If someone dies of one of those what exactly kills him and how? Which of those are medical terms and what meaning exactly do doctors put behind them?
PS: If you have a slightly higher age explanation I'd be ok with it.
PS2: Everyone is awesome, thanks for all the explanations :)
The title.
Hi everyone! I’m a med student and I can’t understand the difference between these two conditions, if there is any; can someone please explain? Thank you!!
Hi everyone there.
I would like to have access to this paper.
DOI: 10.1097/MCC.0000000000000839
Thanks in advance.
It seems there is significant practice variability and opinion in this area. I've been using norepinephrine first (sometimes I titrate on dobutamine if they remain in a low flow state)-- the cardiologist told me when norepinephrine is given alone it prioritizes pressure over flow, which usually improves the blood pressure initially, but potentially causes deterioration thereafter... thoughts?
EDIT: changed levo/levophed to norepinephrine wherever I used it... can’t change the title 🤷🏼♀️
UPDATE: thanks for all of the info! I read through all of the comments and the trials mentioned. I still can’t find anything other than theoretical literature stating that using norepinephrine alone could cause harm. I am still going to use it in cardiogenic shock secondary to MI.
The reading was enlightening. Slightly off topic, but I’m motivated to look harder for valvular sources of cardiogenic shock on my initial bedside echo (god forbid they stay in the ED long enough for a formal echo + formal read). Then I’ll consider changing the meds to match the valvular pathology. Otherwise, I’m probably going to stick with norepinephrine +/- dobutamine during their initial resuscitation in the ED...
I'm sorry for my poor understanding. I understand that since NE has modest beta effect and primarily effects alpha receptors with greater potency, it effects SVR and does not have so much net effect on CO. So if we have AMI causing cardiogenic shock or a situation where force of contraction is already poor, why would NE still be recommended as first line for those type of cardiogenic shock? In those situation, wouldnt one rather prefer something with decreased afterload/SVR AND increased contracility force?
I understand why it's preferred over dopamine for CS because of greater mortality benefit and lesser proarrythmic effects
doi: 10.1097/MCC.0000000000000624
So this is a concept I'm pretty confused about. In NBME 24, they had a patient who has an acute MI with systolic dysfunction/cardiogenic shock and the answer was that his PVR decreased, presumably due to high catecholamine levels. On the Free 120, they had a patient with hypovolemic shock if I remember correctly and it said the patient's PVR increased, even though I would think that both of these scenarios would react in a similar way. Anyone know why PVR increases in hypovolemic shock but decreases in cardiogenic shock? Thanks!
Zanki says within the 1st 24 hours, but an RX qmax question contradicts that. Does anyone know whats going on here?
Here are some screenshots.
https://preview.redd.it/usuuo8tssyo21.png?width=2668&format=png&auto=webp&s=3bf87c08f64374a97fee8e24e1c774e5657bde64
https://preview.redd.it/f8kr9kvvsyo21.png?width=2526&format=png&auto=webp&s=ba0725275beaeb2414d70c5ac0890047329066ab
I'm sorry for my poor understanding. I understand that since NE has modest beta effect and primarily effects alpha receptors with greater potency, it effects SVR and does not have so much net effect on CO. So if we have AMI causing cardiogenic shock or a situation where force of contraction is already poor, why would NE still be recommended as first line for those type of cardiogenic shock? In those situation, wouldnt one rather prefer something with decreased afterload/SVR AND increased contracility force?
I understand why it's preferred over dopamine for CS because of greater mortality benefit and lesser proarrythmic effects
