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Podcast 98 – Cyclic (Tricyclic) Antidepressant Overdose

stormtrooper-pills

I had a crazy case of Tricyclic Overdose while on an overnight shift at Janus General.

Initial and Post-Treatment EKGs

Initial

Initial

Post-Treatment

Post-Treatment

List of Tricyclic Agents from Wikipedia.org

  • Amitriptyline (Tryptomer, Elavil)
  • Amitriptylinoxide (Amioxid, Ambivalon, Equilibrin)
  • Butriptyline (Evadyne)
  • Clomipramine (Anafranil)
  • Demexiptiline (Deparon, Tinoran)
  • Desipramine (Norpramin, Pertofrane)
  • Dibenzepin (Noveril, Victoril)
  • Dimetacrine (Istonil, Istonyl, Miroistonil)
  • Dosulepin/Dothiepin (Prothiaden)
  • Doxepin (Adapin, Sinequan)
  • Imipramine (Tofranil, Janimine, Praminil)
  • Imipraminoxide (Imiprex, Elepsin)
  • Lofepramine (Lomont, Gamanil)
  • Melitracen (Deanxit, Dixeran, Melixeran, Trausabun)
  • Metapramine (Timaxel)
  • Nitroxazepine (Sintamil)
  • Nortriptyline (Pamelor, Aventyl, Norpress)
  • Noxiptiline (Agedal, Elronon, Nogedal)
  • Pipofezine (Azafen/Azaphen)
  • Propizepine (Depressin, Vagran)
  • Protriptyline (Vivactil)
  • Quinupramine (Kevopril, Kinupril, Adeprim, Quinuprine)

Additionally…

  • Amineptine (Survector, Maneon, Directim) Norepinephrine-dopamine reuptake inhibitor
  • Iprindole (Prondol, Galatur, Tetran) 5-HT2 receptor antagonist
  • Opipramol (Insidon, Pramolan, Ensidon, Oprimol) ? receptor agonist
  • Tianeptine (Stablon, Coaxil, Tatinol) Selective serotonin reuptake enhancer
  • Trimipramine (Surmontil) 5-HT2 receptor antagonist and moderate-potency norepinephrine reuptake inhibitor.

And of course, the non-TCA agents…

Pharmacologic Effects of TCAs

K+ Channel BlockadeQTC Prolongation
NE & Serotonin Reuptake InhibitionInitial hypertension quickly followed by hypotension
Na+ Channel BlockadeQRS Prolongation
Hypotension — depresses myocardial contractility
Ventricular dysrhythmias
Brugada-like findings on EKG
Muscarinic Anticholinergic Receptor AntagonismAnticholinergic Toxidrome
AntihistaminergicCNS stimulation or sedation
Alpha1 Adrenergic AntagonismHypotension
GABA-A Receptor BlockadeSeizures

This chart was taken from the excellent Resus Review Blog by Charles Bruen

Sodium Bicarbonate

Increases amount of drug in non-ionized form and may decrease binding to Na-channels (11482860)

May need many, many amps. For some reason the sodium and the bicarb don’t rise significantly in severe toxicity

My goals are QRS duration <100, hemodynamically stable, Na ~150, pH ~7.5

Electrolyte Abnormalities

Beware of hypokalemia and hypocalcemia

Send VBG with lytes at least Q1 hour

Hyperventilation

To promote alkalosis

Hypertonic Saline

If the patient is too alkalotic or out of amps of Bicarb

Sodium Acetate

Can substitute for NaBicarb. This article gives dosing recommendations and precautions. (23636658)

Intubation & Sedation

Be very careful the patient doesn’t become hypercapneic

Sedate with benzo or propofol to raise seizure threshold

Gastric Decon and/or Lavage

If time of ingestion <1 hour ago and airway is protected

We use a commercial device: the Easi-Lav system

Kimberly Clark Easi-Lav

Magnesium

May help, though risk of Torsades is low as long as the patient remains tachycardic

Lidocaine

Even though lidocaine is another Na-Channel Blocker, it actually antagonizes the effects of the TCA-like mediciations. As a Vaughan Williams Class IB agent, For additional information, this review discusses the pertinent issues.(20507243)

VasoPressors

Norepi or Epi

Intralipids

Certainly for cardiac arrest and probably for hypotension/increasing pressor necessity

For this or any other Lipid Question, you need to go immediately to the Lipid Rescue Site

You can find the Lipid Administration Instruction Sheet there, which should be hanging somewhere on the wall of your ED.

