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Unit 2 Pathophysiology. Cardiovascular Diseases
- 1. Cardiovascular Diseases Subject: PATHOPHYSIOLOGY UNIT-II •Prepared by: Mr. Kajale F.V. • (M. Pharm Pharmacology) • SHIVAI CHARITABLE TRUST’S COLLEGE OF PHARMACY.
- 2. HYPERTENSION • Hypertension: •It is also commonly known as high blood pressure, is a serious medical condition that affects millions of people worldwide. It is often referred to as the "silent killer" because it often has no noticeable symptoms, yet it can significantly increase the risk of heart disease, stroke, kidney failure, and other health problems. • Understanding Blood Pressure: • Blood pressure is the force exerted by your blood against the walls of your arteries as your heart pumps blood throughout your body. • Systolic pressure: The top number, which represents the pressure in your arteries when your heart beats. • Diastolic pressure: The bottom number, which represents the pressure in your arteries between heartbeats. • Normal Blood Pressure: • Less than 120/80 mmHg (millimeters of mercury)
- 3. • High BloodPressure Categories: • Systolic pressure between 120 and 129 mmHg Diastolic pressure less than 80 mmHg • Stage 1 high blood pressure: • Systolic pressure between 130 and 139 mmHg or Diastolic pressure between 80 and 89 mmHg • Stage 2 high blood pressure: • Systolic pressure of 140 mmHg or higher or Diastolic pressure of 90 mmHg or higher • There are two main types of hypertension: • Primary (essential) hypertension: • This is the most common type, and the exact cause is unknown. It is likely a combination of genetic and environmental factors, such as: • Family history: Having a family member with high blood pressure increases your risk. • Diet: A diet high in salt, saturated fat, and cholesterol can increase your risk. • Lack of physical activity: Being inactive increases your risk. • Being overweight or obese: Excess weight puts extra strain on your heart and arteries.
- 4. • Smoking: Smokingdamages your blood vessels and increases your risk of high blood pressure. • Excessive alcohol consumption: Heavy drinking can raise your blood pressure. • Stress: Chronic stress can contribute to high blood pressure. • Secondary hypertension: • Kidney disease: Kidneys play a role in regulating blood pressure, and when they are not working properly, blood pressure can rise. • Artery stenosis: Narrowing of the arteries can increase blood pressure. • Hormonal imbalances: Certain hormonal imbalances can also cause high blood pressure. • Symptoms of Hypertension: 1. Headaches 2. Shortness of breath 3. Nose bleeds ,Fatigue 4. Vision changes 5. Chest pain
- 5. CONGESTIVE HEARTFAILURE, • The term congestive heart failure (CHF) is used for the chronic form of heart failure in which the patient has evidence of congestion of peripheral circulation and of lungs. 1. Intrinsic Pump Failure i. Ischaemic heart disease ii. Myocarditis iii. Cardiomyopathies iv. Metabolic disorders e.g. beriberi v. Disorders of the rhythm e.g. atrial fibrillation and flutter. 2. Increased Workload on The Heart i. Increased pressure load: a) Systemic and pulmonary arterial hypertension. b) Valvular disease e.g. mitral stenosis, aortic stenosis, pulmonary stenosis.
- 6. ii. Increased volumeload a) Valvular insufficiency b) Severe anaemia c) Thyrotoxicosis (too much thyroid hormone. ) d) Arteriovenous shunts (abnormal connection between an artery and a vein) e) Hypoxia due to lung diseases. 3. Impaired Filling of Cardiac Chambers a) Cardiac tamponade e.g. Haemopericardium, Hydropericardium b) Constrictive pericarditis. • TYPES OF HEART FAILURE 1. Acute heart failure 2. Chronic heart failure 3. Left-sided and right-sided heart failure 4. Backward and forward heart
- 7. • Acute HeartFailure • Acute heart failure Sudden and rapid development of heart failure occurs in the following conditions: i) Larger myocardial infarction ii) Valve rupture iii) Cardiac tamponade iv) Massive pulmonary embolism v) Acute viral myocarditis vi) Acute bacterial toxaemia. • In acute heart failure, there is sudden reduction in cardiac output resulting in systemic hypotension but oedema does not occur. Instead, a state of cardiogenic shock and cerebral hypoxia develops.
- 8. • Chronic heartfailure • Chronic heart failure develops slowly as observed in the following states: i) Myocardial ischaemia from atherosclerotic coronary artery disease ii) Multivalvular heart disease iii) Systemic arterial hypertension iv) Chronic lung diseases resulting in hypoxia and pulmonary arterial hypertension v) Progression of acute into chronic failure. • In chronic heart failure, compensatory mechanisms like tachycardia, cardiac dilatation and cardiac hypertrophy try to make adjustments so as to maintain adequate cardiac output. • This frequently results in well-maintained arterial pressure and there is accumulation of oedema.
- 9. Left SidedHeart Failure • Left-sided heart failure It is initiated by stress to the left heart. i) Systemic hypertension ii) Mitral or aortic valve disease (stenosis) iii) Ischaemic heart disease iv) Myocardial diseases e.g. cardiomyopathies, myocarditis. v) Restrictive pericarditis. Right-sided heart failure i) As a consequence of left ventricular failure. ii) Cor pulmonale in which right heart failure occurs due to intrinsic lung diseases iii) Pulmonary or tricuspid valvular disease. iv) Pulmonary hypertension secondary to pulmonary thromboembolism. v) Myocardial disease affecting right heart. vi) Congenital heart disease with left-to-right shunt.
