ANTOMYY

Alveolar ventilation

dead space is the air in conducting zone that isn’t available for gas exchange, TV - Dead space = air for gas exchange

Minute ventilation

Breaths per min x TV= MV

Alveolar equation

Breaths per min x (TV - Dead space) = AV

Rate vs depth in alveolar respiration

increase depth and decrease rate of breathing = best way to increase AV

Tidal volume

The amount of air inhaled or exhaled during each breath.

inspiratory reserve volume

The additional amount of air that can be inhaled after a normal inhalation.

expiratory reserve volume

The additional amount of air that can be forcibly exhaled after a normal exhalation.

residual volume

The volume of air remaining in the lungs after a forced exhalation, preventing lung collapse.

functional residual capacity

The volume of air in the lungs at the end of passive expiration, which includes both the expiratory reserve volume and the residual volume.

inspiratory capacity

The maximum amount of air that can be inhaled after a normal tidal volume exhalation, comprising the tidal volume and inspiratory reserve volume.

vital capacity

The maximum amount of air a person can exhale after taking the deepest breath possible, calculated as the sum of the tidal volume, inspiratory reserve volume, and expiratory reserve volume.

Total lung capacity

The total volume of air the lungs can hold, including vital capacity and residual volume.

Respiratory disorders when lower VC= lower TLC

tuberculosis, black lung disease, pneumonia, pulm edema, cystic fibrosis

Obstructive disorders when lower radius = lower flow (lower FEV, VC, RV and TLC)

Conditions like asthma, emphysema and chronic obstructive pulmonary disease (COPD) that cause narrowed airways, leading to decreased airflow and difficulty in breathing.

Forced expiratory volume

% vc exhaled in one second

Daltons Law

Total P = sum of all partial pressure, each gas behaves independently

Henry’s law and Alveolar gas exchange

gases will diffuse into liquid until partial pressure are in equilibrium, always high P to low P

venous pressure

PO2 = 40 mmhg PCO2=46 mmhg in the veins returning to the heart.

Arterial pressure

PO2 = 95 mmHg PCO2 = 40 mmHg in arteries carrying blood away from the heart.

Factors affecting alveolar gas exchange

Pressure gradients —> increase in change of P = increase of diffusion rate (increase in PO2 atm and Po2 arteries)

Factors affecting alveolar change (2)

Diffusion rate, increased fluid/inflammation = lower diffusion

Factors affecting diffusion rate (3)

Surface area, decrease in it causes decrease in difussion

Factors affecting diffusion rate (4)

Ventilation perfusion coupling: poor ventilation —> vasoconstrict to redirect blood flow to open air ways, poor blood flow —> bronchoconstrict locally to redirect blood flow toward open vessels

Venous blood

75% saturated 3 O2/HB = deoxyHb

Arterial Blood

98% saturated, 4 O2/HB = oxyhb

Oxygen

1.5% dissolved in blood, Po2=about 100mmhg

carbon monoxide poisoning

2 O2/HB, CO2 higher affinity for Hb vs O2

Oxygen hemoglobin dissociation curve

Higher Po2: O2 binds tighter, Lower Po2: O2 moves on/off easier

Systemic gas exchange

haldane effect: O2 unloaded from Hb —> deoxyHb has more affinity for CO2 + H+ therefore more loading of CO2+H+ onto Hb

more of Haldane effect

Increased O2 to Hb —> oxyHb has lower affinity for CO2 + H+ so CO2 unloaded in alveoli

Factors affecting unloading and loading of O2

Temperature: increased T (tissues) = increased O2 unloading ( curve goes right)

lower T (lungs) = Increased O2 LOADING (curve shifts left)

Factors affecting unloading and loading of O2 (2)

PH: Bohr effect

increased H+ (tissues)= increase O2 unloading to tissues that need it most

O2 CO2 and the regulation of ventilation

CO2+H2O←→ H2CO3←→ HCO3- + H+

Central Chemoreceptors

In medulla oblongata, increase firing of CC = increased ventilation, Chemo receptors sense H+ derived from CO2 that croses BB

