SEMINAR on Circulatory disturbances.pptx

Circulatory disturbances refer to disorders affecting the normal flow of blood within the body. Proper circulation is essential for delivering oxygen and nutrients to tissues while removing waste products. Any disruption in this process can lead to serious health complications. Circulatory disturbances can result from various conditions, including blood vessel obstruction, abnormal blood pressure, or heart dysfunction.

1. CIRCULATORY DISTURBANCES PRESENTED BY : DR. BHAVIKA ​ UNDER THE GUIDANCE OF DR.NEEMA SHETTY DR.ADITI MATHUR DR.ASHISH BALI DR.TRISHI

2. CONTENT INTRODUCTION TYPES OF CIRCULATORY DISTURBANCES HYPEREMIA AND CONGESTION HAEMORRHAGE SHOCK THROMBOLISM ISCHAEMIA SYNCOPE APPLIED IN PERIODONTICS CONCLUSION REFERENCES

3. INTRODUCTION Circulation is the mechanism of distribution and return of blood to and from tissues in a manner of circular movement. The health of cells and organs critically depends on an unbroken circulation to oxygen and nutrients to remove wastes. However the well being of tissues also require normal fluid balance. Abnormalities in vascular permeability to hemostasis can result in injury even in the setting of an intact blood supply.

4. 1.DISTURBANCES IN THE VOLUME OF CIRCULATING BLOOD Hyperemia Congestion Hemorrhage Shock TYPES 2..CIRCULATORY DISTURBANCES OF OBSTRUCTIVE NATURE Thrombosis Embolism Ischaemia Infarction

5. 1.HYPERAEMIA AND CONGESTION Hyperaemia and congestion are the terms used for localised increase in the volume of blood within dilated vessels of an organ or tissue. Increased volume of blood from arterial and arteriolar dilatation (i.e. increased inflow) is referred to as hyperaemia or active hyperaemia . Impaired venous drainage (i.e. diminished outflow) is called venous congestion or passive hyperaemia . If the condition develops rapidly it is called acute, while more prolonged and gradual response is known as chronic .

6. Abnormal accumulation of blood in the arteriovenous capillary bed causing hyperaemia and passive congestion.

7. Mechanisms involved in chronic venous congestion (CVC) of different organs

8. ACTIVE HYPEREMIA exercise inflammation menopausal flush renal diseases that cause  fluid retention PASSIVE HYPEREMIA heart failure mitral stenosis, a type of  heart disease a blockage in a blood vessel a kink in a vein pneumonia thrombosis CAUSES

9. Active hyperemia does not typically need to be treated, as it is a physiological response to activities such as physical exercise and will improve on its own. Passive hyperemia , however, is caused by other conditions that will need to be treated. Medication for hyperemia causes may include : beta-blockers  to lower  blood pressure digoxin to strengthen the heartbeat blood thinners TREATMENT

10. Haemorrhage is the escape of blood from a blood vessel. The bleeding may occur externally, or internally into the serous cavities or into a hollow viscus. Extravasation of blood into the tissues with resultant swelling is known as haematoma . Large extravasations of blood into the skin and mucous membranes are called ecchymoses. Purpuras are small areas of haemorrhages ( upto 1 cm) into the skin and mucous membrane, whereas petechiae are minute pin head sized haemorrhages . Microscopic escape of erythrocytes into loose tissues may occur following marked congestion and is known as diapedesis. 2.HAEMORRHAGE

11. The various causes of haemorrhage are as under: Trauma to the vessel wall Spontaneous haemorrhage e.g. purpura, acute leukaemias , pernicious anaemia, scurvy. Inflammatory lesions of the vessel wall e.g. bleeding from chronic peptic ulcer, typhoid ulcers,. Neoplastic invasion e.g. haemorrhage following vascular invasion in carcinoma of the tongue. Vascular diseases e.g. atherosclerosis. Elevated pressure within the vessels ETIOLOGY

