In Part I we found that the classic studies of vasovagal syncope, done on fit young subjects, over stated vasodilatation as the dominant hypotensive mechanism. Since 1980, blood pressure and cardiac output have been measured continuously using non-invasive methods during tilt, mainly in patients with recurrent syncope, including women and the elderly. This has allowed us to analyse in more detail the complex sequence of hemodynamic changes leading up to syncope in the laboratory. All tilt-sensitive patients appear to progress through 4 phases: 1 early stabilisation, 2 circulatory instability, 3 terminal hypotension and 4 recovery. The physiology responsible for each phase is discussed. Although the order of phases is consistent, the time spent in each phase may vary. In teenagers and young adults, progressive hypotension during phases 2 and 3 can be driven by vasodilatation or falling cardiac output. The fall in cardiac output is secondary to a progressive decrease in stroke volume because blood is pooled in the splanchnic veins. In adults a fall in CO is the dominant hypotensive mechanism because systemic vascular resistance always remains above baseline levels.