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Dyspnea
Prof Dr / Mohamed Samy Gad
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Dyspnea is a subjective feeling of difficulty breathing
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Pathogenesis of dyspnea
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Mechanical factors
1. Pulmonary congestion :
Interstitial pulmonary oedema which leads to
diminished alveolar compliance (the most
important factor)
Intra-alveolar oedema.
Oedema of bronchial mucosa with or without
bronchospasm.
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2. Low cardiac output leads to fatigue and weakness of
respiratory muscles.3. Hydrothorax leads to mechanical compression of the
lungs.
4. Infra-diaphragmatic causes:
Right sided heart failure, pericardial effusion andconstrictive pericarditis lead to systemic venous
congestionascites and enlarged tender liver which
may elevate the diaphragm and decreases its
mobility.5. Massive pericardial effusion and huge cardiomegaly
occasionally compress the lungs and bronchi.
Mechanical factors
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Nervous factors:
Activation of Hering-Breuer reflex due to
interstitial pulmonary oedemaresult into
tachypnea and dyspnea. {This reflex is
present in normal individuals. In thisreflex , impulses arise from stretched
receptors in the terminal airways at the
end of inspiration, lead to reflex inhibitionof inspiration and passive relaxation of the
chest (expiration)}.
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Nervous factors:
Activation of Churchill-Cope reflex; due to
pulmonary venous congestion. {This reflex
is not present in normal individuals
distension of pulmonary vessels stimulatesJuxta-capillary receptors resulting in reflex
stimulation of respiratory centre causing
tachypnea}.
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Chemical factors:
Hypoxiahypercapneaacidosisstimulate respiratory centre and cause
tachypnea.
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Disturbed V/Q ratio
The well ventilated areas of the lung
should be well perfused with blood and
vice versa. This keeps the V/Q ratio withinthe normal range.
If this is disturbed dyspnea occurs.
This is the main mechanism of dyspneadue to pulmonary cause.
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Types of dyspnea
Types of cardiac dyspnea
Exertional
Paroxysmal nocturnal
dyspnea Orthopnea
Types of respiratory dyspnea
Exertional
Paroxysmal nocturnal
dyspnea Orthopnea
Platypnea
Trepopnea
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Grades of Exertional dyspnoea
Grade1 On doing more than the usual dailyeffort
Grade 2 On doing the usual daily effort
Grade 3 On doing less than the usual daily effort
Grade 4 At rest
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Paroxysmal nocturnal
dyspnea It is a paroxysmal attack of dyspnea that usually
occurs at night, awake the patient 2-3 hours
after sound sleep with marked inspiratory
dyspnea, cough with frothy expectoration,fighting for air. It occurs in attacks, usually
nocturnal due to more opportunity at night to
achieve the time threshold 2- 3 hours neededfor the attack to occur. When it is associated
with wheezes due to bronchospasm it is known
as Cardiac Asthma .
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Pathogenesis of PND
Absorption of oedema fluid that has been
accumulated during the day time ,into the
circulation as a result of elimination of the
effect of gravity and decrease of theelevated venous pressure leading to
increased blood volume and aggravation
of pulmonary congestion. This usuallyneeds 23 hours to occur. (This is the
main mechanism)
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Pathogenesis of PND
Slipping down from high pillows and assuming
the orthopneic position.
Decreased sympathetic activity during sleepand vagal predominance causes reduction of
myocardial contractility.
Night mares may lead to tachycardia, impairedCOP and aggravation of pulmonary congestion.
During sleep there is mild acidemia which
stimulates the respiratory centre.
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PND occurs more commonly in left
ventricular failure and left atrial failuredue to mitral stenosis with atrial
fibrillation.
