Pathophysiology Exam #1

Question 1

How much acid does adults produce in a day? How much acid does a child produce in a day? How does being in a catabolic state affect acid production?

Answer 1

• Adults: produce 1 mEq/kg/day of acids
• Children: 2 – 3 mEq/kg/day
o Children produce more acid than adults, so at greater risk for A-B imbalances & which is why their RR is faster (to blow off more CO2)
• Catabolism: significantly increased
o Pt in a catabolic state (breaking down proteins & amino acids for energy) increases their acid load à so
need to feed them bc until correct catabolism it’ll be hard to correct their A-B imbalance.

Question 2

What are two types of acid that is produced by the body?

Answer 2

• volatile

- non volatile

Question 3

What are the characteristics of volatile acid produced by the body?

Answer 3

• VOLATILE: LARGEST % OF ACIDS
o Volatile acids can chx from one state to another very quickly
o VOLATILE ACIDS COME FROM CO2, A BYPRODUCT OF FAT & CHO (CARB) METABOLISM
o CO2 + H2O -> H2CO3 (carbonic acid)
o CO2, a gas, REGULATED BY LUNGS, hence the name volatile acids

Question 4

What are the characteristics of non-volatile acid produced by the body?

Answer 4

• NON-VOLATILE: SMALLER % OF ACIDS
o From protein metabolism
O SO NON-VOLATILE ACIDS ARE NON-CARBONIC; CONTAIN NO CO2; NOT REGULATED BY LUNGS
o REGULATED BY KIDNEYS
o E.G., sulfuric acid; phosphoric acid; many others

Question 5

What are acids? What is the difference between a strong acid and a weak acid?

Answer 5

ACIDS
• Molecule or ion that DONATES H+ ions (protons) in chemical reactions

• Strong acids: freely dissociate into H+ & anions; e.g., HCl
o Strong acids freely give up their H+ ions
HCl -> H+ + Cl-
Hydrochloric acid when broken down disassociates into H+ & the associated anion Cl-

• Weak acids: minimally dissociate into H+ & anion; e.g., H2CO3 (carbonic acid)
o Weak acids don’t want to give up their H+ ions
H2CO3 ->H+ + HCO3-
Carbonic acid when broken down disassociated into H+ & its associated anion bicarb

Question 6

What are bases? What is the difference between a strong base and a weak base?

Answer 6

BASES
• Molecule or ion that ACCEPTS H+ (protons) in chemical reactions; removes the H+ from the solution
• Examples:
o HCO3- + H+ -> H2CO3
(Bicarb binds to H+ & removes H+ from the solution & become carbonic acid)
o HPO4– + H+ -> H2PO4-
(Base phosphate will accept H+ & become acid phosphate)

• Strong bases (OH- aka hydroxide) react strongly with H+ -> strong bases readily accept H+ ions
• Weak bases (HCO3-) react weakly with H+

Question 7

What are examples of a strong acid and a weak acid?

Answer 7

Strong Acid: HCl
o Strong acids freely give up their H+ ions
HCl -> H+ + Cl- (Hydrochloric acid when broken down disassociates into H+ & the associated anion Cl-)

Weak Acid; H2CO3(carbonic acid)
o Weak acids don’t want to give up their H+ ions
H2CO3 ->H+ + HCO3-(Carbonic acid when broken down disassociated into H+ & its associated anion bicarb)

Question 8

What is the role of proteins in acid base balance?

Answer 8

ROLE OF PROTEINS
• Some amino acids cant accept H+ & donate H+ in certain conditions
• Zwitter ion -> a substance that can accept H+ & liberate H+
• E.G., albumin in the plasma & hgb in RBCs
o Albumin & hgb are proteins that can accept or donate/liberate H+ ions depending on the condition
• Hypoalbuminemic or anemic = met acidosis
o Hypoalbuminemic or anemic -> problem is there isn’t enough protein (albumin) to remove/accept H+
ions from the body’s environment. This leads to met acidosis.

Question 9

Define pH value?

Answer 9

• H+ ion concentration is expressed
as pH value
• pH: Puissance hydrogen (power of hydrogen or H+ concentration)
• pH: negative logarithm of H+ ion concentration

Question 10

In regards to the pH scale, describe what is happening as we move towards the left(towards 10^0) and what is happening as we move towards the right(10^-14)

Answer 10

o As we move to the left on the scale (towards 10^0)
increasing H+ ion concentration & decreasing
hydroxide (OH-) concentration à more ACIDIC
o As move to the right of the scale (towards 10^-14)
decreasing H+ ions concentration & increasing OHion
concentration -> more BASIC

Question 11

Define pH neutral, acidosis and alkalosis:

Answer 11

• pH 7 = neutral; acid = base or H+ ion concentration = OH - ion concentration; we have the same # of H+ as OH-
Ex: HOH (H2O) -> HOH is one H+ ion & one OH-
• pH 7 = base solution

Question 12

What the normal pH value of arterial blood?

Answer 12

• normal pH arterial blood = 7.4 (7.35 – 7.45)

o 7.45 = alkalemia or alkalosis

Question 13

What is the normal pH value of venous blood?

Answer 13

• normal pH venous blood = 7.35
o Venous blood more acidic than arterial bc venous is
carrying more CO2 than arterial, which brings down
the pH

Question 14

What are the pH limits to life?

Answer 14

• limits for life: 7 – 7.7 (???)->however have seen pH

values outside this range & pts have survived

Question 15

What are the pH values of HCl acid, stomach acid, urine and NaOH?

