Neo Hemodynamics- The Oleg Alekseev Legacy 2 Flashcards
ReKap
Changes in the aortic pulse pressure contour can represent the following conditions:
Increased pulse pressure: arteriosclerosis, aortic regurgitation
Decreased pulse pressure: aortic stenosis, mitral stenosis
Increased diastolic blood pressure: mitral stenosis
Decreased diastolic blood pressure: aortic regurgitation, patent ductus arteriosus
Analysis
The correct answer is B. The patient displays a systolic arterial blood pressure (SBP) >140 mm Hg with a diastolic blood pressure (DBP) <90 mm Hg; this is isolated systolic hypertension. It is characterized by increased pulse pressure without greatly elevated DBP. One of the most likely causes is decreased arterial compliance (arteriosclerosis), which is common in elderly patients.
Arteriosclerosis is a pathologic condition caused by calcification and deposition of inelastic connective tissue within the vessel wall. Atherosclerosis is a form of arteriosclerosis associated with lipid deposition and intimal thickening.
Although arteries are considerably less compliant than veins, the arterial tree does stretch to accommodate left ventricular (LV) stroke volume during systole. Energy stored in the arterial walls is then used to maintain forward flow to the capillary beds during diastole (“diastolic runoff”). Arteriosclerosis limits the ability of arteries to stretch under pressure which, in turn, limits diastolic runoff. Peak SBP thus increases to ensure that a greater proportion of stroke volume is transferred to the capillary beds during systole rather than diastole. In the graph, the normal pulse pressure is about 40 mm Hg (SBP of 120 mm Hg − DBP of 80 mm Hg). The pulse pressure has increased to about 80 mm Hg in the patient with arteriosclerosis (SBP 160 mm Hg − DBP 80 mm Hg).
In aortic valve stenosis (choice A), aortic pressure rises very slowly during systole and the pulse pressure is greatly diminished because blood flow through the stenotic valve is impaired.
ReKap
Changes in the aortic pulse pressure contour can represent the following conditions:
Increased pulse pressure: arteriosclerosis, aortic regurgitation
Decreased pulse pressure: aortic stenosis, mitral stenosis
Increased diastolic blood pressure: mitral stenosis
Decreased diastolic blood pressure: aortic regurgitation, patent ductus arteriosus
Analysis
The correct answer is B. The patient displays a systolic arterial blood pressure (SBP) >140 mm Hg with a diastolic blood pressure (DBP) <90 mm Hg; this is isolated systolic hypertension. It is characterized by increased pulse pressure without greatly elevated DBP. One of the most likely causes is decreased arterial compliance (arteriosclerosis), which is common in elderly patients.
Arteriosclerosis is a pathologic condition caused by calcification and deposition of inelastic connective tissue within the vessel wall. Atherosclerosis is a form of arteriosclerosis associated with lipid deposition and intimal thickening.
Although arteries are considerably less compliant than veins, the arterial tree does stretch to accommodate left ventricular (LV) stroke volume during systole. Energy stored in the arterial walls is then used to maintain forward flow to the capillary beds during diastole (“diastolic runoff”). Arteriosclerosis limits the ability of arteries to stretch under pressure which, in turn, limits diastolic runoff. Peak SBP thus increases to ensure that a greater proportion of stroke volume is transferred to the capillary beds during systole rather than diastole. In the graph, the normal pulse pressure is about 40 mm Hg (SBP of 120 mm Hg − DBP of 80 mm Hg). The pulse pressure has increased to about 80 mm Hg in the patient with arteriosclerosis (SBP 160 mm Hg − DBP 80 mm Hg).
In aortic valve stenosis (choice A), aortic pressure rises very slowly during systole and the pulse pressure is greatly diminished because blood flow through the stenotic valve is impaired.
ReKap
Changes in the aortic pulse pressure contour can represent the following conditions:
Increased pulse pressure: arteriosclerosis, aortic regurgitation
Decreased pulse pressure: aortic stenosis, mitral stenosis
Increased diastolic blood pressure: mitral stenosis
Decreased diastolic blood pressure: aortic regurgitation, patent ductus arteriosus
Analysis
The correct answer is B. The patient displays a systolic arterial blood pressure (SBP) >140 mm Hg with a diastolic blood pressure (DBP) <90 mm Hg; this is isolated systolic hypertension. It is characterized by increased pulse pressure without greatly elevated DBP. One of the most likely causes is decreased arterial compliance (arteriosclerosis), which is common in elderly patients.
Arteriosclerosis is a pathologic condition caused by calcification and deposition of inelastic connective tissue within the vessel wall. Atherosclerosis is a form of arteriosclerosis associated with lipid deposition and intimal thickening.
Although arteries are considerably less compliant than veins, the arterial tree does stretch to accommodate left ventricular (LV) stroke volume during systole. Energy stored in the arterial walls is then used to maintain forward flow to the capillary beds during diastole (“diastolic runoff”). Arteriosclerosis limits the ability of arteries to stretch under pressure which, in turn, limits diastolic runoff. Peak SBP thus increases to ensure that a greater proportion of stroke volume is transferred to the capillary beds during systole rather than diastole. In the graph, the normal pulse pressure is about 40 mm Hg (SBP of 120 mm Hg − DBP of 80 mm Hg). The pulse pressure has increased to about 80 mm Hg in the patient with arteriosclerosis (SBP 160 mm Hg − DBP 80 mm Hg).
In aortic valve stenosis (choice A), aortic pressure rises very slowly during systole and the pulse pressure is greatly diminished because blood flow through the stenotic valve is impaired.
In mild-to-moderate mitral valve stenosis (choice D), the aortic pressure wave contour remains unchanged since left atrial pressure increases to compensate for obstructed flow into the LV. Severe mitral stenosis can impair LV preloading and reduce stroke volume to the point where cardiac output is reduced and, thus, peak SBP falls. DBP then rises as a result of systemic vasoconstriction and reduced diastolic runoff.
In patent ductus arteriosus (choice E), a large portion of the blood pumped by the LV is shunted through the ductus arteriosus into the pulmonary artery, which allows the DBP to drop to very low levels before the next heartbeat. It is very unlikely that patent ductus arteriosus would first present in a person of this age as isolated systolic hypertension.
ReKap
Compliance = ΔV/ΔP.
High compliance means that blood vessels are more easily distended by flowing blood.
A decrease in compliance, such as that caused by age-related arteriosclerosis, will cause a compensatory increase in SBP and decrease in DBP, leading to a widened pulse pressure (PP = SBP – DBP).
Analysis
The correct answer is A. Pulse pressure (PP) widens with age due to a loss of arterial compliance.
PP = systolic blood pressure (SBP) – diastolic blood pressure (DBP)
Blood pressure is ideally 120/80 mm Hg, giving a PP of 40 mm Hg. PP in our patient is 155 – 75 mm Hg, or 80 mm Hg.
SBP is determined primarily by left ventricular (LV) stroke volume (SV) and arterial compliance.
Compliance = ΔV/ΔP
DBP is determined primarily by total peripheral resistance (TPR; also known as systemic vascular resistance or peripheral vascular resistance).
The LV ejects blood into the arterial tree during systole faster than it can be distributed to the capillary beds. The large, proximal vessels such as the thoracic aorta and its branches are endowed with elastin which allows them to stretch and distend to accommodate a full SV. Energy stored within the vessel walls then helps drive anterograde flow during diastole, a time during which the LV is relaxing and the aortic valve is closed. Compliance thus helps damp the arterial pressure pulse to maintain even flow throughout the cardiac cycle.
