Chapter 9: Acid-Base Balance

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Welcome to the Deep Dive.

Today we're getting into something really fundamental to how our bodies work, acid -base balance.

Yeah, it sounds maybe a little technical, but honestly,

understanding this is, well, it's crucial.

It really is.

It's like having a key to unlock how so many health processes function.

And knowing this stuff definitely helps you make sense of health information you come across.

Absolutely.

It's like this constant balancing act the body performs.

Pretty amazing, actually.

And for this deep dive, we're using chapter nine of the Saunders Comprehensive Review for the NCLE -XPN Examination Seventh Edition as our guide.

Right.

So we'll pull out the, you know, the really important ideas, how the body regulates things, what happens when it goes wrong, and some key things for healthcare folks to know.

Our mission.

To break it down clearly, make it engaging so you walk away with a solid grasp, not feeling totally overwhelmed.

Okay, let's jump in.

Hydrogen ions, acids, bases.

Where do we start?

Okay.

So the absolute core of this is the hydrogen ion.

H plus any little things, but wow, they determine the pH of our body fluids.

And pH is critical, right?

Keeping it stable is essential for, well, everything to work.

Totally non -negotiable.

It has to stay in a very narrow range.

And pH, that's the scale, one to fourteen, with seven being neutral.

You got it.

It measures how concentrated those H plus ions are.

So below seven, that's what we call the acidosis.

Okay.

And above seven, that's alkaline, or alkalosis, right?

The middle seven, that's neutral.

So more H plus means more acid, lower pH.

Fewer H plus means more alkaline, higher pH.

Makes sense.

Exactly.

So where do these H plus ions come from, and what makes something an acid or a base in this whole system?

Well, acids are basically end products of metabolism.

All the chemical reactions happening constantly.

Okay.

And the key thing is, acids contain H plus ions, and they donate them.

They give them away.

They're the givers.

Got it.

And bases.

Bases are the opposite.

They don't have H plus ions themselves, but they accept them.

They grab onto the H plus ions that acids donate.

So it's this give and take that sets the pH.

Precisely.

That constant interplay determines the balance.

Okay.

We have the players.

H plus, APH, acids donating, bases accepting.

How does the body keep this all perfectly balanced?

It sounds incredibly complex.

It is remarkable.

And we have these really sophisticated systems.

Yeah.

The chapter points out three main ones,

buffers, the lungs, and the kidneys.

Right.

Three different teams working together.

Yeah.

Each with its own job, its own speed.

Let's start with the buffers.

What are they?

Buffers.

I hear that term a lot.

What's their actual role here?

Think of them as the body's rapid response team.

The first line of defense against sudden pH swings in the fluid around our cells.

So they react immediately.

Instantly.

They act like sponges, soak up extra H plus if it gets too acidic, or release H plus if it gets too alkaline.

Immediate correction.

But the source says they get consumed.

What does that mean?

Good point.

It means they're a fast fix, but kind of temporary.

Once a buffer molecule reacts with an H plus ion, it's, well, used up for the moment.

So the body's a bit vulnerable until the other systems, the lungs and kidneys, can step in for the longer term fix and help replenish things.

Buffers also shuttle excess H plus ions to the lungs.

Okay.

Fast fix, temporary, and they transport.

What are the main buffer systems we need to know?

The chapter highlights a few key ones in the extracellular fluid.

First, there's the hemoglobin system.

Inside red blood cells.

Hemoglobin?

Like, for oxygen transport?

Yeah, same molecule.

It uses something called the chloride shift.

Chloride ions move in or out of the red blood cell, depending on oxygen, and bicarbonate ions move the opposite way.

It helps buffer the blood.

Wow.

Okay.

Complex.

What else?

Then there's the plasma protein system.

Works with the liver.

The proteins floating in our blood plasma can grab or release H plus ions as needed, like molecular sponges.

Okay.

Grabbing and releasing H plus carbon makes sense.

Then the big one.

The carbonic acid bicarbonate system.

The source calls this the primary buffer system in the whole body.

The primary one.

Why is it so important?

Because it's the main player keeping our blood pH right around 7 .4.