Answer 15

o HCl acid: pH of 0 -> although need a highly
concentrated solution of HCl
o Stomach: pH of 1. Truly stomach pH is 1 – 3 depending on amt of HCl gastric parietal cells secrete. pH
of stomach is so low to inhibit bacterial growth & kills microorganisms
o Urine: pH 4 – 8, depending on physiologic conditions of body. Able to produce more acidic urine based
on that range than basic urine
o NaOH: pH 14 -> although need a highly concentrated solution of NaOH to achieve pH of 14

Question 16

What is significant about the Henderson-Hasselbalch Equation and what is the formula?

Answer 16

HENDERSON-HASSELBALCH EQUATION
pH = 6.1 + log HCO3-/ CO2 (0.03)

So basically is = to kidney/lungs
• 0.03 is amt of CO2 dissolved in plasma
• Henderson-Hasselbalch equation allows us to calculate pH if have bicarb & CO2 level.

Question 17

To maintain pH 7.4, ___ times more base than acid must be maintained

Answer 17

• to maintain pH 7.4, 20 times more base than acid must be maintained
• pH doesn’t change as long as ratio of base:acid is 20:1
o so if bicarb (base) goes up by a certain ratio & CO2 (acid) goes up by same ratio (keeping a 20:1 ration
b/t bicarb & CO2) ->pH doesn’t chx.
o Bicarb decrease & CO2 decreases in same ratios ->pH stays same
o Bicarb increases & CO2 stays same -> pH increases à alkaline
o CO2 decreases & bicarb stays same ->pH increases à alkaline

Question 18

Define what compensation means in relation to acid base balance:

Answer 18

• Compensation: maintenance of normal pH by increasing or decreasing base to balance increase or decrease
in acid or increasing or decreasing acid to balance increase or decrease in base
o maintenance of pH can can be accomplished by:
-> increasing or decreasing amt of CO2 blowing off
-> increasing or decreasing amt of H+ excreting from body
->increasing or decreasing amt of bicarb reabsorbing from kidneys.
o If have primary resp disorders, kidneys will compensate for that
o If kidneys are cause of primary A-B disorder, respiratory system will compensate for that

Question 19

Work the Henderson-Hasselbalch equation if the HCO3- is 24 and the CO2 is 40

Answer 19

• Example:
o HCO3- = 24 mEq/L
o pCO2 = 40 mmHg
o Solve: 
24/40 (0.03) 
24/1.2
20
6.1 + common log 20
6.1 + 1.3 = 7.4

Question 20

What are three ways the body maintains normal pH and what are the characteristics of each of them?

Answer 20

• Buffer systems: extracellular & intracellular
o Respond with fraction of second
o Buffer system is most rapidly responding system
• Respiratory system is the next to respond
o Acute regulation: 1 – 12 min
o Chronic regulation: 1 – 2 days
• Kidneys are the last to respond
o Respond in hrs to days, but once they do respond, kidneys are the strongest / most powerful system that
manage A-B balance
o Most powerful of all regulatory systems
o Can continue for extended periods to regulate A-B balance

Question 21

What is the definition of a buffer system?

Answer 21

• Buffer system: 2 or more chemicals, so that when a strong acid is added to a solution, the strong acid is
buffered to a weak acid. If a strong base is added to that solution, it’s buffered to a weak base.

Question 22

What are the characteristics of Bicarbonate as related to being a buffer agent?

Answer 22

• Bicarb – carbonic acid buffer system
o Not most powerful, but most important of buffer systems
o CO2 regulated by lungs & HCO3- by kidneys
o CO2↑ + H2O -> (CA) -> H2CO3 -> H+ + HCO3- or
CO2 + H2O

Question 23

What determines which way the formula goes?(as related to Bicarbonate and AB balance?

Answer 23

• CO2 increases formula moves to the RIGHT.

* Bicarb increases formula moves to the LEFT.

Question 24

What is the result when a strong acid(HCl) is combined with a weak base(HCO3-)? What is the outcome?

Answer 24

o Strong acid (HCl) + weak base (HCO3-) -> weak acid (H2CO3) + salt
§ In this example, added a strong acid (HCl) to a solution. It combines with a weak base (HCO3-) &
the result is a weak acid (carbonic acid) & salt as the byproduct
§ Started with a strong acid & buffered it down to a weak acid. That weak acid will have less of an effect on the solutions pH than the strong acid would.

Question 25

What is the result when a strong base(NaOH) is combined with a weak acid(H2CO3)? What is the outcome?

Answer 25

o Strong base (NaOH) + weak acid (H2CO3) ->weak base (NaHCO3) + water § In this example, added strong base (sodium hydroxide) to a solution. It combines with a weak acid (carbonic acid) & yields a weak base (sodium bicarb) with the byproduct being water. § So we’ve taken a strong base added it to a solution & its buffered to a weak base. That weak base has less of an effect on the pH than the strong base would have.

Question 26

In regards to the buffer system, what is the outcome and differences when a weak acid or base is added to a solution as opposed to a strong acid or base?

Answer 26

o OUTCOME: pH minimally changed by weak acid or weak base compared with the stronger acid or base § Buffer system has its limits. Strong acid added to a buffer system & is buffered to weak acid. But, if keep adding strong acid, at some point the buffer system cannot buffer it to a weak acid any more. § So buffer systems have limits à keep adding strong acids & bases to it, there will be a point where it cannot buffer that any more

Question 27

What are the characteristics of protein buffers as related to acid base balance?