With age, the elastic lamina of large vessels breaks down, becoming calcified and mineralized. Many elastin fibers are replaced by collagen, which is significantly less compliant. These changes are known as arteriosclerosis, and have two main effects:
The reduced ability to accommodate blood volume within the arterial tree (during systole for later transfer to capillary beds during diastole) means that the LV must hypertrophy to generate higher peak systolic pressures to achieve greater flow during systole (remember, basal cardiac output has to be maintained at a relatively constant level of 5–6 L/min). SBP increases as a result.
Less stored energy is available to drive forward blood flow during diastole, so pressure drops faster than previously. DBP decreases.
↑ SBP + ↓ DBP = widening of PP
Cardiac output (CO; choice B) is a product of SV and heart rate (HR). Whereas PP is directly proportional to SV, it is largely independent of HR (DBP may be influenced to some degree), meaning that changes in CO can occur independently of PP.
A decrease in myocardial contractility (choice C) would be expected to decrease SV and SBP and, thus, PP would also decrease. PP increases when LV contractility increases, during sympathetic activation, for example.
Decreases in SV (choice D) reduce SBP and PP because a smaller volume of blood enters the arterial system with each heartbeat. PP directly correlates with SV, so PP would not increase if SV has decreased.
A decrease in TPR (choice E), as seen with the onset of exercise, causes SBP and DBP to fall. A compensatory rise in CO would raise SBP, but DBP would remain low and hence PP widens. Although a fall in TPR could explain a widened PP, decreased arterial compliance is a more likely explanation given our patient’s age and history.
ReKap
Coarctation of the aorta is characterized by strong pulses in the upper extremities (radial pulse) and weak, delayed pulses in lower extremities (femoral pulse).
Aortic coarctation with narrowing in the juxtaductal region can produce high thoracic aorta systolic pressures and low abdominal aorta systolic pressures.
Left ventricular hypertrophy is a common complication of coarctation of the aorta due to increased systemic afterload.
Analysis
The correct answer is C. This infant has coarctation of the aorta, which increases left ventricular (LV) afterload and promotes LV hypertrophy.
The discrepancy between upper and lower limb pulses and pressure measurements demonstrates aortic constriction distal to the origin of the left subclavian artery. This creates a resistance to blood flow to the lower extremities and raises systemic vascular resistance. The left ventricle responds with a chronic increase in peak systolic pressure, initiating pathways that lead to LV hypertrophy (i.e., the wall thickness of the LV increases as the myocytes enlarge). A similar process occurs when there is systemic hypertension. The increased blood pressure in the upper body (above the coarctation) also produces arterial hypertrophy, increasing the thickness of the vessel wall and reducing wall distensibility.
Pressure and flow distal to the stricture is decreased, presenting as greatly attenuated pulse pressures in the abdominal aorta and arteries in the lower body. Decreased renal perfusion pressure stimulates renin release from granular cells (juxtaglomerular cells) in the glomerular afferent arteriole, which initiates the renin-angiotensin-aldosterone system (RAAS). RAAS promotes salt and water retention, which helps offset the effects of coarctation on flow by increasing LV preload and further raising aortic pressure proximal to the site of constriction.
Abdominal aortic wall tension (choice A) is a function of perfusion pressure and internal radius (2T = P x r). Coarctation of the aorta reduces pressure in the abdominal aorta and other arteries distal to the constriction, so wall tension is reduced. This effect may be partly offset by dilatation of the aorta distal to the stricture, which increases the internal radius (r), but it is unlikely that wall tension would be increased compared with normal.
Abdominal aortic wall thickness (choice B) is tied to luminal pressure; high perfusion pressures stimulate hypertrophy and increased wall thickness. Coarctation of the aorta reduces pressure in the abdominal aorta, so wall thickness is reduced.
Lower than normal blood flow to the kidneys (choice D), leg muscles (choice E), and other organs below the coarctation is likely, unless the body can compensate adequately for the coarctation via volume loading and LV hypertrophy. With less severe coarctation, which may be asymptomatic until later in childhood, blood flow is normal in these low-pressure areas of the body.
ReKap
The degree of jugular venous distension is directly correlated with the central venous pressure.
Elevated central venous pressure and pulmonary edema in a patient with a history of left myocardial infarction strongly suggest right heart failure secondary to left heart failure.
Analysis
The correct answer is B. This patient has elevated jugular venous pressure (JVP), a classic sign of central venous hypertension, which can be caused by right-sided heart failure. The video shows distension of the jugular vein AKA jugular venous distention (JVD), which directly correlates with central venous pressure (CVP). First, have the patient recline with the head elevated 45 degrees. Then measure the height of the distended portion of the vein above the sternal angle. Finally, add 5 cm (distance from sternal angle to right atrium) to arrive at an estimate for CVP. The normal CVP is less than 8 cm H2O. Points of reference can be measured at the sternum or mid-axillary region (normal values: sternum 0–14 cm H2O; midaxillary 8–15 cm H2O).
To identify a jugular venous pulse, it is important to look for a biphasic pulsation. The pulses correspond with different venous/atrial waveforms, namely the a-wave and v-wave (see figure: the c-wave can be difficult to observe). The a-wave corresponds to right atrial contraction, whereas the v-wave represents right atrial filling during ventricular contraction. This distinguishes the jugular venous pulse from carotid pulsation, which is a single pulsation (systole) and located more medially.
Jugular venous pulsation is defined by the a-wave (right atrial contraction) and v-wave (right atrial filling).
Our patient’s right-sided heart failure is likely secondary to her myocardial infarction two years ago. Though her infarction initially impaired the left side of the heart, the most common cause of right-sided heart failure is left-sided heart failure. Ischemic necrosis of the left ventricular muscle leads to significantly decreased ejection fraction and contractility. Impaired left ventricular function causes fluid to back up into the pulmonary vasculature, presenting as pulmonary edema (producing crackles in the lung bases) and excessive afterload on the right ventricle. This produces chronic volume overload of the right ventricle, eventually leading to right heart failure and consequently elevated JVP. Other causes of elevated JVP include restrictive cardiomyopathy, constrictive pericarditis, and right-sided valvular anomalies.
Capillary oncotic pressure (choice A) is a direct function of plasma protein levels (mainly albumin). Capillary oncotic pressure is the principal force holding fluid in the vasculature in opposition to capillary hydrostatic pressure. A decrease in capillary oncotic pressure allows fluid to leak from the vasculature in turn causing peripheral edema.
Right atrial volume (choice C) is influenced by many aspects of cardiovascular performance (e.g., cardiac output, venous return, total blood volume, and venous compliance). Whether or not atrial volume changes manifest as an increase in right atrial pressure and jugular venous distension depends on vascular fullness, among other factors. Thus, jugular venous distension is not a good way to directly measure right atrial volume.
Increased total blood volume (choice D) can, but does not necessarily, cause jugular venous distension. The latter is a direct reflection of JVP, which is determined in part by blood volume but also by vascular compliance and cardiac function. Thus, jugular venous distension is not a good index of total blood volume.
Venous return (VR; choice E) is a determinant of CVP and JVP, but the effect on these pressures depends on many other aspects of cardiovascular performance (similar to total blood volume and right atrial volume). Thus, JVP is not a good index of VR.
ReKap
The first trimester of pregnancy is accompanied by a 40% to 50% expansion of blood volume.
Expansion occurs through increased fluid retention and leads to hemodilution.
The resulting fall in plasma protein concentration reduces plasma colloid osmotic pressure, which is the principal force for the commonality of peripheral edema in pregnant patients, particularly those of late-term gestations.
