ppy 4

What is in blood

fibrinogen, von willebrand factors (VWF), prothrombin, clotting factors

Sequence when you get a wound

1. wound VWF binds to collagen, 2. platelets bind to collagen via VWF, 3. Binding to collagen activates platelets, 4. A thrombus is formed (platelet plug), does not need thrombin

Thrombin

used for clotting

Thrombus

many platelets piled up

Prothrombin (Xa)

→ thrombin

Fibrinogen (thrombin)

→ Fibrin

Fibrin (XIII)

→ crosslinked fibrin (clot)

Xa

Need to clot

Intrinsic pathways

negative charged surface (platelet lipids), clotting factors, calcium, vitamin K

Extrinsic pathways

negative charged surface (platelet lipids), clotting factors, calcium, vitamin K, tissue factor (thromboplastin)(from endothelial cells)

Effect of aspirin

aspirin inhibits TX2 released by platelets

TX2 is involved in

both platelet aggregation and in contraction of smooth muscle at site of wound (limits blood loss)

Serotonin is involved in

only vascular constriction at site of the wound

When TXA2 is reduced

both platelet aggregation (thrombus formation) and vascular contraction of smooth muscle at site of would is reduced

VWF platelets bind to fibrinogen via VWF (is not direct)

What binds directly to collagen

ADP and TX2

What stimulates the calling in of more platelets to form the platelet plug

TX2 and serotonin

what causes vasoconstriction at site of wound

Blood flow through the systemic circulation

come out through left ventricle into aorta, arteries, arterioles, capillaries, venules, veins, right atrium

Cardiac Output

Stroke Volume x Heart Rate

BP

Cardiac Output x Total Peripheral Resistance

Mean Arterial Pressure

(Systolic Pressure + 2 Diastolic Pressure)/3

Heart muscle AP

1. Sodium channel, sodium channel inactivates and K opens, L-tyoe Ca channels open, L-Type closes, K close

Plateau region, refractory region, repolarization

L type channels open for a brief time during

Filling ventricles

AV open, SL closed (pressure higher in atrium)

Isovolumetric contraction

AV closed, SL closed (pressure higher in aorta)

Ejection

ventricles open (pressure higher in ventricles)

Filling ventricles

PA>PV

Isovolumetric contraction

PA

Ejection

PAPaorta

Preload

directly related to ventricular filling

After load

pressure that the heart must work against to eject blood during systole

TPR

related to BP

Ventricles fill less so less stretch

what happens if preload (EDV) decreases and what can it cause

Less stretch

less overlap of myosin heads with actin sites for myosin binding, kess force of contraction, decrease in Stroke Volume and Cardiac Output

Automanatics effect cardiac output and stroke volume

Parasympathetic

only affects heart rate (decrease cardiac output decrease heart rate)

Sympathetic heart rate

increase cardiac output

Stroke volume up

cardiac output up (sympathetics)

Sympathetic

increase preload venous return, increase contractility, increase cardiac output

AV delay, decrease in conduction velocity

When the heart slows because of parasympathetic activity there is an increase in

The ventricles do not contract at the same time as the atria

There is a delay at the AV node to ensure

During fast heart rate conduction velocity increases

AV delay is less, opposite for slowing of heart rate

Systolic pressure increases, diastolic pressure stays constant

During exercise BP increases because

Blood accumulates in the legs and venous return decreases. This drops EDV (preload) and SV decreases. Decrease in SV results in decrease in CO and drop in BP, You turn on the sympathetic to counter the drip in BP.