It does this with a very specific ratio, 20 parts bicarbonate.

That's HgO3 to one part carbonic acid, H2CO3.

20 to one.

That specific ratio is the key.

That 20 .1 ratio is critical.

It dictates the H plus concentration.

Like a seesaw.

Got to keep it balanced.

How does the body maintain that exact 20 .1 ratio?

This is where the lungs and kidneys really shine.

The lungs control the carbonic acid part by adjusting how much CO2 we breathe out.

Remember, carbonic acid breaks down into CO2 and water.

So breathe faster and deeper, you blow off more CO2, less carbonic acid.

The kidneys on the other hand manage the bicarbonate.

They can choose to keep it or get rid of it, depending on what the body needs.

So lungs carbonic acid control via CO2.

Kidneys bicarbonate control.

Got it.

Is there one more buffer system?

Yep.

The phosphate buffer system.

Found inside cells and in body fluids, especially active in the kidneys.

It works similarly to bicarbonate neutralizing excess H plus ions.

So buffers are the quick responders.

First line.

Now the lungs.

How do they fit into this balancing act?

Lungs are the second line in defense.

And like we just touched on, they work super closely with the buffer systems, especially carbonic acid bicarbonate.

Their main job is controlling carbonic acid by managing CO2 exhalation through breathing rate and depth.

So if things get too acidic, acidosis.

Right.

If pH drops, the lungs kick in, you start breathing faster and deeper.

Hyperventilation basically, to blow off more CO2.

Getting rid of CO2 reduces carbonic acid.

Helps use up those extra H plus ions, nudges the pH back up.

And if it's too alkaline, alkalosis.

Opposite happens.

Breathing slows down, becomes more shallow.

Hyperventilation.

You retain CO2.

Bullying onto CO2 means more carbonic acid forms.

Yep.

Helps neutralize the excess base, brings the pH back down.

It's really quite something how just changing our breathing pattern has such a direct chemical effect.

It absolutely is.

And it's reversible, quick adjustments.

But it's important to remember the lungs mainly handle H plus tied to carbonic acid.

Other types of acid buildup.

That's more a job for the kidneys.

Okay.

Lungs are relatively fast, target carbonic acid.

Now the kidneys, we know they do a lot, but how do they specifically regulate acid base?

Kidneys offer a, let's say, more comprehensive fix.

But they're slower.

It takes hours, even days, for their effects to really show.

Slower but maybe more thorough.

Definitely more thorough and selective than buffers or lungs.

So doing acidosis with too much H plus K, the kidneys secrete those excess H plus ions into the tubules.

Okay.

There they combine with buffers in the urine like phosphate and get fleshed out.

Enduring alkalosis, too much bicarbonate.

Kidneys reverse it.

Excess bicarbonate ions move into the tubules, combine with sodium, and out they go in the urine.

They also selectively regulate bicarbonate in the blood.

They can make more or conserve it, excreting H plus to keep that 20 .1 ratio stable long term.

The chapter also mentions phosphoric acid and ammonia.

How do they fit in?

Right.

Kidneys can also excrete excess H plus as phosphoric acid.

And they can make ammonia from amino acids in the tubules.

This ammonia grabs H plus ions to form ammonium, which is then excreted.

Another way to ditch excess acid.

Wow.

The kidneys are really sophisticated regulators, even if they take their time.

Okay.

One more player mentioned.

Potassium.

How does potassium connect to all this?

Ah, this is a really critical connection.

Potassium plays a big role through exchange.

The body shifts H plus ions in or out of cells to help balance pH.

And potassium often moves in the opposite direction.

It's called transcellular shifting.

Like a swap meet at the cell membrane?

Kind of, yeah.

So in acidosis, lots of H plus in the blood.

Some H plus moves into cells to get out of the bloodstream.

To keep things electrically balanced, potassium moves out of the cells into the blood.

Which increases potassium in the blood.

Exactly.

Can lead to hyperkalemia, high serum potassium.

And an alkalosis?

The reverse.

H plus moves out of cells into the blood to lower the pH.

