Haemodynamic monitoring

• PAP >PAOP
• catheter tip location below the level of the left atrium on a portable lateral chest X-ray
• A and V waves visible within trace (cardiac ripple)
• change in PAOP less than half the change in PEEP during a PEEP trial

am  Ende der Expiration:

bei Spontanatmung ist PAOP der höchste Werte und wird VOR Druckabfall durch Inspiration gemessen

bei Beatmung ist PAOP der niedrigste Werte und wird VOR Druckanstieg durch Respiratorinspiration gemessen

Man geht davon aus, dass am Ende der Expiration die Drücke, die von exterm auf die Pulmonalgefässe wirken, am niederigsten (=0) sind.

Die Venendruckkurve besteht aus 3 positiven Wellen a, c und v; und aus 2 negativen Tälern x und y. Die Venendruckkurve steht in fester Beziehung zum EKG

• a-Welle: Vorhofkontraktion
• c-Welle: Vorwölbung der Trikuspidalklappe zu Beginn der Ventrikelkontraktion
• x-Tal: Kontraktion des Ventrikels, Verschiebung der Ventilebene des Herzens in Richtung Herzspitze, dadurch Abfall des Venendruckes (systolischer Kollaps).
• v-Welle: Füllung des rechten Vorhofes bei geschlossener Trikuspidalklappe
• y-Tal: Öffnung der Trikuspidalklappe, Bluteinstrom in der rechten Ventrikel  dadurch Druckabfall im venösen System (diastolischer Kollaps).

• Fehlende a-Welle: Vorhofflimmern
• Hohe a-Wellen: Erhöhter Widerstand bei der Vorhofentleerung z.B. Trikuspidalstenose, Pulmonalstenose, rechtsventrikuläre Hypertrophie, pulmonale Hypertonie
• Riesige a-Wellen: rechter Vorhof kontrahiert gegen die geschlossene Trikuspidalklappe z.B. ventrikuläre Arrhythmien, Herzblock
• Hohe v-Wellen bei fehlender x-Welle: Trikuspidalinsuffizienz

Wenn die v-Welle der Kurve zu hoch ist dann wird PAOP überschätzt->Messung in der Mitte der a-Welle ergibt besseren medianen Wert. a-Welle am besten mit EKG finden (liegt im PR-Abstand)

• point 1, peak of atrial contraction (a wave);
• point 2, LAP during start of ventricular systole
• point 3, peak of atrial filling (v wave)
• point 4, earliest LAP during ventricular filling;
• line between points 5 and 6, pressure during diastasis.

1. Change in the waveform from pulmonary artery (with systole and diastole) to

a PAOP waveform. Although distinct A and V waves may not always be
identifiable, a low amplitude, oscillating baseline should be visible. A PA waveform should immediately return on balloon deflation

2. Fall in mean pressure; normally, the mean PAOP is similar to or slightly lower than the diastolic PAP (usually within 0-4 mmHg). However, in conditions in which a large V wave is present in the PAOP waveform, the displayed mean value of the PAOP may be higher than diastolic PAP.

3. Blood aspirated from the distal tip of a PAC in the wedge position is highly oxygenated and resembles arterial blood. The PO2 is slightly higher than PO2

of the systemic arterial blood.
The catheter should flush easily to exclude catheter obstruction.
Diastolic
pulmonary artery
pressure is
normally 2-4
mmHg higher than
mean PAOP.
Mean PAOP is
normally lower
than mean PAP

PEEP (including autoPEEP) increases intrapleural pressure (during all stages of the respiratory cycle) causing the measured PAOP to overestimate the actual transmural or filling pressure. With normal lung and chest wall compliance, approximately 50% of the applied PEEP is transmitted to the pleural space and PAOP will rise by less than 50%.

A decreased percentage of PEEP is transmitted if lung compliance is low. Thus in severe ARDS, application of PEEP will have less effect on PAOP measurement.

Any situation where there is increased pulmonary vascular resistance e.g.

• hypoxaemia
• pre-existing chronic lung disease e.g. COPD
• pulmonary embolism,
• ARDS
• sepsis
• primary pulmonary hypertension
• large left-to-right shunts e.g. ASD,VSD.

• Hypervolaemia
• Left heart dysfunction of any cause; LV failure, mitral stenosis/regurgitation, decreased LV compliance
• Cardiac tamponade
• Constrictive or restrictive pericarditis.

