Physiology Exam 3

Pericardium structure/parts

Visceral pericardium, pericardial cavity, parietal pericardium

Pericardial cavity functions

1. Cushions = mechanical protection

2. Allows for heart movement

3. Prevents heart overexpansion

4. (Fluid) reduces friction

5. Defense = physical barrier to infection

Layers of heart composition (outside to inside)

Parietal pericardium → pericardial cavity → visceral pericardium → myocardium → endocardium

Path of deoxygenated blood in the heart:

1. Superior/Inferior vena cava

2. Right Atrium

3. Right Ventricle

4. Pulmonary arteries

Pulmonary arteries carry […] blood

Deoxygenated blood

• Traveling AWAY from the heart = arteries

Path of oxygenated blood in the heart

1. Pulmonary veins

2. Left Atrium

3. Left ventricle

4. Aorta

Pulmonary veins carry […] blood

Oxygenated

• Bringing oxygenated blood from the lungs to the heart

2 classes of circulation:

1. Pulmonary circulation: to and from the lungs to oxygenate blood

2. Systemic circulation: to and from the body (oxygenate tissues)

Parallel Flow

Simultaneous blood flow/supply to different organ systems

The importance of parallel flow:

1. Each organ gets fresh oxygenated blood

2. Heart gets the first tap

3. Independent regulation of blood flow to each organ (Liver, Kidneys)

Coronary circulation

Circulation of blood to the heart and returning it to the right atrium

Coronary circulation TOTAL pathway

Aorta → coronary arteries → capillary beds → coronary veins → coronary sinus → right atrium

Path of oxygenated blood supply to the heart

Aorta → coronary arteries → capillary beds

Path of deoxygenated blood from the heart to the right atrium

capillary beds → coronary veins → coronary sinus → right atrium

Valves - importance

Create a one-way blood flow = prevents backflow

Classes of valves

1. Atrioventricular valves

2. Semilunar valves

Atrioventricular valves

Separate atria and ventricles

• Right atria = tricuspid valve

• Left atria = bicuspid / mitral valve

Semilunar valves

Dictate ventricle outflow

• Right ventricle = pulmonary valve

• Left ventricle = aortic valve

Fibrous skeleton of the heart — ROLES (3)

(Connective Tissue)

1. Structural: surrounds the 4 valves, connects them to the interventricular septum

2. Prevents overstretching of the valves

3. Electrical insulator between atria and ventricles

Why is the left ventricle thicker than the right?

Due to the difference in workload

• Right ventricle — must generate enough force to get blood to the lungs

• Left = must generate much more force to get blood to the rest of the body

Cardiac muscle cell characteristics:

1. Branched

2. Single or binucleated

3. Striated (but not all cells)

4. Intercalated discs

Cardiac muscle cell types

1. Autorhythmic (pacemaker) cells

2. Contractile Cells

Characteristics of Autorhythmic cells:

1. Very small population (1%)

2. Few/no myofibrils = NO sarcomeres = NO force generation

3. Spontaneously generate action potentials = exhibit pacemaker potential

Autorhythmic cells do not contribute […], instead they contribute […]

force; electrical impulses

5 Locations of autorhythmic cells in the heart

1. Sinoatrial (SA) node

2. Atrioventricular (AV) node

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

4. Right and Left Bundle Branches

5. Purkinje Fibers

Characteristics of Contractile Cells

1. 99% of the cells in the heart

2. Myofibrils = sarcomeres = GENERATE TENSION

3. Transverse (t) tubules = extensive and branching

4. Sarcoplasmic reticulum = not as extensive and skeletal

5. Mitochondria are 1/3 their volume

Gap junctions between autorhythmic and contractile cells allows for

electrical passageways

• Passing A.P.

Intercalated discs function

Connect pacemaker and contractile cells into a functional syncytium

Key features of intercalated discs

1. Desmosomes = withstand mechanical stress

2. Gap junctions = allows electrical communication (ions)

T/F: atria undergo excitation-contraction coupling as one

True! Both atria (and both ventricles) relax and contract in unison

Autorhythmic cell action potential characteristics:

1. Spontaneous

2. ALWAYS hit threshold

3. A.P. driven by Na+, K+, and Ca2+

Passage of current flow in the heart:

Autorhythmic cell → current flows via intercalated discs → triggers A.P. in contractile cells

4 Stages to Contractile Action Potentials:

1. Depolarizing Phase: Fast voltage-gated Na+ open (+ enters)

2. Initial repolarizing phase: Fast voltage-gated K+ open (+ leaves)

3. Plateau: A) L-type long-lasting voltage-gated Ca2+ channels open (+ enters)
   B) Slow voltage-gated K+ open (+ leaves)
   **NET RESULT = Plateau!! - efflux = influx

4. Final repolarizing phase: Ca2+ gates close, K+ open = + leaving cel

Absolute refractory period of contractile cardiac cells

Duration = the entire duration of the action potential
- Because cannot have summation/tetanus

Why is the absolute refractory period of cardiac contraction so long?