Answer 27

• Protein buffers o Powerful & plentiful buffers o Albumin & other extracellular proteins o Hgb in RBCs o Amino acids in these proteins can accept or donate H+ ions depending on what body needs at that time o Body in a state of acidosis: those proteins are going to buffer the body fluids by accepting those H+ ions & remove them from the extracellular fluid & increase pH back to normal. o Body in state of alkalosis: proteins will release H+ into body fluids & bring pH down toward normal • Effects of hypoalbuminemia & anemia on A-B balance à talked about earlier

Question 28

What is the movement of H+ and K+ across the cell membrane in response to acidosis and alkalosis?

Answer 28

• Acidosis: H+ into cell & K+ out of cell = HYPERKALEMIA!!! o Hyperkalemia most likely to occur R/T METABOLIC ACIDOSIS o Body in state of acidosis, so have accumulation of H+ in extracellular fluid -> want to shift those H+ into cells. To maintain electrical neutrality a cation has to move out of the cell. H+ move into cell & K+ move out of cell à which can lead to significant • Alkalosis: H+ ion out of cell & K+ into cell o Metabolic alkalosis may cause mild hypokalemia o Alkalosis = deficit of H+ in extracellular fluid à H+ moves out of cell into extracellular fluid & K+ move from extracellular fluid into cell • Not very important in primary respiratory acidosis or alkalosis -> these are only associated with metabolic acidosis & alkalosis

Question 29

What are the treatments for hyperkalemia?

Answer 29

HYPERKALEMIA. o Treatment of hyperkalemia: § First treat the met acidosis (need to fix the problem that started it) § Insulin -> moves K+ into cell & admin dextrose with it § Ca+ -> reestablishes TP. So TP has moved up, so RMP has further to go to elicit a response § Bicarb -> moves K+ back into the cell § Kayexalate § Dialysis

Question 30

How does the respiratory system respond as a buffering system in acid base balance?

Answer 30

RESPIRATORY REGULATION OR A-B BALANCE • Controls CO2 portion of Henderson-Hasselbach equation • Increase in CO2 (caused by hypoventilation) = pH to acidic side • Decrease in CO2 (caused by hyperventilation) = pH to alkaline side • CO2 diffuses into CSF & decreases CSF pH • Central medullary chemoreceptors monitor pH of CSF& increase rate & depth of ventilation • Increase in CO2 -> pH of blood decreases -> pH of CSF decreases; medullary chemoreceptors send msg to medullary inspiratory center to increase rate & depth of ventilations (to blow off more CO2) & bring pH back up towards normal • Opposite happens with decreased CO2 o Decrease in CO2 -> pH of blood increases -> pH of CSF increases (more alkaline); medullary chemoreceptors sense that & decrease rate & depth of ventilations to retain CO2 & bring pH back down toward normal

Question 31

How is the renal system involved in Acid:Base Balance?

Answer 31

• Kidneys are last to respond but are the most powerful • Can excrete urine with pH 4.5 – 8 • Acid urine if more H+ than HCO3 - excreted, which is typical especially in diets high in meat o Eating meat increases acid load & urine pH is more acidic • Alkaline urine if more HCO3- excreted than H+

Question 32

What is the mechanism used by the renal system for acid:base balance?

Answer 32

• Filtered bicarbonate reabsorbed o 99% of bicarb that is filtered from glomerulus into renal tubules is reabsorbed back into the body -> this preserves bicarb load of the body; this isn’t adding NEW bicarb to the body • Synthesis & reabsorption of NEW bicarbonate while buffering & excreting H+ o Buffering & excretion of H+ with inorganic phosphates o Synthesis of ammonia (NH3) & excreting extra H+ as ammonium chloride (NH4Cl)

Question 33

Describe the process of bicarb reabsorption in relation to the renal system involvement with acid:base balance.

Answer 33

• RULE: for every H+ secreted into the tubular lumen & excreted into the urine, a bicarbonate ion & Na+ ion are reabsorbed into the PTC/body fluids • Bicarb reabsorption occurs in proximal tubules in kidneys • Proximal tubule process ->->->->-> • In pic: tubular lumen, tubular cell & PTC • Start with filtered bicarb (filtered through the glomerulus into tubular lumen) • First have H+ that are being actively pumped out of tubular cell into tubular lumen & Na+ pumped out of tubular lumen & into tubular cell -> this is secondary active counter transport. • Have Na+ pumped in & H+ pumped out • Bicarb combines with H+ that was just pumped out into tubular lumen to form carbonic acid. • In presence of CA, carbonic acid breaks down into water & CO2. • CO2 diffuses into tubular cell & combines with H2O (in presence of CA) to form H2CO3- inside tubular cell • That carbonic acid breaks down into H+ & bicarb. • That bicarb is then reabsorbed into PTC & into body fluids. • So, we’re reabsorbing bicarb ->we’re maintaining the bicarb load of the body. 99% of bicarb that’s filtered is reabsorbed back into PTC. • The rule holds true: for each H+ secreted, a Na+ & bicarb are reabsorbed.

Question 34

How is primary active secretion of H+ ions accomplished by the renal system in response to acid:base balance?

