What’s up fellow AMBOSSians! I’m Dr. Zeb, back with another question walkthrough in which
we’re going to review test-taking strategies and important high-yield concepts involving nocturnal
dyspnea, congestive heart failure, reading ABGs, and a bunch of integrated pathophysiology.
Some of these concepts are guaranteed to be tested on your board exams.
I know your time is limited, so let's get to it!
I first like to determine my task by reading the lead-in.
“Which of the following is the most likely underlying
cause of this patient’s current condition?”
Ok, now I’m ready for a pathophysiology question,
so we first need to determine the patient’s diagnosis.
Now, as I’ve explained in other videos, to save time,
I like to read the sentence before to look for confirmatory findings.
“Echocardiography shows a left ventricular ejection fraction of 55%.”
Alright, this matches a normal reading between 50 and 75%, but we should keep in mind that
ejection fraction is preserved. Without any findings to build up
some differentials, let’s read from the top and highlight key info to keep track of it.
This is especially important for shelf,
Step 2 and 3 questions, which often have massive walls of text.
Remember: Usually, only a few pieces of info are all
that are needed to actually answer the question.
Now, yes, highlighting is important, but we need to be efficient and smart about it.
Many years ago, when I first started studying for my Steps, my stems would
often look like the yellow-brick road. I was pretty much Dorothy from the Wizard of Oz.
Highlighting so much actually hurt me since I had a lot of unimportant info included,
which took extra time to process and often confused me.
So I had to learn to control myself and not highlight every little piece of info,
but to focus on the differentiating info, similar to a real clinical scenario actually.
This is one of the reasons we made the key info feature in AMBOSS questions.
It can help train you in identifying what is most important to answer the question correctly.
Now back to the question: “A 68-year-old man comes to the emergency department
because of a 1-week history of worsening bouts of shortness of breath at night.”
Alright, time to put on our thinking caps.
The question writers added a somewhat specific clue here already - shortness
of breath at night - so nocturnal. When clinically reasoning, it’s important
to consider such contrasting descriptors, often referred to as semantic qualifiers.
This is enough to start forming some differentials, including:
pulmonary conditions such as asthma or COPD, cardiovascular like CHF (especially left-sided),
obstructive conditions like sleep apnea, and possibly panic disorder.
Let’s keep these in mind as we continue on,
“He has had a cough for 1 month, occasionally productive of frothy sputum.”
Ok, here’s another key feature, so break out those illness scripts!
Which of these differentials classically causes a cough with frothy sputum?
That’s right! Left-sided CHF
That’s great that we had it memorized by heart… ha, get it… because the heart is….
beep...
But it’s important to understand why,
so we can remember and apply this knowledge better! Let’s dive deeper now.
What happens at night?
People lie down to sleep! Gravity is no longer pulling blood down into the lower extremities
and possibly causing some edema. So the body both redistributes blood volume from the lower
extremities and reabsorbs any excess fluid, increasing the total volume in circulation.
For a healthy heart, this is no big deal. But in CHF, the heart is already struggling
to maintain sufficient cardiac output - it can’t keep up with the excess volume.
In the case of left-sided failure, it backs up into the pulmonary circulation,
leading to elevated pulmonary capillary wedge pressure and pulmonary venous congestion,
and fluid can leak out into the lungs, causing pulmonary edema, dyspnea, and sputum.
If this occurs after an hour or 2 of sleeping, it’s known as paroxysmal nocturnal dyspnea.
In extreme cases, if dyspnea occurs right after lying down, it’s known as orthopnea.
These patients will report relief by sitting up or by sleeping in a more
upright position, for example with extra pillows or even in a chair.
Other mechanisms, such as a depressed respiratory center or adrenergic activity,
may also play a role, but these are less understood and go beyond the scope of your exams.
Already having a diagnosis in mind will help us focus on the
most important info to solidify our hypothesis.
Also, we can’t completely rule out a pulmonary condition like COPD yet,
since a productive cough can occur, so let’s keep that in mind just in case.