Analysis
The correct answer is A. Colloid osmotic pressure drops by ~38% during pregnancy, due to expansion of maternal plasma volume, which increases the likelihood of edema formation. Plasma colloid osmotic pressure (πc), also known as oncotic pressure, is one of four principal forces (Starling forces) controlling fluid movement between blood and the interstitium. Their relationship is described by the Starling law of the capillary:
Colloid osmotic pressure is created by plasma proteins, principally albumin. It is the main force holding fluid within the vasculature, so when πc falls, the tendency for fluid to spill into the interstitial space increases. If the amount of fluid filtering from blood vessels exceeds the ability of the lymphatic system to return it to the heart, peripheral edema develops.
Pregnant women commonly develop peripheral edema because blood volume expands rapidly by 40–50% during the first trimester through fluid retention. The resulting hemodilution reduces albumin concentration, which lowers πc. In addition, The gravid uterus compresses and impairs flow through the inferior vena cava and other smaller veins carrying blood from the lower extremities, which raises Pc in the feet and ankles. Gravitational influences (e.g., a long waitressing shift) potentiate this effect. The combination of low πc and high Pc makes the lower extremities highly susceptible to edema.
Blood volume (choice B) increases ~50% during pregnancy to support left ventricular preloading and the increased need for CO to adequately perfuse the placental bed and other organs most affected by pregnancy (e.g., skin flow increases to dissipate heat).
Fluid retention during the first trimester occurs faster than red blood cell (RBC) production, leading to a decrease in hematocrit (choice C; the “physiologic anemia of pregnancy”). Hematocrit does not affect the likelihood of edema formation, although anemia does decrease blood viscosity and lead to functional murmurs (e.g., the systolic ejection murmur associated with high-output flow across the aortic valve).
Left ventricular afterload decreases, not increases (choice D) during pregnancy due to the addition of a low-resistance circuit to the systemic vasculature (i.e., the placental site) and increased flow to organs supporting the pregnancy (e.g., skin, kidneys, intestines).
Systolic blood pressure (choice E) does not affect the likelihood of edema formation because resistance vessels maintain a stable Pc in the face of changes in arterial pressure over a physiologic range.
ReKap
Mitral stenosis:
Rheumatic heart disease is a common cause of mitral stenosis.
Mitral stenosis reduces the valve orifice surface area and creates resistance to flow between the left atrium (LA) and left ventricle (LV). The LA hypertrophies and generates higher pressures to compensate.
EDV and ESV both fall, the former because of impaired LV filling, the latter because of increased LV contractility and emptying. EF either remains unchanged or may fall slightly.
Analysis
The correct answer is E. The patient is exhibiting early signs and symptoms of mitral stenosis (MS), including pulmonary edema. Characteristic auscultation findings include an “opening snap” caused by restricted opening of the partially fused valve leaflets during diastole, followed by a decrescendo murmur (diastolic rumble) as blood passes through the narrowed valve orifice.
Patients with mitral stenosis usually have a history of rheumatic heart disease (RHD; 50–80% of cases), as noted in this patient. Other rarer causes include valve annulus calcification and congenital conditions that affect the valve. RHD may lead to fusion of the valve commissures and thickening, calcification, and fibrosis of the valve leaflets. These processes gradually narrow the valve orifice, creating resistance to forward flow that impairs left ventricular (LV) filling and reduces LV EDV.
MS typically develops slowly over a period of decades and is paralleled by left atrial (LA) hypertrophy. This allows the LA to develop higher pressures to compensate for the resistance increase. The LV also compensates through a more complete emptying during systole, so ESV typically falls. Because EDV and ESV both decrease, EF typically remains unchanged or may decrease slightly (depending on disease severity). Peak LVP, cardiac output, and PP all remain largely unchanged.
Although LV function may remain largely unaffected by MS, the consequences for the LA, the pulmonary circulation, and the right heart are severe. The increased LA pressure causes chamber dilation and may disrupt conduction pathways, leading to atrial fibrillation (note the patient’s irregular heart rhythm). The pressure is also transmitted back into the pulmonary circulation which results in pulmonary hypertension and edema. The right heart hypertrophies to sustain cardiac output, but may fail as a result of the pressure load.
Increased ESV and EDV combined with decreased LVP and PP (choice A) would be consistent with a patient in congestive heart failure. A failing heart loses contractility (due to the death of myocytes during myocardial infarction, for example) and its ability to sustain a normal LVP and PP is compromised. Volume retention helps compensate by increasing LV preload and EDV, but the loss of contractility means that stroke volume (SV) falls and ESV increases.
The combination of increased LVP but decreased EF (choice B) is suggestive of increased LV afterload, such as seen in aortic stenosis (AS). The reduced valve orifice creates a resistance to outflow that elicits an increase in LVP to maintain cardiac output (CO) and PP. AS stimulates myocardial hypertrophy to meet the needs for increased pressure, but ESV and SV are typically decreased. EDV remains unchanged until the heart begins to fail.
An increase in EDV, EF, LVP, and PP (choice C) is characteristic of chronic aortic regurgitation (AR). An incompetent aortic valve allows blood to flow backward from the aorta to the LV during systole, which contributes to LV preload and raises EDV. AR allows blood to escape the arterial system more easily during diastole, so DBP falls more steeply than normal, which, together with the LVP increase, raises PP.
A decrease in ESV in the setting of increased EDV and EF (choice D) is consistent with mitral regurgitation (MR). The regurgitant valve decreases resistance to left ventricular (LV) outflow, allowing the ventricle to empty more completely during systole and ESV falls. The blood that leaked backward during systole increases atrial pressure and contributes to LV preloading during diastole, so EDV increases.
ReKap
A premature ventricular contraction occurs independently of atrial contraction. Reduced filling time generates reduced stroke volume during this contraction.
The ventricular contraction closes the AV valves, so the atria eventually contract against closed AV valves, producing an abnormally high atrial pressure and “cannon a-waves” on the jugular vein pressure tracing.
Analysis
The correct answer is B. The event labeled “B” on the ECG represents a premature ventricular contraction (PVC). PVCs shorten diastole and thereby reduce left ventricular (LV) filling time and LV end-diastolic volume (LVEDV).
PVCs are relatively common, occurring in virtually all individuals, but their incidence increases with electrolyte abnormalities, hypertension, and heart disease. The tissue damage that accompanies myocardial infarction also increases the occurrence of PVCs. They typically produce few symptoms aside from palpitations, though syncope can occur.
Although the precise mechanism by which PVCs arise is not defined, there are three likely mechanisms:
Structural anomalies in the myocardium create reentrant circuits.
After-depolarizations that are accentuated by electrolyte abnormalities (e.g., hyperkalemia), ischemia, or drugs trigger premature action potentials.
The normal intrinsic pacemaker properties of Purkinje fibers are enhanced by electrolyte abnormalities or sympathetic stimulation.
PVCs can originate from ectopic sites located anywhere in the myocardium. Because all cardiac myocytes are coupled electrically via gap junctions, depolarization at an ectopic site triggers a wave of depolarization that spreads across the entire myocardium. This wave typically travels independently of the His-Purkinje system, so the resulting QRS complexes are usually wide (due to slower myocyte-to-myocyte conduction) and aberrant. PVCs are not usually preceded by P-waves since the electrical impulse originates in the ventricles, rather than the atria.
Premature contraction reduces preload and stroke volume roughly in proportion, so whereas ejection fraction may be reduced during a PVC (choice A), it is affected to a lesser degree than LVEDV.
Ventricular contraction closes the atrioventricular (AV) valves. When PVCs and atrial contractions coincide, the atria contract against closed AV valves. This generates an abnormally high atrial pressure (choice C). The right atrial pressure peak travels backward and can be observed in the jugular vein as a “cannon A wave.”