Mittlerer (PAP-PAOP)/Cardiac output

Aortic regurgitation

Any condition that produces obstruction in the pulmonary veins e.g. tumour, fibrosis, thrombosis

Left atrial mass e.g. large myxoma, thrombus

Mitral valve pathology; stenosis or regurgitation with elevated V wave

Significant tachycardia (heart rate >130 beats/min)

Increased pleural pressure (e.g. PEEP, CPAP especially with associated hypovolaemia or in patients with emphysema)

Catheter placement in West Zone 1 or Zone 2 of the lung.

Decreased left ventricular compliance

• e.g. left ventricular hypertrophy or
• myocardial ischaemia.

• Reduction of pulmonary tree
• pneumonectomy
• massive pulmonary embolism

Q waves may occur as a normal variant and do not always indicate heart disease.

Q waves normally occur in leads I, aVL, V4, V5 and V6.

They are narrow with no notching or slurring and are the result of septal activation.

With normal variance, the depth of the Q wave is <2 mm (2 small squares) in leads I and II and is rarely more

than 1 mm in depth in any of the other leads.

• T wave may be inverted in leads III and aVF and in chest leads V1 and V2 in normal individuals.
• An inverted T wave in leads I, II or V3 to V6 is usually abnormal.

Physiologisch schöpft die untere Körperextremität weniger O2 aus als der Oberkörper (unten geht mehr vom Cardic output durch). In der Sepsis dreht sich das Verhältnis um, weil dann das Splanchnikusgebiet mehr Sauerstoff verbraucht (8% mehr).

Mitralinsuffzienz /Stenose, 

reduzierte linksatriale compliance

verminderte links ventrikuläre compliance

Hypovolämie

Aufzufinden nach T-Welle (wenn korreliert mit EKG) 

bei AV-Dissoziation (Ventrikelkontraktion bereits bei Vorhofkontraktion)

Preload is the wall tension in the ventricle at the end of diastole that represents the final stretch to ventricular muscle.

The Frank–Starling principle states that forcefulness of ventricular contraction is determined by myocardial fibre length at end diastole

Patient in 45 Grad Hochlagerung.

ZVD max. 3cm ab kaudalen Halsende sichtbar

Pressure = flow x resistance.
An elevated intracardiac pressure may be due to an elevated volume or an elevated resistance

mottling= Marmorierung am Knie.

Score 0-5, 0= wenig an Patella, 5 bis Oberschenkel reichend

Hoher Mottling-Score korreliert mit Mortalität

Increased production of lactate:

tissue hypoxia

Increased aerobic glycolysis

Inhibition of pyruvate dehydrogenase (in sepsis)

Methanol/ethylene glycol/propofol toxicity

Thiamine deficiency

Ventolin (aktiviert aerobe Glykolyse)

Lactate buffered solutions used in continuous veno-venous haemodiafiltration (CVVHDF)

Medications (metformin, nucleosidic reverse transcriptase inhibitors, long-term linezolid use, intravenous lorazepam, valproic acid

Haematologic malignancies.

Rechtsventrikulär =ZVD

Linksventrikulär= Pulmo. art. Oklusionssdruck PAOP

Statisches Monitoring

Dynamisches Monitoring:

Schlagvolumenvarianz SVV

systolische Druckvariation SPV (weniger Sensitiv als PPV)

Pulspressure variation PPV (difference between the arterial
systolic and diastolic pressure, variiert bei Beatmung)

GEDV=Globalenddiastolic volume (transpulmonary thermodilution)

LVEDV = Left ventricular end diastolic volume  (Echo)

Fluid responsiveness is frequently defined as an increase in cardiac output ( ≥15% from baseline) with a fluid challenge.

due to the changes in venous tone, intrathoracic pressures, LV and RV
compliance, and geometry that occur in critically ill patients, there
is a poor relationship between the CVP and RV end-diastolic volume.

klassisch

Giant V wave: this occurs with severe tricuspid regurgitation, due to retrograde blood flow
into the right atrium during ventricular systole.

Inspiration: increased intrathoracic pressure -> decreased venous return to the RV.

During inspiration -> LV filling is increased due to
compression of the pulmonary veins. This causes an increase in LV stroke volume.

During expiration the LV stroke volume decreases due to reduced RV filling.

PPV% = 100 x {(PPmax – PPmin )/ (PPmax + PPmin)/2}

PPV >13%

subtracting the intrathoracic blood volume from the intrathoracic
thermal volume

Right ventricular end-diastolic volume (RVEDV) RVEDV is a volumetric measure of
cardiac preload. A recently available pulmonary artery catheter, with a rapid
response thermistor permits nearly continuous assessment of RVEDV, right ventricular
ejection fraction and cardiac output

EF (%) = {(EDV- ESV)/ EDV} x 100

 EF is the percentage of LV diastolic volume ejected with each heart beat.

Einteilung: