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Basic Sciences: Answers
119
specificity was 0.99. The single study conducted in patients evaluated for suspected lung
cancer had a sensitivity of 0.87 and a specificity of 0.90. Pooling all studies, regardless of the
indication for sputum testing, the false-positive rate was 0.09 and the false-negative rate was
0.06.
References
Ammanagi AS, Dombale VD, et al. Sputum cytology in suspected cases of carcinoma of lung
(Sputum cytology a poor man's bronchoscopy!). Lung India. 2012;29:19-23.
Rivera MP, Mehta AC; American College of Chest Physicians. Initial diagnosis of lung
cancer: ACCP evidence-based clinical practice guidelines (2nd edition). Chest.
2007;132(3 Suppl):131S-148S.
1.48 Answer: C
Several Nocardia species, in the family Actinomycetaceae, cause human disease. The
most common human pathogen is N. asteroides, which usually causes pulmonary and
disseminated infection. N. brasiliensis most commonly causes skin infection, particularly in
tropical climates. Infection is via inhalation or by direct inoculation of the skin. Nocardiosis
occurs worldwide in all age groups, but incidence is greater among older adults, especially
men. Person-to-person spread is rare. Lymphoreticular malignancies, organ transplantation,
high-dose corticosteroid or other immunosuppressive therapy, and underlying pulmonary
disease are predisposing factors, but about 50% of the patients have no preexisting disease.
Nocardiosis is also an opportunistic infection in patients with advanced human
immunodeficiency virus HIV infection.
Most clinical laboratories can isolate these microorganisms, but final speciation may be a
challenge and antimicrobial susceptibility testing is especially difficult because of the slow
rate of growth of Nocardia species. Full identification of species and susceptibility testing is
important because of the epidemiologic implications and the difficulties of successfully
treating these infections in immunosuppressed patients. Sulfonamides, including
trimethoprim-sulfamethoxazole, remain the most reliable antimicrobials.
References
Martínez R, Reyes S, Menéndez R. Pulmonary nocardiosis: risk factors, clinical features,
diagnosis and prognosis. Curr Opin Pulm Med. 2008;14:219-27.
Baracco GJ, Dickinson GM. Pulmonary nocardiosis. Curr Infect Dis Rep. 2001;3:286-292.
1.49 Answer: E
Percutaneous transthoracic needle biopsy is a well-established method of obtaining
cytologic and histologic samples from a pulmonary nodule. Properly performed, needle
biopsy is a simple and safe procedure. The risk for pneumothorax is 20 to 40%, but it is rarely
significant enough to require chest tube insertion. Although it is impossible to predict in
whom this will occur, pneumothorax is more frequent and more serious in patients with
severe emphysema and in patients in whom the biopsy is difficult to perform. Minor
hemorrhage and hemoptysis is the other common complication, which is rarely serious. Rare
complications include air embolism and needle tract metastases. Needle biopsy has a high
sensitivity and specificity for malignancy. For benign lesion, a specific diagnosis is less
Shahzad G. Raja
120
common, although with core needle biopsy, the yield of a specific benign diagnosis is
increased.
References
Chung T. Fine needle aspiration of the solitary pulmonary nodule. Semin Thorac Cardiovasc
Surg. 2002;14:275-80.
Wallace MJ, Krishnamurthy S, et al. CT-guided percutaneous fine-needle aspiration biopsy of
small (< or =1-cm) pulmonary lesions. Radiology. 2002;225:823-8.
