Neo Hemodynamics- The Oleg Alekseev Legacy 3 Flashcards
ReKap
Aortic stenosis:
Aortic valve calcification reduces the area of the valvular orifice and creates resistance to LV outflow. The LV hypertrophies and generates high pressures to compensate (LVP increases).
EDV remains largely unchanged, but ESV rises due to a decreased ability to sustain normal EF against the increased resistance.
Arterial blood pressures, including PP, remain largely unchanged.
Analysis
The correct answer is B. The patient presents with aortic stenosis (AS). A pathological decrease in the area of the valve’s orifice creates resistance to left ventricular (LV) outflow. The LV then hypertrophies in order to sustain cardiac output (CO).
AS is typically a disease of older individuals and reflects valve leaflet thickening and stiffening due to inflammation and subsequent calcification (sclerosis). The valve is in a high-pressure, high-velocity part of the vasculature which subjects the valve leaflets to shear stress. Shear stress causes the wear and tear that precipitates such changes. Congenitally bicuspid valves and rheumatic heart disease increase susceptibility to calcification and may cause early-onset disease. AS has several consequences:
Ejecting blood through a narrowed valvular orifice necessitates increased pressure to achieve the higher ejection velocities required to sustain CO at normal levels. LV hypertrophy increases LVP.
Aortic pressure does not change, so a significant pressure gradient develops across the stenotic valve.
Although left atrial (LA) pressure may increase to assist LV preloading, LV hypertrophy reduces wall compliance so EDV remains largely unchanged despite the higher preload.
Stroke volume (SV) decreases since there is less LV outflow and ESV naturally rises as well.
The increase in ESV decreases EF (calculated as (EDV-ESV)/EDV).
Systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP = SBP – DBP) remain largely unchanged, unless there is concomitant heart failure.
Although the patient is currently asymptomatic, AS is evident from the examination findings. The patient has an S4, which reflects LV hypertrophy and increased LV pressure. The systolic crescendo-decrescendo murmur is caused by turbulence associated with blood being ejected at high velocity across the stenotic valve. Finally, the high resistance to outflow means that it takes longer for the LV to achieve the pressure to eject blood into the arterial system, which accounts for the delayed carotid pulses.
Increased ESV and EDV combined with decreased LVP and PP (choice A) is seen in congestive heart failure. A failing heart loses contractility (due to death of myocytes during myocardial infarction, for example) and its ability to sustain a normal LVP, in turn decreasing PP. Volume retention helps compensate by increasing LV preload and EDV, but the loss of contractility means that SV falls and ESV increases.
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 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 (i.e., backward flow), 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.
A decrease in ESV, EDV, and SV (choice E) is suggestive of mitral stenosis (MS). In MS a reduced mitral orifice creates resistance to LV preloading, so EDV falls. An increase in myocardial contractility helps maintain CO by increasing ejection fraction and ESV falls, but SV is still reduced. LVP and PP are maintained near-normal until heart failure occurs.
ReKap
When a person stands up after lying or sitting, blood is forced downward into the lower extremities by gravity.
Venous return and arterial pressure fall, triggering a baroreflex. Sympathetic outflow increases and parasympathetic outflow decreases.
Heart rate, myocardial contractility, systemic vascular resistance, and venous return all increase.
Dizziness and syncope reflect a transient drop in cerebral perfusion pressure.
Analysis
The correct answer is D. Our patient’s dizziness is due to orthostatic hypotension secondary to dehydration and hypovolemia. He has insufficient fluid volume (sometimes seen in patients taking diuretics) to adequately maintain mean arterial pressure (MAP) and cerebral perfusion pressure, resulting in light-headedness and/or syncope. Increased heart rate is part of an autonomic reflex (baroreflex) that attempts to compensate for the pressure drop.
Standing after reclining in bed precipitates the following train of events:
Gravity forces blood downwards, trapping it in the highly compliant veins of the lower extremities.
↓ Venous return → ↓ Central venous pressure → ↓ Left ventricular (LV) preload → ↓ Cardiac output (CO) → ↓ MAP
↓ MAP → ↓ carotid sinus and aortic pressure, sensed by baroreceptors → baroreflex
Baroreceptors communicate via CN IX (glossopharyngeal nerve) and CN X (vagal nerve) to the medulla and baroreflex is effected via parasympathetic (CN X) and sympathetic efferents.
↓ Parasympathetic activity
↑ Heart rate → ↑ CO
↑ Sympathetic activity
↑ Heart rate → ↑ CO
↑ Myocardial inotropy → ↑ CO
↑ Systemic vascular resistance (constriction of small arteries and arterioles) → ↑ MAP (MAP = CO × SVR)
Venoconstriction → ↑ Preload → ↑ CO
Even with the autonomic responses described above, hypovolemia means that the patient is unable to restore MAP sufficiently fast to avoid dizziness upon standing.
Standing leads to a reflex increase in myocardial contractility, not a decrease (choice A). A decrease would further reduce MAP.
Systemic vascular resistance increases, not decreases (choice B) upon standing. Constriction of resistance vessels limits outflow from the arterial system, thereby helping to preserve MAP in the face of reduced CO.
Cerebral blood flow (choice C) decreases upon standing due to a fall in MAP and cerebral perfusion pressure. Patients with orthostatic hypotension may be forced to sit and put their head between their knees in order to restore cerebral flow and avoid syncope.
A baroreflex involves reflex venoconstriction, not venodilation (choice E). Gravity tends to trap blood in the lower extremities, forcing the highly-compliant veins to dilate to accommodate the blood volume, but this is a passive process, not a reflex. Venoconstriction helps offset this effect by limiting venous capacity.
ReKap
Sarcomere length is greatest when left ventricular volume is maximal (e.g., just before left ventricular contraction). This value is best described as the end-diastolic volume (EDV).
Conversely, sarcomere length is shortest at the end of systole.
Analysis
The correct answer is A. Sarcomere length is greatest when the left ventricle is filled with blood (e.g., when left ventricular volume is greatest). This occurs at the end of diastole, just before the left ventricle contracts (point A). The volume of blood in the left ventricle at this point represents end-diastolic volume (EDV).
When venous return to the heart increases, EDV increases (increased preload), and thus sarcomere length increases. Maximal force is generated with a sarcomere length of 2.2 μm. Increasing sarcomere length improves the degree of overlap between actin and myosin filaments, which increases the potential for cross-bridge formation during contraction. This allows the ventricle to contract with greater force to expel the extra volume of blood (Starling’s law of the heart). Lengths larger or smaller than this optimal value will decrease the force the muscle can achieve, which occurs in heart conditions such as hypertrophic cardiomyopathy or hearts with long-standing heart failure.
Point B (choice B) represents rapid ejection following isovolumetric contraction.
Point C (choice C) represents the peak systolic pressure.
Point D (choice D) represents end-systolic volume, which is when the volume of the left ventricle is the lowest. Sarcomere length is the shortest at the end of systole.
Point E (choice E) represents isovolumetric relaxation. The aortic and mitral valves are both closed and there is no change in left ventricular volume. Pressure decreases as the myocardium relaxes.
Point F (choice F) represents the beginning of left ventricular filling as the mitral valve opens.
It is always a pressure difference that causes the valves to open or close.
QRS → contraction of ventricle → rise in ventricular pressure above atrial pressure → closure of mitral valve.
The closure of the mitral valve terminates the ventricular filling phase and begins isovolumetric contraction. The closure of the mitral (and tricuspid) valve produces the S1 heart sound.
Isovolumetric contraction: no change in ventricular volume and both valves (mitral, aortic) are closed. Ventricular pressure increases and the volume is equivalent to end-diastolic volume.
Opening of the aortic valve terminates isovolumetric contraction and begins the ejection phase. The aortic valve opens because the pressure in the ventricle slightly exceeds aortic pressure.
Ejection Phase: ventricular volume decreases, but most rapidly in the early stages. Ventricular and aortic pressures increase initially but decrease later in this phase.
Closure of the aortic valve terminates the ejection phase and begins isovolumetric relaxation. The aortic valve closes because the pressure in the ventricle goes below aortic pressure. Closure of the aortic valve creates the dicrotic notch. Closure of the aortic and pulmonic valves produces the S2 heart sound. (This is a single sound during expiration, but has physiologic splitting during inspiration.)
Isovolumetric relaxation: no change in ventricular volume, and both valves (mitral, aortic) are closed. Ventricular pressure decreases and volume is equivalent to end-systolic volume.
Opening of the mitral valve terminates isovolumetric relaxation and begins the filling phase. The mitral valve opens because the pressure in the ventricle drops below atrial pressure.
Filling Phase: the final relaxation of the ventricle occurs after the mitral valve opens and produces a rapid early filling of the ventricle. This rapid inflow will, in some cases, induce the S3 heart sound. The final increase in ventricular volume is due to atrial contraction, which can be responsible for the S4 heart sound when the atrium contracts against a stiff ventricle (as in a heart with left ventricular hypertrophy secondary to long-standing hypertension).
Aortic regurgitation:
An incompetent aortic valve allows blood to flow backward from the aorta to the left ventricle (LV) during diastole.
The regurgitant flow increases LV preload and end-diastolic volume (EDV). The added volume increases stroke volume and the ejection fraction (EF) on the next beat.
Compensation for the chronic volume overload increases the left ventricular pressure (LVP) and systolic blood pressure (SBP). Aortic pressure falls steeply during diastole due to the regurgitant flow, so diastolic blood pressure (DBP) decreases.
The changes in SBP and DBP cause the pulse pressure (PP) to widen.
Analysis
The correct answer is C. The patient presents with chronic aortic regurgitation (AR), where an incompetent aortic valve allows blood to escape backward from the aorta to the left ventricle (LV) during diastole. The diagnosis of AR is suggested by the blowing diastolic murmur at the left sternal border, which is characteristically best heard with the patient leaning forward. AR usually develops slowly over decades, although it can also occur acutely, most commonly as a result of endocarditis or aortic root dissection. Common causes of chronic AR are a congenital bicuspid aortic valve and calcification that prevents the valve leaflets from coming into close apposition to seal the orifice. AR has several consequences:
The retrograde flow is at the expense of forward flow. Thus, in order to ensure that tissues continue to receive sufficient supply to meet their metabolic needs, the cardiac output (CO) must increase in direct proportion to the backward flow.
The increase in CO results in part from increased left ventricular preloading caused by blood flowing backward through the leaky valve.
End-diastolic volume (EDV) increases as a result, causing ventricular dilatation. The Frank-Starling mechanism ensures that this enhanced preload is pumped out on the next beat (i.e., stroke volume [SV] increases), so the end-systolic volume (ESV) may not be affected to a significant degree. Ejection fraction = Stroke volume/End-diastolic volume, so the ejection fraction (EF) increases also.
Peak left ventricular pressure (LVP) and systolic blood pressure (SBP) increase as the left ventricle hypertrophies to compensate for the diastolic volume and pressure overload.
Blood escaping backward from the arterial system through the regurgitant valve during diastole causes the aortic pressure to fall more steeply than normal, so the diastolic blood pressure (DBP) is decreased.
Pulse pressure ( calculated by SBP – DBP) increases significantly as a result of these changes, which may present as a “water hammer” or bounding peripheral pulse.
Increased ESV and EDV combined with decreased LVP and PP (choice A) would be consistent with congestive heart failure. A failing heart loses contractility (due to 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 SV falls and ESV increases.
The combination of an increased LVP but decreased EF (choice B) is suggestive of increased LV afterload, as seen in aortic stenosis (AS). The reduced valve orifice creates a resistance to outflow that elicits an increase in LVP to maintain CO and PP. AS stimulates myocardial hypertrophy to meet the needs for increased pressure, but the ESV and stroke volume (SV) are typically decreased. EDV remains unchanged until the heart begins to fail.
A decrease in the ESV in the setting of increased EDV and EF (choice D) is consistent with mitral regurgitation (MR). The regurgitant valve decreases resistance to 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 the EDV increases.
A decrease in the ESV and EDV (choice E) is suggestive of mitral stenosis (MS). In MS, a reduced mitral orifice creates resistance to LV preloading, so the EDV falls. An increase in myocardial contractility helps maintain CO by increasing the EF and ESV falls. The LVP and PP are maintained near-normal until heart failure occurs.
ReKap
In a fetus, a relatively high blood oxygen saturation (~85%) is found in the umbilical vein, where initially oxygenated blood (from placental exchange) flows.
High O2 fetal saturations are made possible by fetal hemoglobin (HbF), which has a higher O2 affinity than adult hemoglobin (HbA).
The lowest SO2 in the adult circulation is found in the coronary sinus due to the high rate of O2 extraction by cardiac myocytes.
Analysis
The correct answer is E. The umbilical vein carries blood with an SO2 of 80-90%, whereas the coronary sinus is notable for its low SO2 = (~30%).
In the adult circulation, the highest SO2 levels (~95%) are found in the pulmonary vein, left heart, and aorta. Although PO2 drops to ~40 mm Hg by the time blood reaches the right side of the heart, mixed venous blood O2 saturation (SvO2) is still relatively high at 65-70%. The location with the lowest SO2 in the adult circulation is in the coronary sinus, where the coronary veins converge to dump deoxygenated blood back into the heart. Since the myocardium extracts a very high percentage of O2, the coronary sinus has very low SO2 of ~30%.
ReKap
Mitral regurgitation is characterized by backward flow from the left ventricle (LV) to the left atrium (LA) during systole.
LA pressure rises steeply during systole as a result of retrograde flow.
LV peak pressure must increase to compensate.
Analysis
The correct answer is E. A history of febrile illness with rash and arthritis in a patient from a developing nation is consistent with acute rheumatic fever (ARF). It is likely that she now has rheumatic heart disease, which frequently presents 10 or more years after ARF. The mitral valve is almost always affected, with aortic and tricuspid valve involvement also being common. Valvular disease may cause stenosis, regurgitation, or both.
The patient has mitral regurgitation. Patients classically have a holosystolic murmur, best heard at the apex and radiating to the axilla. Mitral regurgitation is characterized by a rapid increase in left atrial pressure late in ventricular systole caused by the backward flow of blood from the left ventricle (LV) into the left atrium (LA) through a leaky mitral valve.
Pressure tracing of the aortic, atrial, and ventricular pressures in mitral insufficiency (regurgitation).
Mitral regurgitation raises LA pressure, which can elevate pulmonary pressures. This produces pulmonary hypertension and edema with associated chest pain and dyspnea.
The pressure tracings depicted in choice A are characteristic of mitral stenosis, in which a diseased valve impedes LV preloading during diastole. LA pressure rises significantly as a result in order to sustain adequate forward flow, creating a significant pressure gradient across the valve during diastole. Normally, the pressure difference between LA and LV during diastole is minimal (<2 mm Hg). As with mitral regurgitation, patients may present with pulmonary edema and dyspnea due to high LA pressure backing up into the pulmonary vasculature.
Choice B shows the effects of aortic regurgitation on pressures in the aorta, LV, and LA during the cardiac cycle. Aortic regurgitation allows blood to reflux backward from the aorta into the LV, causing aortic pressure to drop off precipitously during diastole. The regurgitant flow manifests as a diastolic murmur. LV peak systolic pressure concomitantly increases to compensate for the reduced forward flow.
