LabQuiz2

bio349 wwu jaci waawaa muscle, cardiac, respiratory

Whole Muscles

organs compromised of muscle fascicles and connective tissues

Within muscles

thick & thin filaments, mitochondria, sarcoplasmic reticulum, myofibril, t-tubules

Sarcomere

unit of structure and function within muscle cell

surrounds myofibrils, stores and releases calcium

Sliding Filament Theory

H-zone and I band shorten (myosin is brought in to m-line and is overlapped by actin)

muscle fiber twitch

-threshold stimulus (Ach) occurs at motor end plate of skeletal muscle

-AP is conducted in all directions along sarcolemma resulting in release of calcium from SR (all-or-none response)

-calcium binds to troponin, makes binding sites on actin available to myosin

-ATP powers each ‘stroke’ of myosin, pulling actin toward center of sarcomere

-results in single contraction of each sarcomere to greatest extent possible

-*can be recorded using electromyography (EMG)

force of whole muscle contraction is what type of response

graded

-vary in strength, not all muscle fibers are stimulated at the same time

-tension varies in different contracting muscle fibers

strength of whole muscle contraction depends on

a. # of motor units recruited

b. tension (force) produced by each muscle cell

1. treppe (thermal kinetic energy)

2. frequency of stim

3. initial fiber length (length-tension relationship)

4. thickness of fiber

c. extent of fatigue

fatigue types

muscular, neuromuscular, central

muscular fatigue

muscle no longer responds to stim

due to chemical changes within cell:

• increase in inorganic phosphate

• accumulation of lactate

• accumulation of k+

• depletion of glycogen

neuromuscular fatigue

at neuromuscular junction

• motor neurons cannot make Ach fast enough to sustain a series of AP

Central Fatigue

CNS no longer sends signals

• motor neurons dont generate AP, even if muscles still respond to stim

• often psych- protective mechanism, e.g stim of inhibitory reflexes via proprioceptors or pain

isotonic contraction

same tension/force, moves a load

concentric: muscle length is decreasing

eccentric: muscle length is increasing during contraction

isometric contraction

same length, force without movement

SA node

atrial depolarization (contraction)

P-wave

ventricular diastole

QRS Complex

ventricular depolarization

(contraction begins)

ventricular systole

T-wave

ventricular repolarization (relaxation begins)

ventricular diastole

What causes the '“lub dub” during the cardiac cycle?

S1 = AV valve close = lub

S2 = semilunar valves close = dub

What causes blood to flow

pressure

BP numbers

normal- 120/8

Systolic and Diastolic Pressure

Systolic Pressure

max pressure exerted by heart when the L ventricle contracts

Diastolic Pressure

lowest pressure experienced by arteries when the L ventricle relaxes

What influences BP?

blood volume- hydrostatic pressure due mostly to plasma volume

cardiac output- heart rate x stroke volume

Blood flow (vessel) is due to ratio of

pressure gradient (ie pulse pressure)/ peripheral resistance

F = P/R

Blood volume

total volume of blood in body ( 5 L)

-RBD (hematocrit) and plasma

-regulated by kidneys (urinary system) and endocrine system- kidneys regulate the amount of water and sodium in the blood

What is required for fluids to move

bulk flow needs pressure gradients

Pulse Pressure

pressure gradient necessary for blood flow

PP = systolic - diastolic

(normally @40 mmHg ie 120-80)

Mean Arterial pressure (MAP)

avg pressure causing blood flow (main driving force for blood through systemic circuit)

can be calculated several ways

= diastolic + 1/3 pulse pressure

What increases resistance to flow

influences perfusion and pressure

1. viscosity

   1. hematocrit, protein, content, etc.

