Podcast thumbnail for Channel Your Enthusiasm

Channel Your Enthusiasm

Claim This Podcast

by Channel Your Enthusiasm

4.9(179 reviews)
33 episodes
Updated Bi-weekly
Accepts GuestsHas Sponsors
37

Podcast Authority

Beta
PoorBased on show quality, social media presence, reviews, charts, and more
Pod Engine
Quality37
Social0
YouTube0
Engagement92

Podcast Overview

<p>A chapter by chapter recap of Burton Rose’s classic, The Clinical Physiology of Acid Base and Electrolyte Disorders, a kidney physiology book for nephrologists, fellows, residents and medical students.</p>

Language

🇺🇲

Publishing Since

1/25/2021

Unlock The Full Podcast Authority Score Report

See how your podcast performs across key metrics

37

Podcast Authority

Beta
PoorBased on show quality, social media presence, reviews, charts, and more
Pod Engine
Quality37
Social0
YouTube0
Engagement92
7
Excellent Areas
1
Good Performance
11
Growth Opportunities
excellent
Episode Length
1h 30m
Performing excellently!
good
Listener Reviews
169 reviews (4.9/5.0)

Recommendations available

Unlock the full report to see detailed tips

poor
Publishing Consistency
Every 61 days

Recommendations available

Unlock the full report to see detailed tips

+16 More Metrics

Unlock comprehensive insights including:

  • • YouTube presence analysis
  • • Social media reach metrics
  • • RSS compliance scoring
  • • Podcast 2.0 features
  • • Technical standards
What's Included in Your Full Report

Detailed Analytics

  • Complete breakdown of all 19 authority metrics
  • Personalized recommendations for each metric
  • Industry benchmarks and comparisons
  • Technical RSS feed analysis and compliance scoring

Growth Strategies

  • Step-by-step action plans for improvement
  • Quick wins to boost your score immediately
  • Pro tips from successful podcasters
Get your free podcast insights report

See how your show performs across every key metric

Instant delivery
No spam
Attract Better Guests

High authority scores make your podcast more attractive to industry leaders and influencers who want to appear on credible shows.

Secure Sponsorships

Sponsors look for podcasts with proven authority and engagement. Your score demonstrates your podcast's value to potential partners.

Grow Your Audience

Understanding your strengths and weaknesses helps you make data-driven decisions to expand your listener base effectively.

1 verified contact email on file for Channel Your Enthusiasm

Pitch yourself as a guest, propose sponsorships, or reach out directly to the host.

Recent Episodes

Episode thumbnail for Chapter Twenty: Respiratory Acidosis

June 3, 2026

Chapter Twenty: Respiratory Acidosis

Host Josh and guest Biff Palmer, MD, discuss the sensing, physiological effects, and molecular responses to elevated CO2 levels in eukaryotes, exploring respiratory acidosis and alkalosis.

