Help: How can left-sided hypertrophy coexist with hypertension?

[pizza100]

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Can someone explain how a patient can have left-sided hypertrophy of the heart along with hypertension?

I thought: left ventricular hypertrophy --> reduced ventricular filling --> reduced stroke volume --> reduced cardiac output --> decreased blood pressure --> no hypertension.

In some of the cases I read, they don't mention heart rate or peripheral resistance, yet they say the patient has left ventricular hypertrophy and hypertension. So, do I have to assume that the heart rate and peripheral resistance are high for that patient? Even if heart rate and peripheral resistance are high, if the ventricular hypertrophy is severe enough, the hypertension should go away, right?

 

[Bacchus]

LVH is a side effect of systemic hypertension. Because there's increased resistance to bloodflow because of the hypertension, left heart ventricle has to remodel and become hypertrophied to push out the blood.

 

[StIGMA]

Ignoring your lack of understanding, your question depends on the magnitude of the decrease in blood pressure. Why would a subtle decrease in blood pressure (say, 10mmHg) cure severe hypertension? Moreover, hypertension is a cause of LVH. You expect hypertension to cure itself by remodeling the heart? Hypertension is caused by many other things, especially peripheral vascular resistance...

 

[pizza100]

Why would a subtle decrease in blood pressure (say, 10mmHg) cure severe hypertension? Moreover, hypertension is a cause of LVH. You expect hypertension to cure itself by remodeling the heart?

I don't expect the decrease in blood pressure due to LVH to be subtle. What if it's so severe that there's very little blood in the left ventricle each time it's filled? Wouldn't that result in dramatic reduction in flow rate and blood pressure?

Yes, I expect hypertension to cure itself when the heart is remodeled so severely. I have a feeling that I am wrong, but I like to know why I am wrong.

I know hypertension causes left ventricular hypertrophy. I just don't understand why LVH wouldn't correct the hypertension.

Thanks Stigma and Bacchus for the replies.

 

[GadRads]

I
I know hypertension causes left ventricular hypertrophy. I just don't understand why LVH wouldn't correct the hypertension.

As someone mentioned above, it's generally an issue with total peripheral resistance. Imagine a case in which the arteries are constricted due to some pathology (atherosclerosis, for example). Although LVH might increase cardiac output, the arterial lumen is still narrowed despite this increase, such as in increased afterload. In this instance, hypertrophy may even worsen hypertension barring some kind of baroreceptor reflex.

 

[BigRedBeta]

Can someone explain how a patient can have left-sided hypertrophy of the heart along with hypertension?

I thought: left ventricular hypertrophy --> reduced ventricular filling --> reduced stroke volume --> reduced cardiac output --> decreased blood pressure --> no hypertension.

And that would be the definition of heart failure...and past a certain point, cardiogenic shock.

The flaw in your understanding is that you're ignoring the other components that go into your blood pressure and cardiac output, and most importantly that the body doesn't like drops in cardiac output.

This is why it's important to understand the relationships between all of those cardiac equations taught in the pre clinical years:

BP=CO x SVR
CO= Stroke volume x HR
Stroke volume determined by Preload, Afterload and contractility (the relationships are less easily expressed, but you need to have a conceptual understanding of the relationships and how the heart will respond).


Go through these sequentially, remembering that cardiac output has to be maintained.

Grossly simplified pathophys
systemic HTN = increased afterload -> cardiac hypertrophy to increase contractility-> stiff ventricle = decreased preload-> decreased stroke volume -> increased HR TO MAINTAIN CARDIAC OUTPUT -> continued HTN

Meanwhile at the same time, other neurohormonal compensatory mechanisms are at play including Renin-Angiotensin, Aldosterone and catecholamine secretion.

The crux of heart failure cardiology is managing this interaction to maintain cardiac output. Critical care goes a step further and can actually alter the demand for cardiac output in addition to affecting CO itself.

 

[JGimpel]

Please excuse my sleep-deprived brain if I miss something basic.

Think of it like creating an onion, but from the outside in. The more layers of onion you create on the inside, the less space you have in there for anything else. Your myocardium reacts the same way, then does whatever it can to keep the most oxygenated blood going to the rest of the body; including increasing the heart rate to keep up the same cardiac output the body is used to.