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Cardiac BronchialAge Any age Usually young age
History Cardiac symptoms Chest symptomsDuration Usually short Usually longTime of attack 2-3 hours after sleep Early morningDyspnea Mainly inspiratory Mainly expiratorySputum Frothy blood tinged Thick pelletsChest examination Basal crepitations Generalized wheezesHeart examination Gallop and murmurs NormalECG Abnormal NormalEffects of drugsAdrenaline Contraindicated Improve the conditionMorphine Drug of choice ContraindicatedAminophylline Improve the condition Improve the condition
Differentiation between cardiac and bronchial asthma
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OrthopnoeaDyspnea that occurs or increases on lying flat, and is
relieved partially or completely by sitting. Cardiac :
Increased venous return on lying flat with elimination
of the effect of gravity that lead to aggravation ofpulmonary congestionactivation of Hering-Breuer
reflex.
Pulmonary:
Disturbed V/Q ratio on lying down due to biapicalpulmonary lesions.
Interference with the action of respiratory muscles.
Abdominal: Elevation of diaphragm.
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The most important cardiac
causes of Orthopnea are LVFand MS.
The most important pulmonarycause of Orthopnea is COPD.
It may be due to increased intra-
abdominal pressure eg. Tense
ascites.
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Trepopnea
It a type of dyspnea that occurs on lying on one
side.
It is usually due to lung lesion that precipitate a
disturbed V/Q ratio on lying to that side.
It is different from preferring to lie on diseased
side to minimize pain.
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Cyanosis
Prof Dr / Mohamed Samy Gad
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Definition
It is bluish discoloration of the skin and
mucous membrane due to increase in the
amount of reduced or abnormal
hemoglobin in the blood.
It is seen in the nail bed, mucous
membrane, ear lobes, lips and fingers.
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THRESHOLD OF CYANOSIS
Approximately 5 g/dL of unoxygenatedhemoglobin called(reduced hemoglobin and is
symbolized HbFe+2 )in the capillaries generates
the dark blue color appreciated clinically as
cyanosis. For this reason, patients who are
anemic may be hypoxemic without showing any
cyanosis and those with polycythemia develop
cyanosis easily.
More than 2 g/dL Methemoglobin (metHb), the
oxidized form of hemoglobin(HbFe+3.)
as low as 0.5 gm/dL sulfhemoglobin levels.
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Types of cyanosis
1. Cen t r a l c ya n o sis:
Is a physical sign causing bluish discoloration of the skin& mucus membranes, caused by lack of oxygen in the
blood, and is associated with cold temperatures, heart
failure, and lung diseases & smothering. It is seen in infantat birth as a result of heart defects, respiratory distress
syndrome, or lung & breathing problems.
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Types of cyanosis
1. Per iph er a l c yan o sis:Is blue tint in fingers orextremities, due to in adequate
circulation. The blood reachingthe extremities is not oxygen
rich. All factors contributing tocentral cyanosis can also cause
peripheral symptoms to appear,however peripheral cyanosis can
be observed without there being
heart or lung failures.
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Differences between central and peripheral cyanosisPeripheralCentral
In body extremities as:
Hands
Finger nails.
Tip of the nose.
lobule of the auricle
Mainly in
Mucous membranes.
Lips.
Tongue.
Hands.
Site
Cold hands.
No clubbing.
Warm hands.
Clubbing is common.
Hands
NormalDecreasedArterial o2pressure
AbsentCommonly presentPolycythaemia
No effect of O2inhalation.Cyanosis is improved except in:
1.Chronic cyanotic heart disease.
2.Abnormal hemoglobin.
The effect of :
1.O2inhalation
It improves the conditionIt worsens the condition1. Exercise
It improves the conditionHas no effect1. Worming
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Special types of cyanosis
Sulfhemoglobinemia
Methemoglobinemia
Differential cyanosis Reversed cyanosis
Unilateral cyanosis
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Sulfhemoglobinemia
Is a rare condition in which there is excesssulfhemoglobin (SulfHb) in the blood. The pigment is a
greenish derivative of hemoglobinwhich cannot be
converted back to normal, functional hemoglobin. It
causes cyanosiseven at low blood levels.
It is a rare blood condition that occurs when a sulfur
atomis incorporated into the hemoglobinmolecule.