Answer 34

• CO2 & water yield carbonic acid & then disassociates into bicarb & H+ • Then H+ are actively pumped out into the tubular lumen This isn’t countertransport of H+; this is primary active transport of H+ out of the tubular cell. • Cl- follows the H+. H+ + Cl- = HCl. HCl acid in the renal tubules. iIf that HCl acid goes thru renal tubules, into kidneys, into ureters, into bladder & out the urethra -> burn on urination if excreting HCl acid. • Luckily those H+ that are actively pumped out into tubular lumen are immediately buffered by bicarb

Question 35

How are H+ ions buffered by inordinate phosphates?

Answer 35

• Phosphate buffer system is composed of HPO4-- (base phosphate) & H2PO4- (acid phosphate) • The phosphate buffers handle the excess H+ when HCO3- isn’t available to combine with H+ • After HPO4-- combines with H+ to form H2PO4 -, it can be excreted as NaH2PO4 (sodium acid phosphate), carrying with it excess H+ à this gets rid of the extra H+; this is one of the ways the kidneys deal with A-B imbalances • In pic have: tubular lumen, tubular cell & PTC • Have Na2HPO4: di-sodium base phosphate. When Na2HPO4 is broken down, it yields base phosphate & 2 Na+. • Base phosphate (HPO4--) combines with H+ to form acid phosphate (H2PO4-). H2PO4- + Na+ = sodium acid phosphate (NaH2PO4), which is eventually excreted into the urine -> this removes H+ ions from body fluids & excretes H+ in urine • At the same time in the tubular cell, have water & CO2 combining to form carbonic acid (H2CO3). H2CO3 breaks down into H+ & bicarb. Bicarb is then reabsorbed back into PTC.

Question 36

In regards to the buffering of H+ with inordinate phosphates, do you see an associated bicarb in the tubular lumen?

Answer 36

No! This is BRAND NEW BICARB being added to body fluids & absorbed into PTC • The rule holds true: for each H+ secreted & excreted into urine, reabsorb one bicarb & one Na+

Question 37

What are the characteristics of the AMMONIA (NH3) – AMMONIUM CHLORIDE (NH4Cl) BUFFERING OF H+?

Answer 37

• Very powerful buffer system in renal tubules that depends on glutaminase enzyme • Generates much NEW bicarbonate • Activity of the enzyme glutaminase, which begins the process, is pH dependent • When pH becomes more acidic: glutaminase is more active -> MORE H+ secreted & excreted; more NEW bicarbonate synthesized & reabsorbed o Increases pH by excreting H+ & creating NEW bicarb • When pH becomes more alkaline: glutaminase is LESS active -> less H+ secreted & excreted; less NEW bicarbonate synthesized & reabsorbed o Decreases pH back to normal by excreting less H+ & creating less NEW bicarb • In this example the pH of body fluid is more acidic -> making glutaminase enzyme more active. • Glutaminase is an enzyme that breaks down glutamine to NH3 (ammonia). NH3 then moves into tubular lumen & combines with H+ to form NH4 (ammonium) • NH4 combines with Cl- yielding NH4Cl à NH4Cl is then excreted in the urine • So we’re getting rid of H+ ions • Also have water + CO2 = carbonic acid, which breaks down in H+ & bicarb à that a BRAND NEW BICARB being added to body fluids & PTC • The rule holds true: H+ secreted into tubular lumen (& eventually into urine) & reabsorbed one bicarb & one Na+

Question 38

What is the significance of high anion gap versus normal anion gap in regards to metabolic acidosis?

Answer 38

• Any time your interpretation of ABG results in metabolic acidosis, have to determine if it’s a normal or high anion gap metabolic acidosis à do this to ID what’s causing the acidosis • Anion gap: Difference in major measured cations (Na+ & K+) & major measured anions (bicarb & Cl-)

Question 39

What is the formula used to determine anion gap?

Answer 39

• AG = (Na+ + K+) – (HCO3- + Cl-)

Question 40

What is a "normal" anion gap?

Answer 40

• Normal AG = 12 – 18 mEq/L o This is assessing the major measured cations & anions (not saying 12 – 18 mEq/L more cations than the anions bc we need chemical neutrality [so cations have to = anions])

Question 41

What is the significance of a high anion gap?

Answer 41

• If AG is increased (> 18 mEq/L), some unmeasured anion is contributing to the gap. That anion must be identified --> have to ID the anion to ID the cause of metabolic acidosis. o As unmeasured anion increases, the Cl- decreases to maintain electrical neutrality o Additionally, the HCO3- decreases as it is used to buffer the acidosis o So, if bicarb is decreasing to buffer the acidosis & Cl- decreases the maintain chemical neutrality, then measured anions gets smaller & cations stays same -> a smaller # of anions is subtracted from cations o So gap b/t measured cations & measured anions increases

Question 42

What is the significance of a normal anion gap?

Answer 42

• Normal AG metabolic acidosis is HYPERCHLOREMIC o normal AG met acidosis is usually caused by decrease in bicarb or an increase in Cl-. o Ex: give NS bolus. This causes hyperchloremic met acidosis bc increase Clo Ex: pt with diarrhea loses lots of bicarb. As bicarb level decreases, the Cl- increases to maintain electrical neutrality.

Question 43

What are some examples of high AG metabolic acidosis & associated unmeasured anion causing the acidosis?