1.50 Answer: A
Bronchial carcinoids are rare, slow-growing neuroendocrine tumours arising from
bronchial mucosa that affect patients in their 40s to 60s. Half of patients are asymptomatic,
and half present with symptoms of airway obstruction, including dyspnoea, wheezing, and
cough, which often leads to a misdiagnosis of asthma. Recurrent pneumonia, haemoptysis,
and chest pain are also common. Paraneoplastic syndromes, including Cushing's syndrome
due to ectopic ACTH, acromegaly due to ectopic growth hormone–releasing factor, and
Zollinger-Ellison due to ectopic gastrin production, are more common than carcinoid
syndrome, which occurs in < 3% of patients with the tumour. A left-sided heart murmur
(mitral stenosis or regurgitation) occurs rarely due to serotonin-induced valvular damage (as
opposed to the right-sided valvular lesions of GI carcinoid). Diagnosis is based on
bronchoscopic biopsy, but evaluation often initially involves chest CT, which reveals tumour
calcifications in up to one third of patients. Indium-111–labeled octreotide scans are useful
for determining regional and metastatic spread. Increased urinary serotonin and 5-
hydroxyindoleacetic acid levels support the diagnosis but are not commonly present.
Only selected cases can be treated endoscopically with laser resection. The complete
surgical resection remains the only therapy with curative intent in the majority of patients.
Parenchyma-sparing resections are indicated whenever possible. Overall survival after
surgery is excellent (5-year rate, 87 to 100%) with low recurrence rate (2 to 11%). N-status
and type of resection seem not to affect prognosis. Local relapse can be treated successfully
with surgery, whereas distant metastases have a poor prognosis even after chemotherapy.
References
Morandi U, Casali C, Rossi G. Bronchial typical carcinoid tumors. Semin Thorac Cardiovasc
Surg. 2006;18:191-8.
Filosso PL, Rena O, et al. Bronchial carcinoid tumors: surgical management and long-term
outcome. J Thorac Cardiovasc Surg. 2002;123:303-9.
1.51 Answer: E
The size of the lesion and the fact that the patient is healthy, asymptomatic and non-
smoker all point towards a benign lung lesion. Hamartomas are the third most common cause
of a solitary pulmonary nodule and the most common benign tumour of the lung.
Hamartomas account for 75% of all benign lung tumours and are composed of tissues
that are normally present in the lung, including fat, epithelial tissue, fibrous tissue, and
cartilage, but they exhibit disorganized growth. Although most hamartomas are asymptomatic
and although they have no malignant potential, bronchogenic carcinoma is an important
differential diagnosis, and an accurate imaging interpretation and diagnosis is important.
Basic Sciences: Answers
121
Peripheral tumours are usually simply observed after the definitive diagnosis, while central
tumours may be excised. The prognosis is excellent.
References
Brandman S, Ko JP. Pulmonary nodule detection, characterization, and management with
multidetector computed tomography. J Thorac Imaging. 2011;26:90-105.
Whyte RI, Donington JS. Hamartomas of the lung. Semin Thorac Cardiovasc Surg.
2003;15:301-4.
Albert RH, Russell JJ. Evaluation of the solitary pulmonary nodule. Am Fam Physician.
2009;80:827-31.
1.52 Answer: D
The patient in this question is in hypovolaemic shock. In hypovolaemic shock, caused by
bleeding, it is necessary to immediately control the bleeding and restore the victim's blood
volume by giving infusions of balanced salt solutions. Blood transfusions are necessary for
loss of large amounts of blood (e.g., greater than 20% of blood volume), but can be avoided
in smaller and slower losses. Volume resuscitation will result in reduced sympathetic
discharge and adequate ventricular filling resulting in reduced total peripheral resistance with
increased cardiac output and cardiac filling pressures.
References
Nunez TC, Cotton BA. Transfusion therapy in hemorrhagic shock. Curr Opin Crit Care.
2009;15:536-41.
Dutton RP. Current concepts in hemorrhagic shock. Anesthesiol Clin. 2007;25:23-34, viii.
1.53 Answer: C
Haemorrhage results in loss of effective blood volume and initiation of sympathetic
adrenal discharge. These will result in reduced pulmonary artery pressure and elevation of
pulmonary vascular resistance.
References
Dutton RP. Current concepts in hemorrhagic shock. Anesthesiol Clin. 2007;25:23-34, viii.
