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INTERAKSI

JANTUNG PARU

INTRODUCTION
UNIT KARDIORESPIRASI
JANTUNG
SISTIM PEMBULUH DARAH
FUNGSI PARU

VENTILASI
LUNG VOLUME
INTRATHORACIC PRESSURE
SURROUNDING PRESSURE
ENDOCRINOLOGIC RESPONSE

MYOCARDIAL RESERVE

CIRCULATING BLOOD VOLUME


AUTONOMIC TONE
BLOOD FLOW DISTRIBUTION

FUNGSI KARDIOVASKULAR

RESPONS KARDIOVASKULAR
TERHADAP
MANUVER VENTILASI MEKANIK

BASELINE DARI FUNGSI SISTIM


KARDIOVASKULAR PASIEN

HUBUNGAN ANTARA AIRWAY PRESSURE,


INTRATHORACIC PRESSURE, DAN LUNG VOLUME

CONSEPT ~ HAS BEEN WIDELY ACCEPTED


PPV - MELALUI AIRWAY PRESSURE
LANGSUNG MEMPENGARUHI HEMODINAMIK
Paw = Pleural Pressure and Lung Volume

wrong assumption

SEBETULNYA
Paw SANGAT TERGANTUNG PADA:
POLA VENTILASI
AIRWAY RESISTANCE
LUNG COMPLIANCE

Paw TIDAK MEREFLEKSIKAN Ppc


(= Transmural LV Pressure)
SECARA AKURAT

LUNG VOLUME
INTRATHORACIC PRESSURE

RESPON HEMODINAMIK
TERHADAP VENTILASI

HEMODYNAMIC EFFECTS OF
VENTILATION
ADA 3 KONSEP DASAR YG HRS DIPAHAMI
1. BERNAFAS = EXERCISE, KEBUTUHAN O2 DAN
ELIMINASI CO2
2. INSPIRASI : INTRAPLEURAL PRESSURE

LUNG VOLUME
3. BERNAFAS SPONTAN : ITP
, SEDANGKAN
VENTILASI TEKANAN POSITIF /PPV: ITP

EFEK HEMODINAMIK AKIBAT


PERUBAHAN PADA VOLUME PARU
PERUBAHAN PADA VOLUME PARU
MENYEBABKAN EFEK PADA:
TONUS SIMPATIS OTONOM
RESISTENSI PEMBULUH DARAH PARU /
Pulmonary Vascular Resistance

TONUS SIMPATIS OTONOM


RESP SINUS ARRHYTHMIA
Inspiration-associated cardioacceleration
Vagally mediated reflex arcs
lung inflation to normal TV <10 cc/kg
heart rate

the

ADH INDUCED FLUID RETENTION

MECHANICAL VENTILATION-INDUCED CHANGES IN


PULMONARY VASCULAR RESISTANCE (PVR)

PVR

Alveolar
compression

Total PVR

Alveolar Vessels

Hypoxic pulmonary
vasoconstriction

Extra-alveolar
vessels

RV

FRC

LUNG VOLUME

TLC

VENTRICULAR INTERDEPENDENCE
50

35

20

LV Pressure (mmHg)

20

10

0
0

10

20

30

40

LV VOLUME (ml)
The effect of increasing right ventricular (RV) volumes on the left
ventricular (LV) diastolic pressure-volume (filling) relationship.
Increase on RV volume decrease LV diastolic compliance

HEMODYNAMIC EFFECTS OF CHANGES IN


INTRATHORACIC PRESSURE ON THE LV FILLING AND
EJECTION PRESSURE
Increasing ITP decreases the
pressure gradient for venous
return and LV gradient

ITP
VENOUS
RETURN

THORAX

LV
EJECTION

ITP
Decreasing ITP increases the
pressure gradients for venous
return and LV gradient

Decrease in ITP that decrease Pra to below zero relative to atm pressure
increase venous return by only a limited amount; increases in ITP
progressively decrease venous return to a complete circulatory standstill

Blood Flow (L/m)

6
5

ITP

ITP

3
2

Venous return
curve

1
-5

0
5
Right Arterial Pressure (mmHg)

10

HEMODYNAMIC EFFECTS OF VENTILATION


BASED ON CARDIOPULMONARY STATUS
Should be clear that:
Spont and PPV have profound hemodynamic
consequences and might even have opposite
effects on the cardiovascular stability in the
different populations of patients
Different modes of mechanical ventilatory
support, by varying degree of the patients
effort and thus changes in WoB and ITP as well
as the level of lung volume, also alter the
hemodynamic response.

