HBAP ExAM 4

12.5-12.9 prep 11b

[12.5 Cardiac cycle] What are the two major phases of the cardiac cycle, and how long does each last at a heart rate of 72 beats/min?

Systole = period of ventricular contraction and blood ejection (about 0.3 sec). Diastole = alternating period of ventricular relaxation and blood filling (about 0.5 sec). One cardiac cycle lasts about 0.8 sec at 72 beats/min.

[12.5 Cardiac cycle] Name the four periods of the cardiac cycle in order, and give the state of the AV valves and the aortic/pulmonary valves in each.

SYSTOLE: 1) Isovolumetric ventricular contraction: AV valves closed, aortic and pulmonary valves closed. 2) Ventricular ejection: AV valves closed, aortic and pulmonary valves open. DIASTOLE: 3) Isovolumetric ventricular relaxation: AV valves closed, aortic and pulmonary valves closed. 4) Ventricular filling: AV valves open, aortic and pulmonary valves closed (atrial contraction occurs at the end of diastole). The phases are identical in both halves of the heart.

[12.5 Cardiac cycle] What happens during isovolumetric ventricular contraction, and why can't the ventricular muscle fibers shorten? When are all heart valves closed?

Ventricles contract but all valves are closed, so no blood is ejected; the walls develop tension and squeeze on the blood, increasing ventricular pressure. Volume of blood in the ventricles is constant and blood is essentially incompressible, so the fibers cannot shorten (analogous to an isometric skeletal muscle contraction: tension, no shortening). All valves are closed ONLY during isovolumetric ventricular contraction and isovolumetric ventricular relaxation.

[12.5 Cardiac cycle] What happens during ventricular ejection, and what is stroke volume (SV)?

Once ventricular pressure exceeds the pressure in the aorta and pulmonary trunk, the aortic and pulmonary valves open and blood is forced into the aorta and pulmonary trunk as the ventricular muscle fibers shorten. Stroke volume (SV) = the volume of blood ejected from each ventricle during systole.

[12.5 Cardiac cycle] What happens during isovolumetric ventricular relaxation (start of diastole)?

Ventricles begin to relax, the aortic and pulmonary valves close (this is the dividing line between systole and diastole as presented), and the AV valves are also closed. No blood enters or leaves the ventricles, so ventricular volume does not change.

[12.5 Cardiac cycle] How does ventricular filling occur, and how much of it occurs before atrial contraction?

AV valves open and blood flows in from the atria. The ventricle receives blood throughout most of diastole, not just when the atrium contracts. Atrial contraction occurs at the end of diastole, after most filling has taken place. In a person at rest, about 80% of ventricular filling occurs before atrial contraction.

[12.5 Cardiac cycle] Mid- to late diastole (left heart): what are the pressure relationships and valve states, and what happens when the SA node discharges?

Atrium and ventricle both relaxed; atrial pressure is slightly higher than ventricular pressure (atrium filling from the veins/pulmonary veins), so the AV valve is held open and blood flows on into the ventricle. Very small pressure differences across open valves produce large flows (little resistance). Aortic valve is closed throughout diastole because aortic pressure is higher than ventricular pressure. Aortic pressure slowly decreases (blood moves out of the arteries); ventricular pressure increases slightly (blood entering). Near the end of diastole the SA node discharges and the atria depolarize (P wave) -> atrial contraction raises atrial pressure -> small extra volume of blood into the ventricle (the 'atrial kick'). Then end-diastolic volume (EDV) is reached = amount of blood in the ventricle at the end of ventricular diastole.

[12.5 Cardiac cycle] Systole (left heart): what events lead to isovolumetric contraction, valve closure, and the opening of the aortic valve?

Depolarization passes from the AV node into the ventricular tissue (QRS complex) -> ventricular contraction. Ventricular pressure rises rapidly and almost immediately exceeds atrial pressure -> AV valve closes (prevents backflow into the atrium). Aortic pressure still exceeds ventricular pressure, so the aortic valve stays closed and the ventricle cannot empty (isovolumetric contraction; all valves closed). Backward bulging of the closed AV valves causes a small upward deflection in the atrial pressure wave. This phase ends when ventricular pressure exceeds aortic pressure -> aortic valve opens and ejection begins. Ejection is rapid at first, then slows down. Blood remaining in the ventricle after ejection = end-systolic volume (ESV).

[12.5 Cardiac cycle] What is the formula for stroke volume, and what are typical resting adult values for EDV, ESV and SV?

