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Chapter 14: Pregnancy and others 125
Table 14.1 Increased IAP in the haematological patient
Growth factor-induced capillary leak syndrome with concomitant large volume
fluid resuscitation and third space sequestration
Chemotherapy-induced ileus, colonic pseudo-obstruction (Ogilvie’s syndrome),
mucositis or gastroenteritis
Sepsis and infectious complications aggravating intestinal and capillary
permeability
Extramedullary haematopoiesis as seen with chronic myeloid leukaemia resulting
in hepatosplenomegaly, chronic IAH and chronic (irreversible) pulmonary
hypertension
The mechanisms of veno-occlusive disease seen after stem cell transplantation
may be triggered by, or related to, increased IAP
Gastroenterology
ACS has been described in patients with toxic megacolon
related to Clostridium difficile, gastroenteritis and perforated
diverticuli. IAP can trigger (re)bleeding of oesophageal varices
in patients with end-stage liver cirrhosis. This justifies the
placement of a nasogastric tube to decompress the stomach
after endoscopy.
ACS has been reported after colonoscopy.
Respiratory
Non-invasive ventilation with the head of the bed elevated to a
45° position has been linked to IAH because of entrapment of
air in the bowel. ACS has been observed during tension
pneumothorax. IAH has been reported in patients with chronic
obstructive pulmonary disease.
126 Section 3: Specific conditions: when to worry more?
Neurology
IAP has been reported to play a role in the malfunction of
ventriculoperitoneal shunts in patients with hydrocephalus.
Cardiology
Prolonged bypass time during cardiac surgery has been linked
to IAH. IAH is seen in chronic cardiac failure and is associated
with worsening renal function. ACS can occur during
extracorporeal life support, and IAP should be monitored.
Devices to induce hypothermia after cardiac arrest use a
closed loop with instillation of cold fluids into the peritoneal
cavity. For safety reasons, these devices limit instillation of fluids
based on IAP, which should be below 15 mmHg.
Gynaecology
Ovarian tumours such as mucous cystadenoma have been
reported to cause ACS (see Figure 14.1).
Reconstructive surgery
IAH and ACS can occur after reconstructive surgery and affect
viability of surgical flaps.
Orthopaedics
IAP has been associated with the activation of abdominal muscles
in highly trained participants during sudden heavy loadings.
Figure 14.1
Chapter 14: Pregnancy and others 127
Miscellaneous
ACS has been reported in scuba diving subjects, in a dog with
babesiosis and in pigs with wheat bloating!
Key points
Common clinical conditions (obesity) and procedures
(laparoscopy, endoscopy, peritoneal dialysis) are associated
128 Section 3: Specific conditions: when to worry more?
with increased IAP and may produce similar symptoms to
IAH or ACS.
Some are not as severe as others and are usually rapidly
reversible.
FURTHER READING
Chun R, Kirkpatrick AW. Intra-abdominal pressure,
intra-abdominal hypertension, and pregnancy: a review.
Annals of Intensive Care 2012; 2(Suppl. 1):S5.
De Keulenaer BL, De Backer A, Schepens DR et al. Abdominal
compartment syndrome related to noninvasive ventilation.
Intensive Care Medicine 2003; 29(7): 1177–81.
0
O
Rourke N, Kodali BS. Laparoscopic surgery during
pregnancy. Current Opinion in Anaesthesiology 2006; 19(3):
254–9.
Schurig R, Gahl GM, Becker H et al. Hemodynamic studies in
long-term peritoneal dialysis patients. Artificial Organs
1979; 3(3): 215–18.
Consequences of intra-abdominal
hypertension: why to worry?
Section 4
Chapter 15
Cardiovascular system and IAH
Introduction
Preload, contractility, afterload and oxygen transport are
abnormal in the critically ill as a result of haemorrhage, fluid
accumulation and direct cellular and organ injury. Inadequate
resuscitation and failure to restore adequate cellular oxygen
delivery through improved end-organ blood flow results in
anaerobic metabolism, ischaemia and the development of
multiple organ dysfunction syndrome.
