Phys Chapter 13

Cardiovascular system

Consists of cardiovascular and lymphatic system

Components of cardiovascular system

Blood

-Transport medium

Heart

-Pump: drives circulation of blood

Blood vessels

-Tubing that conducts blood through circulation

Blood

Represents about 8% of total body weight

Average blood volume = approx five liters

Consists of

-Erythroctyes

-Leukocytes

-Plasma

Erythrocytes

RBC’s

Leukocytes

White blood cells

Platelets

Cell fragments

Plasma = liquid portion of blood

Composed of

-proteins

-nutrients

-hormones

-electrolytes

Plasma proportion of blood

55%

Buffy coat

Platelets and leukocytes

Hematocrit

Erythrocytes

45% of whole blood

Plasma

Mostly water (90%)

-dissolves materials

-acts as fluid for transport

Proteins (7-9%)

-maintain osmotic pressure of blood

-NTK albumins (draw water into/out of the blood)

-lipid transport

-immunity (antibodies)

-clotting factors

-various enzymes

Erythrocytes

Contain hemoglobin (carry oxygen)

No nucleus, organelles

Structure: biconcave discs (greater surface area for diffusion)

Flexible membrane (allows RBCs to travel through narrow capillaries without rupturing in the process)

Erythropoiesis

Occurs in bone marrow

Hematopoietic stem cells (multipotent) (stem cells of one tissue that can become any tissue)

EPO (erythropoeitin)

Workout: kidneys release more EPO (less oxygen) (more aerobically fit)

EPO

EPO is a hormone that stimulates the production of erythrocytes (red blood cells) in the red bone marrow.

How it works

1. Blood oxygen levels decrease (hypoxia).

2. The kidneys detect the low oxygen levels.

3. The kidneys release EPO.

4. EPO stimulates red bone marrow.

5. Red blood cell production increases.

6. More RBCs → greater oxygen-carrying capacity of the blood.

Important things to remember

• Source: Kidneys (primarily).

• Target: Red bone marrow.

• Function: Stimulates erythropoiesis (RBC production).

• Stimulus: Low blood oxygen levels.

Blood typing

Based on the antigen (protein) present on blood cell

A - only A antigens

B - only B antigens

AB - A and B antigens (neither A or B antibodies)

O - neither A or B antigens (can’t have any antibodies because it can’t bind)

Rh - gives you the +/-

Anemia

Below normal O2 carrying capacity of the blood

Causes:

-Dietary deficiencies

-Blood loss

-Bone marrow failure

-Hemolytic anemia (lysing of blood cells)

Leukocytes

WBC’s

Immune system

Thrombocytes

Platelets

Clotting

Thrombocytes

Colorless cell fragments

Come from megakarocyte cell

Function in hemostasts

Thrombopoietin

Thrombopoietin

Making thrombocytes

Hormone produced by liver increases number of megakaryocytes and therefore increases platelet production

Hemostasis

Prevention of blood loss

Involves three steps

1.vascular spasm

2.Formation of a platelet plug

3.Blood coagulation (clotting

Vascular spasm

First step in hemostasis

Reduces blood flow through a damaged vessel

Formation of a platelet plug

Second step in hemostasis

Platelets aggregate on contact with exposed collagen in damaged wall of the vessel

Platelets release ADP which causes surface of nearby circulating platelets to become sticky

Blood coagulation (clotting)

Third step in hemostasis

Coagulation proteins in blood

How is hemostasis prevented

At rest its inhibited by prostacyclin and nitric oxide (both released by healthy, in tact cells)

No damage = no prostacyclin or nitric oxide

Smoking/poor diet (platelets stick)

Clot formation

. Platelets: Promote clot formation

When a blood vessel is damaged:

• Platelets adhere to the damaged vessel wall.

• Platelets activate and release chemicals (including ADP).

• More platelets are recruited.

• Platelets aggregate to form a platelet plug.