So, potassium moves into the cells.

Leading to low potassium in the blood?

Potentially, yes.

Hypokalemia.

So, you absolutely have to monitor potassium levels when there's an acid -base imbalance.

It's a key takeaway.

Definitely noted.

Okay, we've got the regulators down.

Now, what happens when things go wrong?

Let's talk imbalances, starting with respiratory acidosis.

What is that?

Respiratory acidosis means there's relatively too much H plus because the buffer base is low.

The core problem is ventilation.

The lungs aren't getting rid of CO2 efficiently enough.

And what causes that?

The chapter lists quite a few things.

Yeah, box 9 -1 mentions things like asthma, atelectasis collapsed, lung tissue brain trauma affecting breathing control,

chronic lung diseases like bronchitis or emphysema, anything

central nervous system, just plain hypoventilation, pneumonia, pulmonary edema, basically anything hindering good gas exchange.

How might someone look if they have this?

How does the body try to fix it initially?

Well, the body tries to compensate.

You might see them breathing faster and deeper initially, trying hard to blow off that extra CO2, but often it's not enough.

So what are the key nursing actions for respiratory acidosis?

Priority one is always monitoring their breathing.

Watch for distress.

Give oxygen as ordered.

Position them upright.

Semi -fouled helps.

Encourage coughing, deep breathing.

Hydration is important too.

It helps thin secretions.

And crucially,

avoid things that slow breathing further like tranquilizers, sedatives, strong pain meds like opioids,

respiratory treatments, maybe suctioning if needed.

Monitor electrolytes, it's supposed to be potassium,

antibiotics if there's infection and be ready for potentially needing in a debation and mechanical ventilation if it gets severe.

Like if CO2 climbs over 50 and they're in acute distress.

Very proactive.

Okay, flip side, respiratory alkalosis, what's going on there?

Here you have a deficit of carbonic acid, so H plus concentration decreases.

It's usually caused by hyperventilation, breathing too fast or too deep, blowing off too much CO2.

And the causes, box nine to two.

Things like fever, anxiety or hysteria leading to hyperventilation, hypoxia, low oxygen making you breathe faster,

being over ventilated by a machine, even pain can trigger it.

Anything that cranks up breathing beyond what's needed.

How does the body compensate here?

The kidneys try to help.

They'll hold on to H plus ions and start excreting more bicarbonate in the urine to try and bring the pH back down.

And nursing interventions for respiratory alkalosis.

Again, monitor breathing closely.

If anxiety is the cause, emotional support is key.

Breathing techniques can help like voluntary breath holding, maybe re -breathing some CO2 with a mask or if prescribed, a paper bag.

Right, to raise the CO2 level.

Exactly.

If they're on a ventilator, check those settings carefully.

Monitor electrolytes, potassium and calcium this time.

Low calcium can cause muscle spasms or tetany.

So calcium gluconate might be needed and of course treat the underlying reason for the hyperventilation.

Okay, that covers respiratory.

Now metabolic acidosis, what's the issue here?

With metabolic acidosis, the problem isn't primarily the lungs.

It's either losing too much bicarbonate, the buffer base or accumulating other kinds of acids in the body.

Either way, you end up with too much H plus ID.

What kind of things cause this?

Box nine to three.

Big one is diabetes, especially diabetic ketoacidosis, DKA.

You get acid buildup from fat breakdown when insulin is low.

Also too much aspirin, high fat diets, core carb metabolism, malnutrition, kidney failure because kidneys can't regulate acid properly and severe diarrhea, which causes significant bicarbonate loss.

How does the body try to compensate for metabolic acidosis?

The lungs try to help by blowing off CO2.

You often see hyperpnea fast, deep breathing.

A classic sign is cosmos respirations, really deep, regular, rapid breaths.

It's a body's attempt to lower CO2 and raise pH.

And nursing interventions.

Monitor for breathing problems, check their level of consciousness.

Severe acidosis can depress the CNS, track intake and output, manage fluid electrolyte replacement,

safety, maybe seizure precautions.

Monitor potassium closely can actually drop as acidosis corrects itself.