The pressure tracings depicted in choice C are highly characteristic of aortic stenosis. Obstruction of aortic valve outflow causes a compensatory increase in peak LV pressure that is required to maintain adequate cardiac output. Pressure increases in direct proportion to the reduction in valve orifice area and creates a significant pressure gradient between the left ventricle and the aorta during systole.
The pressure tracing profiles in choice D are within normal limits, although peak LV pressure and aortic pressure are both elevated. These tracings are typical of an individual with primary hypertension.
ReKap
Pulmonary capillary wedge pressure provides an indirect estimate of the left atrial pressure.
It can also provide an estimate of left ventricular end-diastolic pressure (preload) except in patients with mitral stenosis.
Analysis
The correct answer is A. When a balloon-tipped catheter (i.e., Swan-Ganz catheter) is “wedged” into a small branch of a pulmonary artery and the balloon is inflated, it provides an estimate of the left atrial pressure. This measurement is known as the pulmonary capillary wedge pressure (PCWP), pulmonary artery wedge pressure (PAWP), pulmonary artery occlusion pressure (PAOP), or simply wedge pressure.
Because inflation of the balloon obstructs all blood flow in the artery branch, distal blood vessels also have no flow. One can think of these distal vessels as physical extensions of the catheter, as they allow blood pressure to be measured on the other side of the pulmonary circulation, i.e., in the left atrium. The PCWP is usually a few mm Hg higher compared to the left atrial pressure, but the general opinion is that PCWP is an important clinical estimate of left atrial pressure. It is usually not feasible to measure left atrial pressure directly because it is difficult to pass a catheter retrograde through the aorta and left ventricle. Left atrial pressure by this technique is commonly used as a measure of left ventricular preload.
Normal PCWP, and hence left atrial pressure, is between 6–12 mm Hg. Thus, our patient presents with elevated left atrial pressure along with evidence of pulmonary edema (muffled lung bases on physical examination). This occurs when pressure builds up within the left side of the heart, resulting in a back-up of fluid into pulmonary vasculature and the lung bases. Causes include congestive heart failure (due to poor left ventricle contractility), mitral stenosis, and acute myocardial infarction. Our patient most likely has mitral stenosis given his history of rheumatic heart fever and the presence of an apical, rumbling diastolic murmur with an opening snap. In contrast, pulmonary causes of pulmonary edema (such as acute respiratory distress syndrome) do not produce elevations of pulmonary wedge pressure, since left atrial pressure is unaffected.
In many instances, the PCWP can provide a reasonable estimate of left ventricular end diastolic pressure (choice B). This is because during diastole, the mitral valve is open, thus equalizing pressures between the left ventricle and left atrium. However, a notable exception is during mitral stenosis, where the pressure in the left atrium (and therefore, the PCWP) is much higher than the left ventricular end diastolic pressure. The difference in pressure is due to the high resistance to blood flow through the stenosed valve.
Left ventricular peak systolic pressure (choice C) occurs when the mitral valve is closed, making it impossible to approximate this pressure using a catheter in the pulmonary artery.
When the balloon at the catheter tip is deflated, the catheter simply measures the pulmonary artery pressure (choice D), which is pulsatile with systolic/diastolic values of 25/8 mm Hg.
Right atrial pressure (choice E) will not be measured from an inflated catheter in the pulmonary artery since the right atrium is proximal to the point of obstruction.
ReKap
Shock is a state of hypoperfusion of the body’s organs and tissues.
There are four types of shock: cardiogenic, distributive, hypovolemic, and obstructive.
Neurogenic shock is a type of distributive shock in which a spinal cord injury causes vasodilation secondary to acute loss of sympathetic vasomotor tone.
Neurogenic shock is usually due to spinal cord injuries from vertebral fractures, resulting in bradycardia, hypothermia, hypovolemia, and warm skin due to the loss of vasoconstriction and disrupted sympathetic reflex to trauma.
Analysis
The correct answer is B. This patient is exhibiting neurogenic shock due to a central nervous system (CNS) injury. Neurogenic shock is a type of distributive shock in which a spinal cord injury causes vasodilatation secondary to acute loss of sympathetic vasomotor tone to the peripheral arteries and veins. Loss of venoconstriction increases venous capacity, whereas dilation of resistance vessels decreases systemic vascular resistance. The net result is decreased venous return, decreased cardiac output, and decreased blood pressure.
Neurogenic shock is usually due to spinal cord injuries from vertebral fractures, particularly of the cervical and high thoracic spine. The typical response to trauma is increased heart rate, cardiac contractility, and catecholamine release from the adrenal glands, all of which is is disrupted due to the spinal injury. This results in relative bradycardia, as seen in this patient, together with warm, flushed skin due to cutaneous resistance vessel dilation. Shock causes the cord injury to worsen as a result of insufficient blood flow. The severity of the injury likely will correlate with the caliber of cardiovascular dysfunction. Careful attention to blood pressure control, oxygenation, and fluid resuscitation are crucial in the treatment of these injuries.
Shock is a state of hypoperfusion and inadequacy of blood flow to dependent tissues. The presentation of shock is variable; the general signs for all types of shock are low blood pressure, decreased urine output, and ultimately confusion.
There are major four types of shock (see table):
Cardiogenic (choice A): caused by the failure of the heart to function as a pump secondary to myocardial damage due to infarction, cardiomyopathy, congestive heart failure, myocardial contusion/concussion, or severe heart valve disease.
Distributive (choice B): commonly caused by a systemic inflammatory response causing dilation of blood vessels throughout the body. Septic, neurogenic, and anaphylactic shock all fall into this category.
Hypovolemic (choice D): the most common type, caused by insufficient circulatory volume. Hemorrhagic shock (choice C) is a subtype of hypovolemic shock.
Obstructive (choice E): due to physical obstruction of the great vessels of the systemic or pulmonary circulation affecting venous return to the heart. Tension pneumothorax and cardiac tamponade are two trauma-related causes of obstructive shock.
[Mnemonic: Obvious Distress Causing Havoc = Obstructive, Distributive, Cardiogenic, Hypovolemic]
The diagnosis of shock needs to be performed quickly and most of the time can be reached with a rapid assessment and without the need for much testing. The treatment of shock is individualized and focused on each type, but is basically aimed at restoring circulatory sufficiency and avoiding tissue damage and/or organ failure.
ReKap
Cardiac function curves (CFC): shift upward and to the left with increased contractility; shift downward and to the right with decreased contractility.
Vascular function curves (VFC): increased blood volume or decreased venous compliance shifts the VFC up and to the right; decreased blood volume or increased venous compliance shifts VFC down and to the left.
Intersection of CFC and VFC is the equilibrium point for the cardiovascular system: the y-coordinate = cardiac output; the x-coordinate = right atrial pressure.
The point where the VFC intersects the x-axis is the mean systemic pressure.
Analysis
The correct answer is E. It is important to approach cardiovascular function curve problems in a systematic manner. The graph in the vignette depicts two types of curves, a cardiac function curve (CFC; e.g., curve 6) and a vascular function curve (VFC; e.g., curve 2).
The CFC shows that a rise in right atrial pressure (RAP) causes cardiac output (CO) to increase. This is because higher atrial pressure drives more blood into the left ventricle, thus raising end-diastolic volume. Remember that higher ventricular volume passively stretches (preloads) myocytes, which increases the force of contraction during systole (Starling’s Law of the Heart, also known as the Frank-Starling relationship). Greater contraction means higher stroke volume, translating to higher CO (CO = stroke volume x heart rate).
The VFC describes how RAP is affected by changes in CO and venous return (VR). The VFC is obtained by measuring the effect of changing CO on RAP (i.e., CO appears on the x-axis and RAP on the y-axis. The axes are then reversed so that the VFC data can overlay the CVC to give the cardiovascular function curves shown above).