12. The effects of blood loss depend upon 3 main factors: i ) The amount of blood loss; ii) The speed of blood loss; and iii) The site of haemorrhage . The loss up to 20% of blood volume suddenly or slowly generally has little clinical effects because of compensatory mechanisms. A sudden loss of 33% of blood volume may cause death, while loss of up to 50% of blood volume gradually over a period of 24 hours may not be necessarily fatal. However, chronic blood loss generally produces iron deficiency anaemia , whereas acute haemorrhage may lead to serious immediate consequences such as hypovolaemic shock . EFFECTS

13. TREATMENT Applying pressure to the wound Use a tourniquet Pack the wound with gauze or a clean cloth if a tourniquet is unavailable  Apply direct pressure to the wound Stitches (sutures) or staples: Surgery:  Surgical procedures may be necessary to stop bleeding from major blood vessels or to repair damaged organs or body tissues Blood transfusion:  Medications:  Medicines help stop and stabilize  blood pressure , which may include tranexamic acid (controls bleeding), vitamin K (promotes blood clotting), and desmopressin (increases blood clotting)

14. A life threatening clinical syndrome of cardiovascular collapse characterised by- An acute reduction of effective circulating blood volume(hypotension) An inadequate perfusion of cells and tissues(hypoperfusion). If uncompensated- impaired cellular metabolism and death. 3.SHOCK TRUE(SECONDARY) SHOCK Circulatory imbalance between oxygen supply and oxygen requirements at the cellular level. Also called as CIRCULATORY SHOCK Transient and usually a benign vasovagal attack resulting from sudden reduction of venous return to the heart caused by neurogenic vasodilatation and consequent peripheral pooling of blood INITIAL(PRIMARY) SHOCK

15. Depending on the causes CIRCULATORY SHOCK can be categorised as- DAVIDSON’S 15 CLASSIFICATION

16. All forms of shock involve following 3 derangements: 16 PATHOGENESIS

17. HYPOVOLAEMIC SHOCK Caused by a reduced circulating volume due to haemorrhagic or non-haemorrhagic causes. Non-haemorrhagic causes- a) Poor fluid intake (dehydration) b) Excessive fluid loss because of vomiting,diarrhoea , urinary loss (e.g. diabetes), evaporation and ‘third-spacing’ (fluid is lost into the gastrointestinal tract and interstitial spaces). Most common form of shock

18. I. MILD SHOCK- Loss of < 20% of blood volume i ) Collapse of the subcutaneous veins of the extremities ii) Feet becomes pale and cool. iii) Sweat in forehead, hand and feet due to adrenergic discharge. iv) Urinary output, pulse rate and blood pressure remain normal. v) Patient feels thirsty and cold. III. SEVERE SHOCK- Loss of blood volume of > 40% i ) Skin of the extremities becomes pale ii) low urinary output, iii) rapid pulse and low blood pressure. II . MODERATE SHOCK- Loss of blood volume from 20 to 40% i ) Oliguria ii) The pulse is ↑ sed iii) Initially the blood pressure remains normal but may fall in the later stage CLINICAL FEATURES

19. 1. RESUSCITATION Establishment of a clear airway and maintaining adequate ventilation and oxygenation. Lowering of the head with support of the jaw to prevent airway obstruction Administration of oxygen 2. IMMEDIATE CONTROL OF BLEEDING TREATMENT

20. 3.EXTRACELLULAR FLUID REPLACEMENT- Ringer's lactate, Ringer's acetate or normal saline supplemented with 1 or 2 ampules of sodium bicarbonate. Rapid replacement of fresh blood after control of haemorrhage 4. DRUGS- ( i ) Sedatives- used to alleviate pain in patients with shock. MORPHINE,BARBITURATES (ii) Chronotropic agents- primarily increase the heart rate. ATROPINE,ISOPROTERENOL (iii) Inotropic agents- improve the strength of cardiac muscle contraction. DOPAMINE,DOBUTAMINE

