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Internal Medicine > January 2021 > Flashcards

January 2021 Flashcards

1
Q

Efficacy of Baricitinib + Remdesivir for COVID?

A

NEJM DEC 2020

RCT by NIH

CONCLUSIONS: Baricitinib plus remdesivir was superior to remdesivir alone in 1) reducing recovery time and 2) accelerating improvement in clinical status among patients with Covid-19, notably among those receiving high-flow oxygen or noninvasive ventilation. The combination was associated with fewer serious adverse events.

Non significant in mortality

Patients receiving baricitinib had a median time to recovery of 7 days (95% confidence interval [CI], 6 to 8), as compared with 8 days (95% CI, 7 to 9) with control (rate ratio for recovery, 1.16; 95% CI, 1.01 to 1.32; P = 0.03), and a 30% higher odds of improvement in clinical status at day 15 (odds ratio, 1.3; 95% CI, 1.0 to 1.6). Patients receiving high-flow oxygen or noninvasive ventilation at enrollment had a time to recovery of 10 days with combination treatment and 18 days with control (rate ratio for recovery, 1.51; 95% CI, 1.10 to 2.08).

Kalil AC, Patterson TF, Mehta AK, et al. Baricitinib plus Remdesivir for Hospitalized Adults with Covid-19. N Engl J Med. 2020 Dec 11. doi: 10.1056/NEJMoa2031994.

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2
Q

What patient population is Baricitinib + Remdesivir treatment beneficial for ?

A

COVID patients on high flow or non-invasive mechanical ventilation

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3
Q

Can Hydroxychloroquine act as an effective post exposure prophylaxis for contacts of COVID confirmed patients?

A

ANNALS OF INTERNAL MEDICINE DEC 2020

RCT

CONCLUSION: This rigorous randomized controlled trial among persons with recent exposure excluded a clinically meaningful effect of hydroxychloroquine as postexposure prophylaxis to prevent SARS-CoV-2 infection.

Among the 689 (89%) participants who were SARS-CoV-2 negative at baseline, there was no difference between the hydroxychloroquine and control groups in SARS-CoV-2 acquisition by day 14 (53 versus 45 events; adjusted hazard ratio, 1.10 [95% CI, 0.73 to 1.66]; P > 0.20). The frequency of participants experiencing adverse events was higher in the hydroxychloroquine group than the control group (66 [16.2%] versus 46 [10.9%], respectively; P = 0.026)

Barnabas RV, Brown ER, Bershteyn A, et al. Hydroxychloroquine as Postexposure Prophylaxis to Prevent Severe Acute Respiratory Syndrome Coronavirus 2 Infection : A Randomized Trial. Ann Intern Med. 2020 Dec 8. doi: 10.7326/M20-6519.

Funded by Bill Gates

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4
Q

FRAMEWORK QUESTION:

What is “post cardiac arrest syndrome”?

A

It is an inflammatory response caused by whole body reperfusion injury following a whole body ischemic event such as cardiac arrest

TIP: Think of cardiac arrest as ischemia to the entire body and ROSC as the trigger for reperfusion. Reperfusion is the principal trigger for the post cardiac arrest syndrome given the injury from oxidants

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5
Q

What are the major organs affected in “post cardiac arrest syndrome”?

A

1) Brain injury:
2) Post arrest cardiac dysfunction
3) Systemic shock - systemic inflammatory response syndrome

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6
Q

Describe the expected hemodynamic state of most patients soon after obtaining ROSC from cardiac arrest?

A

Circulatory shock that can lead to multiorgan failure

“Systemic inflammatory response syndrome” is almost universal following an arrest. Usually apparent with int 24 hours of cardiac arrest. Think of this as “whole body reperfusion injury”

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7
Q

What is the targeted temperature in Targeted Temperature Management?

AKA what does the celsius equate to in Fahrenheit

A

32 degrees to 34 degrees Celsius

Which ends up being 90 - 93

TRICK:

Celsius to Fahrenheit: Celsius X 2 + 30

TIP: Fahrenheit tends to be a higher number for the equivalent celsius. Fahrenheit has more letters in its spelling

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8
Q

How long does Targeted Temperature Management last?

A

12-24 hours only

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9
Q

What patients should Target Temperature Management be used for?

A

Patients who do not awaken after ROSC

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10
Q

What are the only absolute contraindications to targeted temperature management?

A

Pre-existing hypothermia (Defined as < 34 degrees (aka < 93 degrees Celsius)), Major bleeding, and Cyroglobulinemia

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11
Q

What are the main outcomes/benefits derived from Targeted Temperature Management?

A

Studies have shown benefit in 2 arenas:

1) Neurologic recovery
2) Mortality rate

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12
Q

How does shivering during the cooling process affect the efficacy of cooling?

A

It is counterproductive as it produces heat

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13
Q

What is the beneficial end point of Tocilizumab in COVID 19?

A

DEC 2020
NEJM EMPACTA TRIAL
RCT

Addition of tocilizumab to standard care reduces risk of composite of mechanical ventilation and death in adults from high-risk and mostly racial and ethnic minority populations hospitalized with COVID-19 pneumonia

Death, when measured alone, was no different between the 2 groups

Hence, its really reduced risk of mechanical ventilation

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14
Q

What is more likely to present with HA – ischemic stroke vs ICH?

A

ICH

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15
Q

What is the imaging of choice for intracerebral hemorrhage?

A

Non contrast CT is highly sensitive and specific

Clinical tip: Reason it is used in ischemic stroke to rule out hemorrhage

Tip: While CT head is not sensitive or specific for acute ischemic stroke, it is very sensitive and specific for ICH

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16
Q

What structure are make up the basal ganglia?

A

basal ganglia are the caudate, putamen, and globus pallidus in the cerebrum, the substantia nigra in the midbrain, and the subthalamic nucleus in the diencephalon.

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17
Q

Location of ICH helps narrow differential diagnosis of the cause. What is on the differential diagnosis of a patient who presents with ICH in a lobar distribution?

A

Amyloid Angiopathy

Dural AV fistula

AVM

Metastatic brain tumor

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18
Q

What part of the brain does hypertension- induced ICH usually present?

A

4 places:

1) Basal ganglia (Putamen, Globus pallidum)
2) Thalamus
3) Cerebellar hemisphere
4) Pons

Protip: The putamen is the #1 place for hypertensive ICH

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19
Q

Framework Question:

What is the general concern with high BP in the setting of ICH?

A

Higher blood pressure may cause expansion of the hematoma

Clinical tip: lower blood pressure is assumed to reduce size of hematoma, though no evidence

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20
Q

What is the goal BP for patients presenting with ICH?

A
  • if systolic BP of 150-220 mm Hg and no contraindications to BP treatment, reduce systolic BP to about 140 mm Hg
  • if systolic BP > 220 mm Hg, consider aggressive BP reduction with a continuous IV infusion and frequent BP monitoring

ATACH2, INTERACT Trial

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21
Q

What drug class is recommended when lowering BP in patients with ICH?