ECMO

The last resort for tox instability

Want More?

My friends Sean Nordt and Stu Swadron did a great EM:RAP episode on this 2 months ago

Here is a review and guideline article.

Shout-Outs

Medcalc sent me some freebie codes for their new IOS version of the app. Join the mailing list to be in the running (see the area below to sign up for the mailing list)

Daren Lewis of leadingvisually.com designed the wonderful Janus General logo; consider him if you need any message design.

Janus_General_400px_TransparentBG

Now on to the podcast…

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Bibliography

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Podcast 97 – Acid-Base VI – Chloride-Free Sodium

NaCl

Just returned from Castlefest 2013–best ultrasound conference ever!

So last podcast, I bashed on sodium bicarbonate or as John Kellum and David Story call it: chloride-free sodium. This episode I talk about all the good reasons to use NaBicarb.

A physiology quandary

Owen, an anaesthesia registrar, wrote with this comment:

[...On increasing minute ventilation on vented patients with any bicarb given: Great idea and probably what most of us do, but even if you don't then with each breath the patient will be getting rid of more CO2 than previously so there should be more weak acid loss.]

This is one of those situations where I was gobsmacked for a second. When I started to think about this, it seemed intuitively wrong and yet conceptually right. I knew I needed to find someone far smarter than me. I reached out to Mel Herbert, who recommended David Story. Dr Story is Chair of Anaesthesia at the Melbourne Medical School and a physiology god. Here is his response:

Dr. Story, Here is the quandary. As you saw, I did that acid-base show with Dr. Kellum discussing NaBicarb use for the critically ill. Both Dr. Kellum and I believe and the evidence bares out that in a patient who can’t get rid of the excess CO2, there will be negligible changes in pH from the bicarb administration.Now in an apneic patient, I think this is inarguable. However, in a mech. ventilated patient with no resp drive (let’s say a pt we gave NMBs to), I perpetrated the situation would be the same. In response of my listeners brought up this question: If the minute ventilation is kept the same, but the ETCO2 rises (and by extension, the return of CO2 to the alveoli), this would seem to indicate that each breath is actually eliminating more CO2. Say the ETCO2 went from 40 to 80 with the same Vt. Is more CO2 being eliminated and if so, would this alone clear the transitory excess CO2 from the bicarb? This made me think of the opioid overdose patient. As their CO2 rises, are they too eliminating more CO2 with each of their breaths? My cursory understanding has always been simply that CO2 elimination is directly proportional to minute ventilation. That is what i took from West and never really gave it much thought. Now I am thinking and it is puzzling. –Scott

Response from Dr. Story: I agree it is confusing but this is how I see it. I wrote a letter the Anesthesiology years ago on a related topic.

The short answer is it is all relative.

The universal alveolar air equation for any gas (x) is:
PAx = PIx +/- Vx / VA; where PA is alveolar partial pressure, Vx is production or consumption of the gas

For an excreted gas like CO2 this will be:
PACO2 = PICO2 + K (VCO2 / VA)

The constant is due to VCO2 being STPD and VA being BTPS and is about 800 if you are using mmHg and ml/min.

So usually PACO2 = 40, PIcO2 = 0, VCO2 = 250 ml/min and VA = 5,000 ml / min  (10 X 500ml)
Also PACO2 is directly proportional to VCO2 and inversely to Va.
Now if  we give NaBic and Bic forms CO2 VCO2 will increase. If it went up 50% it would be from 250 ml / min to 375 ml / min. If VA is fixed then
PACO2 = 800 X 375 / 5,000 = 60 mmHg

However I agree that Va will go up which will be due to the increase in VCO2, ie the EXPIRED VA will increase

(inspired unlikey = expired when VO2  does not equal VCO2, that is the respiratory exchange ratio does not equal 1, that is what the F in the alveolar gas equation corrects)

Therefore the VA is now 5,125 ml / min

PACO2 = 800 (375 / 5,125) = 58.5 mmHg.