Hardaway RM. Traumatic shock. Mil Med. 2006;171:278-9.
1.54 Answer: C
The vascularly generated shock is caused by loss of blood or other fluids (absolute
hypovolaemia) or by vasodilatation (relative hypovolaemia). Absolute hypovolaemia is
caused by blood loss, plasma loss (burns or other denuding conditions, ascites, hydrothorax
etc.) or dehydration (water deprivation, severe diarhoea or vomiting, excessive sweating,
intestinal obstruction with luminal fluid accumulation, urinary loss of proteins/salt/water,
excessive use of diuretics, hypoaldosteronism etc.). Relative hypovolaemia, sometimes with
universal vasodilatation, is caused by endotoxins (septic shock from viral or bacterial
infections), anaphylactic shock or by a neurogenic vasodilatation (neurogenic shock by severe
pains or stress, anaesthetics or brainstem lesions close to the vasoconstrictor centre).
The reduced delivery of oxygen and nutrients to virtually all cells of the body, is
consequential: The mitochondria synthesise less ATP, the Na
+
-K
+
-pump operates
Shahzad G. Raja
122
insufficiently, the metabolic processing of nutrients is depressed which profoundly depresses
muscular contractions, and finally digestive enzymes destruct the damaged cells. Glucose
transport across the cell membranes in the liver and in the skeletal muscles is depressed
including a severe inhibition of the actions of insulin and other hormones. During progressive
shock the metabolism is reduced and thus the heat energy, so the body temperature tends to
decrease, if the patient is not kept warm. Compensatory mechanisms in shock are called
negative feedback mechanisms, because they operate to counteract the fall in blood pressure.
Baroreceptor responses and many hormonal control systems, that tend to raise the falling
blood pressure, are examples of negative feedback. The gain of a feedback system is defined
as the ratio of the response to the stimulus itself. Decompensatory mechanisms exaggerate the
primary fall in blood pressure. This is called positive feedback. A positive feedback
mechanism can lead to a vicious cycle and death, if its gain is above one. Two examples of
positive feedback in shock are ischaemic brainstem depression and cardiac depression.
Mild shock is a condition, where compensatory reactions can cure the patient without
external help. A latent shock is produced when a healthy blood donor delivers more than the
usual 500 ml of blood for transfusion, but the volume is often replaced within an hour. A
number of negative feedback mechanisms oppose the induced changes of shock. The fall in
mean arterial pressure (MAP) and pulse pressure reduces the stimulation of the high-pressure
baroreceptors in the carotid sinus and the aortic arch. The negative stimulation of the
cardiovascular control centres in the brainstem enhances the sympathetic tone (and reduces
the vagal tone) leading to increased heart rate and contractility as well as to arteriolar and
venous constriction mainly in the skin, skeletal muscles and the splanchnic area. The
bloodflow favours the brain and the heart as long as possible.
Reduced capillary pressure with autotransfusion from the interstitial fluid, thirst and
drinking followed by absorption of fluid from the gastrointestinal tract, and release of
powerful vasoconstrictors such as adrenaline, angiotensin II, vasopressin etc. are all
compensatory mechanisms that counteract shock.
Catecholamines and enkephalins are released from chromaffin granules in the adrenal
medulla. Catecholamines increase the heart rate and the cardiac output by stimulation of the
adrenergic β
1
-receptors in the myocardium. Catecholamines constrict vessels all over the
body by stimulating α
1
-receptors located on the surface of vascular smooth muscles.
ADH (vasopressin) is secreted from the posterior pituitary gland in response to shock,
because the sinoaortic baroreceptors are under-stimulated. Vasopressin is a modest
vasoconstrictor and a strong antidiuretic hormone. The increased ADH secretion causes
increased fluid reabsorption by the kidneys and restores blood pressure and volume.