Just as making muscles work harder in the gym makes them grow larger, the myocardium in your heart hypertrophies, but from the outside in. You could consider this a very simplified version of remodeling. This cycle keeps repeating until the left heart fails to keep up with even the bare minimum oxygen needs for the organs in the body, one consequence of which can be multi-system organ failure.

Increasing PVR can only buy you so much, and remember that it reaches the right atrium first, then gets pushed through into the right ventricle, since atria aren't made to stretch much. Now you have the same problem with the right ventricle, the smaller and weaker of the two, not keeping up with the increased amount trying to pump enough oxygen poor blood into the lungs. The lungs get backed up too and this will create pulmonary hypertension which gets fed back into...the left ventricle and the cycle continues to worsen.

Beta-blockers decrease arterial blood pressure by reducing cardiac output and, in long-term use, also decrease the release of renin from the kidney. The heart doesn't work as hard and the arteries are more relaxed. ACE-Inhibitors lower arteriolar resistance and increase venous capacity thereby decreasing cardiac output like the beta blocker which then lowers stroke volume with the added benefit of lowering resistance in blood vessels in the kidneys. This is why you see them used in people with a history of MI and CHF.

I hope this helps.

 

[dienekes88]

Whoa whoa whoa.

Don't talk to me about LV hypertrophy without mentioning:

1. Volume Overload (Eccentric Hypertrophy) vs. Pressure Overload (Concentric Hypertrophy)
2. WALL STRESS and WALL TENSION
3. Filling pressures

LV Hypertrophy is a response to increased wall tension. Wall stress is maintained in the normal-ish range by increasing LV thickness. Law of LaPlace.

There are usually good physiology/pathophysiology reviews in Circulation.

Read. Read. Read some more. Then go read.

Please excuse my sleep-deprived brain if I miss something basic.

Think of it like creating an onion, but from the outside in. The more layers of onion you create on the inside, the less space you have in there for anything else. Your myocardium reacts the same way, then does whatever it can to keep the most oxygenated blood going to the rest of the body; including increasing the heart rate to keep up the same cardiac output the body is used to.

Just as making muscles work harder in the gym makes them grow larger, the myocardium in your heart hypertrophies, but from the outside in. You could consider this a very simplified version of remodeling. This cycle keeps repeating until the left heart fails to keep up with even the bare minimum oxygen needs for the organs in the body, one consequence of which can be multi-system organ failure.

Concentric hypertrophy, e.g. chronic hypertension, aortic stenosis.

Increasing PVR can only buy you so much, and remember that it reaches the right atrium first, then gets pushed through into the right ventricle, since atria aren't made to stretch much. Now you have the same problem with the right ventricle, the smaller and weaker of the two, not keeping up with the increased amount trying to pump enough oxygen poor blood into the lungs. The lungs get backed up too and this will create pulmonary hypertension which gets fed back into...the left ventricle and the cycle continues to worsen.

Whoa. Where did the discussion of Pulmonary Vascular Resistance come from. If you're going to mention that, please at least mention pulmonary hypertension and include a discussion of the WHO Groups (Evian classification and Dana Point update). You're referencing WHO Group II pHTN, aka Pulmonary Venous Hypertension.

Beta-blockers decrease arterial blood pressure by reducing cardiac output and, in long-term use, also decrease the release of renin from the kidney. The heart doesn't work as hard and the arteries are more relaxed. ACE-Inhibitors lower arteriolar resistance and increase venous capacity thereby decreasing cardiac output like the beta blocker which then lowers stroke volume with the added benefit of lowering resistance in blood vessels in the kidneys. This is why you see them used in people with a history of MI and CHF.

I hope this helps.

Also blockade of chronic sympathetic activation and reduction in myocardial oxygen demand.

And that would be the definition of heart failure...and past a certain point, cardiogenic shock.

Definition of heart failure: clinical syndrome in which the heart is unable to meet the metabolic demands of the body or has to do so with elevated filling pressures.

The flaw in your understanding is that you're ignoring the other components that go into your blood pressure and cardiac output, and most importantly that the body doesn't like drops in cardiac output.

This is why it's important to understand the relationships between all of those cardiac equations taught in the pre clinical years:

BP=CO x SVR
CO= Stroke volume x HR
Stroke volume determined by Preload, Afterload and contractility (the relationships are less easily expressed, but you need to have a conceptual understanding of the relationships and how the heart will respond).


Go through these sequentially, remembering that cardiac output has to be maintained.