Peak LV pressure is decreased (choice D) during a PVC due to the shortened filling time and preload. Peak LV pressure increases with preload due to length-dependent activation of the sarcomere.
The rate of LV pressure development (dP/dt; choice E) would not be greatly affected by a PVC. dP/dt is a direct reflection of myocardial contractility, which is increased by sympathetic stimulation and positive inotropes.
Stroke volume (SV) is decreased (choice F) by a premature contraction due to decreased diastolic filling time. SV increases when preload increases, afterload decreases, or myocardial inotropy increases.
A 25-year-old man with a history of end-stage renal disease receives hemodialysis therapy 3 days each week. Laboratory studies show a hemoglobin of 7.0 g/dL and hematocrit of 25%. The patient is anemic and does not receive erythropoietin. The data shown is obtained from the patient during resting conditions.
Arterial oxyhemoglobin 97%
Arterial partial pressure of oxygen 100 mm Hg
Arterial oxygen content 97 mL oxygen/L blood
Mixed venous oxyhemoglobin 50%
Mixed venous partial pressure of oxygen 35 mm Hg
Mixed venous oxygen content 47 mL oxygen/L blood
Cardiac output 6 L/min
Which of the following is this patient’s resting oxygen consumption?
A. 100 mL/min
B. 150 mL/min
C. 200 mL/min
D. 250 mL/min
E. 300 mL/min
Answer E
ReKap
Fick principle:
VO2 = CO × (Ca - Cv)
VO2 = oxygen consumption, Ca = arterial oxygen content, and Cv = venous oxygen content
Analysis
The correct answer is E. This patient has severe anemia. In order to maintain normal oxygen uptake in the lungs and delivery to tissues, cardiac output (CO) has increased. Oxygen consumption (VO2) can be calculated using the Fick principle:
VO2 = CO × (Ca- Cv)
where Ca is arterial O2 content and Cv is venous O2 content.
Using values from the case history:
VO2 = 6 L/min × (97 mL O2/L - 47 mL O2 /L)
6 L/min × 50 mL O2/L = 300 mL O2/min
Note that each liter of blood loses 50 mL of oxygen as it passes through the tissues. Because 6 L of blood passes through the tissues each minute, and because each liter of this blood loses 50 mL of oxygen, a total of 300 mL of oxygen are used by the tissues each minute. Normal arterial oxygen content is about 200 mL/L, so this patient’s arterial content is reduced by >50% as a result of low hemoglobin content.
The remainder of the answer choices (choices A, B, C, and D) represent miscalculations.
ReKap
Key features of aortic insufficiency include:
Increased pulse pressure (caused by retrograde flow from the aorta to the left ventricle), which may cause signs like head bobbing and a “water-hammer pulse”.
Diastolic murmur best heard along the lower left sternal border.
Aortic regurgitation can occur due to valvular vegetations produced by bacterial endocarditis.
Analysis
The correct answer is D. This patient has a diastolic murmur on the lower left sternal border, which is often heard in aortic regurgitation. Aortic regurgitation (AR) is caused by insufficiency of the aortic valve and is characterized by a wide pulse pressure (the difference between systolic and diastolic pressure).
Aortic, atrial, and ventricular pressure profile in aortic regurgitation. During diastole when the left ventricle is being filled from the left atrium, blood is also entering the left ventricle from the aorta due to the insufficient aortic valve and aortic diastolic pressure decreases precipitously.
During diastole, aortic pressure drops precipitously as the blood flows from the aorta back into the left ventricle (LV) through the incompetent valve. Systolic pressure remains relatively normal or may be elevated because of increased LV preload (from regurgitant volume) during the subsequent contraction. Increased preload also produces chronic volume overload, which can eventually precipitate LV failure. Other clues pointing towards aortic regurgitation include head-bobbing or “water-hammer pulse” found on physical examination, which are manifestations of the increased pulse pressure. Overall mean arterial pressure (calculated as diastolic pressure + 1/3 of pulse pressure) is usually normal or low in aortic regurgitation.
It is also important to evaluate this patient’s clinical context. A middle-aged individual with a history of intravenous drug abuse and presenting with subacute fever, fatigue, and new heart murmur most likely has bacterial endocarditis. Endocarditis results in vegetations on heart valves, (commonly the tricuspid, but any of the four valves can be affected) which can produce regurgitation.
A blood pressure of 50/undetectable mm Hg (choice A) is characteristic of acute shock. The patient would present with signs of end-organ failure (such as oliguria) and an elevated heart rate.
Aortic stenosis is most often associated with reduced systolic pressure and relatively preserved diastolic pressure, such as 95/80 mm Hg (choice B) because the left ventricle is unable to pump a normal amount of blood through a stenotic valvular orifice. Patients present with a systolic ejection murmur in the right upper sternal border that (1) is usually accompanied by thrill, (2) is harsh in quality, and (3) radiates to the carotids. Major causes include age-related calcification and bicuspid aortic valve.
Blood pressure of 120/80 mm Hg or less (choice C) is considered normal in healthy adults, whereas blood pressure of 160/100 mm Hg is considered to be hypertensive. Therefore, blood pressures of 170/100 mm Hg (choice E) and 220/130 mm Hg (choice F) are also considered hypertensive. A blood pressure of 220/130 mm Hg is considered to be a severe condition that may lead to life-threatening end-organ damage if not properly treated (malignant hypertension). Hypertensive mean arterial pressures are unlikely to be caused by symptomatic aortic regurgitation.
ReKap
Anemia reduces blood oxygen-carrying capacity.
Diastolic blood pressure (DBP) falls due to tissue hypoxia and reflexive peripheral vasodilation (↓SVR).
Cardiac output (CO) increases to compensate. Increased SV causes SBP to rise.
Pulse pressure is calculated by SBP – DBP, so pulse pressure (PP) widens in the setting of severe anemia.
Analysis
The correct answer is E. The patient is severely anemic, leading to reflexive systemic vasodilation and widening of pulse pressure. Blood hemoglobin (Hb) concentration is 15–16 g/dL in normal males; a patient is considered to be severely anemic when the Hb concentration falls below 7.5 g/dL.
Pulse pressure (PP):
PP = systolic blood pressure (SBP) – diastolic blood pressure (DBP).
Using the pressure trace below, PP = 120 – 80 = 40 mm Hg.
SBP is determined by left ventricular stroke volume (SV) and cardiac output (CO).
DBP is determined by the ease with which blood can escape the arterial system during diastole, which is determined by systemic vascular resistance (SVR).
PP widens when SV increases and/or SVR decreases.
Anemia limits how much O2 blood can carry, forcing dependent tissues to compensate for the reduced supply through locally-mediated reflexive vasodilation. SVR falls as a result, and PP widens.
The fall in mean arterial pressure caused by increased flow to the periphery triggers a baroreflex, which promotes a compensatory rise in CO through increases in heart rate and SV. The latter contributes to the widening of the pulse pressure by increasing SBP.
CO is increased, not decreased (choice A) in anemia. The rise in CO is needed to supply increased volumes of blood to tissues to compensate for blood’s reduced O2 content. In severely anemic patients, resting CO is increased significantly; this is often called a hyperkinetic circulatory state.
Cyanosis (choice B) refers to a bluish color of the skin and mucous membranes that results from the presence of deoxygenated Hb in blood vessels, especially the capillaries. Cyanosis does not occur in severely anemic patients, despite widespread tissue hypoxia, because color development requires blood to contain at least 5 g/dL fully deoxygenated Hb. Physical examination of anemic patients usually shows their skin, mucous membranes, and conjunctival membranes to be pale due to reduced erythrocytes.
SVR is decreased, not increased (choice C) in anemia because tissue hypoxia stimulates reflexive peripheral vasodilation to increase flow to the tissues.
