Module 7 Study Guide - Physiology I

Everything above, compressed to what you should be able to reproduce without the slides in front of you.

Core ideas¶

Valves are passive one-way doors with no muscle. A valve opens when upstream pressure exceeds downstream pressure and closes when it falls below.
AV valves are the inlets to the ventricles, semilunar valves the outlets. Chordae tendineae and papillary muscles keep the AV valves from prolapsing during ventricular contraction.
Valve disease is mostly left-sided because the left heart sees higher pressures. Stenosis narrows the opening; regurgitation lets blood flow backward.
Arteries carry blood away from the heart and veins carry it toward the heart, whatever its oxygen content.
Systole raises pressure and diastole lowers it. Phase names follow the ventricles, so atrial systole falls during diastole.
Each phase has a static isovolumic stage with every valve closed, then a kinetic stage where volume changes.
On a Wiggers diagram, every valve event sits where two pressure tracings cross.
Ventricular filling has three sub-stages: rapid (passive), reduced (passive), and the atrial kick (active).
CO = HR × SV and SV = EDV − ESV. The autonomic nervous system sets heart rate. Preload, afterload, and contractility set stroke volume.
Preload is about volume and moves the operating point along the Starling curve. Afterload is about pressure and contractility about chemicals, and both shift the curve.
High afterload lengthens isovolumic contraction, which steals time from ejection within a fixed systole and leaves more residual ESV.
Contractility is load-independent and calcium-driven. Ejection fraction and dP/dt max are confounded by preload. ESPVR is the gold standard.
A P-V loop removes time and is read counterclockwise. The right vertical side is isovolumic contraction, the top is ejection, the left vertical side is isovolumic relaxation, and the bottom is filling.
Loop width is stroke volume, the right edge is EDV and preload, and the upper right corner’s height approximates afterload.
ESPVR slope is active end-systolic stiffness, or contractility. EDPVR curvature is passive end-diastolic stiffness, a determinant of preload.

Key terms¶

Interventricular septum: Thick wall separating the low pressure right ventricle from the high pressure left ventricle.
Papillary muscles: Finger-like muscular outcroppings of the ventricular wall that anchor the chordae. Three groups on the right, two on the left.
Chordae tendineae: Fibrous strings tying AV valve edges to papillary muscles, preventing prolapse like the cords of a parachute.
Atrioventricular (AV) valves: Inlet valves into the ventricles. Tricuspid on the right, mitral or bicuspid on the left.
Semilunar valves: Outlet valves out of the ventricles. Pulmonary on the right, aortic on the left. Three cusps each.
Stenosis: Calcified, narrowed valve that is hard to open and close.
Regurgitation (insufficiency): Damaged valve letting blood backwash into the chamber it just left.
Bicuspid aortic valve: Birth defect fusing two aortic cusps. Stenosis develops at much younger ages.
Pectinate muscles: Muscular ridges on the atrial wall that add muscle without much added thickness or weight.
Great vessels: Vessels leading directly into or out of the heart’s chambers: venae cavae, pulmonary trunk and arteries, pulmonary veins, aorta.
Cardiac cycle: All events in the heart in a single heartbeat.
Systole / diastole: Contraction, pressure rises / relaxation, pressure falls. Named for the ventricles.
Isovolumic: Same volume. Every valve closed, so ventricular volume cannot change.
Atrial kick: Active atrial contraction that tops off the ventricles at the end of diastole.
EDV / ESV: Ventricular volume at the end of filling / residual volume left after ejection.
Wiggers diagram: Atrial, ventricular, and arterial pressure plus ventricular volume, tracked over one cardiac cycle.
Stroke volume (SV): Volume ejected in one heartbeat. EDV − ESV.
Cardiac output (CO): Volume pumped per minute. HR × SV, in mL/min.
Preload: Stretch on resting myocytes as the heart fills. Surrogates: LV EDV, LV end-diastolic pressure, atrial pressures.
Afterload: Load the left ventricle pumps against to open the aortic valve. Surrogate: mean arterial blood pressure.
Contractility: Load-independent capacity of myocytes to produce force, set by intracellular calcium.
Lusitropy: Variable rate of relaxation in the heart. Positive with sympathetic stimulation, negative with slow calcium removal.
Inotropy: Variable intensity of contraction in the heart. Virtually synonymous with contractility.
Ejection fraction (EF): SV ÷ EDV × 100. Easy, common, and a poor contractility surrogate.
dP/dt max: Steepest rise in LV pressure during contraction. Cannot separate contractility from preload.
P-V loop: Left ventricular pressure against volume over one cycle, read counterclockwise.
Peak systolic pressure: Highest point on the loop, about two-thirds across ejection.
Compliance / elastance: ΔV ÷ ΔP / ΔP ÷ ΔV, which is stiffness.
ESPVR: End-systolic pressure-volume relationship. Its slope, E_ES, is active stiffness and the gold standard for contractility.
EDPVR: End-diastolic pressure-volume relationship. Its curvature is passive stiffness, a determinant of preload.