“He has type 2 diabetes mellitus and long-standing hypertension.
Two years ago, he was diagnosed with Paget
disease of bone during a routine health maintenance examination.
He has smoked a pack of cigarettes daily for 20 years.
His temperature is 37.0°C (98.6°F), pulse is 110/min, respirations are 25/min,
and blood pressure is 145/98 mm Hg. Current medications include metformin,
alendronate, hydrochlorothiazide, and enalapril. Physical examination shows bibasilar crackles.”
What could this indicate? Pulmonary edema, which matches left-sided failure.
“Cardiac examination shows a dull,
low-pitched sound during late diastole that is best heard at the apex.”
What does this describe? That’s right, an S4 sound - more on this later.
“There is no jugular venous distention or peripheral edema.
Arterial blood gas analysis on room air shows:”
For acid-base disorders, what do we do first? Determine if acidosis or alkalosis
The pH of 7.46 is just above the normal range of 7.35-7.45, so mild alkalosis
What’s next? Determine if respiratory or metabolic. Already the increased respiratory
rate indicates respiratory. But a pCO2 of 29 is lower than the normal range of 35 to 45,
meaning CO2 is being blown out more than normal, so this is respiratory.
Finally, if we want to know if it’s compensated, we look at? Bicarbonate - a buffering conjugate
base that binds excess protons. If we already have an alkaline environment, do you think the body
wants to keep a base around? No, of course not. So we would expect bicarbonate to decrease below 22
to 28, like here with 20, as the kidney excretes it to compensate, typically within a few days.
So the ABG shows compensated primary respiratory alkalosis due to hyperventilation.
Now, to summarize, this patient with a history of long-standing hypertension
has paroxysmal nocturnal dyspnea, a cough productive of frothy sputum,
an S4 heart sound, bibasilar crackles and hyperventilation (suggesting pulmonary edema),
which all indicate acute left heart failure with a normal LVEF of 55%.
So to finish the intermediate step, what’s this patient’s current condition?
Heart failure with preserved ejection fraction, or HFpEF.
I don’t know why, but I like saying that: HFpEF, HFpEF.
Now to answer the question, which of these options contributes to HFpEF?
Impaired myocardial relaxation is correct.
But why is that? Thinking back on our
pathophysiology, how does chronic hypertension affect afterload? It increases it! Remember,
this is the pressure that the left ventricle is pumping against. So if the left ventricle
is having to contract harder to overcome the increased pressure and maintain cardiac output,
what happens to the myocardium over time?
It grows - similar to a bodybuilder’s muscles when lifting more and more weight.
This is known as hypertrophy. More specifically, this thickening of the myocardial wall is called
concentric hypertrophy rather than eccentric, in which the heart increases in size due to dilation.
For concentric, remember compact; for eccentric, remember expand.
There’s likely also some ischemia and fibrosis occurring.
So what happens when the left ventricle wall thickens?
It becomes stiffer, meaning myocardial compliance is reduced and myocardial relaxation is impaired.
What does this do to the end-diastolic pressure and ventricular filling?
The pressure increases and diastolic filling is reduced, leading to diastolic heart failure,
despite a normal ventricular contraction as indicated by the normal EF.
An S4 gallop can arise as the left atrium pumps blood against the noncompliant left ventricle
in late diastole. Symptoms are especially prominent during exertion or tachycardia,
when the ventricle has even less time for filling.
Notice when reviewing this, we’re making mental checkpoints to connect the dots
as we recall the mechanisms. This is a form of elaboration,
which has been shown by learning science to significantly improve learning
and your ability to recall. I highly recommend this as a study technique.
And now, most importantly, what do you call a vegetable that has heart failure?
A hearti-choke….
As you know from my other videos, it’s also important to briefly review
the other options to further connect concepts, strengthen your knowledge,
and identify any gaps, so let’s check them out.
In what condition do we see the destruction of alveolar walls?
