Dyspnea

Prof Dr / Mohamed Samy Gad

Dyspnea is a subjective feeling of difficulty breathing

Pathogenesis of dyspnea

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.

Mechanical factors
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 and constrictive pericarditis lead to systemic venous congestion ascites 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.

Nervous factors:
Activation of Hering-Breuer reflex due to interstitial pulmonary oedema result into tachypnea and dyspnea. {This reflex is present in normal individuals. In this reflex , impulses arise from stretched receptors in the terminal airways at the end of inspiration, lead to reflex inhibition of inspiration and passive relaxation of the chest (expiration)}.

Nervous factors:
Activation of Churchill-Cope reflex; due to pulmonary venous congestion. {This reflex is not present in normal individuals distension of pulmonary vessels stimulates Juxta-capillary receptors resulting in reflex stimulation of respiratory centre causing tachypnea}.

Chemical factors:

Hypoxia hypercapnea acidosis stimulate respiratory centre and cause tachypnea.

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 within the normal range. If this is disturbed dyspnea occurs. This is the main mechanism of dyspnea due to pulmonary cause.

Types of dyspnea
Types of cardiac dyspnea Exertional Paroxysmal nocturnal dyspnea Orthopnea Types of respiratory dyspnea Exertional Paroxysmal nocturnal dyspnea Orthopnea Platypnea Trepopnea

Grades of Exertional dyspnoea Grade 1 Grade 2 Grade 3 Grade 4 On doing more than the usual daily effort On doing the usual daily effort On doing less than the usual daily effort At rest

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 needed for the attack to occur. When it is associated with wheezes due to bronchospasm it is known as Cardiac Asthma .

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 the elevated venous pressure leading to increased blood volume and aggravation of pulmonary congestion. This usually needs 2 3 hours to occur. (This is the main mechanism)

Pathogenesis of PND
Slipping down from high pillows and assuming the orthopneic position. Decreased sympathetic activity during sleep and vagal predominance causes reduction of myocardial contractility. Night mares may lead to tachycardia, impaired COP and aggravation of pulmonary congestion. During sleep there is mild acidemia which stimulates the respiratory centre.

PND occurs more commonly in left ventricular failure and left atrial failure due to mitral stenosis with atrial fibrillation.

Differentiation between cardiac and bronchial asthma

Cardiac
Age History Duration Time of attack Dyspnea Sputum Chest examination Heart examination ECG Effects of drugs Adrenaline Morphine Aminophylline Contraindicated Drug of choice Improve the condition Improve the condition Contraindicated Improve the condition Any age Cardiac symptoms Usually short 2-3 hours after sleep Mainly inspiratory Frothy blood tinged Basal crepitations Gallop and murmurs Abnormal

Bronchial
Usually young age Chest symptoms Usually long Early morning Mainly expiratory Thick pellets Generalized wheezes Normal Normal

Orthopnoea
Dyspnea 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 of pulmonary congestion activation of Hering-Breuer reflex. Pulmonary: Disturbed V/Q ratio on lying down due to biapical pulmonary lesions. Interference with the action of respiratory muscles. Abdominal: Elevation of diaphragm.

 The most important cardiac causes of Orthopnea are LVF and MS. The most important pulmonary cause of Orthopnea is COPD. It may be due to increased intraabdominal pressure eg. Tense ascites.

Platypnea

It a type of dyspnea that occurs on sitting and relieved on lying down. It is usually due to bibasilar pleuro-pulmonary lesions precipitate a disturbed V/Q ratio on sitting.

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.

Cyanosis
Prof Dr / Mohamed Samy Gad

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.

THRESHOLD OF CYANOSIS
Approximately 5 g/dL of unoxygenated hemoglobin 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.

Types of cyanosis

1. Cent r al c yanosis:
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 infant at birth as a result of heart defects, respiratory distress syndrome, or lung & breathing problems.

Types of cyanosis

1.

Per iph er al c yan o sis: Is blue tint in fingers or extremities, due to in adequate circulation. The blood reaching the extremities is not oxygen rich. All factors contributing to central cyanosis can also cause peripheral symptoms to appear, however peripheral cyanosis can be observed without there being heart or lung failures.

Differences between central and peripheral cyanosis

Central Site
Mainly in Mucous membranes. Lips. Tongue. Hands. Hands Arterial o2 pressure Polycythaemia The effect of : Warm hands. Clubbing is common.

Peripheral
In body extremities as: Hands Finger nails. Tip of the nose. lobule of the auricle Cold hands. No clubbing.

Decreased Commonly present

Normal Absent

1.O2 inhalation

Cyanosis is improved except in: 1.Chronic cyanotic heart disease. 2.Abnormal hemoglobin.

No effect of O2 inhalation.

1.
1.

Exercise
Worming

It worsens the condition Has no effect

It improves the condition It improves the condition

Special types of cyanosis

Sulfhemoglobinemia Methemoglobinemia Differential cyanosis Reversed cyanosis Unilateral cyanosis

Sulfhemoglobinemia
Is a rare condition in which there is excess sulfhemoglobin (SulfHb) in the blood. The pigment is a greenish derivative of hemoglobin which cannot be converted back to normal, functional hemoglobin. It causes cyanosis even at low blood levels. It is a rare blood condition that occurs when a sulfur atom is incorporated into the hemoglobin molecule. When hydrogen sulfide (H2S) (or sulfide ions) and ferric ions combine in the blood, the blood is incapable of carrying oxygen.

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).

Sulfhemoglobinemia
Prognosis and treatment The condition generally resolves itself with erythrocyte (red blood cell) turnover, although blood transfusions can be necessary in extreme cases.

Methemoglobinemia
Methemoglobinemia is a disorder characterized by the presence of a higher than normal level of methemoglobin (metHb) in the blood. It may be congenital or acquired due to Anesthetics 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.

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 PDA Cyanosis becomes more apparent.

Reversed cyanosis
Is cyanosis in upper limbs only. Cause: S.V.C obstruction.

Unilateral cyanosis
Caused by local vascular obstruction by (thrombous ,embolism,etc)

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

Causes of peripheral cyanosis

All common causes of central cyanosis Arterial obstruction(e.g. thrombosis or atheroma) Reduced cardiac output (e.g. heart failure, hypovolaemia) Vasoconstriction(e.g. beta-blocker drugs, cold exposure, Raynauds phenomenon) Venous obstruction (e.g. deep vein thrombosis)