Grossly simplified pathophys
systemic HTN = increased afterload -> cardiac hypertrophy to increase contractility-> stiff ventricle = decreased preload-> decreased stroke volume -> increased HR TO MAINTAIN CARDIAC OUTPUT -> continued HTN

Meanwhile at the same time, other neurohormonal compensatory mechanisms are at play including Renin-Angiotensin, Aldosterone and catecholamine secretion.

The crux of heart failure cardiology is managing this interaction to maintain cardiac output. Critical care goes a step further and can actually alter the demand for cardiac output in addition to affecting CO itself.

Cardiac hypertrophy maintains normal-ish wall stress.

Decreased SV and CO also results in a non-osmotic impetus for ADH secretion and volume retention

 

[JGimpel]

Whoa whoa whoa.

Don't talk to me about LV hypertrophy without mentioning:

1. Volume Overload (Eccentric Hypertrophy) vs. Pressure Overload (Concentric Hypertrophy)
2. WALL STRESS and WALL TENSION
3. Filling pressures

LV Hypertrophy is a response to increased wall tension. Wall stress is maintained in the normal-ish range by increasing LV thickness. Law of LaPlace.

There are usually good physiology/pathophysiology reviews in Circulation.

Read. Read. Read some more. Then go read.



Concentric hypertrophy, e.g. chronic hypertension, aortic stenosis.



Whoa. Where did the discussion of Pulmonary Vascular Resistance come from. If you're going to mention that, please at least mention pulmonary hypertension and include a discussion of the WHO Groups (Evian classification and Dana Point update). You're referencing WHO Group II pHTN, aka Pulmonary Venous Hypertension.



Also blockade of chronic sympathetic activation and reduction in myocardial oxygen demand.



Definition of heart failure: clinical syndrome in which the heart is unable to meet the metabolic demands of the body or has to do so with elevated filling pressures.



Cardiac hypertrophy maintains normal-ish wall stress.

Decreased SV and CO also results in a non-osmotic impetus for ADH secretion and volume retention

Looks like a discussion that was meant to be helpful to some medical students got me into a pissing match with a bored resident. I could have said to read Harrison's to get the answers, but took the time to put it in more simplified terms. The rest can decide whose posts are more helpful. You can decide not to be so condescending to others. I can read uptodate and a Chen book too, I just thought explaining it in less technical terms would help.

Please continue to teach us cardiac physiology, oh enlightened resident. This (apparently) non-enlightened resident that tried to help will now bow in your in your grandeur just before I wire up a subclavian.

Enjoy your evening, med students. Don't worry, not all residents are this arrogant. Please check out the many gunner threads on SDN this week for more information.

 

[Doctor Bob]

Whoa. Where did the discussion of Pulmonary Vascular Resistance come from. If you're going to mention that, please at least mention pulmonary hypertension and include a discussion of the WHO Groups (Evian classification and Dana Point update). You're referencing WHO Group II pHTN, aka Pulmonary Venous Hypertension.

Remember to target your response to your audience. The OP is a 2nd year medical student...
At this point most schools are still going through basic pathophysiology and haven't ventured too far into things like the WHO Groups... that tends to get introduced during 3rd/4th years because they are more important to treatment than basic underpinnings of the disease process.

Looks like a discussion that was meant to be helpful to some medical students got me into a pissing match with a bored resident. I could have said to read Harrison's to get the answers, but took the time to put it in more simplified terms. The rest can decide whose posts are more helpful. You can decide not to be so condescending to others. I can read uptodate and a Chen book too, I just thought explaining it in less technical terms would help. Please continue to teach us cardiac physiology, oh enlightened resident. This (apparently) non-enlightened resident that tried to help will now bow in your in your grandeur just before I wire up a subclavian. Enjoy your evening, med students. Don't worry, not all residents are this arrogant. Please check out the many gunner threads on SDN this week for more information.

And you missed your opportunity to take the high road. Teaching is a learned skill also; dienekes88 would benefit more from helpful suggestions on how to improve his/her teaching methods.

 

[dienekes88]

Looks like a discussion that was meant to be helpful to some medical students got me into a pissing match with a bored resident. I could have said to read Harrison's to get the answers, but took the time to put it in more simplified terms. The rest can decide whose posts are more helpful. You can decide not to be so condescending to others. I can read uptodate and a Chen book too, I just thought explaining it in less technical terms would help.