21. Due to primary failure of the heart to pump blood to the tissues. Causes of cardiogenic shock- Myocardial infarction, Cardiac dysrhythmias, Valvular heart disease, Blunt myocardial injury Cardiomyopathy. Resultant decreased cardiac output decreased tissue perfusion & movement of fluid from pulmonary vascular bed into pulmonary interstitial space initially (interstitial pulmonary oedema) and later into alveolar spaces (alveolar pulmonary oedema) CARDIOGENIC SHOCK

22. Skin becomes pale and cool Urine output becomes low. Gradually the pulse becomes rapid and the arterial blood pressure becomes low. Right ventricular dysfunction- neck veins become distended and liver enlarges. Left ventricular dysfunction- broncheal rales and a third heart sound is heard. Gradually the heart becomes enlarged CLINICAL FEATURES

23. 20XX Presentation title 23 Airway must be clear with adequate oxygenation right sided failure caused by a massive pulmonary embolus should be treated with large doses of heparin intravenously. If pain is complained in case of left sided failure proper sedative e.g. morphine should be prescribed. Fulminant pulmonary oedema should be treated with a diuretic. Vasodilators- nitroprusside and nitroglycerin TREATMENT

24. Reduction in preload because of mechanical obstruction of cardiac filling Common causes of obstructive shock- Cardiac tamponade Tension pneumothorax Massive pulmonary embolus Air embolus. Reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in cardiac output. TREATMENT- Pericardial drainage via surgery OBSTRUCTIVE SHOCK

25. Results most often from Gram-negative bacteria entering the body from genitourinary tract, alimentary tract, respiratory tract or skin, and less often from Gram-positive bacteria. Immune system activation and severe systemic inflammatory response to infection Activation of macrophage-monocytes : Lysis of Gram negative bacteria Releases endotoxin, a lipopolysaccharide, into circulation Binds to lipopolysaccharide-binding protein (LBP) LPS-LBP binds to CD14 molecule on surface of monocyte/macrophages TNF-α IL-1 SEPTIC SHOCK

26. Activation of other inflammatory responses: a) Activation of complement pathway: End-products C5a and C3a induce microemboli and endothelial damage. b) Activation of mast cells: Histamine is released which increases capillary permeability c) Activation of coagulation system: Enhances development of thrombi. d) Activation of kinin system: Released bradykinin cause vasodilatation and increased capillary permeability.

27. In early warm shock: cutaneous vasodilatation- decreases systemic vascular resistance- arterial blood pressure falls, but cardiac output increases Body temperature increases due to toxins- the vasculature of the skin dilates, skin remains warm, pink and well perfused. The cutaneous veins remain full. The pulse rate becomes high and the systemic arterial pressure becomes low. Diagnosis is not difficult as this condition is associated with intermittent spikes of fever alternating with bouts of chills. CLINICAL FEATURES

28. In late cold shock: increased vascular permeability due to liberation of toxic products into the centre circulation- hypovolaemia and right heart filling decreases Decrease of flow into the pulmonary vasculature- left heart filling decreases- the cardiac output decreases Clinically it may be difficult to differentiate this type of shock from hypovolaemic shock or from traumatic shock- existence of a septic focus

29. Treatment of infection by early surgical debridement or drainage and by use of appropriate antibiotics Fluid replacement, steroid administration and use of vasoactive drugs TREATMENT

30. Due to allergens like penicillin(most commonly), anesthesia,dextrans,serum injections,stings . Antigen combines with IgE on mast cell and basophils releasing large amounts of histamine and slow releasing substances of anaphylaxis. Clinical features- a) bronchospasm b) laryngeal edema c) respiratory distress d) hypoxia e) massive vasodilation f) hypotension Treatment- administration of oxygen administration of epinephrine administration of antihistamine administration of corticosteroids ANAPHALYTIC SHOCK

