Where Does Blood Get Oxygen? (Pulmonary Capillaries)

Ch 18 notes

Overall architecture: Fig 18.1 in Marieb & Hoehn 9th & 10th editions)

Pulmonary veins and systemic arteries have oxygenated blood. Systemic veins and pulmonary arteries have deoxygenated blood. One way to remember those facts (a way I recommend, since it involves concepts rather than memorization) is to think of a diagram of the entire cardiovascular system (Fig 18.1):

Where does blood get oxygen? (pulmonary capillaries)

Where does it lose oxygen? (systemic capillaries)

What major structures does the blood go through on its way from the pulmonary capillaries (where it gets O2), to the systemic capillaries (where it loses O2)? (It goes through the pulm veins, the left heart, and the systemic arteries)

What major structures does the blood go through on its way from the systemic capillaries to the pulmonary capillaries? (It goes through the systemic veins, right heart, and pulm arteries)

Heart basics

Know layers: epi, myo, endocardial layers. Know chambers, valves, what valves do what, order that blood goes through them. What valves have chordae tendineae & attached papillary muscles, & which don’t? Pericardium. Unique features of cardiac muscle compared to skeletal muscle.

Heart electrical system

Know what causes P, QRS, T waves. Know the major parts of heart’s electrical system: SA, AV nodes, atrioventricular bundle (also known as bundle of His), bundle branches, Purkinje fibers. Know the order in which impulse reach those structures. Know the basic features of the cardiac muscle cell action potential, including the plateau potential and what makes it last a while. What is different about an action potential in a cardiac muscle cell and cardiac pacemaker cell? (Rapid rise of act pot in myocytes is due to Na channels opening; the less rapid rise of the action potential in pacemaker cell is due to opening of Ca channels.) What is the pacemaker potential in a pacemaker cell (slow rise in voltage after an action potential) and what causes it? (Gradual opening of slow Na channels and gradual closure of K channels.) How do sympathetic and parasympathetic nerves affect the cardiac electrical system?

For those interested in more detail on the different ion currents in cardiac myocytes and SA nodal cells, which is beyond the scope of this class, see here for nodal cells and here for myocytes. (Last checked 20160228.)

Wiggers diagram (Fig 18.19 in Marieb & Hoehn 10th ed)

This is my favorite diagram in the chapter. It shows how different aspects of cardiovascular function relate to one another, including how they are temporally related. If you understand this diagram you understand a lot about cardiovascular physiology.

Nervous system regulation (neural regulation) of the heart

Autonomic nerves to heart affect heart rate and contractility. Contractility is the strength of the heart beat, i.e. how hard the cardiac muscle is contracting. Sympathetic nerve fibers release norepi & epi (mostly NE). NE & Epi cause increased HR & increased contractility. Parasympathetic fibers to heart (also called vagal fibers, since they come in the vagus nerve) release ACh, which slows HR. ACh has little effect on contractility. Generally speaking, when sympathetic fibers get more active, parasymps get less active, & vice versa. Bainbridge reflex: a reflex in which atrial stretch causes more activity of sympathetic nerves to heart, which causes more rapid HR. This helps the heart “keep up” when venous return is high.

Hormones that influence the heart

Epinephrine, norepinephrinefrom adrenal medulla (these are sympathetic neurotransmitters as well as hormones)

Thyroxine (thyroid hormone)

Equations

Know the flowing and be able to use them if necessary, perhaps ina rearranged form.

CO = HR * SV

Cardiac output (L/min) = HR (beats/min) x Stroke Volume (ml/beat)

SV = EDV – ESV

Stroke volume (ml) = End diastolic volume (ml) – End systolic volume (ml)

If you know CO and HR you can compute SV, and so forth.

Regulation of Cardiac Output

The equations for cardiac output and stroke volume are relevant here.

What makes CO go up/down? (increase/decrease in HR, increase/decrease in SV)

What makes SV go up/down? This is like asking what makes EDV go up/down, or what makes ESV go down/up. Know the answers. Hint: preload and afterload. What are they? Which, when it rises, makes EDV or ESV rise or fall?