When the heart is arrested and CO falls to zero, pressures in all parts of the cardiovascular system rapidly come into equilibrium at around 7 mm Hg, as shown in the plot above. This pressure is known as mean systemic pressure (MSP; note, in some texts, MSP may be referred to as mean circulatory filling pressure [MCFP], or mean systemic filling pressure [MSFP]).
If the heart is allowed to restart beating following arrest, the ventricles move blood out of the right atrium and venous compartment into the arterial compartment, causing RAP to fall and arterial pressure to rise. RAP declines further as CO increases until a point is reached at which CO becomes limited by VR and a plateau is reached. Since CO is dependent on RAP (as shown by the CFC) and RAP is dependent on CO (the VFC), CO and RAP at any given moment in time are defined by the intersection of the CVC and VFC. This is referred to as the equilibrium point. Only the intersection of curves 2 and 6 (choice E) corresponds to a cardiac output of 5 L/min and a RAP of 0 mm Hg.
As the graph in the question stem suggests, curves 2 and 6 represent only two of numerous possible combinations created by changes in cardiac inotropy or filling pressure.
Changes in myocardial inotropy: Positive inotropes (e.g., epinephrine and other β-adrenergic agonists) shift the CFC upward and to the left. Decreased contractility (e.g., myocardial infarction) shifts the CFC downward and to the right.
Changes in filling pressure: Venous pressure and RAP are determined by venous compliance and blood volume. Increasing blood volume (e.g., blood transfusion) or venoconstriction shifts the VFC upward and to the right. Loss of blood volume (e.g., hemorrhage) or venodilation shifts the VFC downward and to the left.
ReKap
Associate the following findings with their respective diseases:
Weak peripheral pulse is seen with aortic stenosis.
Heaves may be associated with either left ventricular hypertrophy (apex) or right ventricular hypertrophy (left parasternal).
Diastolic murmur is due to turbulence during ventricular filling (such as mitral stenosis or aortic regurgitation).
Decreased S2 heart sound is seen with aortic stenosis.
Loud S3 heart sound is caused by rapid ventricular filling (such as mitral regurgitation or congestive heart failure).
Analysis
The correct answer is E. This patient has aortic stenosis.
Decreased valve area limits cardiac output (CO).
Aortic pressure rises slowly and peripheral pulses are of low amplitude.
Left ventricle hypertrophies to create the high pressures required to maintain CO; ECG shows left axis deviation.
Ejection velocity is greatly increased (Q = ↑ v × ↓ a), leading to turbulence that presents as a systolic murmur.
Typical findings of aortic stenosis include worsening exercise tolerance, angina, syncope or heart failure.
Doppler echocardiography is the test of choice in the evaluation of patients with suspected valvular disease. Echocardiography allows assessment of the valve anatomy as well as of chamber size and ventricular function. Doppler studies permit estimation of pressure gradients and estimations of aortic valve area by using the continuity equation (Q = v × a).
Diastolic murmurs (choice A) are a consequence of turbulence during ventricular filling, such as in mitral stenosis or aortic incompetence. Classically, aortic stenosis is associated with a midsystolic murmur best heard in the aortic area with radiation to the carotid arteries.
Heaves are due to ventricular hypertrophy, and a left parasternal heave (choice B) indicates right ventricular hypertrophy. Aortic stenosis produces left ventricular hypertrophy, thus a sustained apical heave is felt.
The S2 heart sound (choice C) is produced when the aortic valve snaps shut. S2 is soft in aortic stenosis because of the decreased arterial pressures and the poor mobility of the stenotic valve.
The S3 heart sound (choice D) is associated with rapid ventricular filling and may occur either in mitral incompetence or congestive heart failure.
A 62-year-old man comes to the physician because of dizziness, especially after getting up from bed in the morning. He is a non-smoker with a 5-year history of mild hypertension. His treatment regimen includes hydrochlorothiazide and a salt-restricted diet. On physical examination his mucous membranes are dry and his skin shows slightly decreased turgor. Which of the following cardiovascular changes is most likely to occur as he stands up from a supine position?
A. Decreased myocardial contractility
B. Decreased systemic vascular resistance
C. Increased cerebral blood flow
D. Increased heart rate
E. Reflexive venodilation
ReKap
As blood moves through peripheral vasculature, its pressure drops due to systemic vascular resistance (SVR). This relationship is described by a hemodynamic application of the Ohm law:
SVR = (MAP – RAP)/CO
where MAP = mean arterial pressure, RAP = right atrial pressure, and CO = cardiac output.
Analysis
The correct answer is E. This question requires an understanding of the cardiac function curve (Starling curve) and the relationships between different physiologic variables. Ultimately, our goal is to determine systemic vascular resistance (SVR; also known as peripheral vascular resistance or total peripheral resistance).
First, it may help to understand vascular resistance at a conceptual level. We know that blood pressure immediately leaving the heart is high (~100 mm Hg), but when returning to the heart, the pressure is very low (~2 mm Hg). The reason for this drop in blood pressure is SVR, which resides principally in the resistance vessels (small arteries and arterioles). Resistance vessels regulate flow to the capillary beds. The equation that relates pressure and SVR is the hemodynamic application of the Ohm law (V = IR):
Pressure change across the vascular system (ΔP) = Cardiac output (CO) x SVR
Or, rearranged to solve for resistance: SVR = ΔP/CO
We determine CO from the intersection of the cardiac function curve and vascular function curve, which represents an equilibrium point. At point X, the patient has a stable CO of 10 L/min.
To determine ΔP, we need to calculate the difference between the blood pressure as it leaves the heart (mean arterial pressure; MAP) and the blood pressure as it returns to the heart (right atrial pressure; RAP).
This patient’s MAP during the exercise is given as 110 mm Hg. RAP, according to the cardiac function curve (look at the x-coordinate of the equilibrium point, marked X), is 10 mm Hg. Thus, ΔP = 110 – 10 = 100 mm Hg.
Plugging both the CO and ΔP into the original equation, we get our final answer:
SVR = 100 mm Hg / 10 L·min–1 = 10 mm Hg·min·L–1
Ohm’s law is represented in the image above. This figure shows the importance of cardiac output and systemic vascular resistance in determining the pressure gradients within the venous and arterial system.
Knowing VO2 max is irrelevant for answering this question, but this patient’s value is substantially below normal, as is her maximal CO. Be wary of these types of distractors on the examination.
ReKap
Cardiovascular function curves:
Cardiac function curve — increasing preload increases CO.
Vascular function curve — increasing blood volume or decreasing venous compliance increases cardiac preload.
CO supports venous return (VR), and VR supports cardiac preload and CO, so the intersection of the two curves defines how much CO can be generated for any given myocardial contractility, blood volume, and venous compliance.
Analysis
The correct answer is D. The patient’s cardiovascular performance at rest is indicated by the two broken lines that intersect at a cardiac output of 4.5 L/min and right atrial pressure (RAP) of 7 mm Hg.
Cardiovascular function curves depict the interdependence of ventricular and vascular function:
A cardiac function curve (also known as a Frank-Starling curve) shows the effect of preload on cardiac output (CO); its slope and plateau are indices of cardiac contractility.
A vascular function curve shows the effect of varying blood volume and compliance of the blood vessels on CO.
The equilibrium point (i.e., point N in the graph in the vignette), located at the intersection of the two curves, defines the amount of CO that can be supported by available preload, and how much preload (which is dependent on venous return) is generated by the available CO.
Mean systemic pressure (MSP) is the point at which the vascular function curve intersects the x-axis (i.e., at zero CO). MSP is the pressure that exists in all parts of the circulation when the heart stops beating and pressures in all parts of the cardiovascular system have equilibrated.
Interdependence occurs because the heart depends on preload to generate output, and preload is generated by venous return (VR). VR is dependent on CO.
Intersection of cardiac and vascular function curves represents the equilibrium point of cardiac function.