Blood density (choice D) does not significantly change in the setting of anemia. While a reduction in the circulating red blood cell mass does decrease density, this is rapidly offset by an increase in blood proteins and other cellular blood components.
Answer Options:
A. 2
B. 4.
C. 6
D. 7
E. 60
ReKap
The Fick equation calculates flow through an organ.
Since the entire cardiac output (CO) passes through the pulmonary circulation, the Fick equation can be used to calculate cardiac output. The amount of O2 that is picked up by blood per minute (oxygen consumption) divided by the amount of oxygen picked up by each 100 mL portion of the blood flowing through the lungs (arterial-venous oxygen content) provides an accurate estimate of cardiac output.
Analysis
The correct answer is C. Cardiac output can be calculated using the Fick equation as follows:
Cardiac Output = O2 consumption / (arterial O2 content – venous O2 content)
First, it is important to ensure that all units are appropriately converted. Cardiac output is classically expressed in liters per minute (L/min). O2 content is usually expressed per 100 milliliters of blood (mL O2 / 100 mL blood). Thus, the O2 content provided must be multiplied by ten to convert to mL O2 / L blood.
Arterial O2 content = 200 mL O2/L blood
Venous O2 content = 150 mL O2/L blood
Arterial O2 – Venous O2 = 50 mL O2/L blood
The Fick equation for calculating cardiac output can be understood as follows: 300 mL of oxygen are absorbed from the lungs into the pulmonary circulation each minute (i.e., the O2 consumption is 300 mL). Each liter of blood flowing through the lungs picks up 50 mL of oxygen (i.e., the arterial O2 content - venous O2 content). Thus, 6 L of blood must flow through the lungs each minute to absorb this amount of oxygen (6 L of blood per minute x 50 mL O2 per liter of blood = 300 mL O2 per minute).
The Fick equation for determining cardiac output is the most accurate method available and is often used as a standard to test other, less invasive methods.
ReKap
In aortic stenosis, there is resistance to blood flow through the aortic valve.
Therefore, left ventricular pressure (LVP) will increase, as will the workload and the oxygen consumption of the left ventricle.
Left ventricular tissue oxygen concentration is decreased with increased oxygen consumption, which also increases tissue adenosine production, dilating the coronary arterioles.
Analysis
The correct answer is E. The patient has aortic stenosis, a pathologic narrowing of the aortic valve orifice that creates a resistance (AoR) to left ventricular (LV) outflow. The signs and symptoms of aortic stenosis all reflect the need for a chronic increase in LV pressure (LVP) that is required to maintain cardiac output (CO) against this resistance.
Remember that CO must be maintained at a minimum of 5-6 L/min. Since CO = LVP/AoR, if AoR increases, LVP must increase also to maintain CO.
Stroke work: Stroke work is a measure of the amount of work performed by the ventricle to eject blood into the arterial system during a single cardiac cycle (i.e., stroke volume, SV): Work = LVP × SV. Generating a high intraventricular pressure expends more energy than usual, and thus the work increases.
Generating high pressure involves generating greater force during cross-bridge cycling, which expends more ATP than normal. O2 consumption increases as a result.
Increased O2 usage by cardiac myocytes means that O2 extraction from coronary blood is increased, and local tissue O2 levels fall.
An increased workload requires increased ATP expenditure and leads to the accumulation of adenosine (removing the three phosphate groups from ATP yields adenosine). Adenosine acts as a physiologic signal for increased blood flow to meet the O2 needs of a myocardium working at increased pressure. Coronary resistance vessels are particularly sensitive to adenosine. When local adenosine levels rise, the resistance vessels dilate reflexively and flow increases in direct proportion to myocardial demands.
Aortic stenosis is a common valvular disease that has three principal causes:
Congenital – two of the three valve leaflets are fused at birth, forming a bicuspid aortic valve that is prone to premature wear, calcification, and degeneration.
Thickening and calcification of the valve leaflets – the location of the aortic valve in a high-pressure part of the vasculature means that it is vulnerable to hemodynamic damage and subsequent inflammation. The latter leads to progressive calcification, thickening, and stiffening of the valve leaflets, and the commissures may fuse.
Rheumatic disease – Streptococcal infections remain a significant cause of valvular disease in developing nations.
Patients with aortic stenosis typically remain asymptomatic until the valve orifice has been reduced to 1 cm2 or less (normal = 3 – 4 cm2). The left ventricle progressively hypertrophies in response to the chronically increased afterload and a significant transvalvular pressure gradient develops.
Flow velocity through the valve increases in parallel with surface-area reduction, as predicted by the Equation of Continuity:
CO = aN × vN = ↓aS × ↑vS.
In this equation, a and v represent the valve cross-sectional area and flow velocity, respectively, through a normal (N) and a stenotic (S) valve. If CO is to be sustained, a decrease in cross-sectional area means that flow velocity must increase. High-velocity ejection causes significant turbulence, which is audible as a pansystolic murmur (see figure above).
As progressive narrowing of the valve orifice becomes critical and the myocardium is no longer able to generate the pressures required to increase CO above basal levels of CO, patients typically present with exertional angina, dyspnea, and syncope.
Stroke work describes the amount of energy the left ventricle is producing to pump blood across the aortic valve. Patients with symptomatic aortic stenosis require increased stroke work (choices A, B, and C) to maintain normal stroke volume.
Tissue oxygen concentration is inversely correlated with oxygen consumption. Therefore, increased oxygen consumption should not lead to increased tissue oxygen concentration (choice D).
ReKap
During ventricular fibrillation, blood continues to flow passively from the arterial into the venous system until the pressure within the entire circulatory system has equalized at mean systemic pressure (MSP).
During exercise, sympathetic activity causes venoconstriction, which decreases the capacity of the venous system and increases MSP.
Analysis
The correct answer is E. When the heart is suddenly stopped by ventricular fibrillation or any other means, the flow of blood in the circulation ceases within a minute. During the first few seconds, blood flows mainly from the high-pressure arterial system into the low-pressure venous system until the pressures everywhere in the circulation become equal. This equilibrated pressure is called the mean systemic pressure (MSP), which may also be referred to as mean systemic filling pressure (MSFP) or mean circulatory filling pressure (MCFP).
MSP is a function of blood volume and vascular compliance. Compliance is a measure of the relationship between volume and pressure (compliance = ΔV/ΔP). During intense exercise, an increase in sympathetic activity causes venoconstriction, so venous compliance decreases. This increases MSP since the same volume of blood is contained within vessels that are harder to stretch. When MSP is increased, central venous pressure is increased, which increases right atrial pressure (RAP), left ventricular preload, and cardiac output (CO).
MSP is measured at the point at which the venous return curve intersects the x-axis (i.e., at zero CO). Thus, MSP is normally about +7 mm Hg in this woman, and it increased to +20 mm Hg during the exercise, because of increased venous smooth muscle tone. Ventricular fibrillation (V-fib) would cause RAP to rise to a MSP of +20 mm Hg (as shown in the figure) within a minute of onset.
ReKap
The greatest pressure drop in the vascular system occurs across the arterioles.
This is because these are the vessels with the highest resistance.
Analysis
The correct answer is B. Arterioles contribute the largest part of the total peripheral resistance (TPR), also known as systemic vascular resistance (SVR) or peripheral vascular resistance. Vascular resistance is calculated by the hemodynamic application of the Ohm’s law:
R = ΔP ÷ Q
where R is resistance, ΔP is the pressure drop across the vessels, and Q is blood flow through the vessels.
