https://www.youtube.com/watch?v=CwybGwgTm8k

1. By
Dr Mohammud Ibraheem

2. They occur shortly after initial SA bleeding:
A. Acute cardiopulmonary failure
B. Acute hydrocephalus
C. Diffuse cerebral edema
D. Rebleeding
The risk of at least 1 of them during the
acute course is 40%

3. Cardiac manifestations occur in 50%; it
ranges from mild elevation in cardiac
enzymes and ECG changes to obvious
clinical and ECG pathology.
Patients with SAH can present in extremis,
including cardiopulmonary arrest, or milder
initial symptoms but then acutely deteriorate,
often because of aneurysm rupture or acute
hydrocephalus.

4. Within the 1st week, acute LV dysfunction occur in
30%, severe cases lead to significant reduction in
EF and cardiogenic shock (neurogenic
myocardial stunning or stress
cardiomyopathy).
it is secondary to the catecholamine surge, leading
to myocardial cell contraction band necrosis.
Its classic appearance is LV apical akinesis leading
to ballooning of the apex during systole, often
referred to as Takotsubo cardiomyopathy

6.  Patients often have QTc prolongation
followed by T-wave abnormalities and
some will develop a deeply inverted T
wave (cerebral T wave).
 Troponin elevation is seen in up to 30% of
patients with SAH.
Timely diagnosis and treatment of
neurogenic myocardial stunning is important
as the reduced cardiac output can directly
affect cerebral perfusion.

8. They occur in 20% of aSAH patients.
Pulmonary dysfunctions increase the incidence
of vasospasm and fatal medical complications.
 Pneumonia accounts 20% of the pulmonary
complications, pulmonary oedema is seen in
14–23%
 pulmonary embolism in 0.3%.
 Cardiogenic pulmonary edema from
neurogenic myocardial stunning, or, in rare
cases, primary neurogenic pulmonary
edema.

9. Treatment of the underlying disease:
 Occlusion of the aneurysm, salvation of
acute hydrocephalus and, evacuation of
intracerebral hematoma.
 Prevention of secondary brain damage by
maintaining adequate perfusion and
oxygenation.
 Following the initial neurosurgical and/or
interventional treatment, sophisticated
medical diagnostics and treatment is
undertaken to achieve stabilization of the
patient.

10.  ECG, pulse oximetry, invasive BP monitoring
and chest x-ray and lab parameters.
 Advanced monitoring of cardiac function and
volume stat (catheterization of the pulmonary
artery) monitors cardiac output and filling
pressures.
 Less invasive alternatives as thermal
indicator transpulmonary dilution and
continuous pulse-contour cardiac output
(PiCCO) monitoring.
 Echocardiography.
 Continuous transesophageal
echocardiography

11. Cardiopulmonary-compromised patients are
at risk of developing complications due to
fluid overloading, and the careful use of
fluids is necessary.
Any prophylactic induction of hypervolemia
in order to prevent cerebral vasospasm is
contraindicated.

12.  Norepinephrine, epinephrine, and
dobutamine
 If catecholamines are not sufficient,
additive use of alternative inotropic help to
improve cardiac pump function (inhibitors
of phosphodiesterase III (PDE-3) (e.g.
milrinone))
 levosimendan, in a case of refractory
ventricular dysfunction following SAH

13. In cases of cardiac failure refractory to
maximum medical therapy with concomitant
cerebral vasospasm, sporadic reports of the
successful application of intraaortic balloon
pump (IABP) counterpulsation do exist