Please continue to teach us cardiac physiology, oh enlightened resident. This (apparently) non-enlightened resident that tried to help will now bow in your in your grandeur just before I wire up a subclavian.

Enjoy your evening, med students. Don't worry, not all residents are this arrogant.

What is a Chen book, and you should go beyond UpToDate, though I will admit it is usually an excellent overview. We as residents still have to read and re-read. And then go on and broaden our knowledge with a review of the primary literature.

Don't act so butt hurt, man. There is no pissing match. Only education. This is one of the primary issues with training today. You can't correct an intern or resident without some complaint of being condescending or arrogant.

Med students need the exposure to the technical terms, because that is the language that we use to discuss patients. Don't dumb it down for their supposed benefit.

 

[dienekes88]

Remember to target your response to your audience. The OP is a 2nd year medical student...

I both agree and disagree.

They gotta learn it at some point. Best to see it first as a medical student.

Is it more detail than necessary? Probably, but it is a clinical application of physiology that helps the students make the jump from pre-clinical basic science to the ward.

Regarding teaching methods: I do welcome suggestions.

 

[JGimpel]

What is a Chen book, and you should go beyond UpToDate, though I will admit it is usually an excellent overview. We as residents still have to read and re-read. And then go on and broaden our knowledge with a review of the primary literature.

Don't act so butt hurt, man. There is no pissing match. Only education. This is one of the primary issues with training today. You can't correct an intern or resident without some complaint of being condescending or arrogant.

Med students need the exposure to the technical terms, because that is the language that we use to discuss patients. Don't dumb it down for their supposed benefit.

Wow!

If you haven't read a Chen book to really know the ins and outs of cardiac physiology, then please don't act like a cardiologist. You may want to ask a cardiologist (or someone that has trained with them🙂) if he's ever heard of a Chen book. There's definitely more to learn from than uptodate, but that's a great place to start for medical students.

I always appreciated the Attendings that I rotated with in medical school that took the time to put a concept in terms I could understand than the lazy ones that just told me to go read. Maybe I'm the only one.

OK, this resident is taking the high road now.

 

[dienekes88]

Wow!

If you haven't read a Chen book to really know the ins and outs of cardiac physiology, then please don't act like a cardiologist. You may want to ask a cardiologist (or someone that has trained with them🙂) if he's ever heard of a Chen book. There's definitely more to learn from than uptodate, but that's a great place to start for medical students.

I always appreciated the Attendings that I rotated with in medical school that took the time to put a concept in terms I could understand than the lazy ones that just told me to go read. Maybe I'm the only one.

OK, this resident is taking the high road now.

Wouldn't want to be a cardiologist (or even mistaken for one), because that would require being an internist.

For my cardiac physiology, I read Hurst's The Heart. I know it's old school to read a textbook and not a review book, but that's my style. I encourage all students and residents to read text books, published reviews of topics, national guidelines, and the primary literature. Medicine is transitioning right now from self-directed study with the guidance of a senior to hand-feeding the juniors. This is not good. Seniors can't sit with their juniors and go over Sabiston page by page. The role of the senior is to provide a framework within which the details are filled by self-study.

You're not taking the high road if you're calling me lazy. You glossed over the fact that I mentioned most of the important concepts (wall stress, wall tension, concentric vs. eccentric hypertrophy, definition of heart failure, ADH secretion in heart failure, volume retention, chronic sympathetic stimulation, and myocardial oxygen demand) and how they related. I will admit that I didn't go into an exhaustive explanation, but see above: reading still has to happen. Put your ego aside for just one second and try to learn from someone else.

 

[Kaustikos]

Whoa whoa whoa.

Don't talk to me about LV hypertrophy without mentioning:

1. Volume Overload (Eccentric Hypertrophy) vs. Pressure Overload (Concentric Hypertrophy)
2. WALL STRESS and WALL TENSION
3. Filling pressures

LV Hypertrophy is a response to increased wall tension. Wall stress is maintained in the normal-ish range by increasing LV thickness. Law of LaPlace.

The overload in volume causes the increased stress which alleviates the tension. This causes the decreased resistance resulting in decreased PVR.

There are usually good physiology/pathophysiology reviews in Circulation.

Read. Read. Read some more. Then go read.

Concentric hypertrophy, e.g. chronic hypertension, aortic stenosis.