Since the vascular system is a closed, serial circuit, Q is constant as blood flows from one class of vessels to another. Thus, the vessels that cause the greatest pressure drop must have the highest resistance (see figure below).
As blood progresses through the systemic circulation, mean pressure decreases from about 100 mm Hg in the aorta to about 0 mm Hg in the right atrium (see figure). The mean blood pressure is about the same in all portions of the aorta and it only falls by a few mm Hg in the large arteries (choice A). The blood pressure decreases by 10 to 20 mm Hg in the small arteries (choice D) so that blood entering the arterioles has a pressure averaging about 80 to 90 mm Hg. By the time the blood has reached the ends of the arterioles (choice B), the pressure has fallen to about 35 mm Hg. The pressure falls another 25 mm Hg as it flows through the capillary network (choice C), so that blood entering the venules has a pressure of about 10 mm Hg. The blood pressure falls by about 10 mm Hg as it flows through the venous system (choices E and F) to the right atrium.
Answer Options
A. Increased contractility
B. Increased end-systolic pressure
C. Increased pulmonary artery wedge pressure
D. Increased systemic vascular resistance
E. Left ventricular dilation
ReKap
An incompetent aortic valve allows blood to regurgitate backward from the aorta to the left ventricle (LV), which increases preload on the next beat and raises LV end-diastolic pressure (EDP).
Compensation for loss of forward flow includes volume loading and LV hypertrophy, resulting in ventricular dilation.
Hypertrophy and dilation increases ventricular compliance, which allows for enhanced volume loading with little or no increase in EDP.
Analysis
The correct answer is E. The test subject has an incompetent aortic valve (AoV) that has resulted in aortic regurgitation (AR) and left ventricular (LV) dilation. An incompetent AoV allows blood to flow backward during diastole from the aorta to the LV. This regurgitant flow is evident from the isovolumic phases of patient A’s PV loop, which are phases during which both the AoV and mitral valve should have been closed and the LV should be either relaxing or contracting around a fixed blood volume. There is a characteristic increase in LV volume during both phases, indicating regurgitant flow. Although this backward flow contributes to LV preload for the next beat, it is disadvantageous because it reduces vital forward flow.
Pressure-volume loop showing aortic regurgitation (Patient A, red) compared to a healthy individual (Control, blue).
Note also that pulse pressure (PP) is increased in patient A compared with the control. PP is the difference between systolic blood pressure (SBP) and diastolic blood pressure (DBP). Retrograde flow through an incompetent valve bleeds pressure from the arterial system during diastole, so DBP is reduced (DBP is ~75 mm Hg in the control individual and ~65 mm Hg in patient A). The LV must compensate for the loss of forward flow by increasing SBP (SBP is ~130 mm Hg in the control loop, ~ 140 mm Hg in patient A). PP in the control subject is thus 130 – 75 = 55 mm Hg, compared with 75 mm Hg in patient A.
Compensation for loss of forward flow involves extracellular fluid volume loading and ventricular hypertrophy, which allows for increased stroke volume and cardiac output. The LV becomes more compliant as it dilates to accommodate the increased preload, which allows for increased end diastolic volume (EDV) with minimal increase in end-diastolic pressure (EDP; refer to the figure below). EDP for both the control individual and patient A is about 8 mm Hg, but EDV for patient A is 135 mL, compared with 100 mL for the control. Without hypertrophy and dilation, increasing end-diastolic volume from 100 mL to 135 mL would require at least a few mm Hg increase in EDP, since the end-diastolic pressure-volume relationship (EDPVR) steepens with increased volume.
Aortic regurgitation (AR) is relatively common in individuals over 50 years of age; its incidence and severity increase with age. It typically remains asymptomatic even as the LV compensates and dilates. Symptoms of severe AR are those associated with heart failure, including exertional dyspnea, angina, and orthopnea.
Increased contractility (choice A) is incorrect because inotropy has decreased in the PV loop from patient A, as indicated by the slope of the line (end-systolic pressure-volume relationship, or ESPVR) drawn from approximately (0,0) through the end-systolic pressure-volume point. Decreased contractility may be an early indication of failure.
ESP (choice B) is ~115 mm Hg for both loops. End-systolic volume is higher for patient A.
Increased pulmonary artery wedge pressure (choice C) is incorrect because mean pulmonary artery wedge pressure is often used to approximate EDP, which is identical in these two loops. As preloading continues, EDP may increase significantly, which raises pulmonary pressures and may manifest as pulmonary edema.
Increased systemic vascular resistance (SVR; choice D) is incorrect because DBP, which is largely determined by SVR, is lower in patient A than in the control individual. An SVR increase would have made it more difficult for blood to escape and bleed pressure from the arterial system during diastole, so DBP would also have increased.
ReKap
The increase in left atrial pressure that results from mitral regurgitation can cause pulmonary hypertension.
Increases in pulmonary perfusion pressure decrease pulmonary vascular resistance (PVR) by dilating blood vessels that would otherwise be collapsed by the mass of surrounding lung tissue, particularly at low lung volumes.
PVR is normally ~2–3 mm Hg·min·L-1 (~150–250 dyn-s-cm-5).
Analysis
The correct answer is A. The patient has mitral regurgitation, which has caused pulmonary vascular resistance (PVR) to fall from a normal value of ~2–3 mm Hg·min·L-1 (~150–250 dyn-s-cm-5) to 0.74 mm Hg·min·L-1.
PVR can be calculated using a hemodynamic application of the Ohm law (R= V/I) to the cardiac catheterization data included in the vignette. Resistance (R) in the circuit represents PVR. Rearranging the equation gives PVR = ΔP/Q, where ΔP is the pressure gradient (similar to the voltage driving electricity through a circuit) and Q is the cardiac output through the pulmonary vasculature (similar to total current flowing through a circuit).
Q = Cardiac output
ΔP = Mean pulmonary artery pressure – pulmonary capillary wedge pressure (a measure of left atrial pressure)
Mean arterial pressure = diastolic + 1/3 of pulse pressure (i.e., systolic-diastolic), so:
Mean pulmonary artery pressure = 15 + (45 – 15)/3 = 25 mm Hg
PVR = (25 – 21)/5.4 = 0.74 mm Hg·min·L-1
(Multiply by 80 to convert to dyn-s-cm-5 = 59.3)
Mitral incompetence is evident from the diminished S1 (resulting from incomplete valve closure) and a holosystolic murmur (the sound of regurgitant flow during systole). Backward blood flow raises left atrial pressure and pulmonary venous pressure, forcing the right ventricle to generate higher pulmonary arterial pressures in order to maintain forward flow. Pulmonary arteries have much thinner walls than those found in the systemic vasculature, which allows them to be collapsed by the mass of surrounding lung tissue, particularly at low lung volumes. Increasing pulmonary perfusion pressures dilates collapsed vessels, thereby decreasing PVR. Collapsed vessels create unyieldingly high resistance to blood flow.
Over time, pulmonary hypertension can cause pulmonary vascular remodeling which raises PVR, but the elevated pulmonary pressures in this patient are likely secondary to congestive heart failure. Mitral valve incompetence has most likely been caused by, or exacerbated by, heart enlargement and the resulting distortion of the valve annulus.
We can also calculate systemic vascular resistance (SVR) from the data given in the case history (MAP = mean systemic arterial pressure).
SVR = (MAP – right atrial pressure)/CO
MAP = 64 + (124 – 64)/3 = 84 mm Hg
SVR = (84 – 15)/5.4 = 12.8 mm Hg·min·L-1 (choice D)
SVR is normally ~11–15 mm Hg·min·L-1 (~900–1,200 dyn-s-cm-5).
ReKap
The velocity is inversely proportional to the cross-sectional area of a lumen.
A decrease in cross-sectional area will increase velocity.
An increase in cross-sectional area will decrease velocity.
Analysis
The correct answer is C. This patient likely has coronary artery disease. Risk factors include smoking, diabetes mellitus, hypertension, hyperlipidemia, and hypercholesterolemia. Endothelial injury leads to the deposition of plaque in the arteries, which results in obstruction.
This patient shows coronary artery obstruction because velocity has increased seven-fold, indicating a decrease in cross-sectional area by a factor of seven. Thus, the correct answer is choice C, which indicates an artery with a lumen that is one-seventh the size of normal, thus increasing velocity by a factor of 7.
Choices A and B are incorrect because a coronary artery aneurysm would increase the cross-sectional area, not decrease it. Such an increase of cross-sectional area would decrease velocity of flow; this contradicts the data, which showed increased velocity in the affected area.
An obstruction causing the lumen to decrease by 70 times (choice D) would increase velocity by a factor of 70, not 7.
ReKap
Patent ductus arteriosus (PDA) typically causes a continuous murmur throughout the entire cardiac cycle.
The murmur reflects blood being forced through the PDA from the aorta (under high pressure) to the pulmonary artery.
A longstanding, uncorrected PDA may cause congestive heart failure, pulmonary hypertension, and Eisenmenger syndrome.
Analysis
The correct answer is B. The patient most likely has a patent ductus arteriosus (PDA), which is associated with a continuous or “machine-like” murmur. A PDA allows blood to flow backward from the high-pressure systemic circulation into the low-pressure pulmonary circulation. The pressure differential between systemic and pulmonary circuits means that flow is usually from the aorta to the pulmonary artery. The intensity of the murmur roughly follows the rise and fall in aortic pressure occurring during systole and diastole. A PDA is always open, so flow continues throughout the cardiac cycle (i.e., from point 1 to point 6; the two points coincide with the end of mitral valve closure during successive cardiac cycles).
A PDA presents as a continuous, “machine-like” murmur throughout the entire cardiac cycle (systole and diastole).
If left uncorrected, a moderate-to-large PDA can cause pulmonary vascular engorgement that eventually results in pulmonary hypertension and congestive heart failure. If pulmonary pressures continue to increase and ultimately exceed aortic pressure, flow through the PDA reverses, thereby bypassing the lungs. Oxygen-poor, mixed venous blood flowing from the pulmonary artery directly into the systemic circulation results in cyanosis. The combination of a congenital communication between systemic and pulmonary circulations, pulmonary hypertension, and cyanosis is known as Eisenmenger syndrome.
The period between point 1 and point 3 (choice A) represents ventricular systole. Systolic murmurs coinciding with this time period include mitral or tricuspid regurgitation. The murmur is caused by blood being forced backward under pressure from the left ventricle (LV) to the left atrium (LA), or from the right ventricle (RV) to the right atrium (RA) through the respective incompetent valves.
The time period between points 2 and 3 (choice C) coincides with ventricular ejection. Murmurs associated with ejection are systolic and are caused by high-velocity, turbulent blood flow, such as through stenotic aortic and pulmonic valves.
Points 3 and 6 (choice D) define diastole. Diastolic murmurs include those caused by turbulent forward flow through stenotic atrioventricular valves.
Points 5 and 6 (choice E) bracket atrial systole, which is typically associated with a fourth heart sound (S4) caused by blood being forced under pressure into a stiffened ventricle. Atrial contraction can also cause a murmur associated with pressure-assisted flow through stenotic mitral and tricuspid valves.
ReKap
During an isometric contraction, muscle fiber length is held constant.
Left ventricular pressure rises at its most rapid rate, +dP/dtmax, during isovolumic contraction, a time during which intraventricular blood volume remains constant.
Analysis
The correct answer is D. The phase labeled Z in the figure above represents left ventricular (LV) isovolumic contraction (isometric contraction), a time during which LV pressure is rising rapidly and +dP/dtmax reaches a maximal value.
The figure above is known as an LV pressure-volume (PV) loop. The plot records changes in intraventricular pressure during a single cardiac cycle. There is no time axis, so pressure rises and falls in a continuous loop. The figure incorporates all of the important phases, volumes, and valve events associated with the cardiac cycle.
At the beginning of isovolumic contraction, the mitral valve closes and the LV becomes a sealed chamber. The aortic valve has yet to open, so the ventricle is contracting around a fixed volume of blood and muscle fiber length is held relatively constant. The +dP/dtmax commonly reaches values of 3,000 mm Hg/sec during this time in a resting subject. The rate of pressure development, as determined during invasive procedures, is commonly used as an index of LV contractility.
Aortic flow (choice A) does not begin until LV pressure reaches and exceeds aortic pressure, at which point the aortic valve opens. Aortic flow reaches a maximal value during the ejection phase. LV dP/dt is close to zero during this time.
Compliance of the ventricle (choice B) is maximal when the myocardium is fully relaxed, which coincides with diastolic filling.
The maximum negative rate of change of pressure (-dP/dtmax; choice C) occurs during isovolumic relaxation. At the end of ejection, LV pressure drops below aortic pressure and the aortic valve closes. Pressure now decreases rapidly, but the volume remains constant because the mitral valve remains closed until the pressure falls below left atrial pressure.
Ventricular volume (choice E) reaches its maximum value at the end of the filling phase; this is known as end diastolic volume and equates with LV preload.
ReKap
Mitral stenosis:
Left atrial pressure is much greater than left ventricular pressure toward the end of diastole.
Causes include a thrombosed artificial mitral valve, rheumatic heart disease, and atrial myxoma.
Causes pulmonary edema due to elevated back pressure from the left atrium.
Analysis
The correct answer is D. The figure shows that left atrial pressure (LAP) is significantly higher than the left ventricular pressure (LVP) during diastole, which indicates that the mitral valve is obstructing flow (mitral stenosis).
Key points:
During diastole, LAP and LVP should be almost equal in a healthy individual.
Mitral stenosis obstructs forward flow, causing LAP to rise in order to ensure adequate LV preloading.
Turbulent flow through the stenotic valve causes a rumbling, diastolic murmur located at the apex. The stenotic valve may produce an audible opening snap and S1 may be loud.
High LAP causes pulmonary hypertension and pulmonary edema.
LA enlargement leads to progressive fibrosis which disrupts electrical conduction and increases the risk of atrial fibrillation.
Hoarseness may also result because of external pressure on the recurrent laryngeal nerve as it passes the enlarged LA.
In this patient, the mitral valve that was replaced 8 years ago has likely undergone thrombosis, resulting in obstruction of the mitral orifice. Other causes of mitral stenosis include rheumatic fever, atrial myxoma, and rarely, endocarditis.
The pressure tracings in the vignette are not consistent with aortic regurgitation (choice A). Aortic diastolic pressure would be noted to decrease rapidly during diastole due to reflux of blood from the aorta into the LV (figure below). Peak systolic LVP would rise to compensate. This creates a widened pulse pressure.
Aortic stenosis (choice B) usually presents with elevated systolic LVP compared to systolic aortic pressure (figure below). LVP rises to ensure that sufficient blood is ejected through the narrowed valve orifice during systole to meet dependent tissue needs.
Mitral regurgitation (choice C) is characterized by a greatly elevated LA pressure toward the end of ventricular systole (figure below). The increase in pressure is caused by the backward flow of blood from the LV into the LA through the leaky mitral valve. The leak occurs during systole and is characterized by a holosystolic murmur at the apex radiating to the axilla. The LA pressure is normal at the end of diastole because the mitral valve is open and blood flows unimpeded from the atrium into the ventricle.