Organ dysfunction observed during IAH and ACS is the result
of pressure-mediated decreases in cardiac preload and
contractility and increases in afterload. These phenomena
compound the direct compression of organs.
Pathophysiology
Overall cardiovascular effects of IAH
Intrathoracic pressure rises during IAH. Up to 80% of IAP
will be transmitted into the thorax. This leads to compression
of the heart and reduction of end-diastolic volume.
Cardiac output is decreased because of the direct
compression of vascular beds and activation of the
132 Section 4: Consequences of IAH: why to worry?
renin–angiotensin–aldosterone pathway that causes decreased
venous return and increased afterload. Mean arterial blood
pressure may initially increase owing to redistribution of blood
away from the abdominal cavity but will then return to normal or
decrease.
Hypovolaemia and the application of PEEP will exacerbate
the issue. Hypervolaemia will temporarily mask it.
A comprehensive list of IAH effects on haemodynamics is
shown in Table 15.1.
Table 15.1 Cardiovascular effects of IAH – these effects
will be exacerbated in cases of hypovolaemia,
haemorrhage and with increased positive end-expiratory
airway pressure
Diaphragm elevation and cardiac compression ↑
Pleural and intrathoracic pressure ↑
Difficult preload assessment
Pulmonary artery occlusion pressure ↑
Central venous pressure ↑
Transmural filling pressure ↓ =
Intrathoracic blood volume ↓ =
Global end-diastolic blood volume ↓ =
Right ventricular end-diastolic volume ↓ =
Right, global and left ventricular ejection fraction ↓ =
Extravascular lung water ↑ =
Stroke volume variation ↑
Pulse pressure variation ↑
Systolic pressure variation ↑
Inferior vena caval flow ↓
Venous return ↓
Left ventricular compliance and contractility ↓
Chapter 15: Cardiovascular system and IAH 133
Table 15.1 (cont.)
Downward Starling curve shift to the right
Cardiac output ↓
Systemic vascular resistance ↑
Mean arterial pressure ↑↓=
Pulmonary artery pressure ↑
Pulmonary vascular resistance ↑
Heart rate ↑ =
Lower extremity hydrostatic venous pressure ↑
Venous stasis, oedema, ulcers ↑
Venous thrombosis ↑
Pulmonary embolism ↑
Mixed venous oxygen saturation ↓
Central venous oxygen saturation ↓
False negative passive leg raising test ↑
Functional haemodynamic thresholds for fluid responsiveness ↑
IAH and preload
In patients with IAH/ACS, elevated intrathoracic pressure
decreases blood flow in the inferior vena cava and limits blood
return in a pressure-dependent manner. Reduced venous
return has the immediate effect of decreasing cardiac output
because of decreased stroke volume.
The cephalad deviation of the diaphragm compresses the
inferior vena cava as it passes through the diaphragm, further
reducing venous return. This occurs with an IAP as low as
10 mmHg. It is also observed during laparoscopic surgery.
These changes in blood flow are likely to increase the risk of
deep venous thrombosis.
134 Section 4: Consequences of IAH: why to worry?
IAH and contractility
Diaphragmatic elevation and increased intrathoracic pressure
will affect cardiac contractility. Compression of the pulmonary
parenchyma increases pulmonary artery pressure and
pulmonary vascular resistance, and decreases left ventricular
preload. The right ventricular afterload increases and the
thin-walled right ventricle dilates, with concomitant increase
in ventricular wall tension and myocardial oxygen demand
resulting in a decrease in right ventricular ejection fraction.
The interventricular septum may bulge into the left
ventricular chamber, impeding left ventricular filling and
function with further decrease in cardiac output.
Right ventricular dysfunction can become severe in the
presence of marked IAH, leading to significant reductions in left
ventricular contractility.
Figure 15.1 represents the effects of IAP on left ventricular
contractility.
IAH and afterload
Elevated intrathoracic pressure and IAH cause increased
systemic vascular resistance through direct compression of
the aorta and the great vessels. It also increases pulmonary
vascular resistance by compressing the pulmonary
parenchyma.
This explains why mean arterial pressure remains stable in
the early stages of IAH/ACS despite the observed reductions in
venous return and cardiac output.