A

NON vasodilatory drugs – drugs that may vasodilate venous system may worsen ICH by increasing cerebral blood flow (not sure how)

Nicardipine
Clevidipine
Labetalol
Esmolol

CONFUSING since the first 2 drugs are vasodilatory, right?

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22
Q

What percent of strokes are caused by ICH?

A

10%

BUT: 35-45% of these patients are dead at 1 month! Hence, low incidence, high mortality

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23
Q

What is the presentation of the ICH in the putamen?

A

Contralateral hemiparesis
Eyes deviate AWAY from the lesion

Clinical tip: Putamen abuts the internal capsule, through which the corticospinal tract runs through, hence contralateral hemiplegia

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24
Q

What is the presentation of the ICH in the Thalamus?

A

Contralateral hemiparesis
Prominent sensory deficit of ALL modalities
Aphasia
Hemianopia

Specific eye findings

  • deviation of both eyes to the nose (down and inward)
  • Unequal pupils
  • Absence of light reaction
  • Skew deviation (unusual ocular deviation (strabismus), wherein the eyes move upward (hypertropia), but in opposite directions)
  • Ispilateral horner syndrome - interesting that thalamus can lead to horner
  • Absence of convergence
  • Paralysis of upward gaze
  • Retraction nystagmus (when looking upward, the eyes will move in and out of being crossed)

TIP: presentation of thalamic stroke may appear almost identical to MCA stroke + Eye findings

Clinical tip: Thalamus, like the putamen, abuts the internal capsule, through which the corticospinal tract runs through, hence contralateral hemiplegia

Eye findings can help distinguish

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25
Q

What eye findings on exam are characteristic of thalamic ICH?

A

Specific eye findings

  • deviation of both eyes to the nose (down and inward)
  • Unequal pupils
  • Absence of light reaction
  • Skew deviation (unusual ocular deviation (strabismus), wherein the eyes move upward (hypertropia), but in opposite directions)
  • Ispilateral horner syndrome
  • Absence of convergence
  • Paralysis of upward gaze
  • Retraction nystagmus (uncertain how this presents)
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26
Q

Of all the ICH strokes due to hypertension, which part of the brain, if affected, is the most devastating?

A

Pons

Pontine stroke presents and progresses over minutes – deep coma and quadriplegia, locked in syndrome, decerebrate rigiditiy

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27
Q

What is the presentation of cerebellar hemorrhage due to hypertension?

A 
Occipital HA - the one localized head ache to be worried about
Vomiting 
Gait ataxia
Vertigo/Dizziness
**Dysarthria**
**Dysphagia**
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28
Q

What parts of the brain, if ICH occurs from hypertension, place the patient at risk of herniation?

A

Don’t F with Pontine/Cerebellar ICH’s

Pontine ICH

Cerebellar ICH – compression of 4th ventricle

Stupor and altered mental status -> NUS!!!

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29
Q

Framework Question:

What causes the ICH in hypertension?

A

Penetrating arteries in specific parts of the brain – putamen, thalamus, cerebellum and pons – are especially sensitive to hypertension-induced vascular injury

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30
Q

Elderly patient presents with ICH in a specific lobe of the brain – cause?

A

Cerebral amyloid angiopathy

Probably the most common cause of lobar hemorrhage in elderly

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31
Q

ICH in young patient – what is the next test?

A

Urine drug for amphetamines/cocaine

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32
Q

What is the difference between the following:

Intracranial hemorrhage
Intracerebral hemorrhage
Subaracnoid hemorrhage

A

Intracranial is the umbrella term involving SAH, intracerebral hemorrhages

Intracerebral hemorrhages are intraparenchymal bleeds, such as lobar hemorrhages

SAH is NOT intracerebral, but is intracranial

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33
Q

What type of strokes can be caused by stimulant use?

A

ALL of them

  • Ischemic stroke
  • Intracerebral hemorrhage

SAH (due to rupture of pre-existing aneurysm)

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34
Q

What type of intracranial hemorrages are caused by stimulant use?

A

50% intracerebral hemorrhages

50% SAH, hence a young person who presents with SAH may have underlying aneurysm and the addition of stimulants pushed him over the edge

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35
Q

What are the possible locations of intracranial hemorrhages due to anticoagulant use?

A

ANY!

But typically subdural and lobar hemorrhages

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36
Q

What are the possible locations of intracranial hemorrhages due to anticoagulant use?

A

ANY!

But typically subdural and lobar hemorrhages

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37
Q

What are the locations/type of intracranial hemorrhages typical of trauma e.g. fall?

A

Intraparenchymal hemorrhages in the temporal and inferior frontal lobes that will also involve the subarachnoid, subdural and epidural spaces

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38
Q

What malignancies are most commonly associated with ICH?

A

Choriocarcinoma
Malignant melanoma
RCC
Bronchogenic carcinoma

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39
Q

Patient presents with ICH in the setting of taking anticoagulation (or antiplatelets). Reverse?

A

Yes, strong recommendation

E.g. if patient is on VKA, treat with Vit K and PCC (FFP is not available)

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40
Q

What sign on imaging may indicate patient suffering from ICH has ongoing bleeding into hematoma?

A

“Spot sign” which is an enhancement seen within the hematoma which is associated with increased risk of hematoma expansion, mortally and lower likelihood of functional recovery

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41
Q

What platelet count (degree of thrombocytopenia), if present when patient presents with ICH require platelet transfusion to prevent worsening hematoma

A

Plt < 50,000

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42
Q

What size of hematoma in cerebellar ICH usually will require surgical treatment?

A

3 cm

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43
Q

What is the cerebral perfusion pressure goal for patients with ICH?

A

50-70 mmHg

TIP: ½ of the goal BP 140 SBP

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44
Q

Framework question:

How does hyperventilation affect cerebral perfusion pressure?

A

Causes vasoconstriction, hence decreases the perfusion and also the intracranial pressure

Tip: think of hypoventilation, hypercarbia. Brain may interpret that has hypoxia, hence vasodilate, and hence lead to to increase ICP. Hyperventilation decreases CO2 and leads to the opposite

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45
Q

Framework question:

What is an AVM? (in regards to brain)

A

A tangle of vessels located across the cortex or deep within the brain substance. They are a shunt between arterial and venous systems made up of abnormally thin vessels that are mixture of artery/vein in nature.

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46
Q

What is the characteristics of intracranial hemorrhage occurs due to AVMs?

A

Intracerebral hemorrhages that extend to subarachnoid spaces

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47
Q

SAH due to aneurysms are treated with embolization. What about ICH due to AVM?

A

Yes they are as well

NUS consult!

TIP: SAH = AVM treatment

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48
Q

What is the presentation of ICH due to AVM?

A 
Headache
Seizure (30% of the case)

Clinical tip: unlike ICH from hypertension, which seizures are uncommon. In addition, ICH from hypertension presents more like a stroke syndrome

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49
Q

What is the relationship between a dural AV fistula and cortical ischemia or SAH?

