Showing posts with label Critical care. Show all posts
Showing posts with label Critical care. Show all posts

Thursday, May 6, 2021

Mechanical Ventilation- Physiology

Mechanical Ventilation- Physiology


  • Non-Invasive Ventilation is of two types:

  1. CPAP = Continuous Positive Airway Pressure: where continuous pressure is exerted during inspiration and expiration 

  2. BiPAP = Bilevel Positive Airway Pressure: where higher pressures are applied during inspiration and lower pressures during expiration


  • Use of CPAP ­čí¬increases intra-thoracic pressure ­čí¬ decreases Venous Return (VR) ­čí¬ decreased Right Ventricular (RV) preload.

  • PEEP > CVP ­čí¬ Preload decreases

  • PEEP > PAP ­čí¬ Afterload decreases (where PEEP = Positive end expiratory pressure, CVP = Central venous Pressure, PAP = Pulmonary arterial pressure)

  • Cardiac Transmural Pressure = pressure difference between inside of the heart and intrathoracic pressure. When CPAP is given, intrathoracic pressure increases ­čí¬ transmural pressure decreases ­čí¬Afterload decreases


  • CPAP: Increases inspiratory flow ­čí¬ Increases Tidal Volume (TV) ­čí¬ helps in unloading the inspiratory muscles to decrease work of breathing ­čí¬decrease dyspnea


  • Increase in expiratory pressure (like with CPAP) in patients with COPD helps in increasing ventilation and oxygenation. This might seem contradictory (how does increased pressure from the ventilator into the lungs during expiration help in increasing ventilation. It seems counter intuitive!). In order to understand this, think about how PURSED LIP breathing in COPD patients actually help them to breathe better!


  • COPD patients need an additional external PEEP in addition to inspiratory support to improve diaphragmatic function.


  • PRE-OXYGENATION: with 100% O2 for at least 3 minutes helps to prolong the apnea time (Apnea time = time to reach 88 to 90% SpO2). The FRC (functional residual capacity) is the reservoir during the period of apnea. 



  • LUNG INFLATION

  1. Moderate inflation: pulmonary stretch receptors reduce vagal stimulation ­čí¬ moderate tachycardia

  2. Hyperinflation: Stimulates Pulmonary C and J receptors ­čí¬ increased vagal signaling ­čí¬ bradycardia


  • LUNG PROTECTIVE VENTILATION
    - Low Tidal Volume
    - High PEEP (to keep lungs open, prevent alveolar collapse)
    - Low plateau Pressure


  • Esophageal Balloon: Can help in measuring pressures to deliver adequate PEEP and TV.


  • AUTO PEEP
    -Auto PEEP is the difference between alveolar pressure and the pressure at the proximal airway.
    -At the exact end of expiration, ideally, we expect the pressure in the alveoli to be zero as all air should have exited from the alveoli. But when some gas is retained, it leads to the development of Auto PEEP.
    -Auto PEEP is measured by end expiratory hold maneuverer.
    -If elastic forces are high and resistive forces (eg resistance in bronchi etc) are low, auto PEEP is minimal or absent.
    -Increase in resistive forces ­čí¬ passive exhalation time increases to ensure complete emptying of expiratory tidal volume.


  • TIME CONSTANT:
    -Time required for lungs to expire 63% of initial volume during expiration.
    -So total of 3 time constants would be needed to exhale 96% of TV out.
    -So, if we keep Inspiratory: Expiratory time as 1:3, Auto PEEP would not occur.
    -Diseases lung is inhomogeneous and can have different time constants for different parts ­čí¬ Expiratory flow limitation.
    -Flow limitation = dynamic condition that occurs when gas flow cannot be increased by increasing alveolar pressure or reducing airway opening pressure.


  • Dynamic hyperinflation is not the same as air trapping
    -In Asthma, inspiratory activity continues into early expiration ­čí¬ dynamic hyperinflation, without air trapping
    -In Recumbent obese patients, air trapping occurs without dynamic hyperinflation.


  • TRACHEOSTOMY
    -Increased risk of infection as compared to Endotracheal Tube (ET) because:
    1. Lack of humidification
    2. Absence of cough, hence decreased clearance of secretions
    3. Reduced ciliary function
    -Reduced work of breathing as compared to ET because:
    Tracheostomy tubes are smaller, more rigid ­čí¬ less turbulent airflow ­čí¬ reduces expiratory flow limitation, dynamic hyperinflation, auto-PEEP ­čí¬ reducing work of breathing

Written by Amrin Kharawala

Saturday, December 5, 2020

Mechanical ventilation

Terms you need to know

1.       PaO2: Oxygen saturation in arterial blood  (N = 80-100)

2.       PaCO2: Carbon Dioxide saturation in arterial blood (N = 35 – 45)

3.       FiO2: Fraction of inhaled O2 (N = 21% i.e. the fraction of O2 in atmosphere air which we inhale)

4.       PEEP: Positive End Expiratory Pressure – The pressure needed at the end of expiration to keep the alveoli open.

5.       RR: Respiratory rate (N = 12-16)

6.       TV: Tidal Volume (N = 6-8 ml/kg = approx. 500 ml)

Monday, March 30, 2020

COVID-19: Convalescent plasma as a treatment option

As the pandemic of COVID-19 continues, researchers have been looking at treatment options, most recently the use of convalescent plasma has generated a great deal of interest.