Right, because it shifts back into cells.

For DKA specifically, it's insulin, fluids, electrolytes, watching for circulatory collapse.

For kidney disease, maybe dialysis, special diet, low protein, high calorie.

Got it.

Last one, metabolic alkalosis.

What's the story here?

Metabolic alkalosis is a deficit of acid or too much base, so low H plus concentration.

It happens from accumulating bicarbonate or losing a lot of acid.

And the causes,

box nine to four.

Things like diuretics, lots of vomiting or GI suctioning, losing stomach acid,

hyperoldosteronism, taking too much sodium bicarbonate or even massive blood transfusions because the citrate preservative gets converted to bicarbonate.

How does the body compensate for this one?

The lungs try to compensate by slowing down breathing, decreased rate and depth, trying to hold onto CO2 to form more carbonic acid and lower the pH.

And the nursing intervention.

Monitor breathing, watch potassium and calcium levels, safety precautions, meds or IV fluids might be given to help the kidneys excrete bicarbonate.

Be ready for potassium replacement.

And like always, treat the underlying cause.

Okay, we've covered the four big imbalances.

Now arterial blood gases, ABGs, hugely important, right?

Absolutely crucial.

ABGs give you that direct look at pH, CO2, bicarbonate and oxygen levels in arterial blood, essential for diagnosing and tracking these imbalances.

The chapter details assisting with collection.

It starts with vital signs, but then emphasizes the Allen's test.

What is that and why is it so critical?

The Allen's test is a non -negotiable safety step before you stick the radial artery, which is the usual spot for an ABG draw.

It checks if the ulnar artery provides enough blood flow to the hand on its own.

Why check the ulnar artery?

Because if something goes wrong during the radial puncture, say the artery gets damaged, you need assurance that the ulnar artery can still supply the hand adequately.

Otherwise, the hand could suffer serious damage from lack of blood flow,

ischemia.

So how do you do it properly?

Okay, first explain it to the patient.

Then you press down firmly on both the radial and ulnar arteries at the wrist.

Have the patient make a fist several times, the hand should go pale, blanch.

Then came pressure on the radial artery, but release the ulnar artery pressure.

Watch the hand.

Color should return the pinkness within about six to seven seconds.

And if it takes longer?

If it takes longer, that means the ulnar circulation isn't good enough.

You absolutely cannot use the radial artery on that wrist.

Document it, tell the RN and the provider immediately.

You need to find another site, brachial or femoral artery.

Wow, okay.

That test is incredibly important for safety.

What else affects ABG accuracy?

Things like recent changes in oxygen settings,

suctioning within the last 20 minutes or so.

Even the patient's activity level right before the draw can skew results.

Anxiety can affect breathing, so keeping the patient calm helps.

And the sample collection itself, specifics.

You need a special heparinized syringe.

After the draw, apply firm pressure to the site for at least five minutes, maybe 10 minutes, if they're on anticoagulants, prevent bleeding, heutentoma.

You also need to record the patient's temperature and their current oxygen setup on the lab form.

That info helps the lab interpret the results correctly and the sample itself.

Needs to be labeled correctly and transported on ice immediately.

Keeps the gases from changing in the sample.

Okay, got the sample, got the results.

How do we interpret them?

Respiratory versus metabolic.

For respiratory problems, look at the pico -2.

It usually has an opposite relationship with pH.

So if pH is high, alkalosis, pito -2 is usually low.

If pH is low, acidosis, pico -2 is usually high.

Opposite.

pH up, pico -2 down equals respiratory alkalosis.

pH down, pico -2 up is respiratory acidosis.

Okay,

metabolic.

For metabolic, look at the bicarbonate, the HCO -3.

It usually has a corresponding relationship with pH.

So if pH is high, alkalosis, bicarb is usually high, too.

If pH is low, acidosis, bicarb is usually low, too.

Corresponding.

pH up, bicarb up, metabolic alkalosis.

pH down, bicarb down, a metabolic acidosis.

Got it.

The chapter has those pyramid steps, too.

Can you quickly run through those?

Yeah, box nine to five.

Step one, look at the pH.