Stroke volume = end-diastolic volume - end-systolic volume (SV = EDV - ESV). The ventricle does not empty completely. Typical resting adult: EDV = 135 mL, ESV = 65 mL, SV = 70 mL. (EDV = amount of blood in the ventricle just before systole; ESV = amount remaining after ejection.)

[12.5 Cardiac cycle] What happens to pressures during the ejection phase, and why do peak ventricular and aortic pressures occur before the end of ejection?

Aortic pressure rises along with ventricular pressure; very small pressure differences exist between ventricle and aorta because the open aortic valve offers little resistance. Peak ventricular and aortic pressures are reached before the end of ejection and then decrease during the last part of systole despite continued contraction, because the strength of ventricular contraction diminishes (shown by the reduced rate of ejection). Aortic volume and pressure decrease as the rate of ejection becomes slower than the rate at which blood drains out of the arteries into the tissues.

[12.5 Cardiac cycle] Early diastole (left heart): what causes the aortic valve to close, what is the dicrotic notch, and what ends isovolumetric relaxation?

T wave = ventricular repolarization. As the ventricles relax, ventricular pressure falls below aortic pressure (which is still significantly increased by the blood that just entered) -> aortic valve closes. Elastic recoil of the aorta plus blood rebounding against the valve causes a rebound of aortic pressure = the dicrotic notch. AV valve stays closed (ventricular pressure still higher than atrial) -> all valves closed (isovolumetric ventricular relaxation). It ends when rapidly decreasing ventricular pressure falls below atrial pressure -> AV valve opens.

[12.5 Cardiac cycle] Why is early ventricular filling rapid, and how is energy involved?

Venous blood that accumulated in the atrium while the AV valve was closed flows rapidly into the ventricles. Flow is enhanced by a rapid decrease in ventricular pressure: the previous contraction compressed the elastic elements of the chamber so the ventricle tends to recoil outward once systole is over. This expansion lowers ventricular pressure more rapidly and may even create a negative (subatmospheric) pressure. Some energy is stored in the myocardium during contraction, and its release during relaxation aids filling.

[12.5 Cardiac cycle] Why is it important that most ventricular filling is completed in early diastole? (heart rate limit, atrial fibrillation)

Filling is not seriously impaired when the heart beats very rapidly and diastole (total filling time) is shortened. However, at heart rates of about 200 beats/min or more, filling time becomes inadequate and the volume pumped per beat decreases. It also explains why conduction defects that eliminate the atria as effective pumps do not seriously impair ventricular filling in otherwise healthy people at rest, e.g. atrial fibrillation (atrial cells contract in a completely uncoordinated manner, so the atria fail to work as effective pumps).

[12.5 Cardiac cycle] How do pulmonary circulation pressures compare with systemic pressures, and what are the consequences?

Pressure changes in the right ventricle and pulmonary arteries are qualitatively similar to the left ventricle and aorta, but quantitatively much lower. Pulmonary arterial systolic/diastolic pressures are 25 and 10 mmHg vs systemic arterial 120 and 80 mmHg, so the pulmonary circulation is a low-pressure system (lower vascular resistance). The right ventricular wall is much thinner than the left. Despite the pressure difference, the stroke volumes of the two ventricles are the same.

[12.5 Heart sounds] What causes the first and second heart sounds, what do they sound like, and when do they occur?

First sound: soft, low-pitched 'lub' = closure of the AV valves; marks the onset of systole. Second sound: louder 'dup' = closure of the pulmonary and aortic valves; occurs at the onset of diastole. They result from vibrations caused by the closing valves and are normal.

[12.5 Heart sounds] What is a heart murmur, what causes turbulent flow, and what sound do stenotic vs insufficient valves make?

Murmurs = abnormal sounds (can be a sign of heart disease) produced by defects that cause turbulent blood flow instead of normal laminar flow (smooth concentric layers). Causes: stenosis = blood flowing rapidly in the usual direction through an abnormally narrowed valve (high-pitched, whistling murmur); insufficiency = blood flowing backward through a damaged, leaky valve (low-pitched, gurgling murmur); septal defect = blood flowing between the two atria or two ventricles through a small hole in the wall separating them.

[12.5 Heart sounds] How does the timing of a murmur (systole vs diastole) help diagnosis?

Murmur during SYSTOLE suggests: a stenotic pulmonary or aortic valve, an insufficient AV valve, or a hole in the interventricular septum. Murmur during DIASTOLE suggests: a stenotic AV valve or an insufficient pulmonary or aortic valve.