So let's dive in and understand convalescent plasma therapy and its scope:

Convalescent plasma therapy is based on the theory that a patient in the convalescence phase develops antibodies for that disease in their serum, which can be used to treat other patients, after ensuring that safe blood banking practices are being followed.

Historically, convalescent plasma was used as a prophylactic agent against measles. [1] But with the advent of vaccine development and monoclonal antibodies, the use of convalescent plasma went out of practice. It has also been used for scarlet fever [2] and poliomyelitis [3]. The use of convalescent plasma was recommended as an empirical treatment during outbreaks of the Ebola virus in 2014 [4], and a protocol for the treatment of Middle East respiratory syndrome coronavirus with convalescent plasma was established in 2015 [5].

A case series of 5 critically ill patients with laboratory-confirmed COVID-19 and ARDS was done in Shenzhen, China from January 20, 2020, to March 25, 2020. [6] In this study, 5 patients with severe pneumonia (rapid progression and high viral load requiring mechanical ventilation) received SARS-CoV-2 specific antibody (via convalescent plasma), with a binding titer>1:1000 and neutralization titer>40 along with interferon, lopinavir/ritonavir, and methylprednisolone. On 28th March 2020, the FDA gave approval of IND, i.e. Investigatory new drug application to use of convalescent plasma (after approval) to treat critically ill patients. [7]

Friday, June 21, 2019

Understanding Refeeding Syndrome

Refeeding syndrome is a life-threatening metabolic complication of - stay with me - refeeding. It can happen via any route after prolonged starvation.

Who are at risk?
They’re patients with prolonged artifical feeding [parenteral or enteral], malignancy, anorexia and alcoholism.

Why does it happen?
During starvation, the body uses fat and protein for energy. There’s no carbs so there’s little to no insulin.

After refeeding, carbohydrate load causes a spike in insulin level.
Now first prof biochemistry tells you, more insulin means more cellular uptake of phosphate.
That’s it. That low serum phosphate level is the main problem.

How does it present?
Non-specifically and catastrophically. Features are rhabdomyolysis, red and white blood cell dysfunction, respiratory insufficiency, cardiac arrhythmias and seizures.
Left unchecked, it can lead to sudden death.

How do I prevent it?
Identify at-risk patients and give high-dose, high-potency Vitamin C and B complex injection, during re-feeding window.
Monitor vitals and labs closely. Close involvement of nutritionist is ideal.

What if it’s already happened? How do I treat it?
The biggest challenge is management of complications.
As regards phosphate, get the levels back up. Administer oral as well as parenteral phosphate, upto 18 mmol per day.


Thank you, that’d be all.
- Ashish Singh.

Tuesday, April 2, 2019

Pathophysiology: Diabetic Ketoacidosis

Hello guys, here’s a whiteboard summary of how DKA happens.


[Please click on the image to enhance it]

- DKA is a medical emergency. It’s a complication of type 1 diabetes.
- DKA has a triad of hyperglycemia, ketosis [metabolic acidosis] and dehydration.
- Main ketone bodies are beta-hydroxybutyrate and acetoacetate. Acetone is only a minor ketoacid.
- Lactic acidosis also contributes to metabolic acidosis.
- More glucose in blood leads to more glucose filtered into urine causing osmotic diuresis.


- Ashish Singh 

Wednesday, March 6, 2019

HAP and VAP

Pneumonia types — The 2016 Infectious Diseases Society of America (IDSA)/American Thoracic Society (ATS) guidelines distinguish the following types of pneumonia :

●Hospital-acquired (or nosocomial) pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission.

●Ventilator-associated pneumonia (VAP) is a type of HAP that develops more than 48 hours after endotracheal intubation.

Bhopalwala. H

Wednesday, January 2, 2019

In short: Vasopressin in the ICU

Hello!

Here are some quick points + mnemonics on Vasopressin!

1. Effects are preserved during hypoxia and severe acidosis and catecholamine-resistant states.

Mnemonic: Vasopressin presses when other pressors can't press the vasculature anymore.

2. Vasopressin decreases norepinephrine requirement.

3. Onset: fast, offset: fast.
Mnemonic: VasopressIN is IN and OUT fast.

4. It is often weaned off last in patients on multiple pressors for the same reason.

5. Used in:
- Refractory hypotension (potentiates the actions of over vasoconstrictors)
- Esophageal variceal bleed
- Cardiac arrest
Non ICU indications: vWD, DI, hemophilia

That's all!

-IkaN

Tuesday, January 1, 2019

In short: Dexmedetomidine and bradycardia

If a patient who is intubated and sedated develops bradycardia, go through the sedatives list - it might give you a hint on what is causing the bradycardia.

Dexmedetomidine (Precedex) is notorious for causing bradycardia. Another sedative associated with bradycardia is propofol.

That's all!

Will update this post at a later date. What you can do if you are free: Read up on it, write a small post on it and email it to us so we can post it and learn from you :)

-IkaN