Quiz 3 Flashcards
What makes up the inferior mediastinum?
Anterior mediastinum(thymus), middle mediastinum (heart) and posterior mediastinum (lots! arteries, veins, nerves, lymphatics) ; starts at sternal angle- T4 line down to diaphragm
What makes up the superior mediastinum?
Just the superior mediastinum; starts at first rib down to sternal angle- T4 line; Infection from oral region can travel down here; the DANGER SPACE
What makes up posterior mediastinum?
From base of diaphragm and crura; has sympathetic trunk (originates T1-L2)(preganglionic axons, post- ganglionic neurons destined for sweat glands, head, neck, heart, and lungs) superior surface of diaphragm, inferior surface of thorax
Greater splanchnic nerve
(T5-T9) In posterior mediastinum; These sympathetics originate in the lateral horns; course through but don’t synapse in T5-9 ganglia; they gather and course down to abdomen; synapse with a pre-aortic ganglion (ex. celiac or superior mesenteric ganglia)
Lesser Splanchnic nerve
(T10-T11); these sympathetics originate in the lateral horn; course through but don’t synapse in the T10-11 ganglia; they gather and course down to abdomen; synapse with a pre-aortic ganglion (ex. celiac or superior mesenteric ganglia)
Least Splanchnic nerve
(T12); these sympathetics originate in the lateral horn; course through but don’t synapse in the T12 ganglia; they gather and course down to abdomen; synapse with a pre-aortic ganglion (ex. aorticorenal ganglia)
Azygous system of veins
right side of thorax has azygous vein; left side of thorax has accessory hemiazygous vein (above T8) and hemiazygous vein (below T8)
Veins of the mediastinum
SVC, right brachiocephalic vein (arm), azygos vein (T4), posterior intercostal veins, anterior intercostal veins, internal thoracic vein, anastomoses of intercostal veins (connection- in case of blockage- bp builds up and goes through system in a dif. way)
Thoracic lymphatic duct
in mediastinum; cisterna chyli; drains lymph from all tissues of the body except right side of head, neck, chest and arm which are drained by right lymphatic duct
Arteries of the mediastinum
Descending aorta (T4), posterior intercostal arteries, internal thoracic artery (internal mammillary artery), anterior intercostal arteries, anastomosis of intercostal arteries
Organs in the mediastinum
Esophagus (to T10) , trachea and primary bronchi (T4), pulmonary arteries, aortic arch
Aortic arch and it’s branches
(T2, T4) (ascending, descending aorta), brachiocephalic trunk (R. common carotid, R subclavian; exists because arterial system has to go further to go to right side due to heart location on left), left common carotid artery, left subclavian artery
Major veins of mediastinum
SVC, IVC, pulmonary veins , brachiocephalic on BOTH sides, veins bring blood to heart (color just tells you if oxygenated or deoxygenated)
Heart
pericardial sac holds heart; SVC, IVC, or coronary sinus –>R. atrium–> tricuspid (R. AV) valve–>R. ventricle–> pulmonary valve–> pulmonary trunk–> pulmonary arteries–> lungs–> pulmonary capillaries(CO2/O2 exchange in alveolus) –> pulmonary veins–> L. atrium–> bicuspid (mitral, L. AV) valve–> L. ventricle (thicker to pump blood to body)–> aortic valve –> aorta (has 2 coronary arteries coming off of it just above valve)–> systemic arteries–>systemic capillaries (CO2/O2 exchange in systemic tissue)–> systemic veins
Serous membranes
Fibrous pericardium (outermost layer), serous pericardium (more inner, 2 layers, in between there is the pericardial space- has serous fluid for lubrication), parietal pericardium (fibrous parietal pericardium, serous parietal pericardium), visceral pericardium (serous visceral pericardium)
Heart orientation
right atrium forms right border, right ventricle forms the anterior border, left atrium forms posterior border, left ventricle forms inferior border; most left chamber (apex)
Right Ventricle distinguishing factors
In right ventricle there are chordae tendinae and papillary muscles with TRICUSPID VALVE
Atrioventricular valves
(tricuspid/ bicuspid) prevent blood from flowing back into atrium; open when ventricle is filling; ventricle contraction sends blood out through any hole and AV valve snaps shut, preventing back flow into atrium, chordae tendinae and papillary muscles hold valve shut; cause the S1 sound
Semilunar valves
(aortic- middle and pulmonary- most anterior) prevent back flow from great vessels into ventricles; when ventricle relaxes and fills, something needs to prevent aortic flow from reversing (blood pushes down to go down void and catches valves which snap them shut) ; cause the S2 sound
Ventricular Diastole
Chamber fills with blood
Ventricular Systole
Chamber is contracting
Auscultation
Listening to the sounds of the heart; S1 (AV) bottom of heart [mitral on left, tricuspid on right] /S2 (semilunar) top of heart [pulmonary on left, aortic on right]; are sounds made by valves closing; sternal angle (rib 2- under it is 2nd space)-T4 line down to diaphragm
S1 (LUB)
the contracting ventricles caused the AV valves to snap shut
S2 (DUB)
the relaxing ventricles caused the semilunar valves to snap shut
Coronary circulation
coronary arteries, cardiac veins-drain to right atrium
Coronary arteries
right coronary artery–> right marginal artery (anterior), posterior descending (interventricular) artery (PDA) [if RCA supplies PDA heart is right dominant (67%)]; left coronary artery–> left anterior descending (interventricular) artery (LAD)–> left circumflex artery (LCX) (anterior to posterior) [If LCA supplies the PDA the heart is classifed as left dominant (33%)]
coronary artery innervation
sympathetic- vasodilation
parasympathetic- vasoconstriction
cardiac veins
coronary sinus (posterior)–> middle cardiac vein (posterior)–> great cardiac vein (anterior)
Heart innervation (sympathetic)
increases heart rate, increases force of contraction; T1-T4 (thoracic sympathetic cardiac nerve OR cardiopulmonary splanchnic nerve) ; T1–> sympathetic chain–>cervical sympathetic cardiac nerve; T2–> sympathetic chain–>cervical sympathetic cardiac nerve; sympathetic trunk, cardiac splanchnic nerves, cardiac plexus)
Heart innervation (parasympathetic)
decrease heart rate, decrease force of contraction; medulla–> vagus nerve; intramural ganglion; vagus nerve (CN 10), cardiac plexus
Conduction system of the heart
SA (sinuatrial) node–> AV (atrioventricular) node –>bundle of His–> anterior ventricular septum–> apex of heart–> anterior side of ventricles ; ANS to conduction system of heart (medulla–> vagus nerve, thoracic sympathetic cardiac nerve, cervical sympathetic cardiac nerve)
visceral sensory
Visceral motor (efferent) (medulla–> vagus nerve, thoracic sympathetic cardiac nerve, cervical sympathetic cardiac nerve) ; visceral sensory (afferent) (medulla T1-T4) when heart suffers damage body doesn’t know how to react; guesses what is going on; dermatomes T1-T4 (left arm, pectorals)- stabbing feeling, upper chest pain radiating to arm; DULL, DIFFUSE, non-localized pain
Visceral afferent neurons that parallel vagus nerve (heart suffers damage)