Why does BP drop when you suddenly stand up

Pooling blood in lower extremities, decrease in cardiac output

decrease in BP when you stand up

MAP

mean of blood pressure

What could cause a drop in MAP

drop in SV by drop in venous return, drop in heart rate caused by drop in CO (parasympathetic), drop in TPR

P wave

depolarization of atria in response to SA node triggering

T wave

ventricular repolarization

PR interval

delay of AV node to allow filling of ventricles

QRS complex

depolarization of ventricles, triggers main pumping contractions

ST segment

beginning of ventricular repolarization, should be flat

Sympathetic

activates Gs phosphorylate the sodium channel and they open faster

Parasympathetic

activate Gi inhibits adenylate cyclase and cAMP production and beta gammas bind to K channels and slow the closing of these channels

High BP, low albumin, leakage of protein into interstitial fluid

What causes edema in legs?

High BP

hydrostatic pressure

Low albumin

which is decrease in plasma protein which decreases osmotic pressure

BP measurement

first sound systolic pressure, hear sound until you drop below diastolic pressure (no sound)

systolic pressure

first sound (top)

diastolic pressure

no sound (bottom)

A metabolic

no cause relaxation

Stretch responds to either stretch of smooth muscle or lack of stretch smooth muscle contraction

MAP = (SP+2DP)/3

86=(110+2x75)/3

MAP BP 110/75

Conducting zones

bronchi, regulate air flow to alveoli smooth muscle

Conducting zone

Cleans with ciliated cells and mucous cells

Respiratory zone

alveoli, where gas exchange takes place

Partial pressure

% of gas X total pressure

120 = .2 X 600

Total pressure 600 and O2 = 20% find Partial pressure

Take a breath

intrapleural space expands and pressure drops, lungs expand, lung volume increases so alveolar pressure drops relative to Atm pressure and air moves into the lungs

Diaphragm contracts and external intercostal muscles contract

Muscles that move while quiet breathing

Opposite

Muscles that move when you quiet expire

Prevents collapse of lungs, decreases surface tension

What is the role of surfactant

In type 2 cells in the alveoli

Where is surfactant made

Surfactant

does not increase elasticity, increases compliance

Inspiratory reserve volume

when you take deep breath volume taken in

Expiratory reserve volume

blowing air out forcefully

Vital capacity

Title Volume + Inspiratory Reserve Volume + Expiratory Reserve Volume

Inspiratory capacity

Title Volume + IRV + maxim air you can take in

Passive diffusion

Both O2 and CO2 move across membranes by

CO2 flows from

high pressure to low

Normal conditions of CO2

high in capillaries and flow from capillaries to alveoli

O2 flows from

high pressure to low

Chloride shift

1.CO2 is released to alveoli and exhaled, 2. CO2 is converted to HCO3 at tissues to be carried by blood, 3. Shift allows for conversion of CO2 to HCO3 at tissue in tissue 4. Shift of HCO3 to CO2 in lungs

Tissue to lungs (70% HCO3, 20% carbamino HB, 10% dissolved in blood)

How is CO2 transported

Decreased affinity

HB/O2 binding and release increased temp

Increased CO2

decreased affinity

Decreased pH

decrease affinity

Shift graph to the left

increase affinity

Lungs

Want high oxygen affinity in the

Hemoglobin wants

less affinity

Acid, CO2, DPG

shifts to the right, decrease affinity

Immediately O2 levels drop, hyperventilate and lower CO2 so affinity for O2 increases, gives better O2 loading, after a few days DPG levels increase and O2 affinity decreases

What happens if you go up to altitude

If aveouls is poorly ventilated

O2 down, CO2 high then constrict this capillary blood vessle to limit blood flow to this alveolus

If no blood flow to alveoli

O2 high, CO2 low, constrict the smooth muscle of the alvelous that is not perfused and relax the other

Stay unchanged bc increased ventilation

During exercise O2 levels

Lungs are not functioning

you hyperventilate, CO2 builds up and move to right get more H+ acidosis

Metabolic acidosis

lungs are fine if acidic, lungs want to hyperventilate to lower H+ so PCO2 levels are low

Acidosis/Alkalosis

H20+CO2 (CA)= H2CO3 = H + HCO3

Carotid bodies and aortic bodies

peripheral Chemoreceptors located