This patient is in congestive heart failure following his myocardial infarction (MI). MI results in death of myocytes, which reduces overall myocardial contractility. The cardiovascular function curve shifts downward and rightward, reflecting the heart’s reduced ability to generate output at any given preload.
In the days and weeks that follow, the renin-angiotensin-aldosterone system (RAAS) promotes salt and water retention, which increases extracellular fluid (ECF) volume (plasma is an ECF component) to increase left ventricular preload and thereby help support CO.
Myocardial infarction first shifts the cardiac function curve downward and rightward. Vascular function curves shift upwards and rightward to compensate for reduced inotropy.
The patient’s resting CO is below normal for his age and body size, reflecting the effects of MI on cardiac performance. His MSP is elevated to +11 mm Hg (normal MSP is +7 mm Hg) as a result of salt and water retention. The increased blood volume increases central venous pressure and enhances LV preload.
0 mm Hg (choice A) corresponds to RAP under normal conditions. The intersection of the two blue lines shows that an RAP of 0 mm Hg normally supports a CO of ~6 L.
1 mm Hg (choice B) corresponds to the intersection of the normal cardiac function curve and the patient’s current vascular function curve.
4 mm Hg (choice C) roughly corresponds to the start of the patient’s cardiac function curve. The patient’s failing heart is unable to generate CO at this level of preload.
9 mm Hg (choice E) indicates the point at which the normal cardiac function curve plateaus. Further increases in preload do not generate increased CO without a corresponding increase in contractility.
11 mm Hg (choice F), the intersection of the vascular function curve with the x-axis, represents the patient’s current MSP.
ReKap
Left atrial pressure (LAP) can be estimated by measuring pulmonary capillary wedge pressure (PCWP) with a Swan-Ganz catheter.
Remember that left ventricular end-diastolic pressure (LVEDP) normally equals PCWP, which is usually between 4 and 12.
If PCWP is considerably higher than LVEDP, there is a pressure gradient across the mitral valve, indicating stenosis.
Analysis
The correct answer is D. This is a diastolic murmur heard best at the 5th left intercostal space at the midaxillary line (apex), and is indicative of mitral valve stenosis. The pulmonary capillary wedge pressure (PCWP) is elevated to 30 mm Hg and the pulmonary artery pressure is elevated to 45/25 mm Hg (PCWP is measured using a Swan-Ganz catheter and provides an estimate of left atrial pressure, LAP). The left ventricular end-diastolic pressure (LVEDP) is normal but is not equal to the PCWP. A pressure gradient of 25 mm Hg (30 mm Hg − 5 mm Hg) across the mitral valve is a clear indication of mitral stenosis (see figure). The fatigue and shortness of breath result from mild pulmonary edema caused by the increase in pulmonary capillary hydrostatic pressure. It can be surmised that the pulmonary capillary pressure is elevated because pressures are elevated at the arterial and venous ends of the pulmonary circulation. Note: heart sounds can be heard best with headphones.
In aortic regurgitation (choice A), blood flows backward through the aortic valve during diastole when the valve is closed. LVEDP (and PCWP) may be elevated with chronic aortic regurgitation once the myocardium has failed, but aortic regurgitation will not result in an elevated pressure gradient across the mitral valve.
In aortic stenosis (choice B), blood must be ejected from the left ventricle into the aorta through a smaller-than-normal opening, producing a systolic murmur. In aortic stenosis the resistance to ejection of blood is high, so a significant pressure difference develops across the aortic valve. The pressure gradient between ventricular systolic and aortic systolic is normally only a few mm Hg, as seen in this patient, which excludes aortic stenosis.
In mitral regurgitation (choice C), there is a high-pitched, “blowing” systolic murmur loudest at the apex radiating towards the axilla. The characteristic cardiac catheterization finding with mitral regurgitation is a pronounced increase in LAP during ventricular contraction. Normally LAP increases only slightly during ventricular contraction, to about 12 mm Hg. With atrial regurgitation, LAP rises because blood is forced backwards through the incompetent mitral valve; LAP may rise almost as much as left ventricular pressure (LVP) with severe regurgitation. Also, mitral regurgitation is often due to ischemic heart disease (post-MI), mitral valve prolapse, and LV dilation all of which are not clearly evident.
There is no evidence for myocardial infarction (choice E), i.e., peak systolic pressure and LVEDP are both normal. Left ventricular myocardial infarction decreases peak systolic LVP and increases end-diastolic LVP because increased preload compensates for failing contractility.
I don’t know where this came from, but here it is!
ReKap
Aortic regurgitation (AR) is caused by an aortic valve that fails to close fully during systole.
Regurgitant blood flow allows aortic blood pressure to drop rapidly during diastole.
The left ventricle must compensate for lost forward flow by increasing peak systolic pressure, so systolic blood pressure rises also. Pulse pressure widens.
Common causes of acute AR include endocarditis and aortic dissection.
Analysis
The correct answer is A. The patient’s presentation and the pressure tracings are characteristic of aortic regurgitation (AR). The two most common causes of acute AR in a patient with a native (tricuspid) aortic valve are endocarditis and aortic dissection.
The diagram shows aortic pressure (AoP; top broken line), left ventricular pressure (LVP; solid line) and left atrial pressure (LAP; bottom broken line) during a single cardiac cycle. The pressure tracings are notable principally because peak AoP is ~146 mm Hg (peak AoP = systolic blood pressure; SBP) and, more significantly, AoP drops to ~45 mm Hg at the end of diastole (= diastolic blood pressure; DBP). The patient’s blood pressure is thus 146/45 mm Hg rather than a more normal value of 120/80 mm Hg. Note the widening of pulse pressure (PP = SBP - DBP) from 40 mm Hg to 101 mm Hg.
DBP is so low because AR allows blood to reflux backward from the aorta into the LV. Normally, blood flow out of the arterial system during diastole occurs via the various capillary beds that make up the systemic vasculature, which represents a relatively high resistance pathway. Regurgitant flow represents a relatively low resistance pathway (resistance depends on the severity of regurgitation), so aortic pressure drops off precipitously during diastole. The regurgitant flow manifests as a diastolic murmur. LV peak systolic pressure concomitantly increases to compensate for the reduced forward flow.
Aortic dissection causes AR by either involving the valve sinuses or leaflets directly in such a way as to prevent full closure of the valve or by allowing a flap of the aortic wall to prolapse into the valve opening and interfere with normal closure during diastole. The regurgitant blood flow dilates the LV and creates considerable stress that can rapidly lead to cardiogenic shock if not surgically corrected.
Coronary heart disease (choice B) is a common cause of secondary or post-infarction mitral regurgitation (MR). Myocardial infarction leads to volume loading to support LV output by increasing preload. Preloading causes LV dilation which may distort the mitral valve annulus and prevent normal closure. MR causes LA pressure to rise steeply during systole. Peak LV and AoP are usually normal.
Primary hypertension (choice C), like AR, manifests as a rise in both peak LVP and AoP but, unlike AR, DBP typically rises also. Primary hypertension would not cause DBP to fall as depicted in the diagram.
The chordae tendineae provide support for the mitral valve leaflets and prevent them from everting during LV pressure development. Rupture of the chordae tendineae (choice D) can cause acute MR and a rapid rise in LA pressure during systole. The chordae tendineae are often damaged in rheumatic valvular disease. Other causes include Marfan syndrome, endocarditis, and myocardial infarction (through the loss of blood supply to the papillary muscles).
Valvular stenosis (choice E) obstructs forward flow and leads to the development of a significant pressure gradient across the valve. In the case of the aortic valve, LVP would exceed AoP in amounts proportional to the severity of valve narrowing. Mitral stenosis would cause LAP to rise chronically and peak LVP would be reduced, not increased. Valve stenosis alone would not cause a profound drop in DBP.