Vagus nerve pain referred to the craniofacial region (neck, tooth, jaw pain); pain in the mouth might not always be caused by a problem in the mouth
Skeletal Muscle
Attached to bones (or some facial muscles) to skin; single, very long, cylindrical, multi-nucleated cells with obvious striation; voluntary
Cardiac Muscle
Walls of the heart; branching chains of cells; uni- or binucleated cells; striation; involuntary (though can be modulated by ANS), rhythmic
Smooth musle
single- unit muscle in walls of hollow visceral organs (other than the heart); multiunit muscle in intrinsic eye muscles, airways, large arteries; single, fusiform, uninucleated; no striations; involuntary
Striated muscle cells**
Voluntary, attached to bones or skin, very long cylindrical, multinucleated cells, striated (packed with orderly arrangement of myofibrils), not self stimulating (each fiber innervated by branch of somatic motor neuron as part of motor unit), under control of nervous system; high energy requirement (lots of mitochondria, creatine phosphate, myoglobin), fast contracting, no rhythmic contractions; strength increases with stretching; fatigues easily
Cardiac muscle cells **
Involuntary, found only in heart, branching chains of cells connected by porous intercalated discs, with single nucleus and striation, striated (many myofibrils in orderly arrangement), self stimulating (impulse spreads from cell to cell), under control of nervous and endocrine systems and various chemicals, intermediate energy requirement, intermediate speed of contraction yet contraction spreads quickly through tissue due to intercalated discs, rhythmic contractions, strength increases with stretching, doesn’t fatigue
Smooth muscle cells**
involuntary, line walls of most internal organs, single, tapering, cells with a single nucleus, not striated (fewer myofibrils of varying lengths), self stimulating (not individually innervated, impulse spreads from cell to cell), under control of nervous and endocrine systems and various chemicals an stretching, lower energy requirement (fewer mitochondria, etc), slower contracting and rhythmic in some organs producing peristaltic waves along organ, rhythmic contractions, stress- relaxation response, doesn’t fatigue
The motor unit of skeletal muscle
The functional unit of a muscle is the motor unit which is composed of the alpha motor neuron and all of the muscle cells it innervates; the site if innervation is the neuromuscular junction (NMJ); each alpha motor neuron’s axon branch to synapse with up to thousands of different muscle fibers, but each individual muscle fiber is only connected to one alpha motor neuron (allows control over muscle fibers that are recruited); contrasts with cardiac and smooth muscles, whom both undergo rhythmic contractions, and are self stimulating (not innervated, impulse spreads cell to cell)
Sarcoplasmic Reticulum (SR)
intracellular organelle that stores and releases Ca2+ ions (reservoir); terminal cisternae are the enlarged portion of SR nearest the t-tubules; Ca2+ is released from the SR via channels called ryanodine receptors (RyRs); since Ca2+ concentrations in the SR are higher than in cytoplasm, energy (ATP) is required to pump it back into SR via the Ca2+ pump, SERCA (ATP dependent process)
Transverse (T) tubules
smaller tube like structures perpendicular to the sarcolemma (muscle membrane); invaginate into the muscle near the SR in regular intervals; APs propagate down the T-tubules during excitation-contraction coupling
Sarcomere**
extends from one Z disc to the next; an anchor point for actin filaments (myosin/actin)
A-band
the darker band, myosin- containing band; length (~1.5mm) in relaxed muscle does NOT change during contraction
I-band
the lighter band, includes actin filament and Z-disc; shortens during contraction
H-zone
center of the A band, where actin and myosin do not overlap; shortens during contraction
M-line
located in the center of the H zone; accessory proteins anchor myosin to M-line
Titins
anchor thick filaments to Z disc and runs within the thick filaments to the M line; holds thick filaments in place; helps muscle spring back into shape after contraction or stretching
Sliding Filament theory
During contractions, myosin (thick filament) heads form cross bridge connections with actin (thin filaments) which slide the actin filament towards the M-line to shorten the sarcomere in an ATP dependent process (relaxation is also ATP dependent) ; no change in the length of the actin or myosin filaments themselves; both the I band the H zone shorten during contraction; this process is the same in both skeletal and cardiac muscle, but different in smooth muscle
Tropomyosin and Troponin regulating the thin filament
When the muscle is relaxed (when cytoplasmic Ca2+ is low; myosin head at 90 degrees) the actin binding sites are shielded by tropomyosin such that the myosin head can’t bind; when muscle is initially stimulated (when cytosolic Ca2+ increases) Ca2+ binds to troponin and shifts it, pulling tropomyosin protein and exposing the binding sites on actin to allow myosin to form cross-bridges; the higher the Ca2+ concentration, the greater the number of tropomyosin molecules that move to expose myosin binding sites
Initiation of contraction
- Ca2+ levels increase in cytosol 2. Ca2+ binds to troponin 3. Troponin Ca2+ complex pulls tropomyosin away from G-actin binding site 4. Myosin binds to actin and completes power stroke 5. actin filament moves
Cross bridge cycle **
This cycle can continue as long as the muscle is activated, ATP is available, and the limit of shortening has not been reached. Cross bridges cycle independently of one another 1. binding of myosin to actin (Ca2+ activation allows cross bridge formation by binding to troponin) [inorganic phosphate is released] 2. Power stroke (~10nm movement per stroke; actin gets pulled toward middle of sarcomere) [ADP is released] 3. Rigor (myosin in low energy form) [new ATP binds to myosin head; Ca2+ back to storage; for detachment to occur, a new ATP must bind to myosin head and undergo partial hydrolysis] 4. Unbinding of myosin and actin [ATP is hydrolyzed] 5. Cocking of the myosin head (myosin in high energy form) “energized” or “cocked” myosin head: MADPPi [Ca2+ activation allows cross bridge]
Rigor
If cellular energy stores are depleted (as happens after death) the cross bridges can’t detach due to lack of ATP and cycle stops in the attached state. This produces stiffness of the muscle known as rigor. Thus, rigor mortis that sets in shortly after death. Need energy to relax OR contract. Contraction is thus an energy demanding process- lots of ATP is needed
Excitation- Contraction Coupling
The physiological process of converting an electrical stimulus (AP) to a mechanical response (contraction) at the NMJ. 1. Motor neuron AP 2. Ca2+ enters voltage gated channels 3. ACh is released and diffuses across the synaptic cleft and attaches to ACh receptors on the sarcolemma 4. Na+ entry into motor end plate 5. local current between depolarized end plate and adjacent muscle plasma membrane 6. Muscle fiber AP initiated 7. Propagated AP in muscle plasma membrane 8. Ach degradation