Right-sided valvular disease is uncommon, especially in a patient with prior mitral valve surgery. Still, patients may have pulmonic or tricuspid disease if they are drug users or have congenital heart disease. Pulmonic regurgitation (choice E) would cause a diastolic murmur (blood flowing into the right ventricle during diastole), which this patient could have. However, the lesion typically does not cause pulmonary congestion.
Pulmonic stenosis (choice F) would cause a systolic murmur, which this patient does not have. The lesion also would not cause the pulmonary congestion observed in this patient.
ReKap
Aortic pressure at the time of aortic valve opening represents diastolic blood pressure.
On a pressure-volume loop of the left ventricle, the aortic pressure at the end of diastole is represented by the upper-left corner of the pressure-volume loop.
Analysis
The correct answer is C. Aortic pressure at the end of diastole is ~80 mm Hg.
Pressure–volumDuring diastole, the aortic valve is closed and the LV and aorta are separate compartments. LVP rises (diastolic filling), whereas AoP slowly declines as blood flows out of the arterial system to the systemic vascular beds (diastolic runoff). LV contraction closes the mitral valve and there is a brief isovolumic contraction around a fixed volume of blood. When LVP meets and then exceeds AoP, the aortic valve opens and ejection begins. In the graph above, AoP is at around 80 mm Hg at the end of diastole (= diastolic blood pressure, as measured using a pressure cuff and sphygmomanometer).
During ejection, LVP drives an increase in AoP so LVP is slightly higher (~2–3 mm Hg). LVP begins to drop toward the end of systole. Once it falls below AoP, the aortic valve closes and there is a brief isovolumic relaxation before the mitral valve opens and diastolic filling begins. Note that AoP dips briefly following aortic valve closure. This corresponds to the dicrotic notch (or incisura) on a Wiggers diagram, and represents the aortic valve leaflets bulging backward.
e loops (PV loops) plot changes in volume and pressure during a single cardiac cycle. There is no time index, but at a heart rate of 60 beats/min, the loop completes itself in one second. The graph below shows two loops. The solid plot in red shows changes in left ventricular pressure (LVP). Superimposed on this is aortic pressure (AoP), shown as a dashed blue line.
ReKap
A ventricular septal defect (VSD) is the most common congenital cardiac malformation and belongs to the acyanotic group of congenital heart diseases.
Major characteristics of VSD include a left-to-right shunt (which increases oxygen saturation in the right ventricle) and a harsh holosystolic murmur at the left lower sternal border.
Analysis
The correct answer is E. A child with a harsh systolic murmur, no diastolic murmur, and an increased oxygen saturation in the right ventricle most likely has a ventricular septal defect (VSD). VSDs are congenital and are commonly located near the membranous interventricular septum. Hemodynamic consequences include the development of left-to-right shunts (the magnitude of the shunt being proportional to the size of the defect), which may result in the equalization of systolic pressures in the two ventricles. Cardiac catheterization allows for direct visualization and measurement of the shunt and reveals increased oxygen saturation in the right ventricle. Clinically, VSD is associated with a harsh, holosystolic murmur that is heard more readily if there is a residual pressure gradient between the two sides (note: the heart sounds can be heard best with headphones).
Examples of common acyanotic congenital heart defects.
Aortic regurgitation (choice A) and mitral stenosis (choice B) do not generate left-to-right shunts and will not increase oxygen saturation in the right ventricle. These conditions produce diastolic rather than systolic murmurs.
A patent ductus arteriosus (choice C) can initially cause left-to-right shunting, but eventually, as pulmonary vascular resistance increases, a right-to-left shunt may occur. Therefore, cardiac catheterization will fail to show increased oxygen saturation in the right ventricle. The murmur of a patent ductus arteriosus is not holosystolic but a continuous “machinery” murmur; it is readily distinguishable from a VSD murmur.
A patent foramen ovale (choice D) should not be confused with an atrial septal defect, which could account for the increased oxygen saturation on the right side but could not account for the systolic murmur. A patent foramen ovale refers to a residual, slit-like opening between the atria that is patent to a probe but not of hemodynamic significance. In contrast, an atrial septal defect is a much larger opening.
ReKap
Cardiac output = stroke volume × heart rate
Stroke volume is a key measure of cardiac function.
Analysis
The correct answer is D. Cardiac output (CO) is equal to the volume of blood ejected from the heart during each systole (i.e., stroke volume; SV) multiplied by the number of times the heart beats each minute (heart rate; HR).
CO = SV × HR
Therefore, SV = CO/HR, and since CO = 5,000 mL/min and HR = 50/min, SV = 5,000/50 = 100 mL.
Recall that SV is determined by left ventricular preload, afterload, and contractility. HR is regulated by parasympathetic and sympathetic neural input to the sinoatrial node. Measuring SV is one of the initial steps in evaluating cardiac function. Normal SV is between 60 and 100 mL.
ReKap
The lower extremity edema that is common to both pregnant women and patients with hepatic cirrhosis is caused by low serum albumin levels.
Albumin creates a colloid osmotic pressure that helps retain fluid within the vasculature. When albumin levels fall, fluid filters from blood and leads to edema.
In women that are pregnant, albumin levels fall due to fluid retention and hemodilution.
Cirrhosis impairs liver synthetic capacity, so serum albumin concentration is a measure of disease severity.
Analysis
The correct answer is D. Lower extremity edema is common in pregnancy because serum albumin concentration is reduced through fluid retention and hemodilution. Albumin, which is confined to the vasculature by virtue of its large molecular size, creates a colloid osmotic pressure (πc) that helps blood retain fluid. Albumin is synthesized exclusively by the liver. Cirrhosis impairs liver synthetic capacity, so as the severity of the disease worsens, serum albumin concentration falls. The decrease in πc allows excess fluid to filter from blood vessels and accumulate within the interstitium, manifesting as lower-extremity edema and ascites.
Plasma colloid osmotic pressure (πc), also known as oncotic pressure, is one of four principal forces (Starling forces) controlling fluid movement between blood and the interstitium. Their relationship is described by the Starling law of the capillary:
Colloid osmotic pressure is created by plasma proteins, principally albumin. It is the main force holding fluid within the vasculature, so when πc falls, the tendency for fluid to spill into the interstitial space increases. If the amount of fluid filtering from blood vessels exceeds the ability of the lymphatic system to return it to the heart, edema develops.
Anaphylaxis (choice A) increases capillary permeability, allowing fluid and large proteins to escape the vasculature and deplete blood volume with a potentially lethal effect (i.e., shock). Anaphylaxis does not cause edema by decreasing plasma colloid osmotic pressure.
Aortic stenosis (choice B) presents as a crescendo-decrescendo, midsystolic murmur at the left sternal border, but it does not affect the likelihood of edema formation. The murmur noted in pregnant patients is similarly associated with flow across the aortic valve; it is a functional murmur caused by decreased hematocrit (“physiologic anemia of pregnancy”) and blood viscosity. Murmurs caused by a stenotic valve are caused by increased blood velocity, not decreased viscosity.
Congestive heart failure (CHF; choice C), like pregnancy, is associated with increased blood volume, but this does not decrease colloid osmotic pressure. In CHF, the increased blood volume increases venous pressure and cardiac preload, which raises Pc (which increases the likelihood of edema). The volume loading during pregnancy facilitates increased CO but does not raise Pc. In the later stages of failure, hepatic congestion can impair albumin production, but this is secondary to CHF.
Sickle cell disease (choice E) can cause swelling of the hands and feet, but this is related to sickled red blood cells becoming lodged in small vessels, thereby preventing outflow. Sickle cell disease does not affect colloid osmotic pressure.
I have no clue where this card came from, but here is the answer!
