmetry of the Ventricles

Think of form and function! The left ventricle is 3x larger and has a thicker myocardium than the right ventricle.

This is because the left side needs to be stronger in order to pump blood to all the tissues in the body. The right side only pumps blood to the lungs.

Pericardium

Deep two layered serous membrane enclosing the heart. It contains the parietal (outer layer) and the visceral layer (inner layer/epicardium).

Pericardial cavity

Fluid-filled cavity separating the two layers to prevent friction within the pericardium and allows easy movement during heart contractions.

Layers of the Heart

1.) Epicardium

2.) Myocardium

3.) Endocardium

Epicardium

Visceral layer of the serous pericardium

Myocardium

Contractile cardiac muscle cells.

Includes the cardiac skeleton, crisscrossing, interlacing layer of CT. It anchors the cardiac muscle fiber, supports great vessels & valves, and limits the spread of action potentials to specific paths.

Endocardium

Lines heart chamber and valves. It continues with the blood vessels.

Heart septums

Separates the atriums and ventricles. Interatrial septums and interventricular septums.

Heart valves

Unidirectional membranes attached to the heart wall that open and close depending on pressure changes caused by influx of blood in the heart.

There are two atrioventricular (AV) valves and semilunar (SL) valves.

Atrioventricular (AV) valves

When they are open, atrial pressure > ventricular pressure. Blood returning to the heart fills the atria, pressing against the valves. This is what forces them open. As the ventricles fill, the valves hang limply into the ventricles. The atria then contract, forcing additional blood into the ventricles.

When they are closed, atrial pressure < ventricular pressure. When ventricles contract, this forces blood against the valve cups, causing them to close. Papillary muscles contract and chordae tendinae tighten, preventing valve flaps from opening into the atria.

Includes the tricuspid and mitral/bicuspid valves.

bicuspid valve

Transfers blood from right atrium to right ventricle.

tricuspid valve

Transfers blood from left atrium to left ventricle.

Semilunar (SL) valves

When ventricles contract, this forces these valves open, pushing blood into the pulmonary artery and aorta for pulmonary and systemic circulation. When they are open, ventricle pressure > artery pressure.

Includes the pulmonary and aortic semilunar valves.

1.) Pulmonary:

2.) Aortic:

Pulmonary semilunar valves

Transfers blood from the right ventricle to the pulmonary trunk --> pulmonary artery

Aortic semilunar valves

Transfers blood from the left ventricle to the aorta

Heart sounds

There are two: a "lub" and a "dub", associated with the closing of the heart valves.

Lub = AV valves close

Dub = SL valves close

Heart murmurs

Abnormal heart sounds, usually indicating incompetent or stenotic valves. This can be caused my mitral regurgitation.

Mitral regurgitation

Leakage of blood backwards through the mitral/bicuspid valve each time the ventricles contract.

Intercalated disc

Made of desmosomes and gap junctions, they connect cardiomyocytes (heart muscle cells), allowing the heart to function as a syncytium; all cardiomyocytes contract as a unit or none contract at all.

Electrical signals of the Heart

It works on an intrinsic conduction system.

1.) Sinoatrial (SA) node

2.) Atrioventricular (AV) node

3.) Atrioventricular (AV) bundle/Bundle of His

4.) Left and Right bundle branches

5.) Subendocardial conducting network.

Sinoatrial (SA) node

The pacemaker of the heart; generates impulse.

Atrioventricular (AV) node

Where impulse stops for 0.1 seconds, allowing the entry of blood that had not been pumped to ventricles during atrial contraction into the ventricles and carrying the impulse for ventricular contraction.

Atrioventricular (AV) bundle

Also called the Bundle of His, carries impulse from the atria to the ventricles.

Left and Right Bundle Branches

Conduct electrical impulses of the heart through the interventricular septum.

Subendocardial conducting network

Also called Purkinje fibers, they are the depolarizers. They stimulate the contractile cells of both ventricles, causing ventricular contraction.

Difference between contractile muscle cells and pacemaker cells

Contractile muscle cells have a fast response rate. Pacemaker cells have slow response rate and are spontaneous (occur through internal impulse).

Types of cardiac cells

Contractile muscle cells and autorhythmic/pacemaker cells

Cardiac action potentials

1.) Depolarization: Na+ influx through fast voltage-gated channels. This generates action potential.

2.) Plateau phase: occurs due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because there are few K+ channels open.

3.) Repolarization: Ca2+ channels close and K+ channels open, allowing K+ efflux and bringing membrane potential back to its resting voltage

Pacemaker action potentials

1.) Pacemaker potential: slow depolarization due to slow opening of Na+ and closing of K+ channels (membrane potential is NEVER a flat line).

2.) Depolarization: when pacemaker potential reaches threshold, depolarization is caused by Ca2+ influx through Ca2+ channels. This generated action potential.

3.) Repolarization: Ca2+ channels close and K+ channels open, allowing K+ efflux and bringing membrane potential back to its most negative state.

Electrocardiogram (ECG or EKG)

All action potentials are given at the same time and generate three waves...