Renin is secreted from the juxtaglomerular apparatus, when blood pressure and renal
perfusion falls drastically. Renin acts on the plasma protein, angiotensinogen, to form inactive
angiotensin I, which is transformed to the powerful vasoconstrictor, angiotensin II by
angiotensin converting enzyme, ACE. Angiotensin II is a powerful dipsogen and increases
thirst sensation. The rise in normal plasma potassium due to the ischaemia of shock also
releases aldosterone which promotes potassium loss from the kidney by acting on
mineralocorticoid receptors on principal cells in the distal tubule of the nephron.
Adrenocorticotropic hormone (ACTH) and β-endorphins are released into the blood from
the anterior pituitary gland in response to haemorrhage or other forms of stress. ACTH and
endorphins both exaggerate and restrict the development of shock. These opioids depress the
brainstem control centres that normally mediate autonomic responses to stress. Hence,
Basic Sciences: Answers
123
naloxone (an opioid antagonist) improves the circulation and increases the rate of survival
from life-threatening shock. - On the other hand, ACTH has a small aldosterone and a strong
cortisol stimulating effect.
References
Dutton RP. Current concepts in hemorrhagic shock. Anesthesiol Clin. 2007;25:23-34, viii.
Hardaway RM. Traumatic shock. Mil Med. 2006;171:278-9.
1.55 Answer: D
In haemorrhagic shock, blood loss exceeds the body's ability to compensate and provide
adequate tissue perfusion and oxygenation. This frequently is due to trauma, but it may be
caused by spontaneous haemorrhage (e.g., GI bleeding, childbirth), surgery, and other causes.
Most frequently, clinical haemorrhagic shock is caused by an acute bleeding episode with a
discrete precipitating event. Less commonly, haemorrhagic shock may be seen in chronic
conditions with subacute blood loss. Well described responses to acute loss of circulating
volume exist. Teleologically, these responses act to systematically divert circulating volume
away from nonvital organ systems so that blood volume may be conserved for vital organ
function. Acute haemorrhage causes a decreased cardiac output and decreased pulse pressure.
These changes are sensed by baroreceptors in the aortic arch and atrium. With a decrease in
the circulating volume, neural reflexes cause an increased sympathetic outflow to the heart
and other organs. The response is an increase in heart rate, vasoconstriction, and
redistribution of blood flow away from certain nonvital organs such as the skin,
gastrointestinal tract, and kidneys.
Concurrently, a multisystem hormonal response to acute haemorrhage occurs.
Corticotropin-releasing hormone is stimulated directly. This eventually leads to
glucocorticoid and beta-endorphin release. Vasopressin from the posterior pituitary is
released, causing water retention at the distal tubules. Renin is released by the juxtamedullary
complex in response to decreased mean arterial pressure, leading to increased aldosterone
levels and eventually to sodium and water resorption. Hyperglycaemia commonly is
associated with acute haemorrhage. This is due to a glucagon and growth hormone–induced
increase in gluconeogenesis and glycogenolysis. Circulating catecholamines relatively inhibit
insulin release and activity, leading to increased plasma glucose.
In addition to these global changes, many organ-specific responses occur. The brain has
remarkable autoregulation that keeps cerebral blood flow constant over a wide range of
systemic mean arterial blood pressures. The kidneys can tolerate a 90% decrease in total
blood flow for short periods of time. With significant decreases in circulatory volume,
intestinal blood flow is dramatically reduced by splanchnic vasoconstriction. Early and
appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act
to preserve the organism.
Age, medications, and comorbid factors all may affect a patient's response to
haemorrhagic shock. Failure of compensatory mechanisms in haemorrhagic shock can lead to
death. Without intervention, a classic trimodal distribution of deaths is seen in severe
hemorrhagic shock. An initial peak of mortality occurs within minutes of haemorrhage due to
immediate exsanguination. Another peak occurs after 1 to several hours due to progressive
decompensation. A third peak occurs days to weeks later due to sepsis and organ failure (See
also answer to 1.54).