31. Caused by major brain or spinal injury which disrupts brain-stem and neurogenic vasomotor control. Dilatation of the systemic vasculature which lowers the systemic arterial pressure Blood pools in the systemic venules and small veins. The right heart filling and stroke volume decrease. This decreases pulmonary blood volume and left heart filling so that left ventricular output decreases. NEUROGENIC SHOCK

32. Clinical features- skin remains warm, pink and well perfused in contradinction to the hypovolaemic shock. Urine output may be normal. But the heart rate is rapid and the blood pressure is low. Treatment- Elevation of the legs vasoconstrictor drug

33. Traumatized tissues activate the coagulation system and release microthrombi into the circulation- occlude or constrict parts of pulmonary microvasculature to increase pulmonary vascular resistance- increases right ventricular diastolic and right atrial pressures. Humoral products- a generalized increase in capillary permeability- loss of plasma into the interstitial tissue throughout the body- depletes the vascular volume Clinical features- ( i ) presence of peripheral and pulmonary oedema (ii) infusion of large volumes of fluid Treatment- 1. Resuscitation- intubation or mechanical ventilatory support 2. Local treatment of trauma and control of bleeding- similar to hypovolaemic shock. 3. Surgical debridement of ischaemic and dead tissues and immobilization of fractures may be required. 4. Fluid replacement- more fluids required than hypovolaemic shock. 5. Anticoagulation with doses of heparin- One intravenous dose of 10,000 units TRAUMATIC SHOCK

34. Life-threatening complications in shock are due to hypoxic cell injury resulting in immuno-inflammatory responses and activation of various cascades (clotting, complement, kinin). These include the following: 1. Acute respiratory distress syndrome (ARDS) 2. Disseminated intravascular coagulation (DIC) 3. Acute renal failure (ARF) 4. Multiple organ dysfunction syndrome (MODS) With progression of the condition, the patient may develop stupor, coma and death. COMPLICATIONS IN SHOCK

35. 4.THROMBOLISM Thrombosis is the process of formation of solid mass in circulation from the constituents of flowing blood; the mass itself is called a thrombus . Hematoma is the extravascular accumulation of blood clot, e.g. into the tissues. Thrombi may be life-threatening by causing one of the following harmful effects: 1. Ischemic injury 2. Thromboembolism

36. PATHOPHYSIOLOGY

37. Vascular injury exposes the subendothelial connective tissue (thrombogenic) and also causes vasoconstriction of small blood vessels briefly so as to reduce the blood loss. ENDOTHELIAL INJURY

38. Hypercoagulability may occur by the following changes in the composition of blood: i . Increase in coagulation factors, e.g. fibrinogen, prothrombin, factors Va, Vlla and Xa. ii. Increase in platelet count and their adhesiveness. iii. Decreased levels of coagulation inhibitors, e.g. anti thrombin III, fibrin split products. Hypercoagulability of blood

39. Deficiency of antithrombin Deficiency of protein C or S Defects in fibrinolysis Mutation in factor V Secondary (acquired) factors a. Risk factors: i . Advanced age ii. Prolonged bedrest iii. Immobilization iv. Cigarette smoking b. Clinical conditions predisposing to thrombosis: i.Heart diseases ii. Vascular diseases iii. Hypercoagulable conditions iv. Shock Predisposing factors Primary (genetic) factors

40. Resolution Organization Propagation Thromboembolism Fate of Thrombus

41. Cardiac thrombi: Sudden death by mechanical obstruction of blood flow or through thrombo embolism to vital organs. Arterial thrombi: Sudden death may occur following thrombosis of coronary artery. Venous thrombi (phlebothrombosis): These may cause following effects: i . Thromboembolism ii. Edema of area drained iii. Poor wound healing iv. Skin ulcer v. Painful thrombosed veins (thrombophlebitis) vi. Painful white leg (phlegmasia alba dolens ) due to iliofemoral venous thrombosis in postpartum cases 4. Capillary thrombi: Disseminated intravascular coagulation (DIC). CLINICAL EFFECTS