Answer 43

o Shock – lactate * Shock -> decreased perfusion -> anaerobic metabolism -> lactate production. Lactate is the unmeasured anion that’s leading to high AG met acidosis. * As lactate increases, Cl- decreases to maintain electrical neutrality -> causing hyperchloremia. o Cardiac arrest – lactate * cardiac arrest same thing happens -> decreased perfusion -> anaerobic met -> lactate production o Renal failure – a number of anions that are usually renally excreted but cant be bc of kidney fx -> so get anion buildup & cause high AG met acidosis o Lactic acidosis – lactate o DKA – ketone bodies * Ketone bodies are anions that cause a high AG met acidosis * 3 ketone bodies made during DKA: acetoacetic acid, beta-hydroxybutyric acid & acetone * ketone bodies vs ketoacids à ketoacids involved with krebs cycle. Ketone bodies are developed when more acetyl coenzyme A is produced than what can be cycled through Krebs cycle à which is what DKA leads to: production of ketone bodies o Malnutrition/starvation – ketone bodies & others o Salicylate overdose o Ethylene glycol (antifreeze) – metabolites of ethylene glycol that cause the high AG met acidosis

Question 44

In mixed compensation, how do you determine the primary problem and the greatest degree of compensation?

Answer 44

• PaCO2 o Subtract pt PaCO2 value from normal PaCO2 (40 mmHg) o Divide the difference by 40 to determine % chx from normal 40 mmHg – PaCO2/40 mmHg o Note direction of change from normal & how it relates to pt pH value • HCO3- o Subtract pt HCO3- from normal HCO3- (24 mEq/L) o Divide the difference by 24 to determine % chx from normal 24 mEq/L – HCO3-/24 mEq/L o Note direction of change from normal & how it relates to pt pH value • The larger % chax is the primary problem • The smaller % chx is the % (degree) of compensation OR in mixed disorders, the % (degree) of contribution to problem

Question 45

What two components make up mean systemic arterial pressure?

Answer 45

1. Cardiac Output 2. Total Peripheral Resistance Mean systemic arterial pressure= Cardiac Output x Total Peripheral Resistance

Question 46

What two components make up mean cardiac output?

Answer 46

1. Stroke Volume | 2. Heart Rate

Question 47

What two components make up total peripheral resistance?

Answer 47

1. Arteriolar Radius(major influence on PVR) | 2. Blood Viscosity(minor influence on PVR)

Question 48

When blood circulation reaches the ____ the blood pressure is a single digit number.

Answer 48

arterioles

Question 49

The major influence on heart rate is the ANS. The parasympathetic mainly affects HR at the ___ node by what NMT with what receptors? The sympathetic affects HR at these nodes and by what NMT with what receptors?

Answer 49

Parasympathetic --> SA Node --> Ach(neurotransmitter)/M-2(receptor) Sympathetic --> SA Node, AV Node, Ventricular Contractile Fibers --> NE(neurotransmitter)/B-1(receptor)

Question 50

Stroke Volume is influenced by the ___ and ___.

Answer 50

- Sympathetic NS | - LEVD/LVEDP(venous return)

Question 51

What is the cascade determining LVEDV/LVEDP?(4)

Answer 51

1. atrial vol/pressure 2. venous return 3. venous pressure 4. venous tone(sympathetic nervous system activity to the veins) NE/EPI(NMT) a-1/B-2(receptors)

Question 52

What are two determents of venous pressure?

Answer 52

1. skeletal muscle pump | 2. blood volume

Question 53

____ is released from the adrenal medulla when stimulated by the SNS. This further increases the SNS response by increasing HR/SV/CO.

Answer 53

epinephrine(a-1, B-1, B-2)

Question 54

PVR is affected by arteriolar radius and blood viscosity. Arteriolar Radius is affected by the ANS is what two ways and by what means?

Answer 54

1. a-1(increases PVR by decreasing the radius of the arterioles) 2. B-2(decreases PVR by increasing the radius of the arterioles)

Question 55

PVR is affected by arteriolar radius and blood viscosity. Blood viscosity is primarily determined by ____ and that is primarily determined by ____.

Answer 55

- hematocrit | - #of RBC's

Question 56

These 9 things impact arteriolar radius by ___ the arteries.

Answer 56

- oxygen consumption, CO2, H+, K+, bradykinin, histamine, prostaglandins, adenosine, nitric oxide - Favor arteriolar dilation

Question 57

The medulla is located in the _____. What is right below the medulla? What separates the medulla from the spinal cord? What is located above the medulla?

Answer 57

- brain stem - spinal cord - foramen magnum - pons

Question 58

In what part of the vascular bed does the systolic and diastolic pressures narrow until they reach one pressure

Answer 58

Arterioles

Question 59

Mean systemic arterial pressure = ___ x ___

Answer 59

Cardiac output X Total peripheral resistance

Question 60

What sensory nerves stimulate the medullary cardiovascular center?

Answer 60

cranial nerve IX - Glossalpheringeal (internal carotids, baroreceptors, chemoreceptors) cranial nerve X - Vagus (Baroreceptors in aorta)

Question 61

The sympathetic nervous system reacts on the ___ muscles of the arteries and veins

Answer 61

vascular smooth muscle | Arteries that constrict are predominately the medium and small arterioles

Question 62

List five short-term/rapidly acting mechanisms for blood pressure regulation(seconds-minute)

Answer 62

- Baroreceptors (1-2 days they reset to elevated BP) - Chemoreceptors - Right atrium low-pressure receptors/Atrial reflex/Bainbridge reflex - CNS ischemic response - Stress- relaxation response of blood vessels *mechanisms are not working independent of each other, but are working simultaneous at different times*

Question 63

Live four intermediate to long term mechanisms for blood pressure regulation(minutes-hours-days-longer)

Answer 63

-Transcapillary fluid shifts -Renin- angiotensin - aldosterone system -Renal body fluid control mechanisms ->Aldosterone ->Antidiuretic hormone (Vasopressin) ->Pressure diuresis and natriuresis Natriuretic peptides *mechanisms are not working independent of each other, but are working simultaneous at different times*

Question 64

The medullary cardioregulatory center has many innervation...the two primary ones is cranial nerve IX(_____) which brings sensory impulses from the ____, and cranial nerve X(___) that brings sensory impulses from the ___.