A

Patient with dural AV fistula has an arterial connection with venous sinus of the dural. If there is significant enough shunting of arterial blood flow to the venous system, that can cause ischemia. In addition, there can be venous hypertension from excessive flow, leading to SAH.

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50
Q

Framework questions:

What is an action potential?

A

The rise and fall of voltage across a membrane that leads to a characteristic shape

In regards to the cardiac cell, ions travelling through voltage-gated ion channels (aka current) produces the action potential

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51
Q

Framework questions:

How are action potentials and contraction of cardiac cells related?

A

Action potentials are the rise and fall of voltages across a membrane that leads to a characteristic shape

The voltage change from an action potential is the primary signal to trigger the intracellular release of Ca that leads to contraction

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52
Q

Framework question:

Why is it that most antiarrhythmic medications inevitably affect multiple ion channels?

A

The function of many ion channels is both TIME and VOLTAGE dependent

So, though an anti-arrhythmic may target only 1 ion channel, by altering the action potential shape and or duration, other ion channels are inevitably affected

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53
Q

Framework Question:

What are the main driving forces that influence the direction of ions across a membrane?

A

Concentration gradients

Electrical gradients

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54
Q

Framework Question:

What is the transmembrane potential at rest for a cardiac cell? What maintains this transmembrane potential

A

-90mV

Meaning that the inside of the cell is -90mV relative to the outside

Na K ATPase and fixed anionic charges within the cell help maintain this resting membrane potential

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55
Q

Framework Question:

The cardiac cell has a resting membrane potential of -90mV. What is the direction of Na and K in regards to the electrical gradient and concentration gradient?

A

For K:

  • Electrical gradient: K wants to go into the cell since it’s negative
  • Concentration gradient: K wants to leave the cell since the concentration of K is greater within the cell compared to outside

For Na:
- Electrical gradient: Na wants to go into the cell since it’s negative
Concentration gradient: Na wants to go into the cell since the concentration of Na is greater outside the cell compared to inside

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56
Q

Framework Question:

What triggers an action potential?

A

Depolarization of a neighboring myocyte above a certain threshold potential triggers an action potential. The presence of gap junctions lead to the propagation of action potentials from cell to the next, cause neighboring cells to reach their threshold potential and trigger action potentials

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57
Q

Framework Question:

What are the ion channels responsible for each phase of the cardiac action potential?

A

TIP:
The movement of each ion is easy to determine. All you have to do is remember whether the ion is predominantly intracellular or extracellular. In the case of Na (serum Na is 135-145), Na will enter into the cell during an action potential because is predominantly an extracellular ion.

K – mostly intracellular – so will leave the cell
Ca – EXCEPTION – will enter the cell

Phase 0 – Na enters and depolarizes the cell
Phase 1 – K leaves the cell via the “transient outward K channel”
Phase 2 – (plateau) Ca enters the cell via the L type Ca channel/and at the end of phase 3, K leaves the cell again via delayed rectifier channel
Phase 3 – K continues to leave the cell via the delayed rectifier cells

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58
Q

Why is does impulse propagation in the AV node slow down compared to the atria?

Tip: explain by speaking on ion channels

A

Basic concept: the action potentials produced by cells are dependent on the ion channels present on the cells. Hence, action potentials throughout the heart actually differ in morphology.

AV node’s action potential is initiated inward current of Ca which is much smaller compared to the Na current of the atria

Other way to think about it: the speed of an impulse is dependent on the magnitude of the current, the magnitude of the current is dependent on the number of available channels. Hence speed is directly related to channel

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59
Q

What are the 3 factors needed to diagnosis OHS?

A

Obesity: BMI > 30

Hypoventilation: Day time hypercapnia Co2 > 45

Sleep disordered breathing (AKA OSA)

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60
Q

What BMI is considered “severe obesity”?

A

BMI > 40

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61
Q

What is the relationship between OHS and OSA?

A

> 90% of patients with OHS have OSA

Actually 70% of patients with OHS have severe OSA (>30 AHI/hr)

TIP: Think of OHS as OSA that is so bad that it has now spilled over into the day time. It is OSA 24/7

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62
Q

How many AHI’s is considered OSA?

A

Simply 5 events/hour

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63
Q

What is the primary treatment of OHS?

A

PAP – Positive airway pressure

PAP can refer to 3 different things

  • CPAP
  • BiPAP
  • PSV

Watch out! Some, when speaking of NIV, mean Bipap and NOT CpAP

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64
Q

How much weight loss is suggested to lead to resolution of hypoventilation?

A

25-30%

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65
Q

What are the benefits of treating OHS with PAP?

A

Basically the benefits of OSA and correction of daytime hypoxemia (PaO2>55) and hypercapnia

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66
Q

What part of the day is treatment with PAP recommended for patients with OHS?

A

During sleep

But the benefits are actually seen both in the night time AND day time!

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67
Q

What is the consequence of discharging a patient with suspected OHS who presented for acute respiratory failure without PAP?

A

Death

In one study, 3 month follow up showed 10 to 25 % of patients discharged without PAP had died

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68
Q

What is the treatment of choice for patients who present with acute respiratory failure suspected to having OHS?

A

Bipap upon admission
Bipap upon discharge

DIFFERENCE: CPAP is first line for chronic stable ambulatory patients

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69
Q

Does treatment of SAH due to ruptured aneurysm with Tranexamic acid lead to reduced rebleeding? Improved clinical outcomes?

A

LANCET
RCT Dec 2020

Already known to reduce rebleeding, but uncertain if that reduction in rebleeding actually leads to clinical outcomes

1 gm bolus, then 1 gm every 8 hours until after 24 hours or right before aneurysm treatment, which ever came first

We enrolled 955 patients; 480 patients were randomly assigned to tranexamic acid and 475 patients to the control group. In the intention-to-treat analysis, good clinical outcome was observed in 287 (60%) of 475 patients in the tranexamic acid group, and 300 (64%) of 470 patients in the control group (treatment centre adjusted odds ratio 0·86, 95% CI 0·66-1·12)

Conclusion: In patients with CT-proven subarachnoid haemorrhage, presumably caused by a ruptured aneurysm, ultra-early, short-term tranexamic acid treatment did not improve clinical outcome at 6 months, as measured by the modified Rankin Scale

Post R, Germans MR, Tjerkstra MA, et al.Ultra-early tranexamic acid after subarachnoid haemorrhage (ULTRA): a randomised controlled trial.Lancet. 2020 Dec 21. pii: S0140-6736(20)32518-6. doi: 10.1016/S0140-6736(20)32518-6.

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70
Q

Most common cause of congenital hearing loss?

A

Genetic mutations are the most common cause, accounting for 50% to 60% of all cases

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71
Q

Of the genetic causes of hearing loss what is the main inheritance pattern?

