Yes we want a video only on pulse! All these are very basic things but significantly important and everyone should be aware of them ! Thank you for this great video!!
@@MedicosisPerfectionalis you are one hardworking doctor and educator, I must say. I am preparing for MRCP and finding your approach,note and wsy of teaching pretty awesome! NO Stress at all! Though I am much older to you and loving my journey with your notes! God bless you 💥
🚨 Something off topic, if you please. I was recalling one of your previous questions regarding some infection that resembles fungal infection but it's rather caused by bacteria maybe E. Coli and it has the name that falsly suggest a fungal infection. Can you please name the disease and the causative organism behind it? 🙏
@@mari-lay833 it's indeed caused by stap aureus and it goes by the name of Botryomycosis. Thank you for the feedback, i recently recalled what was i asking for (good thing i study a lot 😊)
20:18 Wouldn't DKA increase the respiratory rate rather than decrease it? If DKA causes metabolic acidosis then the rate and depth of ventilations should increase as a compensatory mechanism.
Yes tachypnea does occur for compensation but it will be progressed to bradypnea, let me explain..... The presence of metabolic acidosis will normally generate a respiratory response. The reduction of serum bicarbonate and pH will result in hyperventilation and reduction in carbon dioxide (CO2), partially preventing further fall in pH and bicarbonate concentration. Respiratory compensation for metabolic acidosis will cause the arterial CO2 to decrease by 1.2 mmHg for each 1 meq/L fall in the serum bicarbonate. There is a limit to the lungs’ ability to compensate for metabolic acidosis. Even with serum bicarbonate concentrations below 6 meq/L, CO2 levels cannot fall lower than 8-12 mmHg. Furthermore, the duration of the respiratory compensation is limited by respiratory muscle fatigue. Initially, patients will develop tachypnea, which is increased respiratory rate, leading to decrease in CO2 concentration. With progression of acidosis, respiratory pattern evolves to hyperpnea, which is increased tidal volume, and ultimately, patients will develop a deep, fast and agonal pattern of breathing, named Kussmaul’s respiration. Once patients with DKA develop Kussmaul’s respiration, they are reaching the point of respiratory muscles fatigue, and mechanical ventilation should be considered. Furthermore, patients in DKA are severely “air hungry” prior to intubation, and are at higher risk to develop acute respiratory distress syndrome (ARDS) due to hyperpnea. Mechanical ventilation in these patients is particularly delicate, since a lung protective strategy, with low tidal volumes and controlled transpulmonary pressures, should be maintained, while attempting to increase minute-ventilation until metabolic acidosis is completely corrected. In DKA, respiratory failure is caused by several electrolytes, metabolic and cardiac and lung end-organ damage, hence the bradypnea.. Tdlr:- tachypnea does occur in DKA, but in sever cases the tachypnea is progressed to kussmaul's breathing, which leads to respiratory muscle fatigue in long run, hence respiratory failure, leading to bradypnea
Emergency Medicine Course: www.medicosisperfectionalis.com/
Yes we want a video only on pulse! All these are very basic things but significantly important and everyone should be aware of them ! Thank you for this great video!!
Thank you!
A Pulse video would be wonderful. I have a “Slippery“ pulse per a Chinese medicine doctor.
exactly before my exam THANK YOU !
My pleasure!
Need video on pulse in detail pls🎉
Thank you so much for letting me know!
@@MedicosisPerfectionalis you are one hardworking doctor and educator, I must say. I am preparing for MRCP and finding your approach,note and wsy of teaching pretty awesome! NO Stress at all! Though I am much older to you and loving my journey with your notes! God bless you 💥
❤❤ always my Best, how did you know I was waiting for this lecture ❤❤
Thank you!
Good 👍
Thanks!
Make a video on pulse
Thank you so much for letting me know!
🚨
Something off topic, if you please.
I was recalling one of your previous questions regarding some infection that resembles fungal infection but it's rather caused by bacteria maybe E. Coli and it has the name that falsly suggest a fungal infection. Can you please name the disease and the causative organism behind it? 🙏
I don't know if this is what you're looking for, but all I can think of is mycotic aneurysms caused by Staph. aureus.
@@mari-lay833 it's indeed caused by stap aureus and it goes by the name of Botryomycosis. Thank you for the feedback, i recently recalled what was i asking for (good thing i study a lot 😊)
More videos on pulse❤
Thank you for letting me know!
‘What the French toast are you doing?……’
‘Get your head OUT of your sphincter.’
😂😂😂😂😂😂Omds😅😂😂😂😂
Thank you so much @medicosisperfectionalis😇☺️
My pleasure!
EMS/ EMT/ Paramedics Playlist: ruclips.net/p/PLYcLrRDaR8_fIFkBE_iH_xnXyI0jCqQgT&si=u_AZm-mlYCNm5Ip9
10:09 Another med that can cause bradycardia is digoxin.
Excellent!
Emergency Medicin Playlist: ruclips.net/p/PLYcLrRDaR8_eiv6nwK2Ez2nqxUBDo9tZh&si=pHrO_p7hmLSn6yxM
🚨🚨🚨🚨
More videos are coming!
@@MedicosisPerfectionalis Your channel is a treasure for us, Thank you very much
20:18 Wouldn't DKA increase the respiratory rate rather than decrease it? If DKA causes metabolic acidosis then the rate and depth of ventilations should increase as a compensatory mechanism.
Yes tachypnea does occur for compensation but it will be progressed to bradypnea, let me explain.....
The presence of metabolic acidosis will normally generate a respiratory response. The reduction of serum bicarbonate and pH will result in hyperventilation and reduction in carbon dioxide (CO2), partially preventing further fall in pH and bicarbonate concentration. Respiratory compensation for metabolic acidosis will cause the arterial CO2 to decrease by 1.2 mmHg for each 1 meq/L fall in the serum bicarbonate.
There is a limit to the lungs’ ability to compensate for metabolic acidosis. Even with serum bicarbonate concentrations below 6 meq/L, CO2 levels cannot fall lower than 8-12 mmHg. Furthermore, the duration of the respiratory compensation is limited by respiratory muscle fatigue.
Initially, patients will develop tachypnea, which is increased respiratory rate, leading to decrease in CO2 concentration. With progression of acidosis, respiratory pattern evolves to hyperpnea, which is increased tidal volume, and ultimately, patients will develop a deep, fast and agonal pattern of breathing, named Kussmaul’s respiration.
Once patients with DKA develop Kussmaul’s respiration, they are reaching the point of respiratory muscles fatigue, and mechanical ventilation should be considered. Furthermore, patients in DKA are severely “air hungry” prior to intubation, and are at higher risk to develop acute respiratory distress syndrome (ARDS) due to hyperpnea. Mechanical ventilation in these patients is particularly delicate, since a lung protective strategy, with low tidal volumes and controlled transpulmonary pressures, should be maintained, while attempting to increase minute-ventilation until metabolic acidosis is completely corrected.
In DKA, respiratory failure is caused by several electrolytes, metabolic and cardiac and lung end-organ damage, hence the bradypnea..
Tdlr:- tachypnea does occur in DKA, but in sever cases the tachypnea is progressed to kussmaul's breathing, which leads to respiratory muscle fatigue in long run, hence respiratory failure, leading to bradypnea
First one
Thank you so much!
🤺🚨
More videos are coming!