Shahzad G. Raja
124
References
Dutton RP. Current concepts in hemorrhagic shock. Anesthesiol Clin. 2007;25:23-34, viii.
Hardaway RM. Traumatic shock. Mil Med. 2006;171:278-9.
1.56 Answer: B
In cardiovascular physiology, the baroreflex or baroreceptor reflex is one of the body's
homeostatic mechanisms for maintaining blood pressure. It provides a negative feedback loop
in which an elevated blood pressure reflexively causes blood pressure to decrease; similarly,
decreased blood pressure depresses the baroreflex, causing blood pressure to rise. The system
relies on specialised neurons (barorecptors) in the aortic arch, carotid sinuses, and elsewhere
to monitor changes in blood pressure and relay them to the brainstem. Subsequent changes in
blood pressure are mediated by the autonomic nervous system.
Baroreceptors include those in the auricles of the heart and vena cavae, but the most
sensitive baroreceptors are in the carotid sinuses and aortic arch. The carotid sinus
baroreceptors are innervated by the glossopharyngeal nerve (CN IX); the aortic arch
baroreceptors are innervated by the vagus nerve (CN X). Baroreceptor activity travels along
these nerves, which contact the nucleus of the tractus solitarius (NTS) in the brainstem.
The baroreceptors are stretch-sensitive mechanoreceptors. When blood pressure rises, the
carotid and aortic sinuses are distended, resulting in stretch and therefore activation of the
baroreceptors. Active baroreceptors fire action potentials ("spikes") more frequently than
inactive baroreceptors. The greater the stretch, the more rapidly baroreceptors fire action
potentials. These action potentials are relayed to the nucleus of the tractus solitarius (NTS),
which uses spike frequency as a surrogate measure of blood pressure. As discussed
previously, increased activation of the NTS inhibits the vasomotor centre and stimulates the
vagal nuclei. The end result of baroreceptor activation is inhibition of the sympathetic
nervous system and activation of the parasympathetic nervous system.
The sympathetic and parasympathetic branches of the autonomic nervous system have
opposing effects on blood pressure. Sympathetic activation leads to increased contractility of
the heart, increased heart rate, venoconstriction, and arterial vasoconstriction, which tend to
increase blood pressure by elevating both total peripheral resistance and cardiac output.
Conversely, parasympathetic activation leads to a decrease in heart rate and a minor decrease
in contractility, resulting in a decreased cardiac output and therefore a tendency to decrease
blood pressure.
By coupling sympathetic inhibition with parasympathetic activation, the baroreflex
maximises its ability to reduce blood pressure. Sympathetic inhibition leads to a drop in total
peripheral resistance and cardiac output, while parasympathetic activation leads to a
depressed heart rate and reduced cardiac contractility. The combined effects will dramatically
decrease blood pressure. Similarly, coupling sympathetic activation with parasympathetic
inhibition allows the baroreflex to elevate blood pressure effectively. Sympathetic activation
increases total peripheral resistance and elevates cardiac output, the latter being enhanced by
inhibition of the parasympathetic nervous system.
Baroreceptors are tonically active at mean arterial pressures (MAP) above approximately
70 mm Hg, called the baroreceptor set point. When MAP falls below the set point,
baroreceptors are essentially silent. The baroreceptor set point is not fixed; its value may
change with changes in blood pressure that persist for 1-2 days. For example, in chronic
hypertension, the set point will increase; on the other hand, chronic hypotension will result in
Basic Sciences: Answers
125
a depression of the baroreceptor set point. At a MAP below approximately 50 mm Hg,
baroreceptors are completely silent. The baroreflex may also be responsible for a part of the
low-frequency component of heart rate variability, the so called Mayer waves.
References
Hart EC, Charkoudian N. Sympathetic neural mechanisms in human blood pressure
regulation. Curr Hypertens Rep. 2011;13:237-43.