Peripheral Chemoreceptors

Carotid arteries + aortic arch: stimulus H+, CO2, O2, increased firing when H+ increases and CO2, and when O2 < 60mmhg—-increased ventilation

hypercapnia

arterial PCO2 > 43mmhg

hypocapnia

arterial PCO2 < 37 mmhg

acidosis

ph <7.35

alkalosis

ph > 7.45

hyperventalation

causes by hypocapnia and respiratory alkalosis

Hypoventilation

causes hypercapnia and resp. acidosis

FEEDBACKCHAIN: hypoventilation

increased PCO2 causes increased H+, P. Chemoreceptors, C chemoreceptors which therefor increases ventilation causing PCO2 to decrease

FEEDBACKCHAIN: metabolic acidosis (change in H+_)

Increased H+ causes increased in P chemoreceptors, increased ventilation, increased PCO2 which causes H+ to decrease

FEEDBACKCHAIN: Effect of O2

low O2 (<60mmhg) causes increased P chemoreceptors, increased ventilation which then increases PO2

Digestive function

Process ingested food into a form the body can use like minerals and nutrients

motility

mixing and propulsion

secretion

exocrine (digestive enzyme) + endocrine (hormones)

digestion

mechanical and chemical

absroption

designed to be maximized

Accesory glands

salivary gland, parotid salivary gland, liver, gallblader, pancreas,

Carbs: Polysaccharides + Disaccharides

turn into glucose, fructose, galactose

Protein: Polypeptides

Turn into amino acids

Triglycerides: lipase + glycerol

turn into monoglyceride and 2 free fatty acids

Peritoneum and mesenteries

holds organs in proper orientation

lesser omentum

liver to stomach

greater omentum

covers small intestines

Mucosa (deepest)

lost of surface area

submucosa

major blood and lymph vessels, “submucosal nerve plexus”

muscularis externa

Circular muscle: narrowing motions

myenteric nerve plexus

Longitudinal muscle: shortening muscle

Serosa

innermost layer of the GI tract

Regulates motility

Mysenteric nerve plexus

Regulates secretions

Submucosal nerve plexus

Mouth

first step of the gut

for bitting

incisors

for shredding

canine

for grinding

molars (32 teeths)

Mastication

chew rto prevent chocking and mic with saliva for taste

Salivary glands

parotid, submandibular, sublingual

saliva

1.5L a day

dissolves food for taste

digest starch with amalyse

kill bacteria wiht lysozyme

Pharynx and Esophagus

#2, secretes mucus

Swallowing (delgutition)

1. Tongue compresses (vonluntary)

2. bolus passes down into pharynx

3. upper esophageal sphincter constricts and bolus passes down

organized by medulla oblongata

Peristalis

4. wave of muscle contraction

5. LES sphincter relaxes so bolus can go to stomach

   Weak LES causes acid reflux

Stomach

#3, mostly mechanical digestion

1. longitudinal muscle

2. circular muscle

3. oblique muscle (innermost)

Pyloric sphincter is gate watcher to the duodenum

Receptive relaxation

prepares stomach to recive food

peristaltic waves

pacemaker activity in longitudinal smooth muscle

Peristaltic waves

set by pacemaker activity in longitudinal smooth muscle

Neural/Hormonal input

increased # of AP’s wave = increased force of contraction with no change of rate

chyme

food and gastric secretions

Parietal cells

HCL + intrinsic factors

Chief cells

gastric lipase + pepsinogen

Enteroendocrine cells

Gastrin + paracrine messengers (histamine)

HCL

ph ~1.2

Stimulated by: PSNS, histamine, gastrin

Functions: kills bacteria, denatures protein, activated pepsin+ gastric lipase

pepsinogen

also zynogen and lenzyme precursor

Intrinsic factor

binds vitamin B12 and is absorbed in ileum, if no B12 then lower HB synthesis = pernicious anemia

Chemical digestion

15% protein

10-15% of fat

Cephalic phase

sight smell or thought of food—> PSNS increases to stoamch—> increased gastric motility and exocrine secretions

Gastric phase

Food in stomach increases Ph and amino acid—> increases PSNS and enteric NS which ACH, histamine, and gastrin increases exocrine secretions and gastric motility

Intestinal phase

Chyme in sm intestine—> increased secretin CCK and increased SNS and lower PSNS to stomach = lower gastric secretion and motility to slow stomach emptying

Liver

largest gland

secretes bile

detoxifies blood leaving

Gallblader

Stores and concentrates bile stimulates CCK release (cholecystokinin)