We have had a 50% increase in VCO2 but only a 2.5% increase in VA this will lead to a new equilibrium point in alveolar and arterial CO2 at around 58mmHg.

I have exaggerated the effects of NaBic or as I call it chloride-free sodium to demonstrate the effects as I see it.

Therefore, yes the alveolar ventilation increases due to greater CO2 excretion but it is a relatively small effect on VA. To reduce the PACO2 back to 40 will require a 50% increase in VA. This will be transient as the VCO2 returns to the rate prior to the NaBic infusion.

I hope the above helps. If not let me know.

Cheers

Dave Story

 

So what do I take from all of that? I think regardless of any increase in minute ventilation, the CO2 will eventually go back to baseline after an adminsitration of sodium bicarbonate and you will see the alkalizing effect, but unless you increase the minute ventilation it will take much longer.

Use of Sodium Bicarbonate

If not stored in glass, bicarb containing solutions exchange CO2 and become not so much bicarbonate.

When to use Bicarb

  • Na Channel Blockade in Tox (Slow Push; Hyperventilate if on Vent)
  • Alkalinization for Tox, such as Salicylate Toxicity (Slow Push and then Drip; Hyperventilate if on Vent) [Thanks, Ben!]
  • Non-SIG Acidosis (Drip or IV Fluid)
  • SIG Acidosis (As an IV Fluid)
  • Increased ICP (Drip)
  • Hyperkalemia (As an IV Fluid)
  • Hyponatremia (Drip)

ICP

NaBicarb can be used as a substitute for hypertonic saline in increased ICP (Neurocrit Care 2010;13:24 & Neurocrit Care 2011;15:42). They used 85 ml of 8.4% sodium bicarb infused over 30 minutes.

Why use Isotonic Bicarb as an IV Fluid?

Read this article by Ed Omron (J Intensive Care Med. 2010;25(5):271-80.)

Problems with Bicarbonate Drips

  • Hypokalemia
  • Hypocalcemia

When not to use Bicarb

  • Probably no role in Cardiac Arrest unless you feel the patient has hyperkalemia or toxicologic cause.

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Podcast 96 – Acid Base in the Critically Ill – Part V – Enough with the Bicarb Already

medium_350366151

This is Part V of the EMCrit Acid-Base Talks. If you haven’t listened to the initial series, you may be better off starting there:

Today’s topic comes from a debate I have been having with Steve Smith of the amazing EKG Blog. The main thrust of the debate started with this question…

Does Bicarb Fix pH if You Can’t Increase Minute Ventilation?

pH Equation

When you can adjust PaCO2 to maintain a certain value (i.e. you increase minute ventilation), bicarb will raise pH as evidenced by this animal study (Crit Care Med 1996; 24:827-834). However, if you can’t blow off the CO2 then the effects on pH will not be there (J Pediatr 1977;91(2):287).

In this study, NaBicarb did not correct the pH, while CarbiCarb did (Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis. (Surgery 102:835–839).

This review article recommends against bicarb for permissive hypercapnia (Intensive Care Med (2004) 30:347–356).

This study furthers the idea that NaBicarb is not all that great in closed systems (J Pediatr 1972;80(4):671) and then this discussion explores all of the biochemical reasons why administering bicarbonate as a rapid push in a closed system is a bad idea (J Pediatr. 1972 Apr;80(4):681-2.).

Here is a quote from another review article (Anesthesiology 1990;72(6):1064):

The key concept in the equation [above] is that pH is not related to the absolute value of either bicarbonate concentration nor PCo2, but rather to their ratio.
When exogenous bicarbonate is administered during acidemia, bicarbonate reacts with hydrogen ions to form carbonic acid. Physicochemical equilibrium is shifted, favoring dissociation of carbonic acid to C02 and water. C02 partial pressure increases. The degree of alkaliniza- tion resulting from increased [HC03“] is limited by the rise in Pco2* In (open) systems where increases in PCo2 are prevented (by ventilation) alkalination occurs. When CO2 cannot be eliminated, the pH of the system is only minimally changed. Ostrea and Odel demonstrated in vitro that when isotonic sodium bicarbonate was added to whole blood in a (closed) system where generated C02 could not escape, PCo2 increased and pH was unchanged. Only when C02 was eliminated was the system alkalinized. Similarly, Steichen and Kleinman noted in hypoxic acidotic dogs that administration of 2 mEq/kg of sodium bicarbonate over 3 min when ventilation was unchanged resulted in no net change in arterial pH, although PaCo2 rose from 46 to 61 mmHg. If C02 elimination cannot keep pace with increased C02 generation, administration of bicarbonate during acidemia produces hypercarbia (respiratory acidosis) with little net improvement in pH.