Excitation Contraction coupling in motor endplate
ACh is released and diffuses across the synaptic cleft and attaches to ACh receptors on the sarcolemma 1. AP generated is propagated along the sarcolemma and down the T tubules 2. AP triggers Ca2+ release from the terminal cisternae of SR 3. Ca2+ ions to troponin which changes shape, removing the blocking action of tropomyosin; actin active sites are exposed 4. Contraction: myosin cross bridges alternately attach to actin and detach, pulling the actin filaments toward to center of the sarcomere; release of energy by ATP hydrolysis powers the cycling process 5. Removal of Ca2+ by active transport into the SR after the action potential ends (SERCA) [can shut down 3-4] 6. Troppmyosin blockage restored blocking actin active sites; contraction ends and muscle fiber relaxes
Cardiac Muscle part 2
Cross- striated, elongated, branched cells link to one another at intercalated disks; desmosomes (specialized cell junctions at the intercalated disks - proteins that spot weld the junction and allow force to be transferred and the heart to hold together as it beats despite mechanical stress); Gap junctions (provide electrical conduction to allow beating as single conductive unit [syncyntium]); auto rhythmicity due to intrinsic pacemaker cells( no external innervation required, generate own beat), almost exclusively uses aerobic respiration (large mitochondria thus resistant to fatigue, high myoglobin content since myoglobin can function as an O2 storage mechanism; cardiac tissue is very vulnerable to hypoxia (plasma troponin and myoglobin levels are measured to assess damage over time after heart attacks)
Smooth muscle part 2
Spindle shaped, mononucleated cells under involuntary control of their slow, rhythmic (wave-like) contractions; grouped into sheets on the walls of hollow organs and some vessels; no sarcomeres (not striated), actin fibers attach to the cell wall and the dense bodies in the cytoplasm that serve as anchors. When activated, actin fibers slide over the myosin bundles causing shortening of the cell walls (No troponin present); Ca2+ plays a prominent role in the initiation of contraction, but the source of the Ca2+ differ in smooth muscle vs others (influx through voltage or ligand gated plasma membrane channels and/or efflux from intracellular stores through either RyRs or inositol triphosphate receptors (IP3R) Ca 2+ channels); lacks troponin so Ca2+ binding to troponin does not enable smooth muscle contraction (increased myosin ATPase activity and binding of myosin to actin; crossbridge cycling causes contraction of myosin and actin complexes, in turn causing increased tension along the entire chains of tensile structures, resulting in contraction of the entire smooth muscle tissue.) Relaxation of smooth muscle does not always happen when Ca2+ levels decrease (Dephoshorylation of myosin by myosin light chain phosphatase can lead to relaxation or….; Myosin cross bridges can remain attached to actin despite lowered Ca2+ allowing sustained contractions with little expenditure of energy; Muscle relaxation occurs when the Ca2+-calmodulin complex dissociates or other mechanisms intervene)
Skeletal Muscle Overview
Makes up ~40% of nonfat body weight of the human body; it can help maintain body temp in response to cold (aka shivering) since shivering increases metabolic rate; it is typically attached to bone (tongue is exception); responsible for supporting and moving the skeleton; it is striated (due to sarcomeres); it doesn’t contract without nervous stimulation, is under voluntary control ; high energy demands so fatigues easily
Main events in skeletal muscle contraction**
- AP initiated and propagates through motor neuron 2. AP triggers ACh release at presynpatic membrane of neuromuscular junction 3. ACh diffuses across synpatic cleft from axon terminal to post synaptic membrane in muscle fiber (aka motor endplate) 4. Since Na+ influx> K+ efflux, local depolarization occurs (aka end plate potential- EPP) 5. EPP triggers AP in the skeletal muscle cell that propagates into the t-tubules 6. AP triggers Ca2+ release from sarcoplasmic reticulum 7. Ca2+ binds to troponin on the thin (actin) filament, shifting tropomyosin and revealing the myosin binding sites on the actin filaments 8. energized myosin heads bind to actin and rotate causing shortening (cross bridge cycling) and contraction 9. cytoplasmic Ca2+ falls as it is pumped back into SR causing relaxation in an ATP dependent fashion 10. The cross-bridge cycle is terminated by the loss of calcium from the troponin 11. Tropomyosin translocates to cover the cross-bridge binding sites 12. The calcium returns to the sarcoplasmic reticulum, the muscle relaxes & returns to the resting state
Roles of Ca2+ in muscle contraction
- promotes presynaptic neurotransmitter release 2. Ca2+ released from the SR binds to troponin to initiate sliding filaments 3. Ca2+ promotes glycogen breakdown and ATP synthesis by activating essential enzymes; Thus the same ion that stimulates muscular contraction also activates phosphorylase kinase, which them activates glycogen phosphorylase, which releases Glucose 1 phosphate from glycogen, which can be used to make ATP to support muscular contraction
Sources of ATP production
Free cytosolic ATP provides the immediate source of energy for muscle contractions. However, it is only sufficient to fuel ~ 5-6 seconds of intense activity. Other sources are creatine phosphate, glycogenolysis (anaerobic respiration), or cellular (aerobic) respiration
Creatine phosphate
Direct phosphorylation [couple reaction of creatine phosphate (CP) and ADP to form creatine and ATP]; energy source is CP, no O2 use, 1 ATP produced per CP, creatine; duration of energy provision is 15 s
Glycogenolysis (anaerobic) respiration
Anaerobic mechanism (glycolysis in cytosol–>pyruvic acid–> lactic acid formation) energy source is glucose (from glycogen breakdown or delivered from blood); no O2 used, produces 2 ATP per glucose, lactic acid is released in blood; duration of energy provision 30-60 s
Cellular (aerobic) respiration
Aerobic mechanism in mitochondria; energy sources are glucose (from glycogen breakdown or delivered from blood), pyruvic acid, free fatty acids from adipose tissue, amino acids from protein catabolism; O2 use is required, produces 38 ATP per glucose, Co2, H20; duration of energy provision is hours
Breathing hard after strenuous exercise
During rest or moderate exercise, the O2 is sufficient to support aerobic respiration (using many ATP molecules) but during strenuous exercise, O2 deficiency may develop and lactic acid accumulates as a result of anaerobic respiration; O2 debt is the amount of O2 needed to convert the accumulated lactic acid to glucose and to restore the supplies of ATP and creatinine phosphate (we breath hard after strenuous exercise to get the extra O2 that must be used in the oxidative energy processes to reconvert lactic acid to glucose and to restore the decomposed ATP and creatine phosphate to their original states)
Muscle twitch