ReKap
Aortic stenosis:
↓ Valve surface area.
↑ Transvalvular pressure gradient and left ventricular systolic pressure.
↑ Aortic outflow velocity, leading to turbulence and a crescendo-decrescendo systolic murmur heard best at the right upper sternal border.
Analysis
The correct answer is B. This patient has a systolic murmur best heard in the right upper sternal border, which is consistent with aortic stenosis.
Aortic stenosis:
Aortic valve thickening and calcification → ↓ valve surface area = resistance to aortic outflow.
→ ↑ Left ventricular pressure (LVP) to maintain cardiac output (CO)
→ ↑ Transvalvular pressure gradient,
↑ Aortic outflow velocity (> 2 m/sec is diagnostic) → turbulence and systolic murmur
↑ Left atrial pressure (LAP) to assist preloading.
In severe aortic stenosis, valvular orifice surface area may drop from ~4 cm2 to < 1 cm2, aortic outflow velocity increases from ~0.5 m/s to > 4 m/s, and the transvalvular pressure gradient rises from < 3 mm Hg to > 60 mm Hg (= peak LVP of > 250 mm Hg). Our patient has a peak LVP: aortic pressure gradient of 50 mm Hg (170 mm Hg - 120 mm Hg), which represents severe aortic stenosis.
Aortic stenosis can cause left ventricular pressure to greatly exceed aortic pressure, as more pressure is necessary to overcome the increased resistance from the stenotic valve.
This patient reported chest discomfort and was admitted for suspicion of myocardial infarction. Other common symptoms of aortic stenosis include:
Dyspnea on exertion or decreased exercise tolerance.
Exertional dizziness (presyncope) or syncope.
Exertional angina (can resemble angina from coronary artery disease).
In aortic regurgitation (choice A), blood flows backward through the aortic valve during diastole when the valve should be closed. Peak LVP and aortic systolic pressure are nearly the same with pure aortic regurgitation.
Mitral regurgitation (choice C) represents the backward flow of blood through the mitral valve during systole. Regurgitant flow raises pulmonary capillary wedge pressure (PCWP), which is used as an estimate of LAP.
Mitral stenosis (choice D) creates resistance to blood flow from the LA to the LV during diastole. LAP rises to compensate, manifesting as an increase in PCWP.
Right-sided heart failure is most commonly due to left-sided heart failure: Blood backs up through the lungs and into the right heart. This patient has not yet developed right heart failure. All of the pressure recordings in the right heart and lungs are normal.
Pulmonic regurgitation (choice E) would not affect the pressure gradient across the aortic valve. It may manifest as an increase in peak pulmonary artery pressure (pressure rises to compensate for backflow through the valve).
Pulmonic stenosis (choice F) would not affect the pressure gradient across the aortic valve.
ReKap
Heart failure with reduced ejection fraction:
Myocardial infarction and loss of myocytes reduce contractility which directly decreases peak LVP, SBP, and PP.
Volume retention increases preloading and EDV, which helps compensate for the loss of contractility through the Frank-Starling mechanism.
Reduced contractility reduces LV emptying, so ESV increases and EF falls.
Analysis
The correct answer is A. The patient presents with signs and symptoms of volume overload caused by heart failure (congestive heart failure; CHF). Cardiac failure in this patient is evident from the dyspnea upon exertion, indicating that his ability to increase CO beyond basal levels is severely impaired. Volume loading has increased venous pressure, causing jugular venous distension, elevated BNP levels (an indicator of high blood volume), and pitting edema. He also has pulmonary edema, as evidenced by the bilateral inspiratory rales and the episodes of dyspnea and coughing that wake him from sleep. Although the patient has a history of myocardial infarction (MI), his labs (troponin) and ECG do not indicate an acute event.
Heart failure is a final common pathway for many cardiac pathologies (e.g., MI, as noted in this patient’s history). Myocardial damage has several consequences:
The ability to generate pressure and cardiac output (CO) is reduced (i.e., reduced contractility).
Peak LVP is reduced, which reduces peak arterial pressure and mean arterial pressure.
Reduced arterial pressure activates the renin-angiotensin-aldosterone system (RAAS), which leads to salt and water retention, which increases venous pressure and LV preload.
Enhanced preloading increases EDV, which helps compensate for the reduced contractility through the Frank-Starling mechanism.
Reduced contractility decreases the ability to eject blood during systole, so ESV remains high.
EF = EDV–ESV/EDV. EF, which is a measure of cardiac health, falls (heart failure with reduced ejection fraction; HFrEF).
PP = systolic blood pressure (SBP) – diastolic blood pressure. Since SBP is reduced, PP falls also.
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 need for increased pressure, but stroke volume (SV) is typically decreased and ESV is increased. 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 (i.e., regurgitant flow) allowing the ventricle to empty more completely during systole and ESV falls. The blood that leaked backward during systole increases left atrial pressure and contributes to LV preloading during diastole, so EDV increases.
A decrease in ESV, EDV, and SV (choice E) is suggestive of mitral stenosis (MS). In MS, a reduced mitral orifice creates resistance to LV preloading, so EDV falls. An increase in myocardial contractility helps maintain CO by increasing ejection fraction and ESV falls, but SV is still reduced. LVP and PP are maintained near-normal until failure occurs.
ReKap
A massive pulmonary embolism (PE) can block blood flow through the pulmonary circulation, leading to obstructive shock.
Obstructive shock due to PE usually presents with increased CVP, RAP and PAP, with normal PCWP.
Analysis
The correct answer is D. Sudden hypotension and tachycardia with cold extremities and jugular venous distension (JVD) is consistent with either cardiogenic or obstructive shock. Pulmonary artery catheter measurements show increased CVP, RAP, and PAP, as well as decreased cardiac output and normal PCWP. Elevated right-sided cardiac and pulmonary pressures with normal PCWP are most consistent with a diagnosis of pulmonary embolism (PE). The patient’s prolonged hospitalization and immobility are risk factors for PE.
Massive PEs can block blood flow through the pulmonary circulation, leading to obstructive shock. JVD is caused by elevated CVP, whereas cold extremities are caused by baroreceptor reflex-mediated peripheral vasoconstriction in response to decreased cardiac output and hypotension. Other etiologies of obstructive shock include tension pneumothorax, cardiac tamponade, and constrictive pericarditis.
Cardiopulmonary pressures in relation to different types of shock. Obstructive shock secondary to a PE is characterized by elevated right heart pressures and normal PCWP.
Bacteremia (choice A) can lead to septic shock, which is a form of distributive shock. Bacteremia leads to systemic vasodilation and hypotension without causing significant cardiac dysfunction. Consequently, affected patients often have warm extremities and increased cardiac output due to baroreceptor reflex-mediated tachycardia. Intracardiac pressures are typically low or normal.
Hemorrhage (choice B) can cause hypovolemic shock. A reduction in intracardiac pressure and cardiac output are seen due to the lack of circulating blood volume, JVD would not be present as JVD is a sign of elevated right heart pressures. The extremities would also be cold due to peripheral vasoconstriction.
Myocardial infarction (choice C) can lead to cardiogenic shock. Although cardiogenic shock can present very similarly to obstructive shock (decreased cardiac output, distended neck veins, elevated CVP), cardiogenic shock is usually characterized by an elevated PCWP secondary to increased left heart pressure due to global cardiac dysfunction. Pulmonary embolism does not result in a reduction in the ability of the left ventricle to pump blood.
Spinal cord injury (choice E) can cause neurogenic shock, a type of distributive shock. Injury to the brain and/or spinal cord can disrupt the autonomic pathways leading to systemic vasodilation. In neurogenic shock, there can be a lack of appropriate cardiac compensation due to altered vagal tone and central nervous system injury, leading to an inability to compensate for hypotension with increased heart rate. All intracardiac pressures and cardiac output would be low.
