Mechanical trauma occurs as blood that is released under high pressure stretches the subarachnoid space, compresses the surrounding arteries, and elevates the intracranial pressure. Cerebral vasculature is very sensitive to changes in local environment and vessels constrict as they come in contact with blood. A short-lived constriction of large cerebral arteries is frequently observed in the first minutes after experimental SAH [3]. Blood, in addition, obstructs the passage of cerebrospinal fluid (CSF) and hence increases the risk of acute hydrocephalus, which is observed in as many as 50 % of SAH patients and is associated with poor outcome [4].

Chemical trauma is created by the products of subarachnoid blood lysis. Blood lysis begins within minutes after SAH and results in the appearance of oxyhemoglobin and xanthochromia in the CSF. Hence, xanthochromia is often used for clinical SAH diagnosis when CT scan results are negative [5]. At least three major products of clot lysis are implicated in SAH pathology: oxyhemoglobin, iron, and the recently discovered bilirubin oxidation products (BOXes).

In most SAH patients, cardiac complications appear immediately or develop within a few hours after aneurysmal rupture [22]. These complications include electrocardiographic (ECG) abnormalities, cardiac arrhythmias, and myocardial damage. ECG abnormalities develop within the first 48 h after SAH and reappear at rebleed [23–25]. Prominent ECG abnormalities include P wave abnormalities, prolonged QT interval, ST segment, and T-wave and are associated with poor neurologic grade on admission [26]. Cardiac arrhythmias can occur as the first symptom of acute SAH and are life threatening in 5–10 % of cases [27]. Major rhythmic abnormalities include sinus tachycardia, sinus bradycardia, and premature atrial and ventricular beats [25]. Myocardial injury is found in approximately 30–60 % of SAH patients and is associated with higher mortality [28–30]. Serum creatine kinase (CK)-MB and troponin-1 concentrations that are associated with myocardial injury are frequently increased within 24–48 h in SAH patients [28–30]. In addition, contraction band necrosis, myocardial fragmentation, and focal myocytolysis in the myocardium is found in autopsy of patients who died early after SAH [29–32]. In animals, increased serum CK-MB and cardiac troponin-1 are found as early as 10 min [33], and myocardial damage at 3 h, after SAH [32].

Pulmonary edema, also called neurogenic pulmonary edema, occurs in 10 % of all SAH cases and is a predominant complication in poor grade (Hunt and Hess grade III–V) patients [34]. Pulmonary edema usually develops within hours after SAH; however, a delayed form that appears 3–5 days after SAH is also reported [35]. In animals, leakage of lung capillaries occurs 8 min after injection of blood into the cisterna magna [36]. The nature of mechanisms underlying SAH-related pulmonary edema are cardiogenic (myocardial dysfunction leading to a raised hydrostatic pressure and fluid retention), noncardiogenic (such as acute lung injury or acute respiratory distress syndrome), and neurogenic (pressure of blood on respiratory centers at SAH) [34, 35].

Energy failure after SAH is mostly observed as changes in cerebral energy metabolism as detected in cerebral microdialysis studies. In addition, depletion of high-energy phosphate stores (fall in ATP and ADP and rise in AMP) in the cerebral cortex is noted as early as 6 h after experimental SAH [39, 40]. Cerebral microdialysis studies in animals have established that energy metabolism is disturbed within minutes after SAH, causing depletion of pyruvate and glucose and rises in lactate and in the lactate-to-pyruvate ratio [41, 42]. Similar findings are made in clinical SAH. Sarrafzadeh and colleagues noted that the lactate-to-pyruvate ratio remains significantly high for the first 8 days after SAH in patients with acute ischemic neurological deficits [42].

Energy is required to fuel ATPases to maintain ionic homeostasis across cell membranes. After SAH, as brain energy stores deplete, rapid alterations in ionic distributions across the membranes of brain cells and of cerebral vascular cells occur. In metabolically active neurons and astrocytes, as Na⁺K⁺-ATPases cease to work, intracellular Na⁺ rises and, on reaching a critical point, reverses the operation of the Na⁺–Ca²⁺ exchange carrier, creating increases in intracellular Ca²⁺ and extracellular K⁺. Changes in neuronal ionic content promotes the cortical spreading depolarization and disturbed neurovascular coupling that contributes to the acute pathophysiology of SAH and the later-occurring delayed ischemic neurological deficits (DINDs) [43]. In cerebral endothelial and smooth muscle cells, a pathological rise in intracellular calcium promotes constriction [44, 45]. Other pathological consequences of rises in intracellular calcium include the release of neurotransmitters such as glutamate and activation of enzymes, including ones that are detrimental to cells, such as inducible nitric oxide (NO) synthase (iNOS) and caspases [46, 47].

Although the list of biochemical and molecular mechanisms that activate early and contribute to SAH pathology is long, the key mechanisms are as follows: