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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/Blood
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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.

    http://en.wikipedia.org/wiki/Blood_transfusionhttp://en.wikipedia.org/wiki/Blood_transfusion
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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/Methemoglobin
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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

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