cyanosis.pptx

610 views 22 slides Jan 16, 2024
Slide 1
Slide 1 of 22
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22

About This Presentation

cyanosis,definition,causes,differences between central and peripheral cyanosis,approach to cyanosis


Slide Content

CYANOSIS Dr.G.VENKATA RAMANA MBBS DNB FAMILY MEDICINE

Definition Bluish color of the skin and mucous membranes resulting from an increased quantity of reduced hemoglobin (i.e ., deoxygenated hemoglobin) or of hemoglobin derivatives (e.g., methemoglobin or sulfhemoglobin ) in the small blood vessels of those tissues Criteria Deoxy Hb >5 g% or abnormal Hb ( metHb or sulf Hb ) ± SaO2 <85%. Classification True cyanosis Central cyanosis Peripheral cyanosis Mixed cyanosis Pseudocyanosis

pPseudocyanosis Pseudocyanosis Metals Gold, Silver, Mercury, Arsenic Drugs Minocycline, Chloroquine , Amiodarone Differential cyanosis Cyanosis is seen in only lower limbs PDA with eisenmengerization Reverse differential cyanosis Cyanosis is seen in only upper limbs PDA with eisenmengerization and transposition of great arteries Three by four cyanosis In addition to lower limbs, the left upper limb may also be cyanosed, w hen the patent ductus opens proximal to the origin of left subclavian artery

Intermittent cyanosis Seen in Ebstein’s anomaly Cyclical cyanosis Bilateral choanal atresia Orthocyanosis Development of cyanosis only in upright position due to hypoxia occurring in erect posture Seen in pulmonary arteriovenous malformation Cyanosis absent despite of sufficient reduced hemoglobin In severe anemia, carbon monoxide poisoning

Iron replete cyanosis Iron deplete cyanosis It is compensated erythrocytosis which establishes equilibrium with hematocrit It is decompensated erythrocytosis which fails to establish equilibrium with unstable, rising hematocrit Iron replete cells are deformable Iron deplete cells are less deformable Hyperviscosity symptoms are rare Hyperviscosity symptoms are frequent

Theories of Cyanosis Admixture cyanosis Secondary to shunts Tardive cyanosis Due to reversal of shunt ( eisenmengerization ) Hypoxic cyanosis Due to type 1 respiratory failure Replacement cyanosis Due to abnormal hemoglobins Distributive cyanosis Venous pooling of blood

Hyperoxia Test (Cardiac vs Pulmonary Cyanosis) After giving 100% oxygen for 10 minutes, a repeat arterial blood gas (ABG) is done and if PaO2 is < 150mm Hg then the cause is cardiac and if the PaO2 improves to >200 mm Hg, the cause is respiratory

Central Cyanosis In central cyanosis, the Sao2 is reduced or an abnormal hemoglobin derivative is present Site : Mucous membranes of oral cavity and skin Decreased atmospheric pressure—high altitude Cyanosis usually becomes manifest in an ascent to an altitude of 4000 m (13,000 ft ) Impaired pulmonary function Seriously impaired pulmonary function , through perfusion of unventilated or poorly ventilated areas of the lung or alveolar hypoventilation, is a common cause of central cyanosis This condition may occur acutely, as in extensive pneumonia or pulmonary edema, or chronically , with chronic pulmonary diseases (e.g., emphysema) In the latter situation, secondary polycythemia is generally present and clubbing of the fingers may occur

Anatomic shunts Another cause of reduced Sao2 is shunting of systemic venous blood into the arterial circuit Certain forms of congenital heart disease are associated with cyanosis on this basis Pulmonary arteriovenous fistulae may be congenital or acquired, solitary or multiple, and microscopic or massive The severity of cyanosis produced by these fistulae depends on their size and number They occur with some frequency in hereditary hemorrhagic telangiectasia Sao2 reduction and cyanosis may also occur in some patients with cirrhosis, presumably as a consequence of pulmonary arteriovenous fistulae or portal vein–pulmonary vein anastomoses

In patients with cardiac or pulmonary right-to-left shunts, the presence and severity of cyanosis depend on the size of the shunt relative to the systemic flow and on the Hb-O2 saturation of the venous blood. With increased extraction of O2 from the blood by the exercising muscles, the venous blood returning to the right side of the heart is more unsaturated than at rest, and shunting of this blood intensifies the cyanosis Secondary polycythemia occurs frequently in patients in this setting and contributes to the cyanosis

Methemoglobin Sulfhemoglobin Common causes Ingested medication ( dapsone , antimalarial agents) Local anesthetic Nitrates or nitrites Ingested medication ( dapsone , phenacetin , sulfonamides) Nitrites Typical presentation Cyanosis Neurologic symptoms from headache to coma Respiratory depression Cyanosis Color of the blood Chocolate brown Green Pulse oximetry Inaccurate Inaccurate Arterial blood gas PaO 2  normal Methemoglobin is detected on most machines PaO 2  normal Confirmatory testing Blood gas (arterial or venous) Spectrophotometry or Gas chromatography Management Methylene blue (MB) or Ascorbic acid Supportive (no antidote) Exchange transfusion in severe cases Lack of response to MB

Carboxyhemoglobin Common causes Inhaled CO gas from fires, gas-powered generators, kerosene heaters Smoking Typical presentation Neurologic symptoms from headache to coma Chest pain from myocardial ischemia Headache, malaise Color of the blood Cherry red Pulse oximetry Inaccurate Arterial blood gas PaO 2  normal Carboxyhemoglobin is detected on most machines Confirmatory testing Co- oximetry using arterial blood (in stable patients, venous samples are accurate) Management High-flow or hyperbaric oxygen

Peripheral Cyanosis Peripheral cyanosis is due to a slowing of blood flow and abnormally great extraction of O2 from normally saturated arterial blood It results from vasoconstriction and diminished peripheral blood flow, such as occurs in cold exposure, shock, congestive failure, and peripheral vascular disease Often in these conditions, the mucous membranes of the oral cavity, including the sublingual mucosa, may be spared Site : Nail bed N ose tip E arlobe Outer lips F inger tips Extremities

Peripheral cyanosis

APPROACH TO THE PATIENT Time of onset of cyanosis : Cyanosis present since birth or infancy is usually due to congenital heart disease Central and peripheral cyanosis must be differentiated The presence or absence of clubbing of the digits should be ascertained Pao2 and Sao2 should be determined Spectroscopic examination of the blood should be performed to look for abnormal types of hemoglobin

LAB TESTS CBC CHEST XRAY ECG 2DECHO ABG OXIMETRIC STUDIES SPECTROSCOPE HB ELECTROPHORESIS

TREATMENT OF CYANOSIS Treatment of underlying cause Symptomatic treatment of cyanosis Warming of the affected areas Oxygenation