Fundamental of cardiopulmonary
interaction
SPONT VENT LUNG VOLUME
ITP
IPPV
LUNG VOLUME
ITP
Most hemodynamic differences between spont
ventilation and IPPV reflex differences in ITP and
energy to create this swings
Changes in both lung volume and ITP need to be
considered when assessing the hemodynamic
effects of either spont ventilation or IPPV

The effects of changes in ITP on the LV pressure-volume


relation (ESPVR) when cardiac contractility is normal

LV Pressure

ESPVR
ITP

Decreased
LV Ejection
Pressure

Increased LV
ejection Pressure

Increased LV Preload

ITP
Decreased
LV Preload

Diastolic compliance

LV Volume

ITP

= EDV

, ESV

SV

ITP

= EDV

, ESV

SV

The effects of changes in ITP on the LV pressure-volume


relation (ESPVR) when cardiac contractility is impaired and
volume status is expanded

LV Pressure

ESPVR
Increased LV
ejection Pressure

Decreased
LV Ejection
Pressure

Decreased
LV Preload

ITP

ITP

Increased LV Preload
Diastolic compliance

LV Volume

ITP

= EDV

, ESV

SV

ITP

= EDV

, ESV

SV

ACUTE LUNG INJURY


PEEP sangat diperlukan untuk
mempertahankan distensi alveolus sehingga
oksigenasi arteri lebih baik.
Pada prinsipnya peningkatan tekanan jalan
nafas tidak merefleksikan peningkatan ITP,
namun khusus pada pasien dgn ALI dimana
terjadi penurunan compliance paru dan
dinding dada, maka setiap peningkatan
volume paru oleh ventilasi mekanik akan
meningkatkan ITP.

SINGER AND COWORKERS;

Hyperinflation determine the decrease


in CO, not Paw.
Hyperinflation can be counterbalanced,
in part, by fluid rescucitation that restore
the ITBV to the pre-PEEP level.

Lessard and coworkers:

Compare VC, PC and PC-IRV in 9


ARDS
Because PEEP and TV consistent, the ITP
were similar
Arterial pressure was slightly lower with
PC-IRV compare to VC and PC
But no significant hemodynamic effects
were seen.

Chan and Abraham:

Similar results in 10 ARDS patients


macth for comparable TV and total
PEEP

Abraham and Yoshihara, Poelaert and


colleagues;

Membandingkan mode PC (TV kecil)


dgn VC
Kesimpulan bahwa insiden penurunan
CO lebih sedikit pada pasien yg
menggunakan PC

Christian and coworkers;


APRV (BIPAP) dapat meningkatkan performa
jantung pada pasien dengan ALI/ARDS
Dengan mode APRV maka peak pressure dan
Mean Paw akan lebih rendah sehingga
transmisi ITP akan lebih kecil juga.
Dengan turunnya ITP maka venous return
akan meningkat, selanjutnya performa jantung
juga akan lebih baik, sehingga mengurangi
insiden pemakaian vasopresor untuk
menunjang MAP dan DO2.

COPD
Masalah utama hemodinamik sangat
berhubungan dengan dynamic hyperinflation
Dynamic hyperinflation akan menyebabkan
timbulnya auto/intrinsic PEEP
Auto PEEP + PPV akan meningkatkan
overdistensi alveolar
Ppl
venous return
Asmatic attact/acute on COPD decreased
ITP (mean 30 cmH2O) pulmonary edema
(from PPV to spont)

Intrinsic plus extrinsic PEEP ~


alters hemodynamic function,
except the ext PEEP is delivered
below the intrinsic level of PEEP

Weaning of patients with COPD


Severe COPD may experience
cardiogenic pulmonary edema
during weaning
The cause probably combined
volume overload and increased LV
failure due to decrease LV-EF, and
after diuresis many of these
patients can be subsequently
weaned.

MOHSENIFAR AND COLLEAGUES;

Patients who could not weaned had a


gastric pHi that was substantially
reduced from 7.36 during IPPV to 7.09
during weaning.
Patients who succesfully weaned show
little change in pHi (7.45 to 7.46).
Thus, occult cardiovascular insuffisiency
may play a major role in failure to wean
in critical ill patients