phys exam 2 vocab/things i struggle with

isovolumetric contraction (ventricular systole)

atria is relaxed, ventricles contract, av valves remain close to prevent backflow

ejection (ventricular systole)

atria is relaxed, ventricles contract, blood leaves via open sl valves

isovolumetric relaxation (ventricular diastole)

atria is relaxed, ventricles are relaxed, sl valves are closed

rapid filling (ventricular diastole)

atria is relaxed, ventricles are relaxed, av valves open to allow passive filling

atrial contraction (ventricular diastole)

atria contracts, ventricles are relaxed, av valves are open to allow rest of blood into ventricles

p wave

depolarization of atria

qrs complex

ventricular depolarization, atrial repolarization

t wave

ventricular repolarization

pr segment

av nodal delay

smooth muscle classifications

by location, by contraction patter, by communication with neighboring cells

myocardial contractile cells action potential

depolarizes from na+ into cell, repolarized from k+ leaving cell, long action potential from ca2+

myocardial autorhythmic cells action potential

depolarizes due to ca2+ channels opening

electrical conduction pathway in heart

sa node depolarizes and travels to —> av node —> av bundle —> bundle branches —> purkinje fibers

sinus rhythm

regular rhythm, 60-100bpm

tachycardia

high HR, greater than 100bpm

bradycardia

low hr, less than 60bpm

heart block

electrical signal from av node is partially or completely blocked from reaching the ventricles

Q - cardiac output

volume of blood pumped out by one ventricle in a given period of time

q equation

q = hr x sv

sv - stroke volume

amount of blood pumped by one ventricle during a contraction

sv equation

sv = end diastolic volume - end systolic volume

rate pressure product (rpp) equation

rpp = hr x systolic bp

sns regulation

releases norepinephrine on b-adrenergic rececptors to increase hr, inc na+ influx, positive chronotropic effect

pns regulation

releases acetylcholine on muscarinic receptors to slow hr, inc k+ influx, negative chronotropic effect

preload

degree of stretch before contraction, how much blood has entered the heart at one given time

starlings law

contraction strength increases with increased edv

to inc sv, inc edv why?

increased stretching = increased force. increased force = increased stroke volume

venous return is afftected by

venoconstriction, muscle pumps, ventilation pumps

afterload

resistance of lv ejection to blood

positive chronotropic state

increases the heartrate

negative chronotropic state

decreases the heartrate

ejection fraction

the percent of end diastolic volume ejected in one contraction

ejection fraction equation

ev= sv/edv

map equation

map = diastolic bp + 1/3(pulse pressure)

pulse pressure equation

systolic bp - diastolic bp

affects of exercise on heart

systolic bp increase, diastolic bp does not change

active hyperemia

increased blood flow to tissues based on increased metabolism

reactice hyperemia

decreased blood flow to tissues due to a blockage, must be removed

filtration

fluid movement out of capillaries

absorption

fluid movement into capillaries

blood

ph of 7.35-7.45, temp of 38, 7% of body weight, average is 5-6l (men), 4-5l (women)

albumin

carrier protein, maintains fluid balance. very large

globulin

clotting factors

fibrinogen

forms mesh-like structure in clots

transferrin

iron transport

rbcs

transport oxygen and carbon dioxide

wbcs

help fight of infections

platelets

essential to blood clotting process

steps of platelet plug formation

1. exposed collagen binds and activates platelets

2. activation causes release of platelets factors

3. factors attract more platelets

4. platelets aggregate into platelet plug

intrinsic pathway

12, 11, 9, 10

extrinsic

3,7,10

fibrogen is converted by ______ into _______

thrombin, fibrin

plasminogen converts to ______ which dissolves ________

plasmin, fibrin

type a blood

anti-b antibodies, a antigen

type b blood

anti-a antibodies, b antigen

type ab blood

no antibodies, a and b antigen

type o

anti a and anti b antibodies, no antigens

ventilation

movement of air into and out of the body

respiration

gas exchange

external respiration

gas exchange between lungs and capillaries

internal respiration

gas exchnage between tissues and capillaires

functions of pleural fluid

attach lung to thoracic cage, reduce friction

conduction zone

conducts air to respiratory zone where it is humidified, warmed, filtered. includes trachea, bronchial tree, bronchioles

respiratory zone

exchange of gases between air and blood. includes respiratory bronchioles, alveolar sacs

partial pressure of gas

pgas = patm x % of gas in atomsphere

boyles law

gases move from areas of high pressure to low pressure, a decrease in volume equals an increase in pressure

tidal volume

volume of air moved during a single expiration or inspiration

inspiratory reserve volume

additional volume that you can inspire at the end of a quiet capacity

vital capacity

represents the maximum amount of air you can voluntarily move in and out of your lung with one breath

residual volume

air remaining in lungs at the end of a maximal expiration

primary muscles of inhalation

diaphragm, external intercostals

accessory muscles of inhalation

sternocleidomastoid, scalenes, pectoralis minor, serratus anterior

primary muscles of expiration

none, is driven by relaxation of lungs

accessory muscles of expiration

internal intercostals, transversus thoracis, external oblique, rectus abdominus, internal oblique

during inspiration

the thoracic cavity expands, external intercostals contract, diaphragm contracts. high pressure outside to low pressure inside

during expiration

thoracic cavity reduces, external intercostals relax, diaphragm relaxes. high pressure inside to low pressure outside

compliance

represents relative ease of stretch of lungs and chest wall

high compliance

lungs stretch easily

low compliance

lungs are stiff and hard to inflate

elasticity

tendency of lungs to return to resting state

pulmonary minute ventilation (ve)

volume of air breathed per minutep

pulmonary minute ventilation (ve) formula

ve = respiratory rate (f) x tidal volume (vt)

alveolar minute ventilation (va)

air available for gas exchange

alveolar minute ventilation (va) equation

va = respiratory rate (f) x (tidal volume (vt) x anatomical dead space (vd))

eupnea

normal quiet breathing

hyperpnea

increased respiratory rate/tidal volume with increased metabolism

hyperventilation

increased respiratory rate/tidal volume without increase metabolism

hypoventilaton

decreased alveolar ventilation

tachypnea

respiratory rate less than 24 breaths/min

dyspnea

difficulty breathing

apnea

no breathing

during external respiration, o2 moves

from alveoli (lungs) into blood of surrounding capillaries

during external respiratory, co2 moves

from the blood into the alveoli, where it is then exhaled out of the body

during internal respiration, o2 moves

from the blood into the body tissues/cells which is then used for cellular metabolism

during internal respiratorion, co2 moves

from the body tissues/cells into the blood which carries it back to the lungs

hypoxic hypoxia

low arterial po2

anemic hypoxia

decreased oxygen bound to hemoglobin

ischemic hypoxia

decreased blood flow

histotoxic hypoxia

poisoned cells

emphysema

destruction of alveoli means less surface area for gas exchange