Next up in the #Tweetorial series based on my Hemodynamic Rounds Live lectures Iβll be discussing the basics of mechanical circulatory support (MCS) π
There is a lot of info to cover so this #Tweetorial will be broken up into four parts.
Follow along below for part 1. β¬
There is a lot of info to cover so this #Tweetorial will be broken up into four parts.
Follow along below for part 1. β¬
In this #Tweetorial I will go through the basics of LV function metrics β how do we measure them; how do we understand them & how do we apply them? π
Then we will examine what each device is supposed to do for LV function & understand a couple of pathologic conditions.
Then we will examine what each device is supposed to do for LV function & understand a couple of pathologic conditions.
Weβll start by reviewing shock, its spiral down to death, & the factors involved. β° Weβll also see where hemodynamic support really plays a role.
In AMICS, the first event that occurs is myocardial infarction β severe impairment of left ventricular function. π
Two things happen - Systolic impairment & diastolic impairment. π
Two things happen - Systolic impairment & diastolic impairment. π
With systolic impairment, cardiac output & stroke volume fall. π
Hypotension results. Peripheral & coronary blood flow becomes impaired.
The response to this is systematic vasoconstriction & fluid retention. π§
Hypotension results. Peripheral & coronary blood flow becomes impaired.
The response to this is systematic vasoconstriction & fluid retention. π§
A dramatic fall in the systematic perfusion π¨ & the release of biomarkers & systemic inflammatory response comes next. Biomarkers such as eNOS, iNOS, TNF-a, pro-inflammatory materials reduces further contractility. β¬
We address these two areas with all medical therapies β β Anticoagulants, Arrhythmics, etc. and provide volume resuscitation, inotropy & vasopressors, but that doesnβt always work. π
On the LV diastolic side of the shock cascade - LVEDP goes up as a compensatory mechanism.π This causes LA & PV pressure to β¬ which can cause pulmonary congestion. Hypoxia results, which further promotes ischemia in combination with decreased perfusion. This must be stopped.π«
If this cascade isnβt stopped progressive cardiac dysfunction & death occurs.
At this point we hemodynamic support can be introduced in addition to coronary reperfusion. β½
The hemodynamic syndrome of shock β‘ evolves into a HemoMetabolic syndrome (a term coined by @NavinKapur4). If left unabated shock produces end organ damage and multisystem failure. π€
With circulatory support & systemic perfusion as an early goal to achieve recovery, we focus on normalizing mean arterial pressure. We measure lactates & creatinine to assess the HemoMetabolic state and to evaluate the patientβs prognosis. π
AMI shock necessitates ventricular support & sometimes both LV & RV support & unloading. We measure these looking at filling pressures β The LV with the wedge or PCWP and the RV with RA pressure measurements.
Because of decreased MAP and β¬ LVEDP there is impairment in coronary perfusion resulting in EKG changes & Troponin π.
Finally, as impairment of perfusion persists, renal & hepatic unloading is needed - if we can do it. We see elevation of right sided pressures, abnormal PA hemodynamics, abnormal coagulopathy & liver functions. π
The likelihood of heart recovery is much better the earlier we evaluate and intervene on patients with shock. πβ
If the hemodynamic & metabolic events donβt change the patient will die. That again supports the use of MCS. ββ½
If the hemodynamic & metabolic events donβt change the patient will die. That again supports the use of MCS. ββ½
This concludes part 1 of this #Tweetorial on the Basics of MCS.
Stay tuned for part 2, when we will examine different device options.
Stay tuned for part 2, when we will examine different device options.
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