A

About 80% of inherited hearing loss by autosomal recessive transmission

About 18% by autosomal dominant transmission and about 2% by X-linked recessive transmission

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72
Q

How is the severity of hearing loss graded?

A

Hearing loss can be categorized by severity and type.

Severity is defined by the threshold at which sound is heard.

Mild = 25 to 40 dB.

Moderate = 41 to 70 dB.

Severe = 71 to 90 dB.

Profound = greater than 90 dB.

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73
Q

What are consequences of uncorrected hearing loss?

A

Grade failure, even if mild hearing loss

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74
Q

What is the 1-3-6 rule by the Joint Committee on Infant Hearing?

A

Rule for identification of and intervention for congenital hearing loss

Screening by 1 month
Confirmation by 3 months
Intervention by 6 months

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75
Q

What part of the body, if affected, can cause conductive hearing loss?

A

It can occur at any location from the outer ear (pinna, external auditory canal) to the stapes footplate and oval window.

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76
Q

What is anatomically involved in sensorineural hearing loss?

A

Inner ear (eg, the cochlea) and/or the auditory nerve (cranial nerve VIII).

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77
Q

Framework question:

What is considered the “outer ear”, “middle ear” and “inner ear”?

A

The outer ear, comprising the auricle and external auditory canal (EAC)

The middle ear, comprising the tympanic membrane, ossicles, and the middle ear space

The inner ear, comprising the cochlea, semicircular canals, and internal auditory canals

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78
Q

What image is the gold standard for evaluating ICH?

A

CT is very sensitive for identifying acute hemorrhage and is considered
the gold standard

TIP: Makes sense since it is the first image for suspected ischemic stroke to rule out hemorrhage

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79
Q

2 major risk factors for ICH?

A

HTN and anticoagulant therapy

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80
Q

Which arteries in the brain are sensitive to the effects of HTN?

A

Sites of bifurcations or branches of penetrating arteries, such as lenticulostriate, thalamus, brainstem, thus explaining the commons sites for ICH

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81
Q

What age group of patients are at risk of ICH due to amyloid angiopathy?

A

Elderly

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82
Q

How does amyloid angiopathy cause ICH?

A

Amyloid deposits in tunica media/adventitia of vessels, leading to increased fragility

83
Q

What are features of ICH on presentation that are characteristic for amyloid angiopathy?

A
  • Older age
  • Lobar regions, especially the posterior areas of the brain
  • Multi-focal
  • Recurrent
84
Q

During what part of the natural history of ICH does neurologic decline occur?

A
  • Early on, even within hours – NEUROLOGIC EMERGENCY!

- TIME IS BRAIN

85
Q

What is the gold standard image for evaluating intracerebral hemorrhage?

A

CT Scan

86
Q

What are findings on initial CT scan that are suggestive that the ICH has a secondary cause?

A

SAH

Unusual hematoma shape (non circular)

Presence of edema out of proportion to the early time that ICH is first imaged

Unusual location of hemorrhage

Presence of a mass

87
Q

Patient presents with ICH. Patient takes Warfarin. What is your immediate mgmt?

A

Vitamin K

PCC (if not, than FFP)

88
Q

Patient presents with ICH. Patient takes Warfarin. What is your immediate mgmt?

A

Vitamin K

PCC (if not, than FFP)

89
Q

What is meant by “tunneled” in tunneled CVC?

A

Catheter is “tunneled” under the skin and “terminates” which, in IR terms, refers not to the catheter tip, but rather the exit site on the skin, away from the venous access site (that is, where the vein is punctured)

90
Q

What are the 2 major types of tunneled central venous catheters (CVC)?

A

o With port – AKA a Port is a type of tunneled CVC

o Without port such as tunneled dialysis cathters

91
Q

What is the major difference between what a tunneled CVC with a port and without a port be used for?

A

BOTH can be used for infusion, fluids, nutrition

HD can ONLY be used in tunneled CVC WITHOUT port

92
Q

What are the access sites, that is, the veins used as access for placement of tunneled CVC?

A

o Internal jugular
o Subclavian vein
o Femoral
o TIP: the same places a CVC in the ICU is placed

93
Q

The right IJ is the preferred location for a tunneled CVC. Why?

A

The right IJ leads to a short right brachiocephalic vein that leads to the SVC. However, the left IJ will lead to a long left brachiocephalic vein prior to ending in the SVC

94
Q

What are ABSOLUTE contraindications to tunneled CVC placement?

A

o Severe, uncorrectable coagulopathy
o Uncontrolled sepsis
o Bacteremia

95
Q

What are possible immediate complications of tunneled CVC placement?

A

o Bleeding – bleeding
o Air embolism -> shortness of breath/cardiovascular collapse
o Pneumothorax -> shortness of breath
o Wound dehiscence -> bleeding
o Cather migration/malposition -> can grab chest x ray
o Cardiac perforation -> chest pain/shortness of breath/arrhythmia
o Infection ->

96
Q

Where should the catheter tip of a tunneled CVC end?

A

Cavoatrial junction

97
Q

Patient has suspected air embolism from tunneled CVC placement – what are the immediatre first steps of management?

A

o Trendelenberg position
o Left lateral decubitus
o Aspiration through the CVC

98
Q

What are the 2 main long term complications of tunneled CVC?

A

Thrombosis and infection

99
Q

In the acute setting of atrial fibrillation with rapid ventricular rhythm, when is amiodarone used?

A

In critically ill patients that have atrial fibrillation with rapid ventricular rate without pre-excitation

In addn, it has been used for those with atrial fibrillation and heart failure as well (just like Digoxin)

Beta blockers or NDCC may have hemodynamic effects that are detrimental to patients that are critically ill

100
Q

If patient is hemodynamically unstable and has atrial fibrillation with rapid ventricular rate, what is the treatment of choice?

A

Electric cardioversion (SYNCHONIZED)

Clinical tip: Patient, s/p cardiac arrest and ROSC may have atrial fibrillation with rapid ventricular rate. Cardioversion could be an option

101
Q

In the acute setting of atrial fibrillation with rapid ventricular rate, what are the first line drugs to control rate?

A

IV beta blockers and non-dihydopyridine calcium channel blockers (Diltiazem/Verapimil)

102
Q

Rate control with multiple drugs (BB, NDCC, Amiodarone, Digoxn) fails to control the rate of a patient who has atrial fibrillation and recurrent bouts of rapid ventricular rate. Next step?

A

AV nodal ablation with permanent ventricular pacing is reasonable when pharmacological therapy
is inadequate and rhythm control is not achievable

103
Q

What is the dosing of Amiodarone in the acute setting of atrial fibrillation with rapid ventricular rate if the goal is RATE control? If the goal is RHYTHM control (that is, CV)?

A

TIP: dosing of IV amiodarone in the acute setting depends on the indication – rate control vs rhythm control

Rate control: Same as dead guy dose in ACLS

300mg IV over 1 hour, followed by 10-50mg/hour for the next 24 hours

Rhythm control (AKA cardioversion):

150 mg IV over 10 minutes then 1 mg/min IV for 6 hours, then 0.5 mg/min IV for 18 hours or switch to oral therapy

104
Q

What are the rate control drugs that should not be used if there is a concern for atrial fibrillation with pre-excitation?