Emphysema, a subtype of COPD, which would match the history of long-term smoking,
shortness of breath, and productive cough. But for emphysema, we’d expect reduced lung sounds
on auscultation. In addition, COPD would not explain this patient's S4 heart sound,
and we’d see respiratory acidosis - not alkalosis - due to CO2 retention.
Decreased myocardial contractility was a good consideration, since it's also
a pathophysiologic change in heart failure - but with reduced ejection fraction - or HFrEF.
This commonly occurs with dilated cardiomyopathy or after myocardial infarction. But this patient's
cardiac output is preserved, and despite having risk factors for coronary artery disease (such
as diabetes mellitus, hypertension, and older age), he has no signs of an MI.
Diuretic overdose causes volume depletion, which activates the renin-angiotensin-aldosterone
system (RAAS). Aldosterone then acts on the renal tubules to reabsorb sodium
and excrete potassium and hydrogen, resulting in metabolic alkalosis - not respiratory.
This patient also doesn’t have any notable signs of volume depletion like thirst,
decreased skin turgor, or dry mucous membranes.
Myxomatous degeneration is the most common cause of mitral valve prolapse.
Although severe MVP could eventually lead to heart failure and pulmonary venous congestion
due increased left atrial pressure, this patient doesn’t have typical signs of MVP like chest pain,
palpitations and anxiety, or a high-frequency, midsystolic click heard in the mitral region.
Now this is an interesting option. Because this patient was recently diagnosed with
Paget disease of the bone, he’s at increased risk of developing
systemic arteriovenous fistulas, which can lead to high output cardiac failure.
This rare complication results from the increased vascularity within the abnormal bone
that is undergoing high rates of remodeling. High-output cardiac failure manifests with
features of hyperdynamic circulation such as bounding pulses with a quick upstroke,
subungual capillary pulsations, and venous hums, none of which was reported.
Continuing our reflective practice, let’s briefly consider what other questions could
appear on the exam for a stem like this. Other correct options could have been:
Chronic hypertension
Concentric hypertrophy or any of the consequences we talked about
including elevated left ventricular filling pressures or reduced ventricular filling
They could have just asked for the diagnosis: HFpEF
Note that impaired myocardial relaxation could
have also been correct for another type of cardiomyopathy known as restrictive,
in which the ventricular walls harden but without myocardial hypertrophy.
It’s very beneficial to proactively consider other associations like this so you solidify
your knowledge and you're more prepared on the exam day.
You can read more about congestive heart failure in this AMBOSS article.
So to recap, the key takeaways of this question are:
Formulate differentials for paroxysmal nocturnal dyspnea and know their pathophysiology.
Identify CHF based on common findings, including a history of long-standing
hypertension and signs of pulmonary edema, including paroxysmal nocturnal dyspnea,
a cough productive of frothy sputum, and bibasilar crackles.
And know the types of CHF according to the EF and the associated pathophysiology,
including concentric hypertrophy leading to preserved EF
but diastolic heart failure due to reduced myocardial relaxation and filling.
And as a bonus takeaway: Interpret ABGs to diagnose acid-base disorders by first determining:
If pH is acidic or basic.
Then if respiratory or metabolic based on the pCO2.
And lastly, if compensated based on bicarbonate.
And that concludes this complex question walkthrough - some of these very high
yield topics that will appear on your exam, so I hope you’ve found it helpful.
After getting a lot of positive feedback from the first couple of videos, which I hope you'll check
out, I’m happy to say I’ll continue creating these regularly and extend out into some new styles in
the future. This will all be launched in a new AMBOSS playlist. So subscribe if you want more,
and give the videos a thumbs up or comment if you find them helpful or have any questions.
I’ll also start releasing short highlights from these videos and bonus content in my
social media channels, which you can find in the description below if you’re interested in more.
A lot of you are approaching or in your dedicated study period. I know it’s a challenging time.
It was one of the most difficult yet rewarding in my life.
So keep it up - it will pay off - and stay positive.
You’ve got this.