ReKap
Activation of the renin-angiotensin-aldosterone system (RAAS) in patients with heart failure causes salt and water retention.
Volume retention increases central venous and right atrial pressure.
The resulting increase in capillary hydrostatic pressure causes excessive fluid filtration from the blood to the interstitium, leading to edema.
The presence of a third heart sound (S3), heard best over the apex, is consistent with CHF.
Analysis
The correct answer is D. This patient has peripheral edema in her lower extremities secondary to congestive heart failure (CHF) and increased right atrial pressure (RAP). CHF typically develops when the heart cannot maintain cardiac output (CO) at a level required to support normal arterial perfusion pressures.
↓ Mean arterial pressure (MAP) → activation of the renin–angiotensin–aldosterone system (RAAS).
RAAS promotes salt and water retention.
Volume retention → ↑ central venous pressure (CVP) → ↑ RAP.
↑ RAP → ↑ left ventricular (LV) preload → ↑ CO → ↑ MAP.
Deleterious consequences of ↑ RAP and ↑ LV preload:
↑ RAP → ↑ capillary hydrostatic pressure (pressure backs up into the microcirculation) → peripheral edema (e.g., pedal edema).
↑ LV pressure → ↑ pulmonary capillary hydrostatic pressure → pulmonary edema (e.g., basilar rales).
CHF typically develops when the heart is damaged as a result of myocardial infarction. Heart failure may also occur in the context of heart structural abnormalities (e.g., valvular abnormalities, atrial or ventricular septal defects) or cardiomyopathies (either acquired or inherited).
The patient’s exertional dyspnea is consistent with reduced CO potentially as a result of heart failure. The elevated jugular venous pressure is evidence of increased CVP and RAP. The presence of a third heart sound (S3) on cardiac auscultation, heard best over the apex, is further evidence of CHF. Note that an S3 or S4 can be normal in people under the age of 40 or trained athletes.
The figure below summarizes the Starling forces that govern the rate and direction of fluid movement between blood and the interstitium.
Illustrating demonstrating the starling forces the balance fluid flow in capillaries. Increased plasma hydrostatic pressure and/or decreased interstitial colloid osmotic pressure will predispose to fluid extravasation with resultant edema.
Although decreased interstitial colloid osmotic pressure (choice A) can cause edema, CHF is not associated with this change. Instead, CHF causes increased plasma hydrostatic pressure.
Increased lymphatic flow (choice B) and increased plasma (capillary) colloid osmotic pressure (choice C) would decrease the likelihood of developing edema. In CHF, fluid retention by the kidneys will dilute the plasma and thus decrease plasma colloid osmotic pressure.
Stroke volume (choice E) has no direct role in the formation of peripheral edema and would also be decreased (not increased) in patients with CHF.
ReKap
Septic shock:
Caused by the introduction of bacteria (most commonly gram-negative) into the bloodstream.
Manifests as fever, hypotension, tachycardia, and skin that is warm and flushed.
Can result in both DIC and multi-organ failure.
Analysis
The correct answer is E. The abdominal trauma and surgery have probably introduced gut organisms into the bloodstream, leading to septic shock.
Septic shock:
Multisystem organ failure due to lipopolysaccharide (LPS), which is present in the cell wall of all gram-negative bacteria.
Toxins released by gram-positive bacteria and fungi may also cause septic shock.
LPS binds to a serum protein and stimulates CD14 receptors on endothelial cells and circulating inflammatory cells, eliciting a broad range of end-organ responses, similar to those seen in the trauma patient described here.
It is important to have a high index of suspicion for septic shock as a cause of the DIC in a trauma setting because, unlike other causes of DIC, high-dose intravenous antibiotics would be indicated as part of the supportive therapy. The combination of septic shock and DIC is life-threatening, as many cases progress to multi-organ failure.
Anaphylactic shock (choice A) is brought about by an exaggerated type I hypersensitivity reaction mediated by IgE antibodies bound to mast cells and basophils. The resulting massive release of inflammatory mediators causes systemic vasodilation, an increase in pulmonary vascular resistance, and bronchoconstriction. The pathways involved are complex and not well delineated. Anaphylactic shock would be an unlikely consequence of this patient’s trauma.
Cardiogenic shock (choice B) should be considered in this patient’s differential diagnosis. If he had suffered a myocardial infarction that caused his accident or a cardiac tamponade as a result of the trauma, you would expect him to be in shock when he arrived at the hospital, rather than developing shock three days later. A secondary myocardial infarction or cardiac failure as a result of the accident might cause shock several hours after admission, but would not be expected to cause his DIC. Cardiogenic shock reflects the inability of the heart to maintain output to vital organs. Cardiogenic shock is intrinsic to the heart and usually a consequence of ischemia, arrhythmia, or obstruction.
Hypovolemic shock (choice C) due to hemorrhage in the setting of trauma is a real clinical possibility in this case. If the patient had an unidentified site of moderate bleeding, it is conceivable that shock could develop over a period of hours. However, it would be unlikely to cause DIC. Hypovolemic shock occurs when blood volume decreases to a point at which cardiac output to vital organs can no longer be sustained. Hypovolemic shock is most often due to hemorrhage, fluid loss from burns, severe diarrhea/vomiting.
Neurogenic shock (choice D) can also be in the differential diagnosis in shock after severe trauma, but it usually occurs rapidly and would be seen at the time of the initial examination. Neurogenic shock is an unusual form of shock that occurs in catastrophic nervous-system injuries that cause diffuse vasodilation and hypotension. It is an important cause of disseminated intravascular coagulation, probably secondary to the release of cytokines and cellular degradation products in the setting of massive central nervous system damage. This diagnosis is unlikely because there was comparatively little damage to the head.
The following chart summarizes the various types of shock. PCWP, pulmonary capillary wedge pressure, is a surrogate marker for the left atrial pressure; CO, cardiac output; SVR, systemic vascular resistance.
ReKap
A new-onset third heart sound in an older patient with a history of myocardial infarction suggests congestive heart failure.
Left-sided heart failure is associated with pulmonary edema and dyspnea.
Right-side heart failure produces central venous hypertension with pedal edema, hepatosplenomegaly, and sometimes, ascites.
Analysis
The correct answer is A. A third heart sound (S3) is a low-pitched sound associated with ventricular filling during diastole (see figure). It results from the turbulence generated as atrial blood enters a much larger chamber, as found in the dilated ventricles of congestive heart failure (CHF). CHF is associated with ventricular dilation because low contractility (systolic dysfunction) results in retained end-systolic volume, volume overload, and ultimately, ventricular dilation. The S3 heart sound can also be a normal finding in pregnancy, athletes, and young children.
Figure showing the relationship between cardiac pressure, volume, and electrical changes.
Several findings in this patient should make you concerned about left-sided heart failure (HF). First, she has dyspnea and bibasilar lung crackles, which is indicative of fluid back-up and pulmonary edema. Second, she has a history of myocardial infarction (MI), which can decrease contractility through loss of muscle mass. Finally, she has a displaced point of maximal impulse (PMI) on physical examination, which is suggestive of an enlarged left ventricle. Causes of HF include MI, myocarditis, valvular abnormalities, and drug-induced dilated cardiomyopathy.
Importantly, note that her jugular venous pressure is within normal limits. This is because her left-sided HF has not yet progressed to the right side, though this is the natural course of the disease if poorly managed.
A “soft” (i.e., low intensity) fourth heart sound (S4; choice B) can be a normal finding in some older patients and athletes. The fourth heart sound occurs during atrial contraction immediately preceding S1. An abnormal S4 is usually loud and is heard in people with conditions that increase resistance to ventricular filling, such as concentric ventricular hypertrophy, HTN, aortic stenosis, and restrictive cardiomyopathy.