Episode thumbnail for Chapter Twenty One: Respiratory Alkalosis

March 24, 2026

Chapter Twenty One: Respiratory Alkalosis

<p data-rte-preserve-empty="true" style="white-space:pre-wrap;">References</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Chapter 19, Part 3 August 30, 2023Biff Palmer’s Ted Talk-<a href="https://www.youtube.com/watch?v=XZ-Bb0vMDWs">Why not? Biff Palmer at TEDxSMU 2013</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Anna mentioned this issue of lactic acidosis in a panic disorder: <a href="https://neuro.psychiatryonline.org/doi/10.1176/jnp.13.1.22#:~:text=Lactic%20acid%20production%20decreases%20when,pH%20is%20high%20(alkalosis).&amp;text=This%20effect%20of%20pH%20on,a%20state%20of%20intracellular%20alkalosis">The Lactic Acid Response to Alkalosis in Panic Disorder | The Journal of Neuropsychiatry and Clinical Neurosciences</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047286/">Reminder of important clinical lesson: Lactate: panicking doctor or panicking patient? - PMC</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Melanie regaled the group with an excerpt (page 351) Cohen, J. J., Kassirer, J. P. (1982). Acid-base. United States: Little, Brown.</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Biff Palmer! <a href="https://pubmed.ncbi.nlm.nih.gov/37341662/">Respiratory Acidosis and Respiratory Alkalosis: Core Curriculum 2023</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Melanie loves this study of chronic respiratory alkalosis on participants to traveled to the High ALpine research station on the Jungfraujoch in the Swiss Alps <a href="https://www.nejm.org/doi/full/10.1056/nejm199105163242003">Chronic Respiratory Alkalosis — The Effect of Sustained Hyperventilation on Renal Regulation of Acid–Base Equilibrium | NEJM</a> (and here’s a great picture: <a href="https://www.climate.unibe.ch/services/services_of_cep/jungfraujoch_research_station/index_eng.html">Services: Jungfraujoch Research Station - Climate and Environmental Physics (CEP)</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">JC mentioned that there are cells in the carotid body which are called glomus cells <a href="https://pubmed.ncbi.nlm.nih.gov/35965037/#:~:text=The%20carotid%20body%20(CB)%20is,glomeruli%2C%20innervated%20by%20sensory%20fibers">Neurobiology of the carotid body</a>.</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">JC discussed respiratory alkalosis in cirrhosis and here’s a review he had melanie write that addresses this topic: <a href="https://www.akdh.org/article/S2949-8139(23)00051-4/fulltext">Acid Base Disorders in Cirrhosis - Advances in Kidney Disease and Health</a> and here are some reviews he likes: <a href="https://pubmed.ncbi.nlm.nih.gov/8985264/">The hyperventilation of cirrhosis: progesterone and estradiol effects</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/26011230/">Acid-base disturbance in patients with cirrhosis: relation to hemodynamic dysfunction</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/28523565/">Blood-Brain Barrier Permeability Is Exacerbated in Experimental Model of Hepatic Encephalopathy via MMP-9 Activation and Downregulation of Tight Junction Proteins</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">The finding of respiratory alkalosis in pregnancy is not a new concept. Here’s a study from 1962: <a href="https://www.ajog.org/article/0002-9378(62)90032-7/fulltext">Acid-base balance of arterial blood during pregnancy, at delivery, and in the puerperium - American Journal of Obstetrics &amp; Gynecology</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Melanie reminded us of the Charlie Brown sad face that occurs after bicarbonate infusion and delay in bicarbonate movement to the CSF! <a href="https://www.nejm.org/doi/10.1056/NEJM196709212771201">Spinal-Fluid pH and Neurologic Symptoms in Systemic Acidosis | NEJM</a> (part 2 of chapter 11)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Josh mentioned this report from Andrew Tarulli (a great neurologist previously at BIDMC who has moved to Overlook Hospital in NJ) <a href="https://jamanetwork.com/journals/jamaneurology/fullarticle/789555">Central Neurogenic Hyperventilation: A Case Report and Discussion of Pathophysiology | Allergy and Clinical Immunology | JAMA Neurology</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">He also mentioned this important transporters that affect the pH. <a href="https://pubmed.ncbi.nlm.nih.gov/29956324/">The choroid plexus sodium-bicarbonate cotransporter NBCe2 regulates mouse cerebrospinal fluid pH</a></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><a href="https://www.frontiersin.org/articles/10.3389/fneur.2019.00937/full">Refractory Central Neurogenic Hyperventilation: A Novel Approach Utilizing Mechanical Dead Space</a></p><p data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Outline: Chapter 21</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Respiratory Alkalosis</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Increased pH, low pCO2, variable reduction in HCO3</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Differentiate from metabolic acidosis where pH is decreased</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">(but pCO2 and HCO3 are likewise decreased)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>PATHOPHYSIOLOGY</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Primary decrease in pCO2 when effective alveolar ventilation is increased beyond that needed to eliminate daily CO2 production</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">How does the body respond to hypocapnia</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Mass action</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Reduction in H+ induced by hypocapnia can be minimized by lowering HCO3</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">One: rapid cell buffering</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Two: later decrease in net renal acid secretion → lower HCO3</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">These two strategies explain the difference between acute and chronic respiratory alkalosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Acute Respiratory Alkalosis</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Within 10 minutes, H ions move into extracellular fluid</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">H+ combines with HCO3 → fall in plasma HCO3</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Converted to CO2 and H2O</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">H+ comes from intracellular buffers</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Protein, phosphate, hemoglobin</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">H+ may also come from alkalemia-induced increase in cellular lactic acid production (1)⁉️</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Enough H+ enters ECF to lower HCO3 by <strong>2 mEq for each 10 mmHg decrease in pCO2</strong> (Fig 20-3)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Example: pCO2 falls to 20</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">HCO3 falls by 4 → ~20 mEq/L</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">pH ~7.63</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Not very efficient at protecting pH</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Without compensation pH would be ~7.70</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Chronic Respiratory Alkalosis</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Compensatory ↓ renal H secretion</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Begins within 2 hours</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Not complete for 2–3 days</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Due to parallel rise in tubular cell pH</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Manifested by</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">HCO3 loss</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Decreased NH4 in urine</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>4 mEq drop in HCO3 for each 10 mmHg decrease in pCO2</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Example: pCO2 20 → HCO3 16 → pH ~7.53</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>ETIOLOGY</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Respiration governed by two sets of chemoreceptors</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Central (respiratory center in brainstem)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Peripheral (carotid bodies at bifurcation, aortic bodies at arch)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Central chemoreceptors</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Stimulated by ↑ pCO2 or metabolic acidosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Peripheral