A

NDCC

Digoxin

Amiodarone

Beta blocker (from ESC)

WHY: Basically anything that can block the AV node. Blocking the AV node encourages propagation via the bypass track, which unlike the AV node, doesn’t actually slow down impulses. Hence atrial fib down the bypass tract can lead to such high ventricular rates that it devolves into Vfib or Vtach

According to the AHA 2014 guidelines. No mention of beta blockers

105
Q

Which patients may benefit from addition of Digoxin to their treatment of rate control in atrial fibrillation?

A

Patient’s with HF as it does NOT have a negative inotropic effect

106
Q

In the acute setting of atrial fibrillation with rapid ventricular rate, what are the considerations that need to be accounted for when choosing between using Digoxin vs Amiodarone IV as add on therapy to obtain control?

A

Amiodarone could cardiovert someone, and if a patient is NOT on an anticoagulation, this could be devastating

Digoxin is helpful when patients have underlying heart failure as it does not have a negative inotropic effect. So patients who present with HF and atrial fibrillation with rapid ventricular rate with soft pressures could benefit from Digoxin

107
Q

What type of arrhythmia can amiodarone be used for?

A

BOTH supraventricular and ventricular though only FDA approved for ventricular arrhythmias

Ex: Atrial fibrillation (or any other SVT) and ventricular arrhythmias

Clinical tip: DOSING is the same! 150mg IV over 10 minutes, then 1 mg/min for 6 hours, then 0.5mg/min for 18 hours

108
Q

What is amiodarone’s indications in atrial fibrillation?

A

Acute rate control in atrial fibrillation with rapid ventricular response

Long term rate control (just like beta blocker/NDCC)

Acute rhythm control (aka pharmacologic cardioversion)

Long term maintenance of rhythm control (maintenance of NSR for atrial fibrillation such as after electrical cardioversion)

TIP: It does everything!

109
Q

What class of antiarrhythmics does Amiodarone belong to?

A

Class III which is mainly characterized by blocking the K rectifier channel responsible for repolarization in the phase 3 part of action potential

TIP: however, Amiodarone exhibits properties of all the other classes as well, that is, Na channel blockade, beta blockade and Ca channel blockade

Tip: Salty banana (K and Iodine)

110
Q

What is amiodarone’s main MOA and how should this affect the action potential?

A

Class III which is mainly characterized by blocking the K rectifier channel responsible for repolarization in the phase 3 part of action potential

Therefore it prolongs the action potential and the refractory period

111
Q

How does the dosing of Amiodarone IV for acute tachyarrhythmias differ between treating ventricular arrhythmias vs supraventricular?

A

THE SAME!!!

150 mg IV over 10 minutes then 1 mg/min IV for 6 hours, then 0.5 mg/min IV for 18 hours or switch to oral therapy

112
Q

What is the main FDA approved use of Amiodarone?

A

Ventricular arrhythmias – BOTH treatment and prophylaxis

113
Q

What cardiac adverse effects are associated with Amiodarone?

A

BOTH bradyarrhythmias and tachyarrhythmias

Bradyarrhythmias: bradycardia, AV blocks and IVCD’s which is why it is contraindicated in patients with 2nd and 3rd degree AV blocks and NO pacemakers AND avoided in patients with atrial fibrillation and pre-excitation

Tachyarrhythmias: Can extend QRS and QTc; can lead to Torsades de pointes even with normal QTc BUT for IV formulation, NOT PO

114
Q

What determines if an impulse is propagated?

A

The magnitude of the depolarizing current

In the case of myocytes, that would mean Na channel availability since that determines Phase 0

In the case of AV node, Ca channel availability

115
Q

In terms of ion channels, why does an impulse slow down when reaching the AV node? For example, following the P wave on an EKG, there is a PR interval before QRS

A

The magnitude of the inward current, which occurs through the Ca channel in the AV nodal tissue, is much smaller compared to current generated by myocytes in which the Na channel is the means by which the inward current is created

Lesson: The magnitude of the depolarizing current determines how fast an impulse is propagated

116
Q

Framework question:

What are the 3 conformational states that ion channels go through during an action potential?

A

Open -> Inactivated -> Closed -> Open -> etc.

Open state: Phase 0, during which time ions can flow across (aka current is produced)

Inactivated state: In this state, Na channels can’t reopen until they reassume the closed state

Closed state: during repolarizing, channel goes from inactivated to closed. It is during the closed state that the channel can again open

117
Q

Explain why a restimulation of a cardiac tissue (either atria, ventricular, His purkinje, etc) very early during an action potential does not lead to another action potential?

A

TIP: It’s all about channels

Membrane potential determines amount of Na channels available (AKA voltage dependent)

  • Depolarized – less Na channels recovered from activated state
  • Repolarizing – more Na channels recovered from activated state
  • Resting membrane potential – most Na channels recovered from activated state

Amount of Na channels available determines current

Current determines action potential

During the plateau phase of an action potential, there simply aren’t enough available Na channels. No Na channels, no currents. No currents, no action potentials

118
Q

Why is it that a stimulus that occurs during phase 3 of an action potential leads to an action potential that is small and lower in amplitude?

A

TIP: It’s all about channels

119
Q

How do Na channel blockers affect the amount of Na channels recovered from inactivated state?

A

For a given membrane potential, there are less Na channels recovered from inactivated state

120
Q

What is effective refractory period? (ERP)

A

The longest period during which an extra stimulus fails to produce a propagated response

This is a quantitative description of “refractoriness”

121
Q

What is refractoriness? What is the physiologic basis of refractoriness?

A

The ability for a cell, after depolarization, to not produce another action potential in the face of a stimulus

TIP: Again, it’s all about the channels.

The lack of sufficient Na channels is the basis of refractoriness. But not only sufficient channels, but sufficient channels that have RECOVERED from inactivated state

122
Q

How is the mechanism of refractoriness different between AV nodal cells and mycotyes?

A

Na vs Ca channel
Unrelated to timing vs timing

Depolarization is largely controlled by Ca channels and the current produced by them in AV nodal tissue. Secondly, Ca channels have a slower recovery from inactivated state. So even if there are sufficient Ca channels available, they become ready for re-excitation only after a certain time.

TLDR: Timing and Ca channels

123
Q

What are the three underlying mechanisms of tachyarrhythmias?

A

1) Enhanced automaticity
2) Triggered automaticity
3) Reentry

They can be interrelated, that is, a triggered automaticity may lead to renentry

124
Q

What phase of the action potential if affected will lead to enhance automaticity?

A

Phase 4

For cells that have spontaneous diastolic depolarization, such as AV node and His purkinje cells, the slope of Phase 4 can be increased, leading to enhanced automaticity, basically increased rate

125
Q

What is afterdepolarization? What is triggered automaticity? Their relation?