[12.6 Cardiac output] What is cardiac output (CO), what is its formula, and what is the typical resting example?

CO = volume of blood each ventricle pumps per unit time (usually L/min); in the steady state it is the same in the systemic and pulmonary circuits. CO = heart rate (HR) x stroke volume (SV). Example: 72 beats/min x 0.07 L/beat = 5.0 L/min (typical resting, average-sized adult). Average total blood volume is about 5.5 L, so nearly all the blood is pumped around the circuit once each minute.

[12.6 Cardiac output] What cardiac outputs can be reached during strenuous exercise?

Well-trained athletes: up to 35 L/min (entire blood volume pumped around almost seven times per minute). Sedentary, untrained individuals: 20-25 L/min.

[12.6 Cardiac output] Do heart rate and stroke volume always change in the same direction? Give the example.

No. Example: after blood loss, stroke volume decreases whereas heart rate increases, producing opposing effects on cardiac output. HR and SV are the same for the right and left sides of the heart under steady-state conditions.

[12.6 Heart rate control] What is the inherent SA node rate, why is the resting heart rate lower, and what are chronotropic effects?

Without any nervous or hormonal influence the SA node discharges at about 100 beats/min (inherent autonomous discharge rate). Many parasympathetic and sympathetic postganglionic neurons end on the SA node. Parasympathetic activity (vagus nerves) decreases heart rate; sympathetic activity increases it = chronotropic effects. At rest there is considerably more parasympathetic than sympathetic activity, so the normal resting rate is about 70-75 beats/min, well below 100.

[12.6 Heart rate control] How do sympathetic and parasympathetic stimulation change the SA node pacemaker potential?

Sympathetic: increases the slope of the pacemaker potential by increasing F-type channel permeability (main current = Na+ entering the cell) -> faster depolarization -> threshold reached more rapidly -> heart rate increases. Parasympathetic: slope decreases due to a reduction in the inward current -> threshold reached more slowly -> heart rate decreases. Parasympathetic stimulation also hyperpolarizes SA node cell membranes by increasing K+ permeability, so the pacemaker potential starts from a more negative value (closer to the K+ equilibrium potential) and has a reduced slope.

[12.6 Heart rate control] Which factors other than the cardiac nerves alter heart rate?

Epinephrine (main hormone secreted into the systemic circulation by the adrenal medulla) speeds the heart by acting on the same beta-adrenergic receptors in the SA node as norepinephrine released from neurons. Heart rate is also sensitive to body temperature, plasma electrolyte concentrations, hormones other than epinephrine, and adenosine (a metabolite produced by myocardial cells). These are not as important as input from the cardiac nerves.

[12.6 Heart rate control] What are dromotropic effects, and what general physiological principle does autonomic control of heart rate illustrate?

Sympathetic and parasympathetic neurons also innervate other parts of the conducting system. Sympathetic stimulation increases conduction velocity through the entire cardiac conducting system; parasympathetic stimulation decreases the rate of spread of excitation through the atria and the AV node = dromotropic effects. Principle: most physiological functions are controlled by multiple regulatory systems, often working in opposition.

[12.6 Autonomic effects on the heart] Table 12.5: what are the effects of sympathetic (norepinephrine on beta-adrenergic receptors) and parasympathetic (acetylcholine on muscarinic receptors) nerves on the SA node, AV node, atrial muscle and ventricular muscle?

SA node: sympathetic = increased heart rate; parasympathetic = decreased heart rate. AV node: sympathetic = increased conduction rate; parasympathetic = decreased conduction rate. Atrial muscle: sympathetic = increased contractility; parasympathetic = decreased contractility. Ventricular muscle: sympathetic = increased contractility; parasympathetic = no significant effect (little parasympathetic innervation of the ventricles, so negligible direct effect on ventricular contractility).

[12.6 Stroke volume control] Which variable is more important for determining cardiac output, and what are the three dominant factors that change the force of ejection (stroke volume)?

Stroke volume is the more important variable. A more forceful contraction increases stroke volume by causing greater emptying (ventricles do not completely empty). Three dominant factors: 1) changes in end-diastolic volume (volume of blood in the ventricles just before contraction; the preload); 2) changes in the magnitude of sympathetic nervous system input to the ventricles; 3) changes in afterload (the arterial pressures against which the ventricles pump).

[12.6 Frank-Starling mechanism] What is the Frank-Starling mechanism, and why does it work (length-tension)?

