What is the difference between hypoxic and hypercapnic respiratory failure?
Intensive Care Nephrology
ESRD ptns are particularly vulnerable to severe
COVID-19 (older
age & high frequency of co-morbidity, e.g. DM & HT, in this cohort. The
ASN & ISN
hv issued guidelines and a list of resources to guide nephrologists to provide
life-sustaining DX care. These resources that continue to evolve are frequently
updated, including the following: early
recognition & isolation of individuals with respiratory Sm(s);
ptn separation & cohorting within waiting
areas and within DX unit; use of personal protective equipment in DX unit; with added measures for ptns with
confirmed/suspected COVID-19.
Revise please the abbreviation list on:
https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
Q.429. What is the difference between hypoxic &
hypercapnic respiratory failure?
A. Hypoxic Resp. failure c Failure to
maintain adequate oxygenation.
Hypercapnic
Resp. failure c
inadequate ventilation c Co2 retention.
Q.430. What are the possible modes of
mechanical ventilation in I.C.U.?
A. Modes of Mch.v.:
I. Volume-cycled: certain “tidal
volume” delivered by the ventilator: SIMV (Synchronized
Intermittent Mandatory Ventilator) & CMV (Continuous
Mandatory Ventilation).
II. Pressure-cycled ventilation:
volume is delivered until pre-set maximum pressure is reached = P.C.V. =
pressure controlled ventilation.
III. Flow-cycled
ventilation : “inspiration” continued until a pre-set flow rate is
reached ( P.S.V.) = Pressure Support Ventilation.
CMV:
Minimizes the work of breathing done by the ptn., it is used in ptn. é myocardial ischemia or profound hypoxemia,
e.g. COPD
& tachypnea ptn..
Q.431. What is the etiology of ARDS?
A. Causes
of ARDS:
1) Sepsis Ø the most
common Ø
40 % of cases.
2) SIRS Ø Systemic Inflammatory Respiratory Syndrome.
3) Others Ø Trauma, pneumonia,
burn, DIC, near drowning.
Q.432. What is the pathophysiology of ARDS?
A. Pulm. cpll. endothelium dge:Ø é its permeability + influx of fluid into alveoli.
Neutrophils: activated by [C, IL1,6
,8,10 & TNFa]Ø
inflmm. mediators & highly active oxidative sp. & proteolytic enz. & metabolites of arachidonic a. wch cn
direct-ly injure alveoli & cpll. endothelial cellsØfluid leak é alveoli &
edema formation.
MacrophageØ
Clear alveoli fr. neutrophil Ø Resolution of ARDS.
Thromboxan A2Ø interact é neutrophil Ø Cell aggregation.
Lipo-oxygenase productsØ Permeability ch.ch.Ø Pulm. Vsc. changes Ø Cpll. Leak.
Q.433. What is the effect of ARDS on renal function?
A. ARDS Ø20-40 %ØRenal dysfunction, due
to: [Sepsis- Hemodynamic ins-tability] are
accused, but Mechanical Ventilation itself Ø is FStrong Predictor of
Dgx. of R. dysfunction. (See next Q).
Q.434. What is the effect of “mechanical ventilation” on
renal function?
A. Mechanical ventilation: Ö
1) ê R.B.F.
2) Na+ Retention.
3) ê U.O.
Q.435. What else?
A. Hypercapnea:Ö
Renal V.C. + Nor. release Ø ê RBF.
Systemic V.D. & ê P.R Ø ê RBF.
Q.436. What is the effect of “positive pressure” on renal function in
this situation?
A. Positive
pressure:Ø+ ve intrathoracic
pressure Øê V.R. Øêeffective circulatory vol. & é pulm. Vsc. Pressure & é R.V. afterload Ø
ê C.O. Ø ê RBF.
Q.437.What is the non-hemodynamic
factors affecting renal function?
A. Non-hemodynamic: AKI &
ALI Ø flattening of epithelial cells in canines & R. tub. apoptosis + Incr. biochemical markers of kid. dysfunction
(Rabbit
Model).
Q.438. What humoral changes can be expected due to mechanical
ventilation?
A. Humoral changes due to mechanical ventilation:
1) J ADH ð V.C. (mainly rather H2O retention).
2) J Pl. renin
activity ðK G.F.R. due to: K RBF & H2O retention.
3) K V.R. & K Atrial pressure ð K ANP & K U.O.
- ARDS ð an early manifestation of a SYSTEMIC INFALAMM. process ð MODF
incl. F AKI. BAL in ARDS ð { éTNFa,
IL1B, IL6} in BAL fluid.