A

After depolarization is just as it sounds. It is an abnormal depolarization that occurs AFTER a normal action potential

Triggered automaticity means that the after depolarization reaches a certain threshold and a second action potential is produced. This only occurs after a first normal action potential, the trigger

126
Q

What is DAD? EAD? And their causes?

A

Delayed after depolarization means that the depolarization occurs late, specifically after full repolarization so occurs in phase 4.

This is caused by Ca overload in the sarcoplasmic reticulum. Ca leaks into the cytosol. To get rid of Ca, it uses the Na-Ca exchanger, which brings Na inside the cell in exchange for Ca, thereby depolarizing the cell. Movement of Na into the cell creates a current

Early after depolarization is when the after depolarization occurs early, specifically during phase 3. Multiple ion channels are attributed

127
Q

What is DAD? EAD? And their causes?

A

Delayed after depolarization means that the depolarization occurs late, specifically after full repolarization so occurs in phase 4.

This is caused by Ca overload in the sarcoplasmic reticulum. Ca leaks into the cytosol. To get rid of Ca, it uses the Na-Ca exchanger, which brings Na inside the cell in exchange for Ca, thereby depolarizing the cell. Movement of Na into the cell creates a current

Early after depolarization is when the after depolarization occurs early, specifically during phase 3. Multiple ion channels are attributed

128
Q

How does heart rate affect DAD and EAD?

A

DADs occur more at rapid heart rates

EADs occur more at slow heart rates (aka long action potential) which makes sense since the longer time you are in phase 3, the higher chance you have to having an EAD

129
Q

What is a common underlying contributor to polymorphic ventricular tachycardia – EAD or DAD?

A

EAD since polymorphic ventricular tachycardia is related to prolonged QT, hence long action potential

130
Q

Explain how a WPW can lead to reentrant tachycardia?

A

Normal circumstances:

Sinus node propagates an impulse to both the AV node and the accessory pathway. It is the combination of ventricular activation through both these pathways that leads to the abnormal, prolonged, slurring QRS at NSR

Reentry:

At baseline, AV node and accessory pathway are characteristically different. Accessory pathway has longer refractory period AND lacks decremental conduction. (Def: the more frequently a tissue is stimulated, the slower it conducts)

When a premature impulse is initiated and propagated, the accessory pathway is still refractory. Hence, it travels to the AV node, down the His Purkinje and by the time it reachs the accessory pathway, it is no longer refractory. Hence it goes to the atria, back to the AV node and on and on and on.

131
Q

Can HRS occur in acute liver failure and alcoholic hepatitis?

A

Yes!

Like other consequences of chronic decompensated cirrhosis, HRS, like ascites, can occur in the acute setting of alcoholic hepatitis or acute liver failure

132
Q

What is the definition of the acute kidney injury according to KDIGO?

A

1) Increase of serum Cr by 0.3 within 48 hours
2) increase of serum creatinine by 50% (AKA 1.5 fold increase from baseline) within seven days

Tip: guidelines also define acute kidney injury by urine output, but in the setting of cirrhosis is both difficult and impractical.

133
Q

What is the difference between AKI, AKD and CKD?

A

AKI: 2 or 7 days

1) Increase of serum Cr by 0.3 within 48 hours
2) increase of serum Creatinine by 50% (AKA 1.5 fold increase from baseline) within seven days

AKD: < 3 mos

  • Cr increase <50% < 3 mos
  • GFR < 60 or GFR decrease for 35% or more < 3 mos

CKD: >3 mos
-GFR < 60 for > 3 mos

Simply:
AKI: 2 day or 7 days, purely by Cr
AKD: <3 mos, by GFR or Cr
CKD: >3 mos, purely by GFR

134
Q

GFR, based on Cr equations, underestimate or overestimate GFR?

A

Overestimate

Hence, underestimates the amount of kidney injury to have occurred

135
Q

What is Acute Kidney Disease?

A

In some ways, it is kidney injury that occurs beyond the setting an AKI (2 days or within 7 day), but not beyond the setting that would signify CKD (>3 mos)

It is the injury that precedes CKD

136
Q

In patient’s with AKI, what criteria should be used to define AKI?

A

KDIGO

1) Increase of serum Cr by 0.3 within 48 hours
2) increase of serum creatinine by 50% (AKA 1.5 fold increase from baseline) within seven days

137
Q

What is the difference between Stage I, II and 3 AKI?

A 
Stage I: the same definition as AKI per KDIGO, that is, absolute Cr > 0.3 or >50% increase 
-	Stage1A: Cr<1.5
-	Stage 1B: Cr > 1.5 
Stage 2: Cr 2fold from baseline
Stage 3: Cr 3 fold from baseline
138
Q

What is the recommended volume expansion in patients with cirrhosis and AKI as part of the evaluation of HRS?

A

Albumin 20%, 1g/kg daily for 2 days (max of 100g/day)

139
Q

What biomarker may aid in distinguishing between ATN and HRS?

A

NGAL as it implies tubular damage

140
Q

What is the new proposed pathophysiology of HRS?

A

Combination of microcirculatory dysfunction and inflammation which looks at cirrhosis as not only a circulatory dysfunctional state, but also a pro-inflammatory state

Inflammation from cytokines/chemokines which cause the upregulation of DAMPS and PAMPS which alter the function of the proximal tubules such that they prioritize survival over other functions such as NaCl absorption, so NaCl travel further down the nephon, leading to RAAS stimulation (interesting because in both the old and new theory of the pathophys of HRS, RAAS plays a role)

141
Q

What is the main stay treatment of HRS?

A

Vasocontrictors and albumin

142
Q

Why are vasoconstrictors used in the treatment of HRS?

A

Since the splanchnic vasodilation is a key step in the development of HRS, vasoconstrictors counteract that.

Phys: Though portal hypertension implies a high amount of pressure in the portal system. Splanchnic vasodilation occurs as a consequence of NO that is excreted in response to the portal HTN. This leads not only to local vasodilation, but to systemic vasodilation. Hence, the kidney’s response is to RAAS. It is this localized hypoperfusion that the kidneys are damaged

143
Q

What is the dose of albumin used to treat confirmed HRS?

A

20-40g/day

144
Q

What is the duration of treatment for HRS with vasoconstrictors and albumin?

A

Until a complete response (that is, Scr < 1.5) or 14 days maximum

145
Q

What is the first line vasoconstrictor for the treatment of HRS?

A

Terlipressin

146
Q

What are alternative vasoconstrictors for HRS since the US does NOT carry Terlipressin?

A

If NOT Terlipressin + Albumin

Norepinephrine + Albumin

OR

Midrodrine/Octreotide + Albumin

147
Q

What is considered a complete response to vasoconstrictor + Albumin therapy?

A

SCr within 0.3 of the baseline Cr

148
Q

What is considered a partial response to vasoconstrictor + Albumin therapy?