How about this quote from a strong-ion approach to the use of buffers (Crit Care 2004;8:259):

When ventilation is fixed, however, as commonly occurs in mechanically ventilated patients, the effect of sodium bicarbonate may be to lower arterial pH, as was seen in patients ventilated with a lung protective strategy… [in this study-Am J Resp Crit Care Med 2000;161:1149].

But don’t believe me, let’s Get an Expert…

John Kellum, MDI got to interview John Kellum, MD, master of all things acid-base in the critically ill. You’ll hear more from him in upcoming episodes; this time I asked him the following questions:

  • Does giving NaBicarb actually do anything to the patient’s pH if the patient can’t increase their minute ventilation to blow off the generated PaCO2? (Closed System)
  • Let’s say you can actually can increase pH with NaBicarb, Is there any clinical advantage to actually doing this in an Anion-Gap Acidosis?
  • How about in a patient that received a ton of NS in the ED, should we switch them to a bicarb drip to get SID back in balance?

Even when you Fix the pH with Bicarb, have you done any good in patients with SIG Acidosis?

Probably not!

Advocates of NaBicarb discuss its salutary effects on hemodynamics. However based on the available evidence, there is no reason to think there is any additional effects above those you would see giving hypertonic saline.

Small head-to-head study of NaBicarb and NS showed deleterious effects of the Bicarb (Am J Med. 1989 Jul;87(1):7-14.)

One of the best reviews is by Forsythe and Schmidt in this article (Chest 2000; 117:260–267). Table 1 demonstrating the intracellular effects is particularly relevant.

The other is by Hindman et al. (Anesthesiology 1990;72(6):1064).

If you are going to use it, use it by slow infusion while increasing minute ventilation. Boyd et al. agree and say it better than I can (Curr Opin in Crit Care 2008;14:379).

Severe Acidosis in Trauma Patients

Not fantastic evidence, but in this recent trauma paper (J Trauma 2013;74:45) giving bicarb to severely acidotic patients was associated with increased mortality.

Comments and where they Go…

  • If you have a comment about a podcast, put it in the comments of that podcast–more people will see it that way
  • If you have an unrelated clinical question, put on the EMCrit Google Plus Community Page.

An Amazing Conference is Coming in June 2013:

New York Symposium on Neurological Emergencies and Neurocritical Care

Here is a bibliography of the Literature Reviewed for this Episode

[1] Arieff AI, Leach, W, Park, R, et al. Systemic effects of NaHCO3 in experimental lactic acidosis in dogs. The American journal of physiology. 1982;242: F586-591.

[2] Bersin RM, Chatterjee, K, Arieff, AI. Metabolic and hemodynamic consequences of sodium bicarbonate administration in patients with heart disease. The American journal of medicine. 1989;87: 7-14.

[3] Boyd JH, Walley, KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Current opinion in critical care. 2008;14: 379-383.

[4] Cuhaci B, Lee, J, Ahmed, Z. Sodium bicarbonate controversy in lactic acidosis. Chest. 2000;118: 882-884.

[5] Dell RB. Acid-base effects of hypertonic sodium bicarbonate solutions: a commentary. The Journal of pediatrics. 1972;80: 681-682.

[6] Forsythe SM, Schmidt, GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117: 260-267.

[7] Gehlbach BK, Schmidt, GA. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit – the role of buffers. Critical care. 2004;8: 259-265.

[8] Hindman BJ. Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis: physiologic considerations. Anesthesiology. 1990;72: 1064-1076.

[9] Kallet RH, Jasmer, RM, Luce, JM, et al. The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). American journal of respiratory and critical care medicine. 2000;161: 1149-1153.