1.) P-wave

2.) QRS complex

3.) T-wave

P-wave

On an ECG, this represents the depolarization of SA node, leading to atrial depolarization/atrial contraction. The space between this wave and the next is the delay of impulse at the AV node.

QRS complex

On an ECG, this represents ventricular depolarization occurring at the apex of the heart. The space between this wave and the next indicates the completion of ventricular depolarization/contraction.

T-wave

On an ECG, this represents ventricular repolarization. The space between this wave and the next indicates the completion of ventricular repolarization and cardiac diastole.

What happens during systole?

Contraction

What happens during diastole?

Relaxation

Cardiac cycle

One cycle = the blood flow through the heart during one complete heart beat

Phases of cardiac cycle

1.) Ventricular filling

2.) Ventricular systole

3.) Isovolumetric relaxation

Ventricular filling

(First step of the cardiac cycle) This occurs during cardiac diastole --> atrial contraction/systole. AV valves are open and ventricle pressure is low. 80% of blood passively flows into ventricles. As atrial systole occurs, the atria deliver the remaining 20% of blood to the ventricles.

Ventricular systole

(Second step of the cardiac cycle) As the atria go through diastole, the ventricles begin to contract. At this point, ventricular pressure > artery pressure, opening the semilunar valves and closing the atrioventricular valves.

Isovolumetric relaxation

(Third step of the cardiac cycle) The ventricles relax as the relaxed atria fill. the Blood closes the SL valves. AV valves then open and the cycle begins again at ventricular filling

End diastolic volume (EDV)

Volume of blood in each ventricle at the end of ventricular diastole. Depends on length of ventricular diastole and venous pressure.

End systolic volume (ESV)

Volume of blood remaining in each ventricle after systole. Depends on arterial BP and ventricular contraction strength.

Cardiac Output (CO)

Volume of blood pumped by each ventricle in one minute = heart rate (HR) • stroke volume (SV). The average is 5.25 L/min.

- HR = number of beats per minute (avg. is 75 beats/min)

- SV = volume of blood pumped out by one ventricle with each beat (avg. is 70 mL/ beat)

Stroke volume

Volume of blood pumped out by one ventricle with each beat = end diastolic volume (EDV) - end systolic volume (ESV).

EDV = Volume of blood in each ventricle at the end of ventricular diastole

ESV = Volume of blood remaining in each ventricle after systole.

Factors affecting stroke volume

1.) Preload

2.) Contractility

3.) Afterload

Preload

Factor that affect stroke volume; Degree of stretch of cardiac muscle cells before they contract.

Increased venous return (amount of blood returning to the heart) causes it to increase, ultimately increasing EDV.

Contractility

Factor that affect stroke volume; Contractile strength

Increase caused by sympathetic stimulation --> increased Ca2+ influx --> more cross bridges

Decrease caused by calcium channel blockers

Afterload

Factor that affect stroke volume; Pressure ventricles must overcome to eject blood

How does hypertension affect afterload?

Hypertension = high blood pressure--> increased afterload--> increased ESV --> decreased SV

Sympathetic nervous system's effect on heart rate

Fear/surprise/flight or fight response: release of epinephrine from adrenal gland --> B1 receptors of SA node --> Na+ and Ca2+ influx increases --> pacemaker potential --> depolarization--> increased heart rate

Parasympathetic nervous system's effect on heart rate

Cardioinhibitory center of medulla oblongata send ACh (acetylcholine) through the vagus nerve --> Binds to M2 receptors on the SA node --> opens K+ channels and closes Ca2+ channels --> hyperpolarization --> decreased heart rate

Broad factors that influence heart rate

1.) Size: (age and gender are a function of size); inverse relationship

2.) Exercise: direct relationship

3.) Body temperature: direct relationship

4.) Intra- and extracellular ion concentrations (e.g. Ca2+ and K+) and hormones (epinephrine and thyroxine)

Hypocalcemia

Low calcium levels in blood --> depresses heart rate

Hypercalcemia

High calcium levels in blood --> increases heart rate

Hyperkalemia

High potassium levels in blood --> suppresses electrical activity and can cause cardiac arrest

Hypokalemia

Low potassium levels in blood --> unstable heart rhythms (arrhythmia) causes feeble heartbeat

Epinephrine

Hormone released from adrenal medulla that increases both heart rate and contractility

Thyroxine

Hormone released from the thyroid gland that enhances the effects of epinephrine and norepinephrine

SA node intrinsically fires 100/min; Typical resting heart rate: ~75 beats/min. But why?

The parasympathetic nervous system! The cardioinhibitory center of the medulla oblongata will send acetylcholine through the vagus nerve, decreasing heart rate. At rest, the parasympathetic is active on the sinoatrial nodes. If left to their own devices, the resting heart rate would be 100/min.

Tachycardia

Abnormally fast heart rate (>100 beats/min). If persistent, this may lead to fibrillation.

Bradycardia

Abnormally slow heart rate (<60 beats/min). This is a result of inadequate blood circulation.

Homeostatic response to increase of temperature

As temperature rises, the the brain sends signal from hypothalamus to send blood to the surface. Warm blood flushes into capillary beds, causing heat to radiate from the skin. H2O (sweat)then evaporates off our skin, making us cooler; sweat causes vasodilation via bradykinin in perspiration.