Twitch (the single, brief contraction of a muscle in response to a single AP on its motor neuron); threshold (minimum voltage necessary to produce contraction (a single brief stimulus at that voltage produces a quick all-or-none cycle of contraction and relaxation ex. a twitch)) “all or none” response of motor units (when the motor neuron fires, all of the muscle fibers innervated by its nerve [muscle in that motor unit] will contract (when firing ceases, all of the muscle fibers innervated by the nerve will also cease to contract (motor units contract and relax in an all-or- none manner)
myogram of the skeletal muscle twitch
Latent period(1-2ms, is delay between stimulus and onset of twitch) Contraction phase (period during which tension develops and muscle shortens) Relaxation phase (shows a loss of tension and return of muscle to resting length) Refractory Period (period when muscle will not respond to new stimulus) In skeletal muscle the refractory period is short (2-3ms) and coincides with the depolarization (contraction) phase of the AP (the same motor units involved in the twitch response can’t be fired during this brief phase)
Multiple Motor unit summation (or recruitment)
Examples of graded muscle responses; increasing the strength of the stimulus at a constant frequency to recruit additional motor units and thereby increase the tension developed
Wave (temporal) summation
Examples of graded muscle responses; increasing the frequency of a stimulus that is held at a constant intensity; it is a result of a sustained contraction due to secondary twitch (summed tension) before initial twitch has fully relaxed
Treppe
Examples of graded muscle responses; Incomplete fusion (staircase); form of incomplete fusion of the wave summation at a frequency just below tetanus (still below max tension)
Tetanus
Examples of graded muscle responses;A complete fusion of wave summation, or no relaxation between stimuli (result of depleting calcium); remember Ca2+ is needed to process glycogen and to restore ATP
Fatigue
Examples of graded muscle responses; the result of exhaustion of ATP, buildup of waste products such as lactic acid, and loss of tension despite continuing stimuli; do NOT confuse with rigor
Skeletal muscle mechanics
Tension (the force exerted on an object by a contracting muscle) load (the force exerted on the muscle by an object); thus to shorten the muscle and move the load, the tension generated by the muscle must exceed the load from the object (isotonic (same tension, shorter length)
Isotonic Contraction
The tension (force) generated by the muscle is greater than the load and muscle shortens (once peak tension has developed, the muscle shortens with the constant load; during relaxation the muscle is re-extended by the load) SAME TONE
Isometric contraction
the load exceeds the tension so muscle doesn’t shorten; SAME LENGTH
Muscle length- tension relationship**
At the optimal sarcomere length, the muscle is slightly stretched and there is slight overlap between the myofibrils allowing max overlap of myofilaments and thus producing max number of cross bridges to generate max amount of tension (~80-120% sarcomere length [of total length]); there is also a lower limit (75%) to the contractile ability of the sarcomere and a maximal stretching limit (~170%) of the sarcomere; beyond these upper and lower limits negligible tension develops
Fractionation
All motor units in a muscle do not need to activate for every load. However, the more motor units, or the larger the motor units recruited, the greater the tension (ex. force) developed by the muscle
Henneman’s “size principal”
Motor units are recruited in the order of the size of the motor unit based on the force/ resistance needed; small–> large; motor unit recruitment depends on the demand (ex. load); under load, motor units are recruited from smallest to largest; with lightest intensity exercise, the Type I (slow twitch) motor units are recruited (continuously firing, regardless of intensity [respiration]; ‘slow’ fibers=prolonged activities [maintaining posture, marathons]); when the load is increased, Type IIa (fast twitch) will be recruited to supplement the Type I fibers (“fast” fibers= rapid, powerful actions [jumping, short distance running]); when the load is even greater, the Type IIb are recruited to further supplement Type I and Type IIa motor unit types.
Fast vs Slow Twitch muscle fibers
Skeletal muscles must produce everything from long, sustained contractions to very brief twitches. To accomplish these tasks, there is a mix of slow twitch and fast twitch fivers, with one or the other predominating depending on the demand
Slow twitch (Type I)**
low myosin ATPase activity, slow/low speed/intensity of contraction, high resistance to fatigue, high oxidative (aerobic) capacity, low enzymes for anaerobic glycolysis, many mitochondria, less extensive sarcoplasmic reticulum, many capillaries, high (red muscle) myoglobin content, low glycogen content
Fast twitch (Type II)**
high myosin ATPase activity, fast/high speed/intensity of contraction, low resistance to fatigue, low oxidative (aerobic) capacity, high enzymes for anaerobic glycolysis, few mitochondria, more extensive sarcoplasmic reticulum, few capillaries, low (white muscle) myoglobin content, high glycogen content
Reflex Arcs**
Simple neural pathways connecting receptors (for stimulus detection) to effector organs (site of response) [the responses generated are called reflexes or reflex arcs] May be either somatic (resulting in skeletal muscle contraction) or autonomic (resulting in activation of cardiac or smooth muscle). Most reflexes have 6 basic components: 1. a sensory receptor 2. an afferent neuron 3. an integration center (CNS) 4. an interneuron 5. a motor (efferent) neuron 6. an effector (muscle)
Somatic (spinal) reflexes
Somatic reflexes in skeletal muscle are mediated by the spinal cord and can be used to fine tune muscle tone to do everything from maintain posture to preventing injury; 2 important spinal reflexes are the stretch reflex and the Golgi tendon reflex
Stretch reflexes
Initiate at receptors called muscle spindles which are sensitive to length of muscle as it is stretched. Stretching depolarizes the muscle spindles, which sends AP to the spinal cord, where it synapses and activates the alpha motor neuron; the stretch reflex stimulates the stretched muscle to contract (ex. resist being stretched further); the sensory receptors serving the stretch reflex are classified as proprioceptors, since they are essential for maintenance of posture and muscle tone. When a stretch reflex stimulates a stretched muscle to contract, antagonist muscles that oppose the contraction are inhibited via a process called reciprocal inhibition. The neuronal mechanism that causes this reciprocal relationship is called reciprocal innervation ex. knee jerk or patellar reflex; monosynaptic, stimulated by muscle being stretched, afferent fibers Ia, response is contraction of muscle
Knee Jerk (Patellar) Reflex