Because if the heart could achieve tetanus, there would be no blood flow = lethal

(therefore, no summation possible)

Process of excitation-contraction coupling in contractile cardiac cells

1. Autorhythmic cell A.P. travels to contractile cells = down the membrane

2. L-type Ca2+ voltage-sensitive gated channel opens = Ca2+ enters cell

3. Ca2+ triggers RyR to open SR = more Ca2+ enters cell

4. “Spark” of Ca2+

5. Induces the sliding of filaments = contraction

Relaxation of contractile cardiac cells

(Relies on the removal of Ca2+)

1. Ca2+ stored in SR by Ca2+ ATPase and calsequestrin

2. Ca2+ removed from the cell by NCX antiporter (powered by the gradient from the Na+/K+ ATPase)

How does NCX antiporter work to remove Ca2+ from contractile cells

Antiporter = removes Ca2+ and transports Na+ into the cell (NO ATP, secondary active transport — relies on the conc. gradient from the Na+/K+ ATPase)

The rate of spontaneous excitability of autorhythmic cells […]

Varies — based on the location of the cells

Who sets the pace of depolarizations

Autorhythmic cells with the quickest/highest frequency: “Follow the leader principle”

• In a normal, healthy cardiac tissue — SA node “sets the pace”

Sequence of electrical depolarization

1. SA node depolarizes (spontaneous)

2. Sends depolarization to AV node via the “internodal pathway”

3. Depolarization spreads slowly across BOTH atria, and slows through the AV node

4. Depolarization spreads rapidly to the Apex

5. Depolarize ventricles UPWARD from the apex

AV node

Fibers in the heart that have smaller diameters and fewer gap junctions

Result = slows conduction = allows for the correct coordination between chambers

Fibrous skeleton (role in electrical depolarization)

Connective tissue surrounding the valves = blocks atria and ventricles

****So that ventricles are not effected by the electrical signal of the atria

ECG

Records the electrical activity of the heart

• Composite measurement — the NET of all action potentials

Define the ECG

P wave = Atrial depolarization

QRS complex = ventricle depolarization

T wave = ventricle repolarization

Why is there no atrial repolarization seen on ECG

Because the QRS complex masks it

Direction of conduction and contraction order of ATRIA:

Excite: top to bottom

Contraction: top to bottom (allows to squeeze the blood into ventricles)

Direction of conduction and contraction order of VENTRICLES:

Excite: bottom to top

Contraction: bottom to top (allows blood to be pumped out to body)

Systole

Contraction

Diastole

Relaxing

Cardiac Cycle (5)

1. Passive ventricular filling - AV open

2. Atrial contraction/SYSTOLE

AV Close = lub

1. Isovolumetric ventricular phase/SYSTOLE

2. Ventricular ejection

SL close = dub

1. Isovolumetric ventricular relaxation

Describe the atrial systole phase:

Atria contract = generates higher pressure = allowing blood flow into the ventricles

Ventricular systole stage consists of:

1. Isovolumetric ventricular phase

2. Ventricular ejection

Describe the isovolumetric ventricular phase

Maintains volume while generating tension — no blood flow yet

• AV are closed

When is the “lub” sound of cardiac cycle

Right after atrial systole, at the beginning of ventricular systole

****Ventricle pressure pushes blood against the valves = closing

Describe ventricular ejection phase

During ventricular systole

• Enough pressure is generated to open the SL (semilunar) valves = blood flows out

When is the “dub” sound of cardiac cycle

After ventricular systole

****Ventricle pressure drops = blood backflow fills the cusps

Describe the isovolumetric ventricular relaxation phase

Volume maintained, pressure decreases, and all the valves are closed

THEN: As relaxes, pressure decreases — AV VALVES open when pressure in ventricles is less than the pressure in atria

Stroke volume

Volume of blood pushed out by the left ventricle

• Difference between diastolic and systolic volume

Cardiac output =

Stroke volume * heart rate

Cardiac output can be used as a measure of:

the effectiveness of the heart as a pump

Stroke volume reflects (3)

preload, afterload, and contractility

Preload

The initial stretching of the cardiac sarcomeres in ventricles before they contract

• Length-tension relationship: ideal overlap = maximum tension

Afterload

The pressure that must be exceeded by ventricular contraction for the semilunar valves to open

(The work from the ventricle to actually get blood out)

• Overcoming the pressure = ventricular ejection = pressure exceeds the great vessels

Factors that increase the afterload:

1. Hypertension

2. Narrowing of the vessels or valves

3. Loss of Compliance = stretchability in large vessels

Coronary Artery Disease

Lumen is obstructed = blood flow cannot get to the heart tissue

Autonomic innervation of the heart

Parasympathetic AND Sympathetic innervation

Parasympathetic innervation of the heart:

1. SA node

2. AV node

Sympathetic innervation of the heart

1. SA node

2. AV node

3. Myocardium

Sympathetic regulation of contractility:

Innervation of the myocardium

Contractility of the heart

Ability of the heart to contract

• Influenced by the SYMPATHETIC nervous system = hinges on Ca2+

Myocardial cells contract _____

Together!