Numbers worth knowing¶

Right atrial pressure	~4 mmHg
Left atrial pressure	~8 mmHg
Right ventricle	26/3 mmHg
Pulmonary trunk	25/10 mmHg
Left ventricle	121/7 mmHg
Aorta	120/80 mmHg
Healthy aortic valve opening	3–5 cm²
Severe aortic stenosis	< 1 cm²
Cycle duration	60 ÷ HR s/beat
Tricuspid cusps	3
Mitral cusps	2
Pulmonary and aortic cusps	3 each
Papillary muscle groups, right / left	3 / 2
Pulmonary veins per lung	2
Stages of diastole / systole	3 / 2
Example loop EDV	~130 mL
Example loop ESV	~50 mL
Aortic valve opens	~80 mmHg
Aortic valve closes	~100 mmHg
Peak LV systolic pressure	a smudge above 120 mmHg
Mitral valve events	near 0 mmHg
Peak systolic pressure position	~2/3 across ejection
Thumbs: EF / dP/dt max / ESPVR	2 down / 1 down / 3 up
Age of the VR heart	97 years

Distinctions that get mixed up¶

Pair	How to keep them apart
AV vs semilunar valves	AV valves are inlets from atria to ventricles, held by chordae. Semilunar valves are outlets from ventricles to arteries. Tricuspid and mitral vs pulmonary and aortic.
Stenosis vs regurgitation	Stenosis is a narrowed, calcified valve that is hard to open. Regurgitation is a leaky valve that lets blood flow backward.
Mitral vs aortic regurgitation	Mitral leaks during contraction, back into the left atrium. Aortic leaks after contraction, back into the left ventricle.
Artery vs vein	Direction, not color. Arteries go away from the heart, veins toward it. The pulmonary trunk is an artery carrying deoxygenated blood.
Atrial systole vs ventricular systole	Phase names follow the ventricles. Atrial systole, the atrial kick, happens during diastole.
Isovolumic contraction vs isovolumic relaxation	Both have all valves closed and no volume change. Contraction raises pressure to open the semilunar valves. Relaxation dissipates pressure so the AV valves can open.
Rapid vs reduced filling	Both passive. Rapid when the ventricle is emptier. Reduced when the walls start to fight back.
Preload vs afterload	Preload is volume, at EDV, and moves the operating point along the Starling curve. Afterload is pressure, at ESV, and shifts the curve.
High preload vs high contractility	Both raise force. Preload acts through stretch, contractility through intracellular calcium. dP/dt max cannot tell them apart.
Lusitropy vs inotropy	Lusitropy is rate of relaxation and feeds preload. Inotropy is intensity of contraction and is contractility. Chronotropy and dromotropy are the electrical pair.
Compliance vs elastance	Compliance is ΔV/ΔP. Elastance is ΔP/ΔV, or stiffness, and is what slopes on a P-V graph show.
ESPVR vs EDPVR	ESPVR joins the upper left corners: active stiffness, contractility. EDPVR joins the lower right corners: passive stiffness, ease of filling.
Wiggers diagram vs P-V loop	Wiggers plots pressures and volume against time. The loop drops time and atrial and arterial pressures, plotting LV pressure against LV volume.
Clockwise vs counterclockwise rotation	Counterclockwise is a steeper slope and more stiffness. Clockwise is a flatter slope and less stiffness. Read the loop itself counterclockwise.

Check yourself¶

Name the four chambers and four valves, and trace a drop of blood from the superior vena cava to the aorta.
Explain how papillary muscles and chordae tendineae keep an AV valve from prolapsing, using the parachute analogy.
Why is valvular disease more common in the left heart?
Describe the cycle by which aortic stenosis progresses, and give the opening area of a healthy valve and a severely stenotic one.
Contrast mitral and aortic regurgitation by when in the cycle each occurs and where the blood goes.
Give the definitions of artery and vein that are true 100% of the time, and name a vessel that breaks the color rule.
State the rule for when a valve opens, given P₁ upstream and P₂ downstream.
Reproduce the typical pressures in the right atrium, right ventricle, pulmonary trunk, left atrium, left ventricle, and aorta.
Where does the left atrium sit in a real heart, and where does the inferior vena cava enter the right atrium in the VR heart?
Calculate cardiac cycle duration for a heart rate of 75 beats/min.
Why does atrial systole fall during diastole?
For each of the five stages of the cardiac cycle, give the pressure ordering, the state of both valve sets, and the volume change.
What is the purpose of isovolumic relaxation if no blood moves?
Relate isovolumic contraction and ejection to isometric and isotonic concentric contractions in skeletal muscle.
On a Wiggers diagram, identify the four valve events from the pressure crossings.
Distinguish rapid filling, reduced filling, and atrial kick by mechanism and by the shape of the volume tracing.
Using the example loop (EDV about 130 mL, ESV about 50 mL), calculate stroke volume, then cardiac output at 70 beats/min and ejection fraction.
Define preload, name three surrogates, and list what changes it.
Explain how lusitropy contributes to preload, naming the PKA targets involved.
Explain why high afterload leaves a larger end-systolic volume, using the fixed duration of systole.
Which determinant moves the operating point on the Starling curve, and which two shift the curve?
Why does ejection fraction get two thumbs down and dP/dt max one thumb down as contractility surrogates?
Trace how sympathetic stimulation raises contractility, from norepinephrine to cross-bridges.
Name three ways a positive inotrope can work and three ways a negative inotropic drug can work.
Derive a P-V loop from a Wiggers diagram, and label the four valve events and four phases on it.
On a P-V loop, where do you read EDV, ESV, stroke volume, peak systolic pressure, end-diastolic pressure, and afterload?
How would the loop’s right edge move if preload rose? How would the upper right corner move if afterload rose?
Define compliance and elastance, and explain why slopes on a P-V graph show elastance.
Why does drawing ESPVR and EDPVR require several loops, and what does each line tell you?
A drug rotates the ESPVR counterclockwise. What happened to contractility? A disease rotates the EDPVR counterclockwise. What happened to filling?