[10] Omron EM, Omron, RM. A physicochemical model of crystalloid infusion on acid-base status. Journal of intensive care medicine. 2010;25: 271-280.

[11] Ostrea EM. The influence of bicarbonate administration on blood pH in a “closed system”: clinical implications. The Journal of pediatrics. 1972;80: 671-680.

[12] Rhee KH, Toro, LO, McDonald, GG, et al. Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH. Chest. 1993;104: 913-918.

[13] Steichen JJ, Kleinman, LI. Studies in acid-base balance. I. Effect of alkali therapy in newborn dogs with mechanically fixed ventilation. The Journal of pediatrics. 1977;91: 287-291.

[14] Wilson RF, Spencer, AR, Tyburski, JG, et al. Bicarbonate therapy in severely acidotic trauma patients increases mortality. The journal of trauma and acute care surgery. 2013;74: 45-50; discussion 50.

Now on to the podcast…

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Podcast 95 – Thomas Scalea on Cutting-Edge ICP Management

Thomas Scalea is a legend! He is Physician-in-chief at the Shock Trauma Center in Balitmore. He started the EM program at Kings County in 1991. He is also an excellent doctor and a wonderful person. At the 2012 EMCrit Conference, he gave an amazing lecture on the cutting edge techniques they are using at Shock Trauma for intracranial pressure (ICP) management.

For the basics of ICP Management, check out this prior podcast.

Slides

Here is a pdf of Dr. Scalea’s Slideset

Audio-Only Version

Need just the mp3? Right-click here and choose save-as.

Now on to the podcast…

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Podcast 94 – Has Video Laryngoscopy Killed the Direct Laryngoscope?

Paul Mayo and I seem to have established a tradition of debating each other at the annual Greater NY Hospital Association Critical Care Controversies Conference.

Last year, we debated whether paralytics should be used for emergent intubations.

This year, the topic was Should All Intubations be Performed with Video Laryngoscopy?

I think you will enjoy the debate, because we don’t mind attacking our opponent.

If you enjoyed this podcast and the others on the EMCrit site, please consider supporting the show at CME.EMCrit.org.

Need an audio-only version?

Right click here and choose save-as

Now, on to the debate…

 

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Podcast 93 – Critical Care Palliation with Ashley Shreves

As you know, my motto is maximally aggressive care, ALWAYS! Maximally aggressive curative care and maximally aggressive palliative care. I did a podcast episode on critical care palliation a year or so ago.

At this year’s EMCrit Conference, Ashley Shreves gave the ultimate lecture on the topic. Twenty minutes jam-packed with goodness.

A listener, Don Zweig, wrote with this summary:

  • We (as in ED docs) in general deal with End of Life Care and palliative care situations poorly.
  • Our job as physician is to understand the family goals and values and then give a professional recommendation- it is not to give a menu–they have no medical knowledge to reasonably make this choice.
  • Three things we should never say:
  1.  ”Do you want us to do everything?”  Of course they do, but if you offer “everything” who wouldn’t want mom to get everything? Could they say….”no, whatever you do , don’t do everything for mom!” This also makes the family feel that everything (whatever that entails) is reasonable or possible. Instead use the ‘Pal Care’ approach and say, “What would be most important to you and your mom now?”  On the basis of what you hear make a reasoned professional recommendation.
  2. “Do you want us to resuscitate her?”  This implies that we think it is possible or reasonable to do this!  Since you ask this it must be reasonable.  “You can just bring her back?  Great, go ahead!” Use natural death language.  So it sounds like your mom would want a natural death?  When her heart stops we will not interfere with that process
  3. ” I am so sorry, there is nothing more we can do”  There is a lot that can be done and it involves maximizing comfort and minimizing suffering. They need palliative care or hospice.    So call a consult and give palliative meds.
  • Try to get private room and take them off the monitor!  There is no place for monitor in the dying patient for which you are providing comfort care.
  • Treat discomfort with morphine or dilaudid in very small doses.  Double every 15 minutes until decreased suffering.

Addendum

This amazing post on the blog Expensive Care is a must read on the topic of the ethics of CPR

Need an Audio-Only version?

Right-Click here and choose save-as

Now on to the Vodcast…

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Join the EMCrit G+ Community Page

If you have a comment or question about one of the podcasts, chuck it into the comments section.