A

Improvement in stage of AKI (example, improvement from stage 2 AKI to Stage 1) but SCr still > 0.3 from baseline

149
Q

What is the best therapeutic option for patients with HRS?

A

Liver transplant

150
Q

What are the 3 necessary components of a re-entry circuit such as AVRT?

A

1) Anatomically defined circuit
2) Heterogeneity in the refractoriness among regions of the circuit
3) Slow conduction in one part of the circuit

151
Q

What are the 4 ways in which antiarrhythmic drugs may treat arrhythmias that are caused by enhanced automaticity?

A

By altering the 4 determinants of spontaneous pacemaker discharge

1) Increase maximum diastolic potential – aka hyperpolarize the cell so that the beginning of phase 4 starts at a more negative potential and so for the same given slope, it takes longer to reach the threshold potential that initiates an action potential. Overall, phase 4 is prolonged
2) Decrease phase 4 slope. This will lead to longer phase 4 to reach threshold potential. Phase 4 is prolonged
3) Increase threshold potential – means phase 4 has to reach a higher threshold prior to the initiation of an action potential. Overall phase 4 is prolonged
4) Increase action potential duration which basically prolongs phase 3

152
Q

What drug treats enhanced automaticity by increasing maximum diastolic potential?

A

Adenosine and acetylcholine

153
Q

What drug treats enhanced automaticity by decreasing phase 4 slope?

A

Beta blockers

154
Q

What drug treats enhanced automaticity by increasing threshold potential?

A

Blockade of Ca or Na channels

155
Q

What drug treats enhanced automaticity by prolonging action potential?

A

Blockade of K channels

156
Q

What are the 2 major ways antiarrhythmics suppress arrhythmias due to DAD’s and EAD’s? (AKA triggered automaticity and afterdepolarizations)

A

1) Inhibit the inward current that is responsible for the upstroke – Block Na or Ca channels to prevent upstrokes

Tip: all about the channels. No channels, no upstrokes

2) Inhibit afterdepolarizations

157
Q

What mechanism of antiarrhythmics terminate the arrhythmias cause by anatomically determined re-entry?

A

Blocking the action potential propagation – aka slowing the conduction

In the case of WPW, blocking the AV node with beta blocker or CCB or adenosine will do the trick

158
Q

What mechanism of antiarrhythmics terminate the arrhythmias cause by functionally determined re-entry?

A

Increase refractoriness.

Slowing the conduction can lead to the development of reentrant arrhythmias and in the functionally defined circuits slowing conduction may only change the pathway and not extinguish the circuit

159
Q

How do antiarrhythmics prolong the refractory period?

A

1) Block Na channels. This leads to less Na channels available to induce another impulse

2) Prolonging the action potential, whether by Na channels or any other means, will prolong refractory period
a. Ex: Ca channel blockers in the SA/AV node
b. Ex: blockers of the delayed rectifier currents (K channels in phase 3)

160
Q

Framework Question:

What is meant by “state dependent ion channel block”?

A

Ion channels undergo conformational change between 3 different states: closed, open and inactivated

The ability of a drug to block an ion channel is dependent on the conformational state, that is, drugs will only have affinity to block ion channels in certain states. Na channel blockers only bind to ion channels in the “open” or “inactivated” state

Hence, the efficacy of a drug to block a certain ion channel is dependent on the state of the ion channel, that is, “state dependent ion channel block” and factors that promote longer duration of time in those desired states

161
Q

Na channel blockers are able to block ion channels in which conformational state?

A

Inactivated and open states

Hence, during each action potential, during the diastolic interval (phase 4), Na channel blockers dissociate and the block is released

162
Q

Na channel blockers – how is efficacy affected by increased heart rate?

A

Increased heart rate allows less time for Na channel blockers to dissociate – dissociation rate – so blocking is increased

Lesson: dissociation rate determines efficacy of Na block

163
Q

Na channel blockers – how does ischemia affect the efficacy?

A

Ischemia is a state of depolarization. And in depolarized states, rate of recovery from block is slowed down. Hence, Na blocking efficacy is increased

Rate of recovery refers to the rate at which an ion channel goes from open -> inactivated -> closed state

Lesson: rate of recovery from block affects the efficacy of ion channel blockers

164
Q

Framework Question:

What main antiarrhythmic property leads to prolonged QT?

A

The QT interval is measured from the beginning of the QRS to the end of the T wave. It encompasses both depolarization and repolarization. ANY mechanisms that prolong the action potential duration can prolong the QT interval. This is often done by prolonging Phase 3, which is most commonly and foremost done by blocking the delayed potassium rectifier channel (IKr)

Lesson: Malfunction of ion channels may lead to an intracellular excess of positively
charged ions, i.e. either by an inadequate outflow of potassium ions or by an excessive inflow of sodium ions.The intracellular excess of positively charged ions prolongs ventricular repolarization and results in QT interval prolongation on the ECG. Hence the second way QT can be prolonged by drugs is by increase in the late Na current which slows intraventricular conduction

165
Q

What is the MOA of calcium channel blockers such as Diltiazem, Verapamil?

A

It’s all in the name – calcium channel blocker.

It blocks Ca channels predominantly in the nodal tissues, such as SA/AV node.

Slows conduction velocity and increases refractoriness

166
Q

Confused:

What are ways to extend refractory period of cardiac cells?

A

1) Extending the action potential: prolonging phase 3 or non-nodal cells with K channel blockers
2) Slowing conduction velocity: Calcium-channel blockers reduce the slope of phase 4 (referring to nodal tissue), thereby decreasing the rate of spontaneous depolarization, which reduces the rate of pacemaker firing. These drugs also decrease the slope of phase 0, which slows conduction velocity within the AV node. Overall, decreasing slope of 4 and 0 leads to slow conduction velocity, which leads to a longer ERP.

167
Q

What is the MOA of QT prolongation from Na blocking agents?

A

Malfunction of ion channels may lead to an intracellular excess of positively
charged ions, i.e. either by an inadequate outflow of potassium ions or by an excessive inflow of sodium ions. The intracellular excess of positively charged ions prolongs ventricular repolarization and results in QT interval prolongation on the ECG. Hence the second way QT can be prolonged by drugs is by increase in the late Na current which slows intraventricular conduction

Given the structural similarity between K+ and
Na+ channels, it is possible that
K+ channel blocking drugs also bind to Na channels

168
Q

What is portal hypertensive gastropathy?

A

Pathology of the gastric mucosa due to portal hypertension that can lead to slow bleeding

169
Q

What is the cause of the bleeding from PHG?

A

Portal hypertension is a prerequisite for the development of portal hypertensive gastropathy (PHG). The pathogenesis of PHG may be related to both congestion and hyperemia in the stomach. This is supported by the finding that gastric mucosal blood flow is increased in patients with cirrhosis and PHG compared with those without PHG

Because the gastric mucosa in the setting of PHG is friable, bleeding may occur when ectatic vessels rupture (though PHG is an uncommon cause of significant bleeding in patients with portal hypertension)

170
Q

What does PHG look like in endoscopy?