You're forgetting essential hypertension, chronic hypotension, mitral regurg, tricuspid regurg, pulmonary artery stenosis

Whoa. Where did the discussion of Pulmonary Vascular Resistance come from. If you're going to mention that, please at least mention pulmonary hypertension and include a discussion of the WHO Groups (Evian classification and Dana Point update). You're referencing WHO Group II pHTN, aka Pulmonary Venous Hypertension.

Pulmonary Vascular Resistance causes left sided hypertrophy.

Also blockade of chronic sympathetic activation and reduction in myocardial oxygen demand.

No, it's increased diastolic time so the coronary arteries have more time to absorb nutrients like Oxygen, Fat, Lipids, Proteins, Glucose, Ketones, Acids, Bases.

Definition of heart failure: clinical syndrome in which the heart is unable to meet the metabolic demands of the body or has to do so with elevated filling pressures.

Wait... which one? Left sided? Right sided?

This is why it's important to understand the relationships between all of those cardiac equations taught in the pre clinical years:

BP=CO x SVR
CO= Stroke volume x HR
Stroke volume determined by Preload, Afterload and contractility (the relationships are less easily expressed, but you need to have a conceptual understanding of the relationships and how the heart will respond).


Go through these sequentially, remembering that cardiac output has to be maintained.

Grossly simplified pathophys
systemic HTN = increased afterload -> cardiac hypertrophy to increase contractility-> stiff ventricle = decreased preload-> decreased stroke volume -> increased HR TO MAINTAIN CARDIAC OUTPUT -> continued HTN

Meanwhile at the same time, other neurohormonal compensatory mechanisms are at play including Renin-Angiotensin, Aldosterone and catecholamine secretion.

The crux of heart failure cardiology is managing this interaction to maintain cardiac output. Critical care goes a step further and can actually alter the demand for cardiac output in addition to affecting CO itself.
Cardiac hypertrophy maintains normal-ish wall stress.

Decreased SV and CO also results in a non-osmotic impetus for ADH secretion and volume retention

What's ADH?


.

 

[jdh71]

I'm going to hop into the douchefest to inquire how does an increase in pulmonary vascular resistance cause left ventricular hypertrophy?

 

[BigRedBeta]

Definition of heart failure: clinical syndrome in which the heart is unable to meet the metabolic demands of the body or has to do so with elevated filling pressures.

Which would be reasonably assumed to be the case when " reduced cardiac output --> decreased blood pressure --> no hypertension. " as per the OP. I suppose there could be instances that don't, but in general, such a decrease in CO is going to be associated with some sort of exercise intolerance. As someone in pediatrics, I admittedly don't have much experience with the NYHA classifications, but seems most patients would be on the spectrum.

Decreased SV and CO also results in a non-osmotic impetus for ADH secretion and volume retention

Agreed

 

[Doctor Bob]

I'm going to hop into the douchefest to inquire how does an increase in pulmonary vascular resistance cause left ventricular hypertrophy?

After the VSD causes the PVR to reach a critical level and the flow reverses then... errrr.... hmmm.....

No wait, the PVR causes a backup of pressure and leads to liver congestion; the congestion causes enlargement of the abdominal organs and increases the pressure on the abdominal aorta increasing systemic resistance.... errr..... hmmm.....

 

[SpecterGT260]

I don't expect the decrease in blood pressure due to LVH to be subtle. What if it's so severe that there's very little blood in the left ventricle each time it's filled? Wouldn't that result in dramatic reduction in flow rate and blood pressure?

Yes, I expect hypertension to cure itself when the heart is remodeled so severely. I have a feeling that I am wrong, but I like to know why I am wrong.

I know hypertension causes left ventricular hypertrophy. I just don't understand why LVH wouldn't correct the hypertension.

Thanks Stigma and Bacchus for the replies.

Pressure is not by any necessity dependent on CO. It is more directly related to the elastic recoil of vessels and the outflow rate (not the inflow). With a slow outflow (as is true in hypertension) the heart doesn't have to move much volume at all to maintain pressure. Furthermore, the organs are the primary determinant of blood pressure, so even when hypertrophy gets bad enough as to reduce output (which doesn't happen right away. Output in hypertrophy is essentially normal early on), the kidneys are sending signals to increase BP.

I think your issue is that you assume the wall stiffness is an immediate consequence of hypertrophy and you aren't considering the fluid dynamics that cause hypertension.