The ventricle contracts more forcefully during systole when it has been filled to a greater degree during diastole: all other factors being equal, stroke volume increases as end-diastolic volume increases (ventricular-function curve; also called Starling's law of the heart). It is essentially a length-tension relationship: greater EDV = greater stretch of ventricular sarcomeres before contraction = more forceful contraction. Difference from skeletal muscle: the normal resting point for cardiac muscle is NOT at its optimal length but on the rising phase of the curve, so greater filling stretches the fibers more and increases the force of contraction. (At very high volumes force and stroke volume decline, as in skeletal muscle.)

[12.6 Frank-Starling mechanism] What additional mechanisms link stretch to force in cardiac muscle cells, and what is the physiological significance of the Frank-Starling mechanism?

Stretching cardiac muscle cells toward their optimum length (besides changing thick/thin filament overlap): decreases the spacing between thick and thin filaments (more cross-bridges can bind during a twitch), increases the sensitivity of troponin for binding Ca2+, and increases Ca2+ release from the sarcoplasmic reticulum. Significance: at any given heart rate, an increase in venous return (flow of blood from the veins into the heart) automatically increases EDV and therefore stroke volume and cardiac output. It maintains the equality of right and left cardiac outputs: if the right side suddenly pumps more blood than the left, the increased flow returning to the left ventricle automatically increases left ventricular output, so blood does not accumulate in the pulmonary circulation.

[12.6 Sympathetic regulation] What is contractility, which factors increase it, and how does it differ from the Frank-Starling mechanism?

Contractility = the strength of contraction at any given end-diastolic volume (do not confuse with contraction = the process of generating force in muscle). Sympathetic nerves are distributed to the entire myocardium; norepinephrine acts on beta-adrenergic receptors to increase ventricular contractility; plasma epinephrine acting on these receptors does too. The increased force and stroke volume are independent of a change in EDV. Extrinsic factors that increase force at a given EDV have inotropic effects. The Frank-Starling mechanism does NOT reflect increased contractility. During sympathetic stimulation the Frank-Starling mechanism still applies, but stroke volume is greater at any given EDV (more complete ejection of the EDV).

[12.6 Sympathetic regulation] What is the ejection fraction (EF), and what other effects does sympathetic stimulation have on ventricular contraction and relaxation?

EF = SV / EDV (ratio of stroke volume to end-diastolic volume). Averages 50-75% under resting conditions in a healthy heart; increased contractility causes an increased EF (one way to quantify contractility). Sympathetic stimulation also makes contraction and relaxation of the ventricles occur more quickly (and increases the maximum force developed). Because sympathetic activity also increases heart rate (less time for diastolic filling), the quicker contraction and relaxation partially compensate by making a larger fraction of the cardiac cycle available for filling.

[12.6 Sympathetic regulation] What is the cellular mechanism by which sympathetic stimulation increases myocardial contractility?

Norepinephrine/epinephrine bind beta-adrenergic receptors -> G-protein-coupled cascade -> adenylyl cyclase -> cAMP -> activation of cAMP-dependent protein kinase, which phosphorylates proteins involved in excitation-contraction coupling: 1) L-type Ca2+ channels in the plasma membrane; 2) the ryanodine receptor and associated proteins in the sarcoplasmic reticulum membrane; 3) thin filament proteins, in particular troponin; 4) thick filament proteins associated with the cross-bridges; 5) proteins involved in pumping Ca2+ back into the sarcoplasmic reticulum. Result: cytosolic Ca2+ rises more quickly and reaches a greater value during excitation, Ca2+ returns to its pre-excitation value more quickly, and rates of cross-bridge activation and cycling are accelerated = stronger, faster contraction.

[12.6 Stroke volume control] What is afterload, and how does it affect stroke volume?

Afterload = how hard the heart must work to eject blood; the arterial pressure is a 'load' the contracting ventricular muscle works against (like a muscle lifting a weight). Proportional to aortic pressure for the left ventricle and pulmonary artery pressure for the right ventricle. The greater the load, the less the contracting fibers can shorten at a given contractility, so increased arterial pressure tends to reduce stroke volume (in certain situations). In the normal heart, several inherent adjustments minimize this influence; but alterations in vascular resistance and long-term increases in arterial pressure (high blood pressure, heart failure) can weaken the heart and influence stroke volume.

[12.6 Cardiac output] Summary: which factors increase cardiac output and how are they controlled?

CO = SV x HR. Heart rate: increased by sympathetic input to the SA node and plasma epinephrine (chronotropic action); decreased by parasympathetic input to the SA node. Stroke volume: increased by increased end-diastolic volume (preload) via the Frank-Starling mechanism, and by increased contractility (increased sympathetic stimulation or epinephrine, via increased myocardial cytosolic Ca2+); can be reduced by increased afterload.