Is it high alkalosis or low acidosis?

Step two, look at the pico -2.

Is it opposite to the pH change?

Yes, it's likely respiratory.

If not, go to step three.

All right.

Step three, look at the bicarbonate, HCO -3.

Does it correspond with the pH change?

If yes, it's likely metabolic.

Simple steps.

What are the normal ABG values again?

Table nine to three.

Normal pH, 7 .35 to 7 .45.

Normal pico -2, 35 to 45 millimil HT.

Normal bicarbonate, HCO -3.

21 to 28 milli QL.

Normal powa tube, oxygen.

80 to 100 millimilo HT.

But remember, altitude can affect that powa tube.

And table nine to four just summarizes how these change in the different imbalances.

Okay.

And that critical thinking scenario on page 87, the Allen's test, where color takes 20 seconds to return.

Yeah, 20 seconds is way too long.

Normal is six, seven seconds.

It signifies insufficient ulnar circulation.

Big red flag.

So the action is?

Don't use that radial artery.

Report the finding immediately to the RN and notify the provider.

They need to choose a different site for the ABG draw.

Safety first.

Absolutely.

Lastly, the practice questions.

Let's hit a few highlights to reinforce things.

Maybe define terms if needed.

Okay.

Question 46 gives pH 7 .55, bicarb 22, betho 30.

High pH, low pitho, that's respiratory alkalosis.

So you'd encourage slower breathing to retain CO2.

Makes sense.

Question 48 asks the purpose of the Allen's test.

Oh, we know that.

It's to check the ulnar artery circulation for collateral flow.

Question 49, patient with NG tube suction.

Risk four.

Metabolic alkalosis.

You're suctioning out stomach acid, hydrochloric acid.

Losing acid makes you more alkaline.

Question 50, severe diarrhea.

Risk four.

Metabolic acidosis.

Diarrhea means losing lots of bicarbonate from the gut.

Loss of base leads to acidosis.

Question 51, DKA patient with deep regular rapid breathing.

What's that called?

That specific pattern is Cussmalls respirations.

It's distinct from just hyperapnea, fast deep breathing, bradypnea, slow breathing, apnea, no breathing, or chain stokes, that cyclic pattern.

Cussmalls is the body's attempt to blow off CO2 in metabolic acidosis like DKA.

Good distinction.

Question 52, COPD patient.

Most likely imbalance.

Respiratory acidosis.

COPD impairs CO2 removal, so CO2 builds up.

Increasing carbonic acid and lowering pH.

Question 54, respiratory alkalosis.

What other lab might be abnormal?

Low potassium, like 3 .0 Meql.

Remember that shift.

H plus leaf cells and alkalosis.

K plus enter cells, lowering serum potassium, hypokalemia.

Tetany has muscle spasms from low calcium, which can sometimes happen with alkalosis, but low potassium is a more direct expected finding.

Right.

And 55, which AVGs show respiratory acidosis.

You need low pH and high pico -2.

So pH 7 .25 acidosis and pico -2, 50 millimillihg, high CO2, fits the bill.

Perfect.

That really helps tie it all together.

Yeah, working through those questions definitely reinforces how to apply the concepts.

So there we have it, a really thorough deep dive into Chapter 9 from the Saunders Review, covering acid -base balance from top to bottom.

We hit the regulators' buffers, lungs, kidneys, the imbalances, acidosis and alkalosis, both respiratory and metabolic.

Their causes, signs, interventions.

The importance of AVGs, how to assist with collection safely, including that critical Allen's test, how to interpret the results.

Plus key nursing concepts, safety points, priorities, and we walk through those practice questions.

We aim to cover everything in the chapter.

We really did.

We didn't skip any sections.

OK, so here's something to think about.

Consider just how precisely your body maintains this acid -base equilibrium constantly, without you even noticing.

What other automatic processes inside you might be way more interconnected and complex than we usually realize?

It's definitely food for thought.

The body's interconnectedness is just incredible, always striving for balance.

Thanks so much for joining us on this deep dive.

We hope this gave you a really solid, clear understanding of this vital piece of physiology.