 

[SpecterGT260]

Whoa whoa whoa.

Don't talk to me about LV hypertrophy without mentioning:

1. Volume Overload (Eccentric Hypertrophy) vs. Pressure Overload (Concentric Hypertrophy)
2. WALL STRESS and WALL TENSION
3. Filling pressures

LV Hypertrophy is a response to increased wall tension. Wall stress is maintained in the normal-ish range by increasing LV thickness. Law of LaPlace.

There are usually good physiology/pathophysiology reviews in Circulation.

Read. Read. Read some more. Then go read.



Concentric hypertrophy, e.g. chronic hypertension, aortic stenosis.



Whoa. Where did the discussion of Pulmonary Vascular Resistance come from. If you're going to mention that, please at least mention pulmonary hypertension and include a discussion of the WHO Groups (Evian classification and Dana Point update). You're referencing WHO Group II pHTN, aka Pulmonary Venous Hypertension.



Also blockade of chronic sympathetic activation and reduction in myocardial oxygen demand.



Definition of heart failure: clinical syndrome in which the heart is unable to meet the metabolic demands of the body or has to do so with elevated filling pressures.



Cardiac hypertrophy maintains normal-ish wall stress.

Decreased SV and CO also results in a non-osmotic impetus for ADH secretion and volume retention

PVR = peripheral vascular resistance, in this case. 🙄👍

Edit... maybe not. His post was unclear there. If he was discussing pulmonary it is more of an academic discussion. But increasing pulmonary resistance actually lowers pre load so I don't see how it fits in here so I'm still saying the relevant discussion is focused on the periphery.

 

[JGimpel]

In a week, neither you nor anyone else seemed to have ever heard of these books are a senior-level interventional cardiologists or CT surgeon's review texts, so here you go. You can postulate how I happened to know of them on your own. A good start may be that the way that this would have happened is if that resident's attending thought he was ready to browse through one of his because he thought I knew far beyond the basics to get something out of them. Just sayin'

Yes, right now you're getting the guidance of a senior.
Get reading.

 

[Doctor Bob]

Yes, right now you're getting the guidance of a senior.
Get reading.

... really?

If you haven't read a Chen book to really know the ins and outs of cardiac physiology, then please don't act like a cardiologist.

Unless you've taken and passed the Cardiology Board Certification exam, then please don't act like a cardiologist.

 

[SpecterGT260]

 

[jdh71]

Unless you've taken and passed the Cardiology Board Certification exam, then please don't act like a cardiologist.

Well. To be fair, sometimes you have to act like the cardiologist because they won't.

You ever sometimes feel like if they can't stent it, they aren't really all that interested in helping a brother out??

 

[JGimpel]

... really?



Unless you've taken and passed the Cardiology Board Certification exam, then please don't act like a cardiologist.

My comment was directed at one person, diene, that claimed to have a superior grasp of the information the OP asked about than I due to my simplification of the general physiology. This was characterized as "dumbing-down" the information to the others interested in the information. If anyone else took offense to what I said, I apologize.

I'm sure the brunt of people taking offense to what's been posted on this thread would be the way one poster, diene, spoke of myself and other posters. The point is that copying and pasting links and quotes from texts into a post, then belittling those who want things actually explained to them in language at their level of training is not good practice anywhere.

Framingham, ALLHAT, Rhythm vs. Rate, Sick-Sinus, CHADS, etc!

I can do the same listing of topics, but it doesn't really help anyone either.

I've actually run the wires and put in a stent or two under very close observation by a cardiologist that I was working with after I was able to draw out and explain something similar to what I outlined above. Before you ask, I passed on actually inflating the stent. I held my breath as he went past 7 and left it at that. I, however, definitely don't claim to be anywhere near the level of knowledge that he or any of his peers were. He let me borrow his books for the remainder of the time with him and the Chen books are definitely the ones he wanted to challenge me with. There are more of them, but the two above are ones I had experience with.

I'm definitely referring to myself as guiding diene on how to treat others with respect as and encouraging him to attempt read at a higher level, but then teach it to the level of his audience. His advice on getting a topic and researching further is also repeated, this time to have a good enough understanding of the topic to be able to be able to explain it to others well enough to be understood without being as condescending.

To the OP, you'll be fine with your Harrison's and UptoDate for now. If you have an interesting case, look up the topic in more detail at that time and be prepared to discuss it with your attending the next day.