Izzo JL Jr, Taylor AA. The sympathetic nervous system and baroreflexes in hypertension and
hypotension. Curr Hypertens Rep. 1999;1:254-63.
1.57 Answer: A
Angiotensin is an oligopeptide in the blood that causes vasoconstriction, increased blood
pressure, and release of aldosterone from the adrenal cortex. It is a powerful dipsogen. It is
derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver.
It plays an important role in the renin-angiotensin system. Angiotensin I is converted to
angiotensin II through removal of two terminal residues by the enzyme Angiotensin-
Converting Enzyme (ACE, or kininase), which is found predominantly in the capillaries of
the lung. ACE is a target for inactivation by ACE inhibitor drugs, which decrease the rate of
angiotensin II production. Other cleavage products, 7 or 9 amino acids long, are also known;
they have differential affinity for angiotensin receptors, although their exact role is still
unclear. The action of angiotensin II itself is targeted by angiotensin II recptor antagonists,
which directly block angiotensin II AT
1
receptors. Angiotensin II is degraded to angiotensin
III by angiotensinases that are located in red blood cells and the vascular beds of most tissues.
It has a half-life in circulation of around 30 seconds, while in tissue, it may be as long as 15-
30 minutes. Angiotensi II has a number of effects throughout the body. These include:
Cardiovascular effects
It is a potent direct vasoconstrictor, constricting arteries and veins and increasing
blood pressure.
Angiotensin II has prothrombotic potential through adhesion and aggregation of
platelets and production of PAI-1and PAI-2.
It has been proposed that angiotensin II could be a cause of vascular and cardiac
muscle hypertrophy.
Neural effects
Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ of
the brain, decreases the response of the barorecptor reflex, and increases the desire
for salt.
It increases secretion of anti-diuretic hormone (ADH) in the posterior pituitary and
secretion of ACTH in the anterior pituitary.
It also potentiates the release of norepinephrine by direct action on postganglionic
sympathetic fibres.
Adrenal effects
Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a
hormone that causes the kidneys to retain sodium and lose potassium.
Shahzad G. Raja
126
Elevated plasma angiotensin II levels are responsible for the elevated aldosterone
levels present during the luteal phase of the menstrual cycle.
Renal effects
Angiotensin II has a direct effect on the proximal tubules to increase Na
+
resorption.
Although it slightly inhibits glomerular filtration by indirectly (through sympathetic
effects) and directly stimulating mesangial cell constriction, its overall effect is to
increase the glomerular filtration rate by increasing the renal perfusion pressure via
efferent renal arteriole constriction.
References
Diz DI, Arnold AC, et al. Angiotensin peptides and central autonomic regulation. Curr Opin
Pharmacol. 2011;11:131-7.
Head GA, Saigusa T, Mayorov DN. Angiotensin and baroreflex control of the circulation.
Braz J Med Biol Res. 2002;35:1047-59.
1.58 Answer: D
In order to calculate cardiac output from the available data we apply Fick principle. Fick
principle involves measuring:
Whole body oxygen consumption (VO
2
) per minute using a spirometer (with the subject
re-breathing air) and a CO
2
absorber
the oxygen content of blood taken from the pulmonary artery (representing venous
blood)
the oxygen content of blood from a cannula in a peripheral artery (representing
arterial blood)
From these values, we know that:
VO
2
= (CO x C
A
O
2
) – (CO x C
V
O
2
)
where CO = Cardiac Output, C
A
O
2
= Oxygen concentration of arterial blood and C
V
O
2
=
Oxygen concentration of venous blood.
This allows us to say
CO = VO
2
/ C
A
O
2
- C
V
O
2
CO = 500/0.24-0.16
CO = 500/0.8
CO = 6.25 L/min
References
Mathews L, Singh RK. Cardiac output monitoring. Ann Card Anaesth. 2008;11:56-68.