Answer 64

* IX(glossopharyngeal---->carotids (baroreceptors/chemoreceptors) * X(Vagus)--->aorta(baroreceptors)

Question 65

Parasympathetic output from the medullary cardioregulatory center primarily affects the ___ node of the heart.

Answer 65

SA node

Question 66

Preganglionic fibers are very ____ and Postganglionic fibers are very ___.(length)

Answer 66

- long | - short

Question 67

Sympathetic fibers have ____ preganglionic fibers than parasympathetic. One activated the SNS affects these areas of the heart.

Answer 67

- shorter | - SA node, AV node, ventricular contractile fibers of the heart

Question 68

Besides affecting the heart, ones the SNS is activated it also innervates the ___ ___ to release these neurotransmitters in these amounts.

Answer 68

- adrenal medula - Epi(80%)/NE(20%) these NMT circulate in the blood further intensifying the SNS response

Question 69

The SNS that terminates on vascular smooth muscle has this affect.

Answer 69

-maintain vascular tone and BP(so cause vasoconstriction in the medium and small size arteries and arterioles)

Question 70

Baroreceptors monitor _____/_____ in these two places.

Answer 70

- stretch/pressure | - Carotid sinuses of internal carotids(operate MAP 60-100-not stimulated by MAP

Question 71

What pressures do the carotid baroreceptors operate at? At what pressures do the arctic baroreceptors operate at?

Answer 71

- carotid-->60-180 mmHg | - aortic--->90-210 mmHg

Question 72

When the blood pressure is increased, impulses are sent via CN #9 and CN #10 which combine and form the ___ and terminates in the ___.

Answer 72

- tractus solitarius | - medullary nucleus solitarius(sensory portion of the medullary cardiovascular regulatory center)

Question 73

Increased MAP excites __________ in the medullary cardiovascular regulatory center which results in?

Answer 73

- central medullary alpha-2 receptors(clonidine/precedex) | - decreased SNS outflow and increased PNS outflow

Question 74

Decreased MAP less _______ in the medullary cardiovascular regulatory center which results in?

Answer 74

- less excitation/inhibition of central medullary alpha-2 receptors - increased SNS outflow and decreased PNS outflow

Question 75

What is the sequence of events of the response of the cardiovascular medullary response to increased MAP?

Answer 75

• Increased BP/increased pressure in aortic arch and carotid sinuses and increased stimulation of baroreceptors • Increased action potentials/nerve impulses transmission to medullary cardiovascular regulatory center • Increased activation of central medullary alpha-2 receptors • Decreased SNS and increased PNS outflow • Decreased heart rate • Decreased strength of ventricular contraction -- Decreased stroke volume --Decreased cardiac output • Arterial dilation – Decreased SVR • Venous dilation -- Decreased venous return -- Decreased LVEDV/preload(Frank Starling Mechanism) --Decreased LV stretch – Decreased SV – Decreased CO • Decreased adrenal medulla epi and norepi secretion – decreased SNS response • Decreased MAP Occurs via the tracts solitarius to the nucleus solitarius

Question 76

What is the sequence of events of the response of the cardiovascular medullary response to decreased MAP?

Answer 76

* Decreased BP/decreased pressure in aortic arch and carotid sinuses and decreased stimulation of baroreceptors * Decreased action potentials/nerve impulses transmission to medullary cardiovascular regulatory center * Decreased activation of central medullary alpha-2 receptors * Increased SNS and decreased PNS outflow * Increased heart rate * Increased strength of ventricular contraction -- Increased stroke volume --Increased cardiac output * Arterial constriction – Increased SVR * Venous constriction -- Increased venous return -- Increased LVEDV/preload --Increased LV stretch – Increased SV – Increased CO * Increased adrenal medulla epi and norepi secretion – Increased SNS response * Increased MAP

Question 77

Baroreceptors reset in _____ days to the pressure they are exposed to.

Answer 77

1-2 days *so not important for long-term regulation of BP*

Question 78

Chemoreceptors are located in the ____ and the ____ bodies and are not stimulated until the BP is

Answer 78

Chemoreceptors in aortic(arch) bodies and (bifurcation)carotid bodies (outside the aorta and carotids, so small blood vessels permeate aorta and carotids to perfuse the chemoreceptors) • Not stimulated until BP

Question 79

The peripheral chemoreceptors monitor ___, ___, and ___; which are affected by _____.

Answer 79

- PaO2, PaCO2, pH - decreased BP • Decreased BP = ↓PaO2, ↑PaCO2, ↓pH

Question 80

The chemoreceptors located in the aortic arch and the internal carotid are stimulated when the PaO2 was ____?