• All of none - because of functional syncytium

Myocardial cells produce […] contractions based on […]

Graded contractions

• Based on the amount of Ca2+ in contractile cells

(Therefore: altering Ca2+ = alters contraction)

Effect of the sympathetic regulation of contractility:

Increases the Ca2+ available AND/OR the rate of SLIDING

Mechanism of sympathetic regulation of contractility

1. Norepinephrine (binds beta receptor) activates protein kinase A (pka)

2. pka phosphorylates 4 protein targets to increase contractility (influences Ca2+)

   1. L-type Ca2+ voltage-gated channel open longer

   2. RyR release channel enhanced Ca2+ release

   3. Ca2+ ATPase works faster (collection of Ca2+ more effective = can move more often)

   4. Myosin ATPase = makes it go faster

4 Protein Targets of PKA

1. L-type Ca2+ voltage channel

2. RyR channel

3. Ca2+ ATPase

4. Myosin ATPase

Heart rate is regulated by

Sympathetic and parasympathetic innervation

Sympathetic [inc/dec] heart rate

INCREASES heart rate

2 mechanisms of sympathetic nervous system to increase heart rate

1. Increases the rate of spontaneous depolarization of SA node

2. Makes it easier to excite the AV node: velocity of conduction increases

Mechanism of sympathetic influence on heart rate

1. Norepinephrine binds the beta receptor IN THE NODE CELLS

2. Triggers the 2nd messenger = targets channel protein

3. Na+ is let into the cell = FASTER rate of depolarization

The sympathetic nervous system impacts:

1. Contractility (therefore - stroke volume)

2. Heart rate

Beta Blockers

Limits the ability of the body to respond to the sympathetic nervous system by limiting the effects of norepinephrine/epinephrine = reduces heart rate

Parasympathetic regulation of cardiac output

Heart rate

Parasympathetic [inc/dec] heart rate

DECREASES heart rate

2 mechanisms the parasympathetic uses to decrease heart rate

1. Decreases the rate of spontaneous depolarization of the SA node

2. Makes it harder to excite the AV node

Mechanism of parasympathetic influence on heart rate

1. Acetylcholine binds receptor:

A) Increases the K+ leaving = hyperpolarizes (inhibits action potentials from autorhythmic cells)

B) cAMP decreases = Na+ gates close = less Na+ flows into the cell = SLOWS depolarization

Vascular system overview (main kinds + key role)

1. Arteries: Pressure Reservoir (expandable)

2. Arterioles: Variable resistance (can selectively restrict/relax)

3. Capillaries: exhange

4. Venules

5. Veins: Volume reservoir (expandable)

4 Main materials of blood vessels

1. Endothelium - single layer

2. Elastic Tissue - elastin protein = stretches

3. Smooth Muscle - control diameter

4. Fibrous Tissue = primarily collagen = tensile strength

Capillaries =

Just endothelium

• Very very simple to maximize exchange

Elastic arteries

Ex: Aorta, pulmonary artery …

• Stretch = when ventricles contract (bc = ejects blood)

• Recoils = when ventricles relax

FUNCTION = pressure reservoir

Have thick bands of elastic connective tissue

Muscular arteries

Ex: Most arteries in arterial circuit

• Less elastic (than aorta) = less able to expand and recoil

• Thick smooth muscle layer = capable of vasoconstriction AND vasodilation

• Deliver blood to organs

Microcirculation:

Control of capillary bed perfusion

Microcirculation is controlled by:

Metarterioles = partially surrounded by smooth muscle AND the precapillary sphincters

• Less exchange when sphincters are contracted

• Level of control MUST be on the metarteriole/sphincter level BECAUSE capillaries are too simple to control it

3 ways for things to move between bloodstream and interstitium

1. Diffusion

2. Transcytosis

3. Bulk flow

Transcytosis

Method of bringing solutes across the endothelium

1. Through vesicles

2. OR — some vesicles fuse together to create temporary channels

3 types of capillaries:

1. Continuous

2. Fenestrated

3. Sinusoid

Continuous capillaries

Most common

• Have gaps in the endothelial cell junctions = create leakiness

• Allow SMALL solutes

Fenestrated capillaries

Found in the kidney, small intestine, endocrine glands

• Have large pores (fenestrations)

Sinusoid capillary

Found in the bone marrow, spleen, liver

• Extremely large openings in the endothelial and basement membrane

• **Allows for large substances: proteins and BLOOD CELLS

Route of fluid exchange:

Arteriole → Net filtration (moving out) → Net absorption (in) → Venule

OR: can go into LYMPH after Net filtration (then into venous circulation)