1. CYANOSIS PRESENTED BY THIRUMURUGAN E Msc CVT

2. CYANOSIS Cyanosis is derived from the colour ‘cyan’, which comes from ‘kyanous’, the Greek word for blue. Definition:  Cyanosis is bluish discoloration of skin and mucous membrane  caused by increased quantity of reduced hemoglobin > 5g/dl

3. Threshold of cyanosis  It is the minimal concentration of reduced Hb In the capillary blood that leads to appearance of cyanosis. Threshold cyanosis = 0.5 (reduced Hb in arterial blood + reduced Hb in venous blood).

4. Basics  Deoxygenated blood -From right ventricle enters into lungs  In lungs (alveolus)  Co2 –ejected off by exhalation  O2-inhaled (it deoxygenated the blood )  Then oxygenated blood enters into left side of heart  From left side of heart supplies the tissue  Tissue uses the oxygen and form a byproduct co2

6. Hemoglobin  It is a protein consist of heme molecules acts as glubin chain.  Each glubin chain contains of 4 irons (fe2+)  Each of 4 iron it reversible binds with one oxygen molecule.

7. Hemoglobin Hb in 2 forms –deoxyHb and oxyHb  – In DeoxyHb- globin units are tightly bound(TENSE CONFIGURATION) –which has reduces the affinity of Hb molecule to Oxygen  When 1 st oxygen is bound- the bonds holding globin chains are released producing RELAXED CONFIGURATION  Which exposes more oxygen binding sites leading to high fold affinity to oxygen binding.

8. OXYGEN DISSOCIATION CURVE  When relation between po2 and %of Hb saturation is plotted on graph we get –oxygen – haemoglobin dissociation curve.  Its shows that % of Hb saturation increases with increase in po2  Relationship-not linear.

9. SIGMOID SHAPED CURVE - CAUSE  When 1 molecule of O2 combines with Hb, affinity of Hb increases & so on  This is called Co-operative binding Kinetics.  Due to this O2-Hb dissociation curve is Sigmoid.

10. SIGMOID SHAPED CURVE  Loading Zone – Related to process of O2 uptake in lungs.  Even Po2 falls below 60 mmHg saturation is still 90%, so loading zone provide margin of safety

11. SIGMOID SHAPED CURVE  Unloading zone – related to O2 delivery in tissue, steep portion below Po2 60mmHg

12. SHIFTS IN O2-HB DISSOCIATION CURVE Shift to Right:  Decreased affinity of Hb for O2. Causes:  Decreased PH  High temperature  Example-central cyanosis

13. SHIFTS IN O2-HB DISSOCIATION CURVE Shift to left increased affinity of haemoglobin for oxygen. (eg -lungs ) have high affinity of oxygen, later goes into muscle it reduces its affinity.( Causes –  Decreased Temperature Example –pheripheral cyanosis

14. Types of Cyanosis CYANOSIS PERIPHERAL CENTRAL

15. MECHANISM OF CYAOSIS- Stagnant hypoxia  It results from deficiency of blood flow through tissues  EX:PERIPHERAL HYPOXIA

16. Stagnant hypoxia

17. PERIPHERAL CYANOSIS

18.  Usually indicates stasis of blood flow in the periphery with normal arterial O2 saturation.  But widened arteriovenous (AV )O2 difference.  Reduced HB in the skin exceeds 4g/dl.

19. PERIPHERAL CYANOSIS  Avo2 difference:  Difference in arterial blood and venous blood  Difference in Arterial blood –amount of oxygen delivered to the tissue.  Difference in venous blood-amount of oxygen leaving the tissue.  Represent-how much oxygen is extracted at time.

20. PERIPHERAL CYANOSIS  It is most prominent in cool exposed areas that may not be well perfused, such as extremities particularly Nail beds Nose Limbs  Immersion of the limbs in warm water for several minutes reverse cyanosis

21. ETIOLOGY of PERIPHERAL CYANOSIS (secondary) EXPOSURE TOCOLD OBSTRUCTION LVF DECREASED CO

22. Mechanism  Normal systemic arterial oxygen saturation and increased oxygen extraction.  resulting in a wide systemic arterio-venous oxygen difference (av 02 difference).  The increased extraction of oxygen results from sluggish movement of blood through the capillary circulation.

23. PERIPHERAL CYANOSIS  Sites Tip of nose Ear lobules Outer aspect of lips, chin, cheek Tips and nail beds of fingers, toes Palms, soles

24. Central cyanosis

25. MECHANISM OF CYANOSIS- Hypoxic hypoxia  Rate of diffusion of O2 to tissues is decreased  O2 tension and O2 content decrease in arterial and venous blood

26. Hypoxic hypoxia

27. Central cyanosis  Pathologic condition caused by reduced arterial oxygen saturation.  Involves highly vascularized tissues, such as the lips and mucous membranes, through which blood flow is brisk and the arterio-venous difference is minimal

28. OXYGEN SATURATION Normal oxygen saturation in arterial blood is 95% Normal oxygen saturation in normal mixed venous blood is 70% Oxy-haemoglobin =13.3g of 14g/dl Reduced haemoglobin =0.7g/dl Oxy-haemoglobin =9.8g of 14g/dl Reduced haemoglobin =4.2g/dl

29. OXYGEN SATURATION Mean of reduced Hb : (arterial and mixed venous blood )=0.7+4.2/2=2.45g/l. Hence colour of normal skin is pink.