Cholley BP, Payen D. Noninvasive techniques for measurements of cardiac output. Curr
Opin Crit Care. 2005;11:424-9.
Basic Sciences: Answers
127
1.59 Answer: D
In order to calculate stroke volume from the available data we apply Fick principle first
to calculate cardiac output. Fick principle involves measuring:
Whole body oxygen consumption (VO
2
) per minute using a spirometer (with the subject
re-breathing air) and a CO
2
absorber
the oxygen content of blood taken from the pulmonary artery (representing venous
blood)
the oxygen content of blood from a cannula in a peripheral artery (representing
arterial blood)
From these values, we know that:
VO
2
= (CO x C
A
O
2
) – (CO x C
V
O
2
)
where CO = Cardiac Output, C
A
= Oxygen concentration of arterial blood and C
V
= Oxygen
concentration of venous blood.
This allows us to say
CO = VO
2
/ C
A
O
2
- C
V
O
2
CO = 500/0.24-0.16
CO = 500/0.8
CO = 6.25 L/min
Next, cardiac output = stroke volume x heart rate
Stroke volume = 6.25/70 x 1000
Stroke volume = 90 ml approximately
References
Mathews L, Singh RK. Cardiac output monitoring. Ann Card Anaesth. 2008;11:56-68.
Cholley BP, Payen D. Noninvasive techniques for measurements of cardiac output. Curr
Opin Crit Care. 2005;11:424-9.
1.60 Answer: B
Pulmonary vascular resistance (PVR) is calculated by using the formula:
PVR = Mean pulmonary artery pressure – Pulmonary capillary wedge pressure
Cardiac output
In order to calculate PVR from the available data we apply Fick principle first to
calculate cardiac output. Fick principle involves measuring:
Whole body oxygen consumption (VO
2
) per minute using a spirometer (with the subject
re-breathing air) and a CO
2
absorber
the oxygen content of blood taken from the pulmonary artery (representing venous blood)
the oxygen content of blood from a cannula in a peripheral artery (representing arterial
blood)
Shahzad G. Raja
128
From these values, we know that:
VO
2
= (CO x C
A
O
2
) – (CO x C
V
O
2
)
where CO = Cardiac Output, C
A
O
2
= Oxygen concentration of arterial blood and C
V
O
2
=
Oxygen concentration of venous blood.
This allows us to say
CO = VO
2
/ C
A
O
2
- C
V
O
2
CO = 500/0.24-0.16
CO = 500/0.8
CO = 6.25 L/min
Next, Mean pulmonary artery pressure = Diastolic pressure + 1/3 (Systolic pressure –
Diastolic pressure)
Substituting the values we get
Mean pulmonary artery pressure = 15 + 1/3 (25-15)
Mean pulmonary artery pressure = 15 + 3.33 = 18.33
Finally, PVR = 18.3-5/6.25 = 13.5/5.25 = 2.0 resistance units (mm Hg/L/min)
approximately.
References
Mathews L, Singh RK. Cardiac output monitoring. Ann Card Anaesth. 2008;11:56-68.
Cholley BP, Payen D. Noninvasive techniques for measurements of cardiac output. Curr
Opin Crit Care. 2005;11:424-9.
1.61 Answer: C
Stroke volume is calculated by using the following formula:
Cardiac output = stroke volume x heart rate
Cardiac output is calculated by using the following formula based on Fick principle:
VO
2
= CO x (C
A
O
2
-C
V
O
2
)
where VO
2
= oxygen consumption, CO = cardiac output, C
A
O
2
= arterial oxygen content and
C
v
O
2
= mixed venous oxygen content, respectively.
Substituting the values in this formula we get:
300 mL/min = CO x (20-15) mL/100 mL
CO = 300 x 100/5 mL/min
CO = 6000 mL/min
Next, stroke volume is calculated as follows:
6000 mL/min = stroke volume x 100 beats/min
Stroke volume = 6000/100 mL/min
Stroke volume = 60 mL/min