Question 81

What is the response by the chemoreceptors when the PaO2 decreased

Answer 81

* Impulses from carotid bodies through sensory portion of CN IX(Glossopharyngeal) and from aortic bodies through sensory portion of CN X (Vagus) to tractus solitarius to nucleus solitarius * Integration in the medullary cardiovascular regulatory center tends to decrease SNS and increase PNS/vagal outflow, which would slow the heart rate. * HOWEVER . . . * HOWEVER, integration of a number of simultaneous physiologic mechanisms, such as systemic catecholamine release in response to low oxygen, tend to activate the SNS, which overrides the medullary CV regulatory center * THUS, the outcomes are variable but tend to be: * Increased heart rate * Increased strength of ventricular contraction -- Increased stroke volume -- Increased cardiac output * Arterial constriction – Increased SVR * Venous constriction -- Increased venous return -- Increased LVEDV/preload --Increased LV stretch – Increased SV – Increased CO * Increased adrenal medulla epi and norepi secretion – Increased SNS response * Increased MAP * NOTE: Outcomes vary from person to person based on a number of variables

Question 82

The right atrium low pressure receptors(Bainbridge reflex) minimize changes in MAP related to changes in ___ ___.

Answer 82

Blood volume

Question 83

The RA and the PA are normally ____-pressure areas.

Answer 83

low

Question 84

The R atrium low-pressure receptors(Bainbridge Reflex) are stimulated by?

Answer 84

increased MAP

Question 85

What is the outcome of stimulation of the Bainbridge Reflex?

Answer 85

* OUTCOMES: Overall, antagonistic to baroreceptor response. * Dilation of afferent arterioles – increased GFR – increased UOP * Deceased ADH secretion – increased UOP and vaodilation * Decreased aldosterone – increased sodium and water excretion and decreased vascular volume(getting rid of excess vascular volume) * Increased natriuretic peptides production, which will decrease vascular volume and decrease BP (see later content about natriuretic peptides) * Direct pressure on SA node – increased heart rate(heart doesn't have as long to fill so decrease pressure) * Impulses through sensory portion of vagus to medullary cardiovascular regulatory center * Increased SNS outflow and no change in PNS/vagal outflow * Increased HR , FOC, SV, and CO * Increased venous return, which decreases venous volume

Question 86

When blood volume and pressure are increased, the is dominant; when blood volume and pressure are decreased, the is dominant.

Answer 86

- Bainbridge reflex | - baroreceptor reflex

Question 87

When is the central nervous system Ischemic response activated and what activates it and what is the outcome?

Answer 87

-last ditch effort • Decreased blood flow (ischemia) to medullary cardiovascular regulatory center as result of ↑CO2 and ↓O2 • Neurons of medullary CV regulatory center come maximally excited secondary to direct effects of ischemia • Maximal SNS outflow • Widespread systemic vasoconstriction of all arteries and veins to attempt to increase MAP • Activated when MAP

Question 88

What is the goal of the central nervous system ischemic response and what is the outcome if it fails?

Answer 88

* GOAL: Maintain blood flow to brain * If brain blood flow does not increase, brain neurons become severely ischemic and die within 3 – 10 min. * MAP falls, vasoconstriction lost, death follows

Question 89

Stress-Relation response of Blood Vessels causes __________ and is a ______ to ______ regulation of MAP.

Answer 89

• Continued stretch on vascular smooth muscle leads to reflex relaxation and decrease in pressure • Short-term to intermediate regulation of MAP

Question 90

With intermediate-long term mechanisms for BP regulation, transcapillary fluid shifts has this affect on capillary hydrostatic pressure in response to increased MAP?

Answer 90

increased capillary hydrostatic pressure

Question 91

With intermediate-long term mechanisms for BP regulation, transcapillary fluid shifts has this affect on capillary hydrostatic pressure in response to decreased MAP?

Answer 91

decreased capillary hydrostatic pressure

Question 92

How does transcapillary fluid shifts respond overall to an increased MAP? What is the result?

Answer 92

• Increased MAP • Increased capillary hydrostatic pressure at arterial and venous ends of capillaries(more fluid removed from vascular system) • Increased filtration into interstitium on arterial end and decreased absorption from interstitium on venous end(why those with chronic HTN=dependent peripheral edema) • Decreases systemic volume and MAP

Question 93

How does transcapillary fluid shifts respond overall to an decreased MAP? What is the result?

Answer 93

• Decreased MAP • Decreased capillary hydrostatic pressure at arterial and venous ends of capillaries(less fluid being moved from the vascular beds) • Decreased filtration into interstitium on arterial end and increased absorption from interstitium on venous end • Increases systemic volume and MAP

Question 94

Renin is produced by these types of cells and in response to these two things.

Answer 94

- juxtaglomular cells - decreased tubular filtrate flow rate - decreased sodium content of the filtrate

Question 95

As BP decreases tubular filtrate flow rate ____ and tubular filtrate sodium content ____. This stimulates ____ secretion.

Answer 95

- decreases, decreases | - renin

Question 96

Renin converts angiotensinogen to _____, which is converted to _____ by _____.

Answer 96

- angiotensin I - angiotensin II - angiotensin converting enzyme(ACE)

Question 97

Where is ACE produced?

Answer 97

endothelium of arterioles...the majority of arterioles are located in the lungs....so most ACE comes from lungs.

Question 98

Angiotensin II is a _______ which _____ BP.

Answer 98

- potent vasoconstrictor | - increases BP

Question 99

Epi/NE directly acts on the ___ which ___ renin secretion.

Answer 99

- GMC | - increases

Question 100

In what three ways does angiotensin II affect BP regulation?

Answer 100

1. Potent vasoconstriction of arteries and veins 2. Direct effect on renal tubules and peritubular capillaries causing renal reabsorption of Na and H2O 3. Secretion of aldosterone which favors renal reabsorption of Na and H2O.