2. vessel diameter (tone)

   1. resistance = 1/r^4

3. vessel length

autonomic NS

sympathetic (epi and ne)

-increase HR

-vasodilation/vasoconstriction

what local metabolites cause vasodilation

NO

histamine

K+

bradykinin

cardiac output controllers

intrinsic and extrinsic factors (nervous and endurance)

total peripheral resistance

intrinsic and extrinsic control

blood volume controllers

primarily controlled by endocrine and urinary systems

Intrinsic mechanisms on cardiac output and peripheral resistance

frank-starling law of the heart

sa node responds to stretch

local control of vessel diameter

frank-starling law of the heart

-strength of contraction is proportional to muscle fiber stretch (length-tension relationship)

more venous return = larger contraction/stroke volume

sa node responds to stretched

-increased AP frequency

-increased HR

local control of vessel diameter

-metabolic changes, elevated K+, histamine, temp, etc.

-myogenic stretch

extrinsic mechanisms that influence cardiac output and peripheral resistance

-sympathetic (norepinephrine) and parasympathetic (Ach) influences on the heart

-NE with epinephrine to prolong the effects of sympathetic response on blood vessels

-endocrine influences on blood volume

—adh and aldosterone, singly or as part of the RAAS

—natriuertic peptides

circulatory shock

lack of blood volume

1. hypovolemic (low blood volume)

2. cardiogenic (heart failure)

3. vasogenic (loss of tone in blood vessels)

4. neurogenic (nervous system failure)

vital organ function preservation at oxygen deprivation

-bradycardia/mammalian dive reflex occurs when

1. breath is held

2. face is submersed in ice cold water and/or

3. occular pressure increases

main components of external respiration

1. ventilation: air is moved into and out of the lungs

2. gas exchange b/w alveolar air and pulmonary capillaries

3. transport of gases to and from tissue cells

4. gas exchange b/w capillaries and tissue cells (responding to metabolic need via homeostatic mechanisms)

pressure differences

negative pressure in thoracic cavity

visceral and parietal pleura adhere to each other with a thin film of serous fluid

muscles of inspiration

sternocleidomastoid (elevates sternum)

scalenes group (elevate upper ribs)

pectoralis minor

external intercostals

diaphgragm

muscles of expiration

diapghram

internal intercostals

abdominals

quadratus lumborum

rate of diffusion

available surface area x concentration gradient/ resistance of membrane x thickness of membrane

other respirator functions

• enhances venous return

• enables speech

• sense of smell

• filters and removes airborne debris

• involved in water and heat loss

• ph regulation

how is respiratory measured

oxygen saturation

lung volumes

affects respiratory volumes

architecture: skeltal build, sex, height, muscle strength

age: muscle strength and elasticiy of body wall

extensibility: during inhilation of lungs and thoracic bod wall = compliance

elasticiy of lungs during exhalation

respiraory disfucntion

obstructive: interfeere with ventilation or difficulty emptying, include chronic obstructive pulmonary disease (asthma, bronchitis)

restrictive: interfere with gas exchange or difficulty filling

asthma

inflammation and bronchospasm

difficult expiration due to mucus build up

irritant

• intrinsic: infection, pullition

• extrinsic- alergens like pollen, animal dander

cystic fibrosis

hereditary

chloride pumps are made but not inserted into membrane

• dehydrations and overly sticky mucus layer

• pancreas— no section of digestive enzymes

• small intestine- compromised digestion adn nutritent absorption

• respiratory tract- congestion, chronic infection, pulmonary collapse

muscular dystrophy

• reduced viatl capacity

• short shallow breathing

• normally compensate by increasing respiratoy rate

• unable to compensate because muscle function is compromised

pneumonia

• fluid accumulation within/around alveoli

• commonly due to bacterial or viral infection

• also accidentl aspiration food or vomit

congestive heart failure

• fluid accumulation around alveoli

• fluid build up in pulmonary circuit

• poor gas exhange

sickle cell disease

hereditary

-misfolding of b-globin chain of hb

due to irregualar shape of RBC, increased risk of capilary obstruction

at lungs- microcirculation obstruction in pulmonary capillaties