chemoreceptors</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Stimulated by hypoxia (and acidosis)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Thus hyperventilation can be produced by</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Hypoxemia</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Anemia</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Reduction in arterial pH</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Other stimuli</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Pain</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Anxiety</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Mechanoreceptors</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Direct stimulation of respiratory center</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Table 21-1</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Hypoxemia</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Respiratory response occurs in stages</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Stage 1</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Peripheral chemoreceptor activation</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Hyperventilation → respiratory alkalosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Increased cerebral pH inhibits central respiratory center</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Limits hyperventilation</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">No significant hyperventilation until pO2 &lt; 50–60 mmHg</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">If lung disease prevents pCO2 reduction</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Hypoxia stimulates ventilation at PaO2 &lt; 70–80 mmHg</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Stage 2⁉️</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Persistent hypoxemia → ↓ HCO3</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Lowers pH toward normal</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Removes alkalosis inhibition</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Allows greater ventilatory response</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Pulmonary Disease</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Common in pneumonia, PE, interstitial fibrosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Also pulmonary edema (though acidosis more common)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Hyperventilation may be due to hypoxemia</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Often not corrected by oxygen</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Other contributors</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Mechanoreceptors in airways, lungs, chest wall</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Signals via vagus nerve</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Juxtacapillary receptors (interstitium)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Irritant receptors (epithelium)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Activated by inflammation or inhaled irritants</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">(asthma, pneumonia)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">These contribute to dyspnea even without hypoxia</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Direct Stimulation of Medullary Respiratory Center</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Cortical input (psychogenic hyperventilation)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Retained amines in hepatic failure (not prostaglandins⁉️)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Bacterial toxins (gram-negative sepsis)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Salicylates</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Progesterone (pregnancy, luteal phase)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Persistent acid CSF after rapid correction of metabolic acidosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">NaHCO3 raises extracellular pH</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Peripheral chemoreceptors reduce ventilation → ↑ pCO2</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">CO2 crosses BBB rapidly, HCO3 does not</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Brain senses ↑ pCO2 → ↓ CSF pH</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Paradoxical prolongation of hyperventilation</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Neurologic disorders</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Pontine tumors → local acidosis → ↓ CSF pH → ↑ ventilation</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Hypocapnia in acute cerebral accidents</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>Mechanical Ventilation</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Overventilation can cause respiratory alkalosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Correct by</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Increasing dead space (no explanation given 🤷🏻‍♂️)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Decreasing tidal volume</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Decreasing respiratory rate</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>SYMPTOMS</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Due to increased CNS and peripheral nerve excitability</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Lightheadedness</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Altered consciousness</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Paresthesias (extremities, circumoral)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Cramps</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Carpopedal spasm</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Syncope</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Cardiac</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Supraventricular and ventricular arrhythmias</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Mechanisms</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Impaired cerebral function</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Increased membrane excitability</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">↓ cerebral blood flow</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">35–40% reduction if pCO2 drops by 20 mmHg</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Psychogenic hyperventilation symptoms</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Dyspnea</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Headache</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Chest pain</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Symptoms more prominent in <strong>acute disease</strong> (rapid pH change)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Electrolytes</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">↓ phosphate (as low as 0.5–1.5 mg/dL)</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Due to intracellular shift</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Increased glycolysis → ↑ phosphorylated compounds</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>DIAGNOSIS</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Tachypnea</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">But could be acidosis or alkalosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Consider sepsis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Compensation equations can be ambiguous</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Example: 7.48 / 20 / XX / 16</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Could be chronic respiratory alkalosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Or acute respiratory alkalosis + metabolic acidosis 😖</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Case 21-1</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">5-year-old with AMS, playing with aspirin</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;"><strong>TREATMENT</strong></p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Usually not necessary</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Do NOT give</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Respiratory depressants</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">HCl</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Paper bag rebreathing</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">↑ inspired CO2</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Can correct acute respiratory alkalosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">If chronic → may leave patient with metabolic acidosis</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">Can treat with NaHCO3</p><p class="" data-rte-preserve-empty="true" style="white-space:pre-wrap;">“Give a mouse a cookie” 😉</p>