42. 5.ISCHAEMIA Ischaemia is defined as deficient blood supply to part of a tissue relative to its metabolic needs. The cessation of blood supply may be complete (complete ischaemia) or partial (partial ischaemia). Hypoxia : oxygen deprivation in muscles MALNUTRITION- Failure to remove waste products

43. 1. Anatomic pattern 2. General and cardiovascular status Anaemias (sickle cell anaemia, in particular) ii) Lowered oxygenation of blood (hypoxaemia) Senility with marked coronary atherosclerosis Cardiac failure Blood loss Shock. 3. Type of tissue affected Brain (cerebral cortical neurons, in particular). Heart (myocardial cells). Kidney (especially epithelial cells of proximal convoluted tubules) FACTORS DETERMINING SEVERITY OF ISCHAEMIC INJURY

44. Syncope is the sudden transient loss of consciousness and postural tone with spontaneous recovery. Loss of consciousness occurs within 10 seconds of hypoperfusion of the reticular activating system in the mid brain. SYNCOPE

45. Identify at-risk patient Reduce Stress Treat patient in a supine position Ensure profound local anesthesia Use local anesthetic agents containing a vasoconstrictor congruent with the patient’s functional capacity Prevention:

46. Signs and symptoms Adrenergic component Anxiety Pallor Pupillary dilation Palpitation Cholinergic component Diaphoresis (perspiration) Nausea Salivation Bradycardia Hypotension Sudden, brief loss of consciousness Seizure (rarely)

47. Emergency response: Place patient in Trendelenburg position, i.e., head and chest slightly below a line parallel to the floor and feet slightly elevated Administer oxygen Sudden, brief loss of consciousness Stimulate cutaneous reflexes Cold towel compresses to forehead and back of head Administer aromatic ammonia inhalant Reevaluate vital signs TREATMENT

48. If patient’s condition deteriorates Notify EMI Monitor vital sign. If at any time the patient becomes unresponsive, no normal breathing, and no palpable pulse consider the diagnosis of cardiac arrest Immediate CPR and defibrillation congruent with current recommendations Signs of recovery: vital signs return to baseline values, patient is alert Signs of deterioration: vital signs unstable, mental status labile

49. Dental considerations in cardiovascular patients Relationship of cardiovascular disease and periodontitis Periodontitis has been proposed as having an etiological or modulating role in cardiovascular and cerebrovascular disease, diabetes, respiratory disease, and adverse pregnancy. Another indirect effect of periodontal infection that may explain the association between periodontal disease and heart disease is that periodontal organisms ( Tannerella forsythia and Porphyromonas gingi valis ) contain heat-shock protein-60 which cross-react with the heart. These antibodies to heat-shock proteins of periodontal bacteria are cross-reactive that is exposed in an injured endothelium or atheromatous plaque.

50. Dental management Consulting the physician regarding the current medical status, medication, and patient management during periodontal therapy Detailed family history of cardiovascular disease, history of hypertension, medications, duration and antihy pertensive treatment history, severity of disease, and its complications Followed by short morning appointments, premedication with anxiolytics or prophylactic nitroglycerin, nitrous oxide-oxygen sedation, and slow delivery of an anesthetic with epinephrine (1:1,00,000) coupled with aspiration.

51. CONCLUSIONS Circulation failure of severe   is the main cause of death. Early and appropriate circulation support is very important to reduce mortality. Patients with a wide variety of cardiovascular diseases are frequently encountered in dental practice and it is necessary to treat them. Safe and effective dental management of such patients requires close medical and dental coordination, an understanding of the potential hazards during dental treat ment , knowledge of drugs used in treatment of cardiovascular diseases, and the potential adverse effects of drugs commonly used in periodontal practice.

52. REFERENCES Textbook of Pathology HARSH MOHAN Textbook of Periodontology CARANZA 14 th EDITION Textbook of periodontology PERIOBASICS Dental considerations in cardiovascular patients: A practical perspective