Sudden stretch of a muscle results in: 1. muscles spindles detect stretch of muscle 2. sensory neurons conduct AP to spinal cord 3. sensory neurons synapse directly with alpha motor neurons 4. Alpha motor neurons conduct AP to the muscle, causing it to contract and resist being stretched. The muscle that contracts is the muscle that is stretched
Extrafusal Fibers
Subtype of skeletal muscle fibers; make up the bulk of muscle, innervated by alpha motor neurons, provide the force for muscle contraction; ALPHA MOTOR NEURONS INNERVATE AND STIMULATE EXTRAFUSAL SKELETAL MUSCLE
Intrafusal fibers
Subtype of skeletal muscle fibers; Encapsulated in collagen sheaths to form the muscle spindle; innervated by gamma motor neurons (as well as the afferents of group Ia and II sensory neurons): are subdivided into: 1. nuclear bag fibers (nuclei collected in bag like bundles in middle of fiber; detect fast, dynamic changes in muscle length and tension; innervated by group Ia afferents (fast)) 2.Nuclear chain fibers (nuclei are arranged in single row (chain); detect static changes in length and tension; innervated by slower group II afferents as well as the fast group Ia afferents); GAMMA MOTOR NEURONS INNERVATE THE MUSCLE SPINDLE INTRAFUSAL FIBERS
Golgi (Deep) Tendon Reflex
Tendon reflexes- initiated at receptors in the tendon called Golgi tendon organs (GTO) and sensitive to tension in tendon caused by muscle contraction; GTOs depolarize in response to the tendon being stretched, but inhibit the alpha motor neuron (stimulates the contracted muscle to relax by inhibiting the agonist (Ib) motor neuron in the contracted muscle (relieving tension on the tendon); The antagonist muscle’s efferent motor neuron is reciprocally stimulated causing contraction to balance movement; THE GOLGI TENDON REFLEX IS A PROTECTIVE FEEDBACK MECHANISM TO PREVENT TENDON DAMAGE; Disynpatic, stimulated by muscle contraction, afferent fibers are Ib, response is relaxation of the muscle ex. clasp knife
Muscle spindle (measures muscle length)
Muscle tone is fine-tuned by this sensory organ; 3 major components: specialized intrafusal muscle fibers, sensory terminals (group Ia and II afferents [proprioceptors]), motor terminals (gamma motor (efferent) neurons; remember stretch reflex activates efferent alpha motor neurons when muscle is stretched causing contraction of the muscle; The finer the movement requirement, the greater the number of muscle spindles in a muscle
Golgi Tendon Organ (measures muscle tension)
Muscle tone is fine-tuned by this sensory organ; Sensory terminals (a single group of Ib sensory (afferent) fibers; Golgi tendon reflex inhibits efferent alpha motor neurons when the muscle is contracted causing relaxation of the muscles to prevent injury
Flexor withdrawal
After touching hot stove or stepping on a nail; polysynaptic, stimulated by pain, afferent fibers are II, III (or Adelta fibers) and IV(C fibers); response is ipsilateral flexion, contralateral extension
Pleural Membranes (muscles, organs, etc.)
External, internal, innermost intercostal muscles innervated by spinal nerves segmentally at each level ventral rami (intercostal nerves) and are supplied by intercostal arteries that arise from (anterior) internal thoracic and (posterior) descending aorta; lungs surrounded by pleural membrane (sac), bronchial tree
Pleural membranes are like
Two plates of glass and a drop of water (tension, hard to pull apart, but can slide them) have parietal pleura with serious fluid in between then visceral pleura touching lungs; if you break the seal, air moves in (pneumonthorax) and you get a collapsed lung
Parietal pleura
4 regional names reflecting adjacent surfaces: cervical parietal pleura, costal parietal pleura, diaphragmatic parietal pleura, mediastinal parietal pleura
Visceral pleura
Invests lungs and fissures; tightly adhered, no potential space
Pleural Space
potential space, serous fluid (prevents friction)
Root of lung
aka. The hilum; parietal and visceral pleura are contiguous here [ not covered with pleura]
Costadiaphragmatic recess
Exhale- Diaphragm relaxes, moves up, decreases lung volume, pleura layers meet (disappear); Inhale- diaphragm contracts, pulls down, increases lung volume, pleural layers pull apart (reappears)
Innervation (parietal pleura)
Parietal pleura- has pain receptors- somatic innervation; intercostal nerves; cervical and costal parietal pleura BUT diaphragmatic and mediastinal parietal pleura are innervated by phrenic nerve [PHRENIC NERVE IS THE ONLY SOMATIC NERVE THAT REFERS PAIN] If pain fibers are activated in between diaphragmatic and mediastinal parietal pleura would feel referred pain at (C3,4,5 keep diaphragm alive- collar, a little bit of shoulder)
Innervation (visceral pleura)
Visceral pleura- autonomic, stretch receptors only; visceral afferent neurons to brain stem (along parasympathetic pathways) visceral afferent neurons to T levels (along sympathetic pathways)
Right lung
Upper lobe, horizontal fissure, middle lobe, oblique fissure (goes to posterior), lower lobe
Left lung
heart takes up space so this one is smaller; upper lobe, oblique fissure, lower lobe with lingula (little tongue)
Airways (conduction)
Trachea, carina (branching point), primary bronchi (right is shorter and more vertical [more likely to get aspirated objects lodged into] while left is longer and more horizontal (left lung is pushed to side by heart)), secondary bronchi (right has 3 branches (upper, middle, lower) while left has 2 (upper and lower) which = # lobes), Tertiary bronchi (# tertiary bronchi= # bronchopulmonary segments) PROGRESSIVE BRANCHING OF BRONCHI MATCHES LOBULAR STRUCTURE OF LUNGS
Innervation of bronchi (sympathetic)
Bronchodilation (T1) via epinephrine; also increases blood flow to lungs (vasoconstriction in GI tract, skin, etc. increased vascular pressure)
Innervation of bronchi (parasymathetic)
Bronchoconstriction via CN X to medulla
Bronchi continue branching to respiratory portion of airways
Bronchioles, cartilage (terminal bronchioles lack- lack support so don’t have something to hold it open- difficulty breathing due to reduction of airflow to alveolar sacs ), smooth muscle; Alveolar sac is site of gas exchange [where O2 is stored] pulmonary arteries carry deoxygenated blood (CO2) –> Pulmonary capillaries [exchange]–> pulmonary veins carry oxygen rich blood to left atrium while trachea (airway) carries CO2 out of body
Boyle’s law
Pressure varies inversely with volume; volume increased, therefore pressure decreased Or volume decreased therefore pressure is increased
Diaphragm muscle
Primary muscle of respiration; at rest/relaxed (when breath out), protrudes up but when muscle contracts (when breath in) diaphragm goes down; esophagus, descending aorta, and inferior vena cava pass through; innervated by the phrenic nerve (C3,4,5 keep the diaphragm alive) FUNCTION: TO INCREASE THE VOLUME OF THE LUNGS; inhale (diaphragm goes down) exhale (diaphragm goes up); also functions as separator
Thoracic anatomy and Boyle’s Law