But I get a ton of clinical cases and questions by email or the contact form that have not been covered on a podcast yet. I love this–it exposes me to some great cases I would never hear about otherwise. Problem is, up until this point, it has been a 1 on 1 conversation. This is sort of a waste because nobody else benefits except you and me. So in the future, when you have a  case or question like this, I would love it if you posted to the Google Plus EMCrit Community page. This allows a few things:

  1. it allows my answer to be seen by a much larger group of people
  2. it allows folks smarter than me to chime in as well
  3. it keeps a record of these case interactions so I can refer people to them in the future

So how do you do it? Easiest way to learn is to watch this video:

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Podcast 92 – EMCrit Intubation Checklist

Checklists

Since Peter Pronovost’s landmark study on how a simple checklist can nearly abolish central line infections, checklists have been the darling of the medical literature. But central lines generally are for elective procedures, allowing us the time and patience to run through the list. Can we gain the same safety and cognitive benefits in an adrenaline-laden procedure like intubation? Hell yeah!

It all starts with the EMCrit Intubation Checklist

preview of the emcrit airway checlist

Download the checklist

The Components

HOp Killers

Here is the wee on the HOp Killers: Hemodynamic Kills, Oxygenation Kills, and pH Kills

RSI or Awake? · DSI? · RSA? · ICP/Vascular?

Are the peri-intubation medications ready?

RSI Meds

Push-Dose Pressors

What is the plan for unexpected difficult or failed airway?

Can the cricothyroid membrane be palpated?

What is the plan for post-intubation sedation?

Is the patient positioned adequately?

from AirwayCam Site

from AirwayCam Site

Would the patient benefit from pre-intubation NGT?

Skills of Intubation

Laryngoscopy

Cricothyrotomy

Video

Bougie-Aided Cricothyrotomy

Video

Post Intubation Management

Building Checklists

The Checklist Project and their Checklist for Checklists

Other People’s Intubation Checklists for Inspiration

The EMCrit checklist drew inspiration and aid from these other checklists. Shoulders of giants and such…

Did you like this post? Then tweet the hell out of it

Need the Audio only version

Right Click here and Choose Save-as

Now, on to the podcast…

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Podcast 91 – Treatment of Aortic Dissection

Aortic Dissection

Lower Dp/Dt and Blood Pressure

Control Pain with fentanyl

Control Heart Rate/Inotropy with esmolol

See the esmolol drip sheet (YOU MUST CHECK ALL NUMBERS WITH YOUR OWN PHARMACY)

Control Blood Pressure

With in order of preference: clevidipine, nicardipine, nitroprusside, nitroglycerin

What about if the patient can’t get beta-blockers?

What about labetalol?

A-lines

Why is the Patient’s Blood Pressure Low?

  • Myocardial Infarction

Andy Neill thankfully addressed my erroneous assumption that MIs in Dissection would only be right coronary infarctions

Does an anterior STEMI rule out dissection? – Emergency Medicine Ireland

and check out this article as well (J Emerg Trauma Shock 2011;4:273-278)

  • Site of Blood Pressure Measurement

  • Rupture of the Aorta

  • Aortic Insufficiency

  • Pericardial Tamponade

Neurodeficits

Intubation

Do a high-icp/vascular intubation (More to come on this)

(1) SMACC CLUB
http://lifeinthefastlane.com/2013/01/so-you-wanna-know-about-smacc-club/

(2) PK SMACC-talks (the deadline has been extended)
http://smacc.net.au/pk-smacc-talk/
entries so far: http://smacc.net.au/category/pk-talk/

 

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Podcast 90 – Mind of the Resuscitationist Series: Cliff Reid’s Own the Resus Room

Cliff Reid is the prototypical resuscitationist; he rocks! He has discussed his philosophies on previous episodes:

And of course, Cliff’s blog, resus.me, is some of the best retrieval and resuscitation information around.

I brought Cliff up to speak in my Critical Care Track at the 2012 Essentials of Emergency Medicine. Mel Herbert was kind enough to give me permission to post the lecture here. I think you’ll love it as much as I do.

Need the audio-only version of Cliff’s talk? Right click the link and choose save-as.

Now, on to the podcast…

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