• Platelets also help activate clotting factors involved in coagulation.

Clotting factors

Always present in blood plasma in inactive precursor form

Vessel damage that exposes collagen initiates cascade of reaction that involve successive activation of clotting factors

-Convert fibrinogen to fibrin

Two pathways for blood clot formation

Intrinsic pathway:

Activated by exposed collagen (platelets stick to collagen)

Extrinsic pathway:

Released from damaged tissue (releases tissue factor)

Final outcome:

Fribrinogen (soluble) →fibrin (insoluble)

Factor X stuff

Factor X →Factor Xa

Prothrombin →thrombin

Fibrinogen →Fibrin

Thrombin converts fibrinogen to fibrin (?)

Now can form clots

blood thinner

Prevents blood clots (inactivates factor X)

Pain meds ex. aspirin (also a blood thinner) could bleed out (aren’t clotting)

Fibrinogen vs fibrin

Fibrinogen (soluble) dissolves in plasma

Fibrin (insoluable) forms the mesh that forms the clot

Purpose of valves

Prevents backflow

R AV valve shut: more pressure in vents than atria

When pressure is greater behind the valve it does what

Opens

When pressure is greater in front of the valve what happens

It closes

Systole

Contracting

Diastole

Relaxing and filling

In systole what valve is open

Open

Aortic and pulmonary (semilunar) valves.

Closed

Mitral (bicuspid) and tricuspid (AV) valves.

In diastole what is happening to the pulmonary semilunar valve

During ventricular diastole, the pulmonary semilunar valve is CLOSED.

Why?

1. The ventricles relax.

2. Ventricular pressure decreases.

3. Pressure in the pulmonary trunk becomes higher than pressure in the right ventricle.

4. The pulmonary semilunar valve closes to prevent blood from flowing backward into the right ventricle

Events of systole

Isovolumetric contraction

-Ventricles contract, but no blood ejected

-Blood pressure rises above pressure in atria

-Atrioventricular valves shut

-all valves shut

Ejection

-Blood pressure in ventricle exceeds pressure in arteries

-Blood flows out of ventricles, causing pressure in ventricles to fall

-semilunar valves open

Events of diastole

Isovolumetric relaxation

-Pressure in ventricles drops below arterial pressure

-Semilunar valves prevent backflow of blood

-No change in ventricular volume

Rapid filling

-Pressure in ventricles falls below atrial pressure

-AV valves open, allowing blood to flow into ventricles

Atrial contraction

Electrical activity of heart

Heart beats autorhythmicity

Two specialized types of cardiac muscle cells

-Autorhythmic cells

Do not contract

Initiate AP’s and spread impulse throughout heart

-Contractile cells

99% of cardiac muscle cells

Do mechanical work of pumping

Normally do not initiate own AP’s

Sequence of electrical activity of heart

1.SA node

AP spreads throughout right and left atria

2.AV node

Conduction delay

Why? Want to give atria time to contract

3.Bundle of His

4.Purkinje fibers

Spread to non-conducting ventricular cells through gap junctions

Draw out the autorhymicity picture

Okay

Draw out myocardial cell picture

Okay

Excitation-contraction coupling in cardiac muscle

-Components of both skeletal and smooth muscle

-Gap junctions located in intercalated discs

Excitation-contraction coupling in cardiac muscle is the process that converts an electrical signal (action potential) into a mechanical contraction.

The BIG thing to remember is that calcium entering the cell triggers more calcium to be released from the sarcoplasmic reticulum (SR).

Look at picture on slide 34 and then draw it out

Refractory period in the heart

Why important?