End of expiration, no air movement Pb=0, Pb=P(alv), Palv=0, diaphragm is up; During inspiration, air flows in Pb= 0, Pb>P(alv), P(alv)= -1 [alveolar volume increases] thorax expands, diaphragm contracts; AS AVEOLAR VOLUME INCREASES, P(alv) DECREASES, creating a pressure gradient; end of inhalation, No air movement, Pb=0, P(alv)=0; when diaphragm drops down, pulls parietal pleura down and visceral membrane and lungs expand passively; suction type of event; muscles increase thoracic volume; during expiration, air flows out, Pb=0, P(alv)> Pb, P (alv)= 1 (alveolar volume decreases), thorax recoils, and diaphragm relaxes squeezing lung volume down
Accessory muscles in Thoracic anatomy and Boyle’s law
Intercostals and serratus anterior ; ribs are elevated and pushed out “bucket handle movement up” ; also scalenes and sternocleidomastoid- help pull ribs up- more breathing space; superior and anterior movement of sternum (pump handle upward movement)
Respiratory Tract
System of tubes which functions to conduct air from the atmosphere to alveolar membranes; gas exchange with the blood takes place across these membranes, can be divided into 2 functional components: 1. The conducting zone (nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles) and funnels down to 2. respiratory zone (respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli) The upper respiratory tract would be the nasal cavity to the start of the larynx while the lower would be the larynx through to the lungs (respiratory zone is contained totally down here)
Ventilation of the Respiratory tract
Ventilated through the creation of a localized negative pressure environment, which draws air in because of Boyle’s law [inspiration]- actively expand the chest cavity (lungs) increasing it’s volume and decreasing pressure in relation to external atmosphere. Elasticity of lungs allows expiration during quiet breathing to be a passive process (no muscle work)- allows thoracic cavity to rebound back, forcing some (but not all) air out; the “seal” on the thoracic cavity allowing manipulation of the internal pressure is why punching holes in thoracic cavity wall is BAD
Upper respiratory tract: nasal passage
Possible to be a mouth breather, but one gets most air through nasal passages. Functions: warms and humidifies the inspired air, removal and retention of pathogens/particulate matter [anything bigger than 5-10nm tends to impact the naso pharynx because of their momentum and do not make the curve], olfaction, serves as a trap to drain out paranasal sinuses and lacrimal ducts; 2 chambers separated by nasal septum (cartilage and bone); turbinates (bone shelf projections, force air into a regular steady flow over mucosal surfaces [slow air to help warm and humidify]) mucosa [ lamina propria has complex capillary loop system releases heat to warm inspired air; seromucus glands release water to humidify air and produce mucus to trap particulate air impurities, lots of IgA produced by plasma (B) cells]
Respiratory epithelium
Upper respiratory tract (nasal cavity); type of epithelium in nasal passage; ciliated pseudostratisfied columnar epithelium; covers middle and interior turbinates as well as rest of conducting portion of the system
Olfactory epithelium
Upper respiratory tract (nasal cavity); type of epithelium in nasal passage; specialized epithelium (pseudostratisfied) covering superior turbinate and roof of nasal cavity; olfactory neurons (ciliated bipolar olfactory neurons with membrane chemoreceptors (axons form olfactory nerve, CN I); supporting cells (pseudostratisfied columnar cells that support olfactory cells); basal cells (stem cells which replace ON every 2-3 months [can revive epithelium]); brush cells (columnar cells with microvilli; afferent connection to CN V (trigeminal)) lamina propria contains Bowman’s glands (olfactory glands)- produce liquid (acts as solvent) facilitates odor detection
Lower respiratory tract: Larynx
Passage for air between pharynx and trachea; rigid wall for protection reinforced by cartilage; cartilage movements participate in sound production during phonation; also serves as a gate for GI and respiratory passages; has epiglottis (gate; serves to prevent swallowed food from entering larynx); lingual surface has stratified squamous epithelium, transitions to respiratory epithelium that covers vestibular folds ( sometimes stratified squamous found a little bit if use a lot); vestibular folds contain glands and lymphoid nodules, vocal cords covered with stratified squamous , containing large vocal muscles
Histology of Vestibule of nasal cavities
Stratified squamous, keratinized to non- keratinized; sebaceous/sweat glands; hyaline cartilage; vibrissae (stiff hairs) and moisture both filter and humidify air
Histology of Most areas of nasal cavity
Respiratory epithelium; seromucus glands; bone and hyaline cartilage; rich vasculature and glands; warm, humidify and clean air
Histology of superior areas of nasal cavity
Olfactory epithelium; serous (Bowman’s) glands; bone (ethmoid); solubilize and detect odorant molecules in the air
Histology of nasopharynx
Respiratory and stratified squamous ; seromucous glands; bone and skeletal muscle; conduct air to larynx; pharyngeal and palatine tonsils
Histology of larynx
Respiratory and stratified squamous ; mucous glands; elastic and hyaline cartilage. ligaments, skeletal muscle; site for phonation; epiglottis closes while swallowing
Histology of trachea
Respiratory epithelium; mucous glands; C shaped rings of hyaline cartilage; smooth muscle (trachealis); conduct air to primary bronchi entering lungs, mucous associated lymphatic tissue
Lower respiratory tract: Trachea
Larynx to carina (keel; ridge formed by the division of 2 primary bronchi); 16-20 C shaped hyaline cartilage rings; these keep it from collapsing, which would be “quite bad”; 100-120mm long; 25mm diameter; at the border with the esophagus (located dorsally) the ends of the C are joined by smooth muscle, called the trachealis
Layers of the Trachea
- mucosa (respiratory epithelium- pseudostratified ciliated columnar; has terminal bars [junctions between cells- zonula adherins, desmosomes, and gap junctions]; cell type (~30% each): mucous goblet cells produce mucus; basal (short) cells are progenitor cells; and ciliated columnar cell push trapped particulate matter up and out) 2. Lamina propria (tunica fibromusculocartilaginea) mixed seromucus glands are located in the submucosa and contribute to humidification of air and also trapping contaminants 3. Tunica adventita (CT layer; holds everything together)
Trachea support structures
C shaped cartilage stabilizes trachea while maintaining tracheal rigidity; the trachealis (smooth muscle) is found joining the 2 ends of the C rings and runs the length of the trachea, next to esophagus; it serves to compress the trachea slightly (important for more easily allowing swallowing and narrow the opening so air can be expelled with more force ex. coughing, swallowing)
Lower respiratory tract: bronchial tree
Primarily inside lungs and main event of respiration; from the trachea, it branches a total of 23 times, with each branching decreasing gradually in diameter (ranging from 25 mm at the trachea to 0.5mm at the level of the terminal bronchioles); branching serves to funnel the continually warmed and humidified air into a wider cross sectional surface area to facilitate gas exchange