[12.7 Measuring cardiac function] What is echocardiography, what can it detect, and is it invasive?

Ultrasonic waves are beamed at the heart and the returning echoes are electronically plotted by computer to produce continuous 2- and 3-dimensional images of the heart throughout the entire cardiac cycle. It can detect abnormal functioning of cardiac valves or contractions of the cardiac walls and can measure ejection fraction (assesses wall and valve function). It is noninvasive because everything used remains external to the body.

[12.7 Measuring cardiac function] What is cardiac angiography, how is it done, and what is it used for?

Invasive technique: a thin, flexible tube (catheter) is temporarily threaded through an artery or vein into the heart; a liquid containing radiopaque contrast material is injected through the catheter during high-speed x-ray videography. Useful for evaluating cardiac function and for identifying narrowed or completely blocked coronary arteries (patency) - assesses coronary artery patency and blood flow.

[12.8 Vascular system overview] What are the major functions of the vascular system, and which general principle of physiology is highlighted?

The heart provides the overall driving force for blood movement, but the vascular system has a major function in regulating blood pressure and distributing blood flow to the various tissues. Elaborate branching and regional specializations of the vessels efficiently match blood flow to metabolic demand in individual tissues. Principle: structure is a determinant of function.

[12.8 Vascular system overview] What is the endothelium, where is it found, and how does vessel wall structure differ between capillaries and other vessels?

Endothelium = a smooth, single-celled layer (lining) of endothelial cells in contact with the flowing blood; the one structural component common to the entire circulatory system, from the heart to the smallest capillary. Capillaries consist only of endothelium and associated extracellular basement membrane. All other vessels have one or more layers of connective tissue and smooth muscle (in addition to the endothelial lining).

[12.8 Vascular system overview] What are the functions of endothelial cells (Table 12.6)?

1) Physical lining of heart and vessels to which blood cells do not normally adhere. 2) Permeability barrier for exchange of nutrients, metabolic end products and fluid between plasma and interstitial fluid; regulate transport of macromolecules and other substances. 3) Secrete paracrine agents acting on adjacent vascular smooth muscle: vasodilators (prostacyclin, nitric oxide [EDRF]) and vasoconstrictors (endothelin-1). 4) Mediate angiogenesis (new capillary growth). 5) Central role in vascular remodeling (detect signals, release paracrine agents acting on adjacent cells in the vessel wall). 6) Contribute to formation and maintenance of extracellular matrix. 7) Produce growth factors in response to damage. 8) Secrete substances that regulate platelet clumping, clotting and anticlotting. 9) Synthesize active hormones from inactive precursors. 10) Extract or degrade hormones and other mediators. 11) Secrete cytokines during immune responses. 12) Influence vascular smooth muscle proliferation in the disease atherosclerosis.

[12.8 Vascular system overview] What is the function of each vessel type in Figure 12.31 (large artery, arteriole, capillary, venule, large vein)?

Large artery: low-resistance, conducting vessels. Arteriole: main resistance vessels; controls distribution of blood flow. Capillary: exchange of gases, fluid and nutrients; uptake of waste and secretory products from cells. Venule: WBCs are released into tissues during inflammation and infection; capacitance vessels. Large vein: low-resistance, high-capacitance vessels.

[12.8 Vascular pressures] How do blood pressures change along the systemic and pulmonary circuits, and why?

Pressure falls as blood flows from the ventricles through the capillary beds back to the atria; by the time blood reaches the atrium, most of the pressure originally generated by ventricular contraction has dissipated. Reason: the blood vessels offer resistance to flow from one point to the next, so the average pressure at any point is lower than upstream toward the heart. Systemic arterial pressure is higher than pulmonary arterial pressure; the pulmonary circuit has lower vascular resistance.

[12.9 Arteries] What is the structure of the aorta and other systemic arteries, and what are their two major functions?

Thick walls containing large quantities of elastic tissue (also some smooth muscle); can be viewed most conveniently as elastic tubes. Function 1: large radii suit them as low-resistance tubes conducting blood to the various organs. Function 2 (related to elasticity): act as a 'pressure reservoir' that maintains blood flow through the tissues during diastole (ventricular relaxation) because of elastic recoil of the thick arterial walls.

[12.9 Arteries] What is compliance, and what determines the pressure inside an elastic container such as a balloon?