30. Central cyanosis  Arterial oxygen saturation <85%  O2 SATURATION –FURTHER DROPS TO LOWER LEVELS.  Since it is the absolute quantity of reduced Hb in blood that is responsible for cyanosis.

31. Central cyanosis  Higher the total hb content,greater is tendency towards cyanosis (ex- polycythemia )  Cyanosis may be absent in patients with severe anaemia (hb <33%) DESPITE MARKED OXYGEN DESATURATION.

32. Central cyanosis  Association :  central cyanosis often associated with polycythemia  Sites: Involves entire body Tongue (margins & undersurface) Inner aspects of lips Mucous membranes of gums, soft palate, cheeks

33. PATHOGENESIS of Central cyanosis 1- Decreased arterial oxygen saturation: -Due to inadequate oxygenation - owing to impaired pulmonary function (pulmonary venous blood is not fully saturated ) - -Inhalation of 100% oxygen may clear cyanosis -This is called Anoxemic cyanosis -Example: pulmonary disorders

34. PATHOGENESIS of Central cyanosis 2- Decreased arterial oxygen saturation: -Due to Intracardiac right to left shunt -and pulmonary venous blood is fully saturated -This is called shunt or Admixture cyanosis -Example: Cyanotic CHD

35. PATHOGENESIS of Central cyanosis 3- Decreased arterial oxygen saturation: -Due to replacement of normal by abnormal hb. -This is called replacement cyanosis. -EX- Methemoglobinemia

36. Differential cyanosis  Condition where some part of the body receives more hypoxic blood than others  Cyanosis confined to lower limbs  or no cyanosis of arm and face, typically seen in 1- PH with right to left shunt Through PDA. Example – If the ductus is proximal to left subclavian artery (Then right hand is less cyanosed than left hand and both the feet.

37. PDA  Left to right shuntpulmonary HTreversed shunt (Rt Lt shunt)  Desaturated blood from the ductus enters the aorta (distal to the left subclavian artery),sparing the brachiocephalic circulation

38. PDA ..

39. CYANOSIS Differentiation of cyanosis of cardiac origin from that of pulmonary causes 1-Tachypnea: -In CHD there is no other signs of respiratory distress expect tachypnea. 2- Cheyne strokes breathing can occur both in heart and respiratory failure. 3- Arterial blood gas analysis in pAtIENT with cyansosis also helps in differentiating cyanosis of cardiac origin from that of respiratory cause.

40. ABG

41. MIXED CYANOSIS  Presence of both peripheral and central cyanosis.  Example :Chronic cor pulmonale (rv dilation and hypertrophy due to PAH )due to fibrosis of lung  Lung lesion tends to produce central cyanosis  While associated with right heart failure tends to cause peripheral cyanosis

42. METHEMOGLOBINEMIA  NORMAL PHYSILOGY: Major function of Hb transport of oxygen from lungs to body tissues, mediated by reversible binding of molecular oxygen to heme iron Heme iron of deoxy Hb must be in ferrous state to allow reversible binding with oxygen. This ferrous iron is continually subjected to oxidant stress (resulting in formation of ferric hemoglobin i.e.methemoglobinemia)

43. METHEMOGLOBINEMIA  Methemoglobinemia is incapable of reversible oxygen binding. Etilogy: nitrites-nitroprusside aniline dyes- shoe dyes,crayons Drugs-anesthetics and analgesic Presentation: Slate grey cyanosis

44. METHEMOGLOBINEMIA Diagnosis : When a sample of venous blood is agitated in air for 15min, Characteristic chocolate brown color is formed. SPECTROSCOPE

45. METHEMOGLOBINEMIA TREATMENT : Slow infusion of 1-2mg /kg body wt of 1% freshly prepared methylene blue in normal saline. Decrease the methemoglobinemia levels Withdrawal of offending drugs

46. TREATMENT  Goals- Provide adequate tissue oxygen and CO2 removal.  Principles- Establish airway Ensure oxygenation Ensure adequate ventilation Correct metabolic abnormalities Alleviate the cause of respiratory distress

47. TREATMENT  Monitor Airway, breathing, circulation (ABCs)  with respiratory compromise, establish an airway & provide supportive therapy (e.g., oxygen, mechanical ventilation)  Monitor Vital signs

48. Hoarseness

49.  It is not related to cardiovascular disease. Occurs in :  mitral stenosis,  aortic aneurysm,  pericardial effusion  Intubation related (post cardiac surgery)

50. Hoarseness  Mitral stenosis: due to compression of laryngeal nerve  Aortic aneurysm: compression of laryngeal nerve  Pericardial effusion related to myxedema,