Patients with right-sided HF have signs of central venous hypertension including pedal edema (choice D), hepatic congestion with hepatosplenomegaly, i.e., enlargement of the liver and spleen (choice E), and ascites (choice C). However, this patient presents without jugular venous distension, which makes the possibility of right-sided HF less likely. Pedal edema, hepatosplenomegaly, and/or ascites can also occur in patients with renal, hepatic, or venous conditions not associated with cardiac disease.
ReKap
Exercise causes sympathetic activation, which increases CO.
Sympathetic stimulation of the myocardium increases HR and inotropy. Increased inotropy manifests as a shift upward and to the left in the CFC.
Sympathetic stimulation of the veins decreases their capacitance, which raises MSP and left ventricular preload. These changes manifest as a rightward shift in the VFC.
The decrease in SVR that results from dilation of resistance vessels controlling flow to active muscles also causes the VFC to rotate clockwise.
Analysis
The correct answer is B. The increase in cardiac output (CO) and right atrial pressure (RAP) depicted by the intersection of the dashed lines in the figure (point Z) result from activation of the sympathetic nervous system (SNS) during exercise.
The plots defined by their points of intersection describe how CO is limited by venous return (VR) and how VR is limited by CO. The interdependence of CO and VR locks the cardiovascular system at the intersection (equilibrium) points.
The cardiac function curve (CFC) is better known as a Starling curve. It describes the preload-dependence of left ventricular (LV) output.
The vascular function curve (VFC) describes the effects of VR (which is dependent on CO and the ease with which blood travels through the vasculature) on RAP. RAP equates with LV preload.
The pressure at which the VFC intersects the x-axis = mean systemic pressure (MSP). MSP reflects the “tightness” or “fullness” of the vasculature. It is determined experimentally by arresting the heart (CO = 0 L/min) and letting pressure in all parts of the system equilibrate. MSP is normally around +7 mm Hg.
The point of intersection between a CFC and a VFC defines how much CO can be supported by any given preload (RAP), and vice versa.
SNS activation during exercise modifies both curves. In the present example, a resting equilibrium point gives a CO of 5 L/min, supported by 0 mm Hg of RAP. Exercise shifts the equilibrium point (point Z) to give a CO of ~18 L/min at an RAP of 2 mm Hg.
Several different physiologic mechanisms contribute to the increase in CO that is necessary to support exercise.
Heart rate (HR): ↑ SNS activity and ↓ parasympathetic activity → ↑ HR
LV contractility: ↑ SNS activity → ↑ contractility → ↑ stroke volume
Venoconstriction:
↑ SNS activity → venoconstriction → ↓ venous capacity and ↑ venous pressure (note MSP shifts from 7 mm Hg to 20 mm Hg) → ↑ LV preload
Tensing abdominal muscles and rhythmic contraction of active muscles compresses veins (extravascular compression) and forces blood back to the heart.
Note that the VFC also rotates upward (increased slope) during exercise because systemic vascular resistance (SVR) has decreased. SVR decreases due to the vasodilatory effects of metabolites being generated by exercising muscle.
A blood transfusion (choice A) increases central venous pressure and RAP, which shifts the VFC to the right. The CFC may reflexively drop downward and to the right to maintain a stable CO, but it would not shift leftward.
Heart failure (choice C) lowers the CFC (decreased contractility). The resulting decrease in blood pressure activates the renin-angiotensin-aldosterone system (RAAS), causing volume retention. The VFC shifts progressively rightward as a result, increasing MSP.
Hemorrhage (choice D) reduces blood volume, which decreases MSP and shifts the VFC to the left. Severe hemorrhage can culminate in hypovolemic shock, which impairs myocardial contractility through hypotension and inadequacy of coronary perfusion.
Spinal anesthesia (choice E) blocks SNS output and venodilates, which decreases MSP and shifts the VFC to the left. Myocardial contractility decreases also, which shifts the CFC downward.
ReKap
The area enclosed by the left ventricular (LV) pressure-volume loop is equal to the work output during a single cardiac cycle.
Aortic stenosis increases LV afterload and stroke work.
Oxygen demand is directly related to cardiac work.
Analysis
The correct answer is E. The area enclosed by a ventricular pressure–volume (PV) loop is equal to the stroke work of the ventricle during a single cardiac cycle. This patient has aortic stenosis, which raises left-ventricular (LV) afterload and thus requires higher peak systolic pressures. This raises LV oxygen consumption despite the fact that stroke volume (SV) has not changed. Oxygen demand is directly related to work performed during systole.
SV is equal to the difference between the amount of blood in the ventricle prior to systole (end-diastolic volume; EDV) and the amount of blood in the ventricle at the end of systole (end-systolic volume; ESV). Note that the EDV is 125 mL and the ESV is 50 mL in plot X; SV is thus 75 mL. Plot Z (which is representative of aortic stenosis) shows that the EDV and ESV have both increased by similar amounts, so SV is still 75 mL.
Choices A and B are incorrect because the EDV (the lower right point of the curve) is shifted to the right. Increased EDV and diastolic pressure represents increased preload rather than decreased preload. Also, SV is unchanged in the patient.
Choice C is incorrect because stroke work is increased in the patient (the area within the PV loop is increased). The area represents stroke work.
Choice D correctly represents that stroke work is increased. However, SV is unchanged.
Choice F correctly describes that oxygen consumption is increased, but it is incorrect because SV remains normal.
ReKap
Mitral regurgitation:
An incompetent mitral valve allows blood to flow backward from the left ventricle (LV) to the left atrium during systole.
Regurgitant blood flow contributes to preload for the next beat and increases LV end-diastolic volume.
End-systolic volume falls due to decreased resistance to LV outflow.
There is no isovolumic phase to the cardiac cycle because the LV is never a closed vessel in this pathology.
Analysis
The correct answer is D. The patient presents with a history and murmur consistent with mitral regurgitation (MR), whereby an incompetent mitral valve allows blood to escape backward from the left ventricle (LV) to the left atrium (LA) during systole.
MR has several notable consequences for the LV. The regurgitant valve decreases resistance to LV outflow, so afterload is reduced. This allows the ventricle to empty more completely during systole and end-systolic volume (ESV) falls. The blood that leaked backward during systole increases left atrial pressure and contributes to LV preloading during diastole, so end-diastolic volume (EDV) increases. Stroke volume (SV) = EDV – ESV, so MR leads to an increase in SV.
The increased preloading means that peak LV pressure (LVP) and systolic blood pressure (SBP) remain unchanged, despite the regurgitant flow. Diastolic blood pressure (DBP) is determined by ease of outflow from the arterial system and is not affected by MR. Pulse pressure (PP), which is equal to SBP – DBP, is not usually affected by MR.
Although rheumatic heart disease is the most common cause of MR in many parts of the world, degenerative mitral valve disease, infective endocarditis, trauma, and certain drugs are more typical causes of MR in developed countries. Infective endocarditis can cause valve scarring and prevent the valve leaflets from closing fully at the beginning of systole. Patients typically remain asymptomatic because LV function is preserved. Common presenting symptoms include atrial fibrillation caused by LA dilation, which distorts electrical conduction pathways.
Increased ESV and EDV combined with decreased LVP and PP (choice A) would be consistent with a patient with congestive heart failure. A failing heart loses contractility (due to 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 SV falls and ESV increases.
The combination of increased LVP but decreased SV (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, SV, and PP (choice C) is characteristic of 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 raises PP.
A decrease in ESV, EDV, and SV (choice E) is suggestive of mitral stenosis (MS). In MS, a reduced mitral orifice creates resistance to LV preloading, so EDV falls. An increase in myocardial contractility helps maintain CO by increasing ejection fraction and ESV falls, but SV is still reduced. LVP and PP are maintained near-normal until failure occurs.