Compliance = how easily a structure stretches = change in volume / change in pressure (Compliance = deltaV/deltaP). The pressure in the balloon depends on 1) the volume of water and 2) how easily the balloon can stretch. A thin, stretchable balloon takes large quantities of water with only a small increase in pressure; a thick, hard-to-stretch balloon shows a large pressure increase even with a small quantity of water.

[12.9 Arteries] How do the arteries act as a pressure reservoir during the cardiac cycle (one-third rule)?

During systole only about one-third of the stroke volume leaves the arteries; the rest remains in the arteries, distending them and increasing arterial pressure. When ventricular contraction ends, the stretched arterial walls recoil passively like a deflating balloon and blood continues to be driven into the arterioles during diastole; arterial volume and pressure slowly decrease. The next contraction occurs while the walls are still stretched, so arterial pressure does not decrease to zero.

[12.9 Arterial blood pressure] Define systolic pressure, diastolic pressure and pulse pressure, and how are they recorded and felt?

Systolic pressure (SP) = maximum arterial pressure, reached during peak ventricular ejection. Diastolic pressure (DP) = minimum arterial pressure, just before ventricular ejection begins. Recorded as systolic/diastolic, e.g. 120/80 mmHg (both average about 10 mmHg lower in females than males). Pulse pressure = SP - DP (120 - 80 = 40 mmHg). It is felt as a pulsation in the arteries of the wrist or neck: nothing is felt during diastole, but the rapid pressure increase at the next systole pushes out the artery wall, and this expansion produces the detectable pulse.

[12.9 Arterial blood pressure] What determines the magnitude of pulse pressure, and what does arteriosclerosis do to it?

Three most important factors: stroke volume, speed of ejection of the stroke volume, and arterial compliance. Pulse pressure is greater if the volume ejected increases, if the speed of ejection increases, or if the arteries are less compliant (stiffer). Arteriosclerosis = stiffening of the arterial walls that progresses with age: increases systolic and decreases diastolic pressure, so pulse pressure increases (often after age 40).

[12.9 Arterial blood pressure] What is mean arterial pressure (MAP), how is it calculated, and why is it important?

MAP = average pressure during the cardiac cycle. NOT halfway between SP and DP, because diastole lasts about twice as long as systole. At a typical resting heart rate: MAP = DP + 1/3 (SP - DP) = diastolic pressure plus one-third of the pulse pressure. Example: 80 + 1/3 (40) = 93 mmHg. Important because it is the average pressure driving blood into the tissues over the entire cardiac cycle. 'Mean arterial pressure' needs no specific artery because the aorta and other large arteries offer negligible resistance, so mean pressures are similar everywhere in the large arteries of a person lying down.

[12.9 Arterial blood pressure] How does arterial compliance affect pulse pressure vs MAP, and which is the better diagnostic indicator of arteriosclerosis?

Compliance is an important determinant of pulse pressure but typically has no major influence on MAP. As compliance changes, systolic and diastolic pressures change in opposite directions: low compliance (arteriosclerosis) with an otherwise normal circulatory system = large pulse pressure (higher systolic, lower diastolic) but a MAP close to normal. Therefore pulse pressure is usually a better diagnostic indicator of arteriosclerosis than MAP.

[12.9 Measuring blood pressure] How is blood pressure measured with a sphygmomanometer, and what are Korotkoff's sounds?

Inflatable cuff with a pressure gauge around the upper arm; stethoscope over the brachial artery just below the cuff. Cuff is inflated above systolic pressure: the artery is completely compressed and no blood flows (no sound). Air is slowly released. When cuff pressure falls just below systolic pressure, the artery opens slightly for a brief time at peak systole; blood flow through the partially compressed artery is at very high velocity (small opening, large pressure difference) and turbulent, producing vibrations = Korotkoff's sounds heard through the stethoscope.

[12.9 Measuring blood pressure] Which cuff pressures correspond to systolic and diastolic pressure, how do the sounds change, and how do Korotkoff's sounds differ from heart sounds?

Systolic pressure = cuff pressure at which sounds are first heard (soft, tapping, intermittent). As cuff pressure decreases, the duration of flow in each cycle becomes longer (sounds loud, tapping, intermittent, then a low muffled continuous sound). Diastolic pressure = cuff pressure at which sounds disappear, because flow is continuous and nonturbulent through the open artery. Korotkoff's sounds are NOT the same as heart sounds (which are due to closing of cardiac valves). Automated home monitors are of adequate accuracy to assess trends in one's own blood pressure.