A

Snake like mosaic pattern that may be superimposed with red signs, a sign of severe PHG

171
Q

What are key differences in endoscopic findings that distinguish PHG from GAVE (Gastric Antral Vascular Ectasia)?

A

GAVE is located in the gastric antrum, that is, the area before the pylorus.

PHG is located at the opposite end, that is, the proximal stomach in the body and antrum

In regards to appearance, GAVE is characterized by red spots WITHOUT a mosaic background

172
Q

What is the characteristic of a GI bleed from PHG?

A

PHG and every form of enteropathy might be clinically important because they are sometimes responsible for insidious blood loss (chronic iron deficient anaemia) and in exceptional cases even overt acute bleeding.

173
Q

What is treatment for GI bleed from PHG?

A

NSBB and iron supplementation for chronic iron loss

174
Q

How is acute GI Bleed from PHG treated?

A

Same is EVH as dictated by small uncontrolled studies

Yes, that means: octreotide/PPI/Abx ppx

175
Q

What is the next step of management for a patient with persistent GI bleed from PHG despite NSBB?

A

TIPS

176
Q

When we speak about “gastric varices”, what are the different types?

A

GOV1 – esophageal varices extending below the cardia into the lesser curvature

GOV2 – esophageal varices extending below the cardia and into the fundus - cardiofundal varices

IGV 1 – isolated in the fundus

IGV 2 – isolated anywhere other than the fundus

177
Q

What are the most common type of gastric varices?

A

GOV 1 – makes up 75% of the cases

178
Q

Which gastric varices have more severe hemorrhaging?

A

GOV 2 – cardiofundal varices

179
Q

If cardiofundal varices are discovered on endoscopy, what underlying disease process must be evaluated?

A

Splanchnic venous thrombosis

180
Q

What type of GI bleed, in the acute setting, should be treated just like a GI bleed from EVH?

A

PHG

Acute gastroesophageal hemorrhage of ANY type

Makes sense because in all those situations, patient has underlying cirrhosis and from presentation alone, you can’t tell if it is EV vs the others. In regards to GOV1 and 2, they both are extensions of EV, so it makes sense to treat them the same

181
Q

What is the recommended rate of correction for hyponatremia? What is the limit of correction for hyponatremia per day?

A

Both European and US guidelines agree that 10 mEQ/day is the maximum change

US guidelines differ in that they adjust the limit for patients at “high risk” for ODS – no more than 8 mEQ/day

182
Q

What is the fluid recommended to treat acute hyponatremia?

A

HTS 3% over 10 minutes in the US, over 20 minutes in the UK x3 as needed

183
Q

How does 3% HTS treat acute, symptomatic hyponatremia? (Explain the physiology)

A

In acute hyponatremia, neurologic symptoms arise from cerebral edema given the shift of fluid from the extravascular space to the intracellular space.

HTS leads to increased tonicity of the extravascular space, causing fluid shifts from intracellular to extracellular

184
Q

What certain clinical scenarios can lead to acute hyponatremia?

A 
Postoperative period 
Exercise
MDMA
Haloperidol
Thiazide diuretics 
Desmopressin 
Oxytocin 
IV Cyclophosphamide
Transurethral or hysteroscopic use of irrigants such as glycine, sorbitol or mannitol which can be absorbed and cause fluid shifs
185
Q

What is the indication to using 3% HTS for the treatment of hyponatremia?

A

Severe symptoms regardless of acute or chronic

186
Q

What is the dosing, frequency and rate at which 3% HTS should be administered for symptomatic hyponatremia?

A

100ml HTS 3% over 10 minutes up to 3 times

187
Q

What level of Na is considered “severe hyponatremia”?

A

Na < 125

188
Q

What duration of hyponatremia is considered “acute”?

A

< 48 hours

189
Q

What is the expected Urine Na level in patients with hypovolemic hyponatremia?

A

Urine Na < 30

Explanation: in hypovolemic and even hypervolemic hyponatremia (effective blood volume is low), the body will respond with Na retention

190
Q

What can cause pseudohypnatremia?

A

Fat – hypercholesteremia
Protein – high protein concentration
Glucose – hyperglycemia

191
Q

What is the expected Urine Na and Urine Osm for a patient with SIADH?

A

Urine Na > 30
Urine Osm > 100

Remember, “I” means inappropriate. Hence, in the setting of hypoosmolality, what is appropriate is getting rid of free water (Urine Osm <100) and retaining Na (Urine Na < 30)

192
Q

In the algorithm of diagnosing the cause of hyponatremia, when is volume status evaluated?

A

AFTER Urine Na and Urine Osm is evaluated

Volume status is notoriously difficult to assess from a PE standpoint

193
Q

What other urine lab may help diagnose SIAD?

A

FeUrea > 12% highly specific and sensitive

194
Q

What is the algorithm in evaluating a patient with Hypnatremia?

A

Acute or symptomatic?

Urine Osm > 100 Or Urine Osm < 100
-	Urine osm < 100: appropriate 
o	Low solute intake 
o	Primary polydipsia 
o	Beer potomania 
-	Urine osm > 100: inappropriate 
o	Eval Urine Na

Urine Na > 30 OR Urine Na < 30
- Urine <30: Na retention which indicates low effective blood volume (hypervolemia) or true hypovolemia
- Urine > 30:
o SIADH
o Endocrine causes: Adrenal insuff, Hypothyroid
Wasting syndrome: renal salt wasting or cerebral salt wasting

195
Q

What is the pathophysiologic cause for neurologic symptoms in acute severe hyponatremia?

A

Cerebral edema and inability of the neurons to have adapted to the shift in fluid

196
Q

What are measures to lower serum Na when it is overcorrected?

A

Hypotonic fluids or Desmopressin

197
Q

When should hyponatremia overcorrection be corrected?

A

When limit for Na change in one day is surpassed

> 10 mEQ/day
8 mEQ/day (if high risk for ODS)

198
Q

Is there a difference in the limit of Na correction between acute and chronic hyponatremia?

A

According to the European guidelines, in acute symptomatic hyponatremia, there may not be a restricted limit! Crazy!

In chronic, there is a limit – 10 meQ/day (8 meQ/day if high risk for ODS)

199
Q

What is the cornerstone treatment for chronic hyponatremia?

A

Free water restriction (1 L/day)

200
Q

What are the 2 mechanisms by which to treat chronic hyponatremia?

A

Reduced free water intake and increase free water renal excretion

201
Q

What are the indications of treating hyponatremia with HTS?

A

Severe symptoms, regardless of whether the hyponatremia is acute or chronic

202
Q

How does urea aid in the treatment of hyponatremia due to SIAD?

A

Urea causes osmotic diuresis and free water excretion

203
Q

Expected urine labs for SIADH

A

Urine Osm >100

Urine Na > 30

Internal Medicine (6 decks)

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