Episode thumbnail for Chapter Nineteen: Metabolic Acidosis, part 3

February 22, 2026

Chapter Nineteen: Metabolic Acidosis, part 3

Joel and Roger, along with Anna, Josh, Melanie, Amy, JC, and Lety, discuss metabolic acidosis, covering renal tubular acidosis types, mechanisms, clinical manifestations, and treatments, offering insights into diagnosis and management.

33 total episodes available with 5 transcripts

Recent guests on Channel Your Enthusiasm

Guests from recent episodes — sign up to see every guest that has ever appeared on this show.

Helbert Rondon

Guest

Deep-dive analytics for Channel Your Enthusiasm

Frequently asked questions

Have a different question and can't find the answer you're looking for? Reach out to our support team by sending us an email and we'll get back to you as soon as we can.

What is Channel Your Enthusiasm?
<p>A chapter by chapter recap of Burton Rose’s classic, The Clinical Physiology of Acid Base and Electrolyte Disorders, a kidney physiology book for nephrologists, fellows, residents and medical students.</p>
How often does this podcast release new episodes?

This podcast updates bi-weekly.

Where can I listen to this podcast?

This podcast is available on 9 platforms including Apple Podcasts, Spotify, and more. You can also use the RSS feed directly.

Does this podcast accept guests?

Information about guest appearances is not available.

Legal Disclaimer

Pod Engine is not affiliated with, endorsed by, or officially connected with any of the podcasts displayed on this platform. We operate independently as a podcast discovery and analytics service.

All podcast artwork, thumbnails, and content displayed on this page are the property of their respective owners and are protected by applicable copyright laws. This includes, but is not limited to, podcast cover art, episode artwork, show descriptions, episode titles, transcripts, audio snippets, and any other content originating from the podcast creators or their licensors.

We display this content under fair use principles and/or implied license for the purpose of podcast discovery, information, and commentary. We make no claim of ownership over any podcast content, artwork, or related materials shown on this platform. All trademarks, service marks, and trade names are the property of their respective owners.

While we strive to ensure all content usage is properly authorized, if you are a rights holder and believe your content is being used inappropriately or without proper authorization, please contact us immediately at hey@podengine.ai for prompt review and appropriate action, which may include content removal or proper attribution.

By accessing and using this platform, you acknowledge and agree to respect all applicable copyright laws and intellectual property rights of content owners. Any unauthorized reproduction, distribution, or commercial use of the content displayed on this platform is strictly prohibited.