Question 101

Vasoconstriction of arteries and veins by angiotensin II favors.....?

Answer 101

-increased venous return->increased MAP->increased RBF

Question 102

Renal reabsorption of NA and H2O favors.....?

Answer 102

-increased vascular volume->increased venous return(preload/SV/CO)->increased MAP->increased RBF

Question 103

How does increased RBF affect renin?

Answer 103

decreases the production of renin secondary to negative feedback.

Question 104

What are the two most important stimuli increasing secretion of aldosterone from the zone glomerulosa from the adrenal cortex?

Answer 104

1. increased potassium 2. angiotensin II also stimulated by a lesser extent by: 3. decreased sodium 4. Adrenocorticotropic hormone(ACTH)

Question 105

Where specifically is aldosterone produced?

Answer 105

* Adrenal cortex | * Zona glomerulosa: outer layer of cells of adrenal cortex secretes aldosterone

Question 106

What are the effects of aldosterone secretion?

Answer 106

• Late distal tubules and cortical collecting tubules - >Increased reabsorption of sodium from tubular filtrate into peritubular capillaries - >Water follows sodium secondary to osmotic gradient - >INCREASED VASCULAR VOLUME AND MAP - >ALSO, potassium and hydrogen secretion and excretion into urine *STEROID BASED HORMONE SO IT IS LIPID SOLUBLE*

Question 107

What causes ADH(antidiuretic hormone)? | two things?

Answer 107

• Increase in body fluid osmolality • A decrease in the vascular volume by about 20% is a potent stimulus for ADH/vasopressin secretion

Question 108

ADH(vasopressin) acts on two receptors to help increase BP...what are they and what is the effect once they are stimulated?

Answer 108

• V-1 receptors: Vasoconstriction(vasoconstriction of smooth muscles) of arteries and veins(remember like alpha-1) • V-2 receptors: Increased tubular reabsorption of water to increase vascular volume and blood pressure(remember there are two kidneys)

Question 109

ADH is synthezied where?

Answer 109

hypothalamus--->posterior pituitary

Question 110

As BP increases GMF increases which increases????

Answer 110

urine ouput *this is why the first line tx for HTN is to decrease venous volume by administering a diuretic*

Question 111

Where are natriuretic peptides secreted from in humans?

Answer 111

* Atrial Natriuretic Peptide (ANP) * Brain Natriuretic Peptide/B-TYPE NATRIURETIC PEPTIDE(BNP) * BNP is synthesized and secreted primarily by cells in the cardiac ventricles in humans

Question 112

Natriuretic peptides favor.......?

Answer 112

favor a decrease in BP *does not play a role in raising BP*

Question 113

So what causes Atrial Natriuretic Peptide(ANP) secretion?

Answer 113

- increased plasma sodium level/hypervolemia which - increases venous return which - causes right atrial distention which - increases right atrial pressure which - stimulates right atrial condiocytes to secrete ANP

Question 114

What are the four effects of ANP secretion?

Answer 114

1. posterior pituitary--->decreases ADH secretion which favors diuresis leading to decrease ECFV(decreased MAP)*also inactivates circulating ADH* 2. adrenal cortex--->decreases Aldosterone secretion which decreases natriuresis leading to decrease ECFV(decreased MAP) 3. kidneys--->decreases renin which decreases angiotensin II which decreases vascular constriction, decreases BP*also inactivates circulating angiotensin II* 4. blood vessels--->causes vasorelaxation which decreases BP 5. heart--->decreases strength of contraction, decrease HR, decrease preload, decrease afterload, decrease BP

Question 115

If a person experiences massive hemorrhage and BP is 20-30s what mechanism is responsible for attempting to increase BP?

Answer 115

The Ischemic response which causes maximum systemic outflow

Question 116

Do natraetic peptides favor increase in BP or a decrease in BP?

Answer 116

they favor a decrease in BP

Question 117

A decrease in pCO2 and a decrease in HCO3 leads to what change in pH?

Answer 117

no change

Question 118

In long term acidosis, do you have an increase H+ secretion from the body or a decreased?

Answer 118

Increase in renal secretion(reabsorbs and synthesizes bicarbonate

Question 119

Which of the following buffer hydrogen in tubular filtrate? Hydrochloric acid, HCO3, Ammonia, Phosphates?

Answer 119

HCO3 Ammonia Phosphates

Question 120

What is the cause of a primary hypercholemic or normal AG acidosis?

Answer 120

prolonged vomiting/prolonged diarrhea(getting rid of bicarb in stool)

Question 121

What type AF acidosis in DKA?

Answer 121

high AG metabolic acidosis

Question 122

What are the associated anions that are causing the chloride levels to decrease and are causing the high AG?

Answer 122

ketone bodies(acetone/acidic acid/hydrogenous???)

Question 123

If the ABG results does not match the H&P what do you do?

Answer 123

redraw

Question 124

What types of substances is released from the Zona Glomerulosa?

Answer 124

Aldosterone

Question 125

Does Aldosterone favor an increase or a decrease in Na reabsorption?

Answer 125

Increase in Na reabsorption

Question 126

Does an increase in sodium reabsorption increase or decrease vascular volume?

Answer 126

increase

Question 127

Does an increase or decrease in BP stimulate renin secretion?

Answer 127

decrease

Question 128

If the diagnosis is a metabolic acidosis, what is the next thing we need to determine?

Answer 128

Determine the AG(normal or high?)