When hydrogen sulfide(H2S) (or sulfideions) andferricions combine in the blood, the bloodis incapable
of carrying oxygen.
http://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Hemoglobinhttp://en.wikipedia.org/wiki/Cyanosishttp://en.wikipedia.org/wiki/Sulfurhttp://en.wikipedia.org/wiki/Atomhttp://en.wikipedia.org/wiki/Hemoglobinhttp://en.wikipedia.org/wiki/Hydrogen_sulfidehttp://en.wikipedia.org/wiki/Sulfidehttp://en.wikipedia.org/wiki/Ionhttp://en.wikipedia.org/wiki/Ferrichttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Oxygenhttp://en.wikipedia.org/wiki/Oxygenhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Ferrichttp://en.wikipedia.org/wiki/Ionhttp://en.wikipedia.org/wiki/Sulfidehttp://en.wikipedia.org/wiki/Hydrogen_sulfidehttp://en.wikipedia.org/wiki/Hemoglobinhttp://en.wikipedia.org/wiki/Atomhttp://en.wikipedia.org/wiki/Sulfurhttp://en.wikipedia.org/wiki/Cyanosishttp://en.wikipedia.org/wiki/Hemoglobinhttp://en.wikipedia.org/wiki/Blood8/13/2019 22.10 Dysnea and Cyanosis
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Sulfhemoglobinemia
Sulfhemoglobinemia is usually drug induced. Drugs associated with
sulfhemoglobinemia include acetanilid,
phenacetin, nitrates, trinitrotoluene and sulfur
compounds (mainly sulphonamides). (i.e.
overdosing of sumatriptan).
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Sulfhemoglobinemia
Prognosis and treatment
The condition generally resolves itself with
erythrocyte (red blood cell) turnover,
although blood transfusionscan be
necessary in extreme cases.
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Methemoglobinemia
Methemoglobinemia is a disorder characterizedby the presence of a higher than normal level of
methemoglobin(metHb) in the blood.
It may be congenital or acquired due toAnesthetics such as benzocaine and Xylocaine
,Benzene, Certain antibiotics (including
dapsone and chloroquine), Nitrites (used as
additives to prevent meat from spoiling).
Treatment: Methylene blue,Ascorbic acid,
Hyperbaric oxygen therapy, Exchange
transfusions.
http://en.wikipedia.org/wiki/Methemoglobinhttp://en.wikipedia.org/wiki/Bloodhttp://www.nlm.nih.gov/medlineplus/ency/article/002404.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002375.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002923.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002923.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002923.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002923.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002375.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002404.htmhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Methemoglobin8/13/2019 22.10 Dysnea and Cyanosis
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Differential cyanosis
Is cyanosis only in the lower limbs (upper
limbs show little or no cyanosis).
Causes:
1.Patent ductus arteriosus (PDA)
2.Coarctation of the aorta with PDACyanosis becomes more apparent.
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Reversed cyanosis
Is cyanosis in upper limbs only.
Cause: S.V.C obstruction.
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Unilateral cyanosis
Caused by local vascular obstruction by
(thrombous ,embolism,etc)
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Causes of central cyanosis
CARDIAC CAUSES
Congenital:
Congenital cyanotic heart
diseases Acquired:
Heart failure
Ruptured interatrial or
interventricular septum.
Respiratory causes
Low amount of inspired
oxygen
Hypoventilation Impaired diffusion
Impaired perfusion
Shunt: Pulmonary AVMs
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Causes of peripheral cyanosis
All common causes of central cyanosis
Arterialobstruction(e.g. thrombosis or
atheroma)
Reduced cardiac output (e.g. heart failure,
hypovolaemia)
Vasoconstriction(e.g. beta-blocker drugs, cold
exposure, Raynauds phenomenon)
Venousobstruction (e.g. deep vein thrombosis)
http://en.wikipedia.org/wiki/Arterialhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Hypovolaemiahttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Venoushttp://en.wikipedia.org/wiki/Deep_vein_thrombosishttp://en.wikipedia.org/wiki/Deep_vein_thrombosishttp://en.wikipedia.org/wiki/Venoushttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Hypovolaemiahttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Arterial