Allow heart to relax and fill

ECG represents

Recording electrical activity of cardiac impulse that reaches body surface

-Not a direct recording of a single AP in a single cell at a single point in time

ECG uses

Determines HR/diseased states

Coronary circulation

Muscle is supplied with oxygen and nutrients by blood delivered to it by coronary circulation, not from blood within heart chambers

Coronary vessels = Provide bloody supply to heart during diastole

-During systole, coronary vessels are compressed by contracting heart muscle

Coronary blood flow normally varies to keep pace with cardiac oxygen needs

Vascular tree consists of

Arteries

Arterioles

Capillaries

Venules

Veins

Most blood in veins or arteries

Veins

Important to get blood back to the heart

Layers of arteries/veins

Tunica externa

Tunica media

Tunica interna

Arteries

Low resistance elastic conduits

-Due to large radius, arteries offer little resistance to blood flue

Pressure reservoir

-Act as pressure reservoir to provide driving force for blood

(expand/recoil)

Arterioles

Function

-Distribute cardiac output among systemic organs, depending on needs

• Vasoconstriction

• Vasodilation

If they constrict/dilate then more gets into capillaries

Controlled by intrinsic and extrinsic factors

Arteriole pressure

High resistance (no flow)

Moderate resistance (moderate flow)

Low resistance (large flow)

Capillaries

Thin walled, extensively branched

-Maximized surface area and minimized diffusion distance

Function:

Site of exchange blood and surrounding cells

Only tunica media

Types of capillaries

Continuous - tight, less leakage (skin, muscle, lung, CNS)

Fenestrated - windows/holes that allow more through (Exocrine glands, renal glomeruli, intestinal mucosa)

Discontinuous - large openings/ more can pass through (liver, spleen, bone marrow)

Veins

Return blood to heart

Blood reservoir

Structure:

-Large radius offers little resistance to blood flow

Low pressure system

Valves (don’t let blood drop)

Veins and gravity

Veins have low blood pressure so they need help getting blood back to the heart

1. One way valves - ensure blood travels in the correct direction towards the heart

2. Skeletal muscle pump - skeletal muscles contract which pushes blood up towards the heart

3. Respiratory pump

Coronary artery disease

Leading cause of death in the US

-Due to atherosclerosis (plaque builds up)

Risk factors:

Carcinogens - free radicals (expose collagen), smoking, obesity, diabetes

Lymphatic system

Fluid (most of it should be picked up) (some left behind) LS picks it up

Aids immune system

Removal of interstitial fluid and return uni-directionally to heart

Absorbs and transports fatty acids

Lack of lymphatic system function

Leads to edema

Extreme edema = elephantiasis

What is happening in an ECG - P, QRS, T

P wave	Atrial depolarization → atria contract
PR segment	AV node delay; electrical signal is briefly slowed before reaching ventricles
QRS complex	Ventricular depolarization → ventricles begin contracting
QRS complex	Atrial repolarization also occurs but is hidden by ventricular depolarization
ST segment	Ventricles are fully depolarized and contracting (ejection phase occurs during this period)
T wave	Ventricular repolarization → ventricles begin relaxing

PR segment

Conduction delay - Ventricles are filling

What is happening during the ST segment

During the ST segment, the ventricles are depolarized. This corresponds to the period when ventricular contraction and blood ejection are occurring.

Draw out excitation coupling in cardiac cells

Compare the structure and function of arteries, veins, and capillaries.

Include:

• Wall thickness

• Pressure

• Lumen size

• Presence or absence of valves

• Main function

Feature	Arteries	Veins	Capillaries
Wall thickness	Thick	Thin	One cell thick
Pressure	High	Low	Low
Lumen	Narrower	Wider	Very narrow
Valves	No	Yes (especially in limbs)	No
Function	Carry blood away from heart	Carry blood toward heart	Exchange gases, nutrients, and waste

Define vasoconstriction and vasodilation.

Also, explain what happens to:

• Vessel radius

• Resistance

• Blood pressure

	Vasoconstriction	Vasodilation
Vessel radius	Decreases	Increases
Resistance	Increases	Decreases
Blood pressure	Generally increases	Generally decreases

MAP equation

CO x TPR