Homeostatic response to decrease in temperature

Through vasoconstriction, blood is shunted to deeper, more vital organs (i.e. the thoracic and abdominal regions). This causes extremities to get colder first. When you're shivering, muscles are contracting, generating heat.

Capillaries

Vessels between arteries and veins that contact tissue cells. They are made of endothelium with basal lamina.

They exchange gases, nutrients, waste, hormones, etc.

The tunica intima is 1 cell layer thick.

Intrinsic mechanisms

Metabolic or myogenic controls distribute blood to individual organs and tissues.

Extrinsic mechanisms

Neuronal or hormonal controls that maintain mean arterial pressure (MAP) and redistribute blood during exercise and thermoregulation.

Vasodilation

Widening of blood vessels.

1.) Intrinsic mechanisms

a. Metabolic

- decrease in O2

- increase in CO2, H+, and K+

- prostaglandins

- adenosine

- nitric oxide

2.)Extrinsic mechanisms:

a. Neuronal

- decrease in sympathetic stimulation

b. Hormonal

- atrial natriuretic peptide

Vasoconstriction

Narrowing of blood vessels

1.) Intrinsic mechanisms

a. Myogenic

- stretch

b. Metabolic

- Endothelins

2.) Extrinsic mechanisms

a. Neuronal

- increase in sympathetic stimulation

b. Hormonal

- angiotensin II

- antidiuretic hormone

- epinephrine

- norepinephrine

Lumen

Central blood-containing space of blood vessels

Tunica intima

Internal layer of blood vessel walls. It contains endothelium that lines the lumen of all vessels.

Tunica media

Middle layer of blood vessel walls. It is made of smooth muscle and elastin. This is what is affected by vasodilation and vasoconstriction, affecting blood flow and pressure.

Tunica externa

The outer layer of the blood vessel. It is made of collagen fibers.

Types of arteries

(From closest to heart--> furthest from heart)

1.) Elastic arteries

2.) Muscular arteries

3.) Arterioles

Elastic arteries

Closest arteries to the heart. Have a large lumen as well as a large, thick wall. They are made of elastin.

The aorta and its major branches are elastic arteries.

Muscular arteries

They are distal from the heart, but not as distal as arterioles. They have a thick tunica media with more smooth muscle that is active in vasoconstriction.

Sphincter

Muscles that control whether blood with flow into the capillaries. If they're open, blood flows through true capillaries. If they're closed, blood bypasses the capillaries.

Arterioles

The furthest away from the heart. They lead from the capillary beds via vasodilation and vasoconstriction.

Venule

Formed when the capillary beds unite. They are the first vessels coming from the capillaries.

Capacitance vessels

Also called blood reservoirs. They are small veins that come from the venules.

Venous valves

Flaps within the veins that allow the blood to flow only in one direction

How is blood moved through the arteries?

Pressure generated by cardiac contractions

How is blood moved through the veins?

Skeletal muscle pumps and venous valves

Venous insufficiency

Pooling of blood in the veins. This is why people tell you to stand up and walk around when sitting for a prolonged period time or when people wear compression socks after surgery.

Blood pressure (BP)

Force per unit area erected on wall of blood vessel by blood; measured in mmHg. Clinically, it is measured as a systemic arterial in large arteries near the heart, typically the brachial artery.

Average blood pressure

120 --> systolic pressure

80 --> diastolic pressure

Systolic blood pressure

Pressure that is the result of ventricular systole

Diastolic blood pressure

Pressure that is the result of ventricular diastole

Mean arterial pressure (MAP)

[Systolic pressure + 2(Diastolic Pressure]/3

Average = 93.3

Why isn't the mean arterial pressure not the average between systolic and diastolic pressure?

We spend a longer time in diastole than systole.

Sphygmomanometer

An instrument used for measuring blood pressure, typically consisting of an inflatable rubber cuff that is applied to the arm (brachial artery) and connected to a column of mercury next to a graduated scale, enabling the determination of systolic and diastolic blood pressure by increasing and gradually releasing the pressure in the cuff. Sounds are heard with stethoscope.

Applied pressure > systolic pressure: the artery is closed; there are no sounds

Applied pressure = systolic pressure: artery is partially open/opening and closing; sounds are heard

Applied pressure = diastolic pressure: the artery is fully open; there are no sounds

Blood Flow (BF)

Volume of blood flowing over a period of time in ml/min = ΔP/R

ΔP = change in pressure

R = resistance

Resistance (R)

Friction with vessel walls caused by...

1.) blood viscosity

2.) total blood vessel length

3.) blood vessel diameter (temperamental)

R = 1/r^4

r = radius

You take a vacation to the Swiss Alps. What impact might this have on blood flow?

1.) Tissue hypoxia—> less O2—> increase in blood vessel diameter and radius—> resistance decreases —> flow increases (initially and right away)

2.) higher altitude = less oxygen —> EPO activation—> more RBC production—> higher blood viscosity—> increase in resistance—> decrease in flow (occurs eventually)