If you're asking about pathophysiology (which I hope you are otherwise I typed a lot of this for nothing):
Distributive shock implies that the problem lies in the distribution of oxygen to the tissue, i.e. outside of the pump mechanism. This is usually seen in septic, anaphylactic and neurogenic shock. There is widespread vasodilation and this is the underlying cause of the hypotension and shock. In septic shock there is also reduced tissue uptake of oxygen due to toxins but as far as the pump mechanism is concerned it only recognises the need to push more blood out. The end result is what is known as "high output" cardiac failure because the intact pump increases CO to try and compensate for the decreased TPR due to vasodilation. Increased venous return is not a given, while it may be increased initially due to the effect of the pump, there can be venous pooling due to vasodilation.
EDIT: To clarify, as a result of vasodilation: "CO falls in late septic shock because the drop in preload severely outpaces the increased contractility and heart rate." (paraphrasing SDN user
venko)
Hypovolemic shock and cardiogenic shock are not entirely the same, so it's prudent to discuss them separately.
Hypovolemic shock implies that the intravascular volume is depleted, which is the underlying cause of hypotension and shock. Again, the pump mechanism only recognises the need to push more blood out, but there is almost no blood to push in this case. The end result is what is known as "low output" cardiac failure because the intact pump tries to increase CO, but as you know CO = HR x SV and in this case there is no volume. Hence there is only an increase in HR, and a net decrease in CO due to a severe lack of volume. In an attempt to preserve blood pressure with what little intravascular volume is there, there is vasoconstriction. Contrast this with distributive shock where vasodilation was the cause and not an effect. Venous return is decreased simply because there is nothing to return and hence you have
collapsed jugular veins.
Cardiogenic shock implies that the pump mechanism is at fault, which is the underlying cause of hypotension and shock. This could be obstructive e.g. tamponade or non obstructive e.g. congestive heart failure. The end result is what is known as "low output" cardiac failure because the damaged pump cannot put out an effective SV, and in turn this causes decreased CO. Hence there may be only an increase in HR with a net decrease in CO. The rest of the pathophysiology remains the same as hypovolemic shock because the tissues don't care why they are not receiving oxygen. The difference is that in cardiogenic shock you will often see
distended jugular veins due to the backup of blood behind the ineffective right heart.
To sum it up,
1. Distributive shock = decreased TPR (vasodilation) causing increased CO (including tachycardia) and hence possibly increased venous return.
2. Hypovolemic shock = decreased CO (due to low intravascular volume) causing vasoconstriction, (ineffectual tachycardia) and decreased venous return
3. Cardiogenic shock = decreased CO (due to pump failure) causing vasoconstriction, (ineffectual tachycardia) and decreased venous return (but with jugular venous distension)
The basic mechanism of shock is that tissues don't care why they're getting less oxygen from the blood and as a result of hypotension the body tries to increase CO and vasoconstriction takes place to maintain blood pressure. The differences in the types of shock depend on which aspect of this physiological compensation is deranged and causing the shock.