Lower respiratory tract general characteristics
As one descends there are alterations: 1. epithelium height and complexity decreases 2. cartilage rings are replaced by isolated blocks or irregular plates and then go away all together at the level of the bronchioles 3. trachealis muscle is replaced with bundles of smooth muscle that spiral around the airways 4.amount of elastic fibers and smooth muscle proportionally increases. Goblet cells and glands (secretion) proportionally decrease
Conducting zone structures
Lumen diameter decreases; Decrease in cartilage, glands, goblet cells, and height of cells (ciliated simple columnar in bronchioles–> cuboidal in terminal bronchioles)as go down but increase in smooth muscle, elastic tissue, and bronchus associated lymphatic tissue (BALT or MALT)
Bronchi
There are 2 which branch off trachea; no gas exchange takes place at the level of the bronchi; not identical (right bronchus is shorter and wider and branches differently); the right primary (main) bronchus has 3 secondary (lobar) branches and then multiple tertiary (segmental) ones; the left has only 2 secondary branches before dividing into multiple tertiary bronchi; each tertiary bronchus supplies an isolated “bronchopulmonary segment” of the lung; there are 3 layers: 1. mucosa (respiratory epithelium gives way to simple ciliated columnar as descend) 2. lamina propria (smooth muscle, elastic tissue, primary: cartilage rings, giving way to plates in secondary down 3. Adventitia (CT)
Bronchioles
Smaller bronchi; ciliated simple cuboidal epithelium (shorter) with some goblet cells; no cartilage, very prominent smooth muscle; sustained constriction here is bad
Terminal bronchioles
End of conduction; some simple cuboidal ciliated cells; club cells (club shaped, non ciliated, secretory granules (surfactant), formerly “clara” cells, secrete surfactant/antimicrobial peptides, progenitor cell population; no cartilage, some smooth muscle, but not as prominent
Respiratory zone
respiratory bronchioles, alveolar ducts, alveolar sacs, alveolus; ~300 mil alveoli account for most of the lung’s volume and are the main site for gas exchange with blood
Transition Zone
From bronchiole to terminal bronchiole (conduction) to respiratory bronchiole (respiration); simple squamous or low epithelium in respiratory bronchiole- needed for gas exchange
Alveoli
The structural and functional unit of lung; large surface area (specialized for gas exchange); 300 mil/lung; increase surface area for gas exchange; thin, low (simple squamous) epithelium; thin walled sacs, separated by inter-alveolar septa; alveoli are connected by alveolar pores (pores of Kohn) which can serve to distribute air evenly, equalizing pressure, also will help prevent total loss of ventilation in the event of bronchioles being blocked, but also allow the spread of bacteria and neoplasms
Alveolar cell types
Type I pneumocyte (alveolar cell): physically makes the (very thin) membrane for gas exchange; constitute around 95% of the alveolar surface (make up the membrane); joined by right junctions
Type II pneumocyte (alveolar cell): large cuboidal cells, make surfactant, serve as progenitor cells for tissue renewal
Dust cells: basically a macrophage located in the alveoli
Histology of bronchi
respiratory epithelium transitioning to simple cuboidal; goblet cells; prominent spiral bands of smooth muscle, irregular cartilage plates; repeated branching, conduct air deeper into lungs
Histology of bronchioles
simple ciliated cuboidal to columnar; goblet/club cells; prominent circular layer of smooth muscle, no cartilage; conduct air, important in bronchioconstriction and bronchiodilation
Histology of terminal bronchioles
transitioning to simple cuboidal, ciliated; club cells; thin, incomplete circular layer of smooth muscle, no cartilage; conduct air to respiratory portion of lungs; clara cells with protective functions
Histology of Respiratory bronchioles
simple cuboidal, club cells, scattered alveoli; fewer smooth muscle fibers, mostly around alveolar openings; conduct air deeper, but with some gas exchange and protective Clara cells
Histology of Alveolar ducts and sacs
Simple cuboidal between alveolar ducts; bands of smooth muscle around alveolar openings; gas exchange, some conduction
Histology of Alveoli
Low epithelium, Type I and II alveolar cells (pneumocytes), no muscle or skeletal support; network of elastic and reticular fibers, site of all gas exchange; surfactant from Type II pneumocytes, dust cells
pH basics
pH is defined as the negative log (10) of the effective H+ ion concentration of a given solution; thus on a pH scale, 1 numerical change= 10 fold change in the concentration of H+ of a solution; pH=7 or a perfectly neutral, is the pH of pure water at 25C when H+ and OH- ions are present in a 1:1 ratio; physiological pH (pH of the plasma/interstitial fluid) is 7.4 or slightly alkaline
Definitions of Acids/bases
Arrhenius: acids increase H+ ion concentrations in aqueous solutions, bases increase OH= in aqueous solutions
Bronsted-Lowry: Acids donate protons, while bases accept protons (but do not necessarily increase OH- concentration)
Lewis: Acids accept electron pairs, bases donate electron pairs
Most acid/bases we consider in a physiological context are ‘weak’[ donate relatively few of their H+/OH- ions ex H2S, NH2] as opposed to ‘strong’ [completely dissociate in solution ex HCl, NaOH]
Critically important as our ability to keep our pH regulated is due to the buffering capacity of our body fluids; if we had a lot of strong acids/bases it would be difficult to buffer
Biological importance of pH regulation
Altered H+ concentrations have a range of biological effects, most of them somewhat contrary to life; this is because protons tend to be highly reactive and there are many H+ binding sites found in and around cells; These include (but not limited to): protein folding and confirmation, ion currents, ligand receptor interactions, muscle contraction (ex. lowered intracellular pH causes elongation AP/ refractory periods and decreased contraction in cardiac myocytes), cell proliferation, most biochemistry operates best at physiological pH ranges; if patient were to have even pH of 6.8 or 7.8 serum, they would be very near death
Physiological sources of Acid
Na+ concentration in the ECF is around 3.5 mil times that of H+, further the normal range of variation is around 1 milionth that of Na+ [tightly regulated]; acids are produced from a variety of life processes (aerobic and anaerobic metabolism) ; aerobic metabolism is the source of Co2, which dissolved in aqueous environment of the blood forms H2CO3 which is a weak acid [CO2 +H20 H2CO3 HCO3- + H+; normally this rxn is not energetically favorable, but carbonic anhydrase on RBCs speeds the rxn forward, helping dissolve CO2 in blood, facilitating transport. Carbonic acid is referred to as Volatile acid (removed from lungs); all other acids produced are nonvolatile (removed from kidneys); MORE CO2 MEANS A POTENTIALLY LOWER PH IN SERUM