Q.439. Can u please summarize the aforementioned factors affecting renal function in ARDS patient? <
A. Factors
affecting “renal function” in ARDS patients: ¯¯
1) Sepsis.
2)
Hemodynamic instability.
3) Mechanical ventilation:Ø
ê R.B.F.
Na+ Retention.
ê U.O.
4) Hypercapnea:Ø
i. Renal V.C.
+Nor. release Ø
ê RBF.
ii. Systemic V.D. & ê P.R Ø
ê RBF.
5)
Positive pressureØ+ve
intrathoracic pressure Øê V.R. Øê effective circ-ulatory
vol. & é pulm. Vsc. pressure & é R.V. afterload Ø ê C.O.Ø ê RBF.
6)
Non-hemodynamic : AKI & ALIØ flattening of epithelial
cells in canines & R. tub. apoptosis + incr. biochemical
markers of kid. dysfunction.
7)
Humoral changes due to mechanical ventilation:
J ADH ð V.C. (mainly rather H2O retention).
J Pl. renin activity ðK G.F.R. due to :K RBF & H2O retention.
K V.R. & K
Atrial pressure
ðK ANP & K U.O.
Q.440. What is the role of “pulmonary cytokines” in AKI?
A. Pulm. cytokinesØ [TNFa, IL. 1,2,8, ,فيات 128 , Interferon g , granulocyte, macrophage colony stimulating f.] Ø All
hv bn ass. é R. injury in isch./ reperfus-ion model.
Generally, during COVID-19 pandemic, ptns receiving home DX should hv their
regular follow-up visits performed via telemedicine rather than in-clinic visits. Moreover, home
visits by health care professionals shd be minimized or hold. Pnts should hv at least
two weeks of DX supplies with proper medications in case they hv to self-isolation.
If in-person visit is clinically indicated,
proper infection control measures for the outpatient unit should be applied with
limitation of the number of ptns seen per day. Non-urgent procedures should be postponed.
The ASN has provided guidelines for nephrologists caring for hospitalized
patients requiring DX for ESRD and AKI, adherence to the suggested guidelines is advised:
Ptns e COVID-19
should be co-localized on a floor or ICU,
if possible. Co-localization within adjacent
rooms can enable one DX nurse to
simultaneously deliver DX for > one ptn. If ptn is in a negative-pressure isolation
room, then one HDX nurse will need to be dedicated for the care of that ptn in
a 1:1 nurse-to-ptn
ratio. If possible, ptns with suspected/confirmed COVID-19 who’re not critically ill shd be dialyzed in
their own isolation room rather than being transported to the in-ptn DX
unit.
Video & audio streams should be used to troubleshoot alarms
from outside the room to minimize the need for DX nurse or the
nephrologist to enter an isolation room. CRRT is preferred among critically
ill ptns in ICU who hv ESRD/AKI.
Even among ptns who’re hemodynamically stable and who cd tolerate intermittent HDX (IHD), CRRT or
prolonged intermittent renal replacement therapy (PIRRT),
also called sustained low-efficiency DX (SLED),
should be performed instead, depending upon machine & staffing availability.
As CRRT or PIRRT can be managed
without 1:1 HDX support. This would potentially help decrease wastage of personal protective equipment and limit exposure among HDX nurses. With CRRT capacity overwhelming, CRRT machines can be used to deliver prolonged
intermittent ttt (eg, 10 hs rather than continuous)
with higher flow rates (eg, 40-50 mL/kg/h). This will enable CRRT machine
to be more available for care of another ptn after terminal dysinfection. If
available, HDX or CRRT machines are scarce,
clinicians may need to consider ttt of AKI with PD. Ptns with suspected/confirmed
COVID-19 who
develop AKI, and an emphasis should
be placed on optimizing volume status to exclude and ttt pre-renal (functional) AKI while
avoiding hypervolemia, wch may worsen ptn’s
respiratory status. Ptns with AKI with no
need for DX should be managed on a limited contact bases. Physical evaluation
and U/S studies should be coordinated e primary/consulting teams to minimize contact, as much as possible. Ptns
receiving ACEi/ARBs) should continue their therapy (unless there’s a contra-indication
e.g. hyperkalemia or hypotension). There’s no evidence that
stopping ACEi/ARBs limit the severity of COVID-19.
Pts e stage 4/5 CKD who’re referred for DX access placement should undergo their
procedures as planned (not hv their planned procedure deferred).
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