pH of blood serum
Importance of controlled pH in blood serum; an overabundance of H+ ions in the blood is called acidemia [refers specifically to blood] Acidosis is the blanket term for the conditions leading to acidemia; A lowered H+ concentration in the blood is alkalemia; Alkalosis is the blanket term for the conditions leading to alkalemia; Blood pH doesn’t tell you much about the amount of conjugate base/acid in the blood, but mainly the ratio between them (and thus how much H+ present); both of these conditions have undesirable effects and so the free H+ ion concentration in serum is controlled by: lungs (can remove CO2; relatively fast- minutes), kidneys (remove H+, retain HCO3-; slow (days)), buffering (resist pH change; can’t remove; instantaneous); does not remove H+, reversible for alkalosis
Systemic Regulation of pH: Lungs
Increased levels of H+ ions are rapidly detected: a change in pH from 7.4 to 7 results in a 4-5x increase in alveolar ventilation (breathing more rapidly, heart beating faster to feed lungs); decreased H+ levels (raised pH) causes respiratory depression, causing a retention of CO2. This has less of an impact, as the resulting lowered O2 levels also stimulate respiration/ ventilation; While fast acting, the lungs can only deal with volatile acid (arising from CO2) as nonvolatile acids have nothing to do with CO2 or carbonic acid
Systemic Regulation of pH: Kidneys
The kidneys are a hugely powerful organ system- mainly because they can remove or retain ‘stuff’ in the blood (ex. urine depending on what is or isn’t in it and how much of it there is); they are relatively slow acting however, generally taking days to exert an effect in response to a significant challenge, although they continually function to maintain homeostasis; renal regulation of pH therefore is a matter of excreting or retaining acid or base (urine can be acidic/basic); the kidneys can thus also deal with nonvolatile acids; quantitively, the retention of HCO3- is actually more important than H+ excretion in terms of renal control of pH [EXCRETING 1 HCO3- IS BASICALLY THE SAME AS ADDING 1 H+] The kidneys can also produce ‘new’ HCO3- by metabolizing glutamine, which makes ammonium (NH4+) and HCO3- ; in the case of too alkaline a pH, H+ can be retained and HCO3- excreted
Systemic Regulation of pH: Key Buffer systems
Bicarbonate (important in buffering the extracellular fluid)
phosphate (important in buffering the intracellular fluid and in the tubules of the kidneys [also in blood, but not enough to make difference]) and
proteins (generally negatively charged and this can absorb free H+ ions, maintaining pH, both in intracellular and extracellular environments [ex. deoxy hemoglobin in RBC is an important buffer]
Buffering
A buffer is a substance that is capable of absorbing and releasing H+ ions depending on ambient conditions; consider: a free acid divested of its H+ can then accept an H+ (making it a conjugate base)
Carbonic acid: H2CO3 H+ + HCO3- [or in this instance bicarbonate and hydrogen]; thus to understand buffering we need to think about the dissociation constant of an acid ex. its propensity to disassociate (Ka= [H][A]/ [HA]) ka is a ratio depending on the concentration of component parts. This value is the inverse of the association constant ; buffer systems can resist pH change in either direction. The addition of OH- would react with free H+ resulting in H20 and resisting an increase in pH
Henderson- Hasselbalch
pH=pka+log [A-]/[HA]; demonstrates mathematically the relationship between pH, disassociation constant (how keen things are to split up) and relative amounts of free/bound H+ ions; if the ratio of [A-]/[HA] is equal then the pH= pka; buffers are most effective [ex. have the greatest capacity to accept or donate H+ ions) when the pH=pka, within a +/- 1 pH range because the quotient of H+ ions is right around where the buffer most able to take on or remove them from solution, causing resistance to change in pH; buffers can’t change pH per se, as they do not dispose of H+ or OH- ions but rather help a solution (ex. blood) RESIST a pH change; this is critical as it is a rapidly acting first line of defense against sudden (and possibly fatal) pH shifts
Intracellular pH regulation
Is just as important as that of the ECM for normal cellular function; ion transporters (many), protein buffering, and the phosphate buffer system are the most important regulators; slightly more acidic inside cell (pH 7.1) which happily corresponds to the pka of the phosphate buffer system, allowing it to operate at peak performance [ H2PO4 H+ + HPO42-] active under low IC pH is Na+ in and H+ out OR 2 HCO3- in; active under high IC pH is Cl- in and HCO3- or OH- out
Systemic Acidosis/Alkalosis: Respiratory
Respiratory acidosis/alkalosis refers to those conditions pertaining to increase or decrease in blood CO2 (and thus carbonic acid); due to buffering, even a fair increase in blood CO2 and therefore free H+ is almost completely and immediately buffered unit it can be lowered again through the lungs/kidneys ; hyper/hypoventilation can cause respiratory acidosis/alkalosis and may be acute or chronic; particularly for chronic conditions, the kidneys must try to compensate but often can’t totally restore pH. Thus many hospitalized patients have pH imbalance related conditions
Hypoventilation: Acidosis
Decreased CO2 clearance, decreased serum pH, increased renal excretion of H+ and retention of HCO3-, causes obstructive lung disease, CNS trauma, narcotics, insufficient ventilation, polio
Hyperventilation: alkalosis
Increased CO2 clearance, increased serum pH, decreased renal excretion of H+ and retention of HCO3-, causes anxiety, stroke, pain, over-ventilation, hypoxemia
Systemic acidosis/alkalosis: Metabolic
Disturbances in blood pH that relate to HCO3- levels instead of CO2 are referred to metabolic; these generally have their roots in kidney function, although can relate to other systems; the lungs will try to compensate for this and therefore metabolic acidosis/alkalosis will have respiratory manifestations
Metabolic acidosis
Abnormal loss of HC03-, decreased serum pH, increased ventilation to try and remove CO2, causes diarrhea, renal insufficiency, and excessive lactic acid
Metabolic alkalosis
Abnormal retention of HCO3-, increased serum pH level, respiratory depression (to some extent) retention of CO2, causes excessive vomiting (loss of stomach acid), hypokalemia, mineralocorticoids
Mixed acid base disorders
When more than one simple disturbance in acid- base exist; ex. heavy vomiting, causing a loss of stomach acid and therefore a metabolic alkalosis due to overabundance of HCO3-, however this vomiting could also result in a loss of blood volume, and thus an increase in lactic acid due to poor perfusion of tissues, ultimately resulting in metabolic acidosis; Salicylate poisoning often involves acute stimulation of the respiratory center, causing respiratory alkalosis, but also resulting in an accumulation of endogenous, non volatile acids, resulting in metabolic acidosis