- 11. • Backward andForward Heart Failure • Backward Heart Failure:(Left-sided Heart Failure) • In this condition, one of the ventricles (usually the left ventricle) fails to pump out all the blood that enters it. As a result, the ventricular filling pressure increases, leading to systemic or pulmonary edema (fluid accumulation in the body or lungs). • Essentially, the heart struggles to effectively move blood forward, causing fluid to back up. • This type of heart failure is associated with congestion and increased pressure in the circulatory system. • Forward Heart Failure:(Right-sided Heart Failure) • In forward heart failure, the heart is unable to pump out enough blood to meet the body’s cellular needs. As a result, excess fluid retention occurs, leading to edema (swelling) in various parts of the body. The heart’s inability to deliver sufficient blood to tissues and organs results in symptoms related to inadequate perfusion.
- 13. • Ischemic HeartDisease • Arteriosclerosis is a general term that refers to the thickening and hardening of the arteries. Cause: • Loss of elasticity: Over time, the arteries naturally lose some of their elasticity, making them less flexible. • Scar tissue buildup: Injuries or inflammation in the arteries can lead to scar tissue formation, contributing to stiffness. • Calcium deposits: Calcium can build up in the arterial walls, further stiffening them. I. Senile arteriosclerosis (affects arteries) II. Hypertensive arteriolosclerosis (affects arterioles) III. Monckeberg's arteriosclerosis (Medial calcific sclerosis) (affects arteries) IV. Atherosclerosis (affects arteries)
- 14. • Angina • Anginapectoris, commonly known as angina, is a type of chest pain that occurs when part of the heart muscle doesn’t receive enough oxygen-rich blood. • It serves as a symptom of coronary artery disease, which develops when the heart’s arteries become partially or completely blocked. The discomfort associated with angina is often labeled as squeezing, pressure, heaviness, tightness, or pain in the chest. It may feel like a heavy weight pressing down on the chest. • Pathophysiology: • Angina arises from myocardial ischemia, a state where the heart muscle is deprived of adequate oxygen-rich blood. The most frequent cause is coronary artery disease (CAD), characterized by atherosclerotic plaque buildup narrowing or occluding the coronary arteries supplying the heart. Additionally, coronary artery spasm and severe anemia can contribute to angina development.
- 15. o Types ofAngina i) Stable or typical angina ii) Prinzmetal’s variant angina iii) Unstable or crescendo angina i. Stable or typical angina • Stable or typical angina is characterised by attacks of pain following physical exertion or emotional excitement and is relieved by rest. The pathogenesis of condition lies in chronic stenosing coronary atherosclerosis that cannot perfuse the myocardium adequately when the workload on the heart increases. • During the attacks, there is depression of ST segment in the ECG due to poor perfusion of the subendocardial region of the left ventricle but there is no elevation of enzymes in the blood as there is no irreversible myocardial injury.
- 16. ii. Prinzmetal’s variantangina • This pattern of angina is characterised by pain at rest and has no relationship with physical activity. • The exact pathogenesis of Prinzmetal’s angina is not known. It may occur due to sudden vasospasm of a coronary trunk induced by coronary atherosclerosis, or may be due to release of humoral vasoconstrictors by mast cells in the coronary adventitia. iii. Unstable or crescendo angina • Also referred to as ‘pre-infarction angina’ or ‘acute coronary insufficiency’, this is the most serious pattern of angina. It is characterised by more frequent onset of pain of prolonged duration and occurring often at rest. It is thus indicative of an impending acute myocardial infarction. • Multiple factors are involved in the pathogenesis of unstable angina which include: stenosing coronary atherosclerosis, complicated coronary plaques (e.g. superimposed thrombosis, haemorrhage, rupture, ulceration etc), platelet thrombi over atherosclerotic plaques and vasospasm of coronary arteries.
- 18. • Myocardial Infarction(MI) • Myocardial infarction (MI), commonly referred to as a heart attack, represents a critical cardiovascular event arising from significant coronary artery obstruction. • This obstruction dramatically reduces blood flow to a segment of the heart muscle, leading to ischemia (oxygen deprivation) and subsequent cell death (infarction) in the affected region. • Etiology: • Atherosclerosis, the progressive buildup of plaque within the coronary arteries, is the leading cause of MI. Plaque formation narrows the arterial lumen, ultimately leading to critical stenosis and compromised blood flow. • Symptoms: 1. Chest pain or discomfort, which may radiate into the shoulder, arm, back, neck, or jaw. 2. Shortness of breath, nausea, feeling faint, cold sweat, fatigue, and decreased consciousness. 3. Neck pain, arm pain, or feeling tired.
- 20. • Respiratory system:Asthma • Asthma is a chronic inflammatory disease of the airways in the lungs. These airways, called bronchi, become inflamed and narrowed, making it difficult to breathe. This can lead to symptoms like wheezing, coughing, shortness of breath, and chest tightness, particularly at night or during exercise. • Symptoms: • Wheezing: A whistling sound during breathing, caused by narrowed airways. • Coughing: Especially at night or early morning, often productive (with mucus). • Shortness of breath: Difficulty catching your breath, a feeling of suffocation. • Chest tightness: A sensation of pressure or tightness in the chest. 1. Extrinsic (atopic, allergic) asthma: It usually begins in childhood or in early adult life. Most patients of this type of asthma have personal and or family history of preceding allergic diseases such as rhinitis, urticaria or infantile eczema. Hyper sensitivity to various extrinsic antigenic substances or allergens is usually present in these cases. e.g. house dust, pollens, animal danders, moulds etc.
- 21. 2. Intrinsic (idiosyncratic,non-atopic) asthma • This type of asthma develops later in adult life with negative personal or family history of allergy, negative skin test and normal serum levels of IgE. • Most of these patients develop typical symptom complex after an upper respiratory tract infection by viruses. Associated nasal polypi and chronic bronchitis are commonly present. 3. Mixed type • Many patients do not clearly fit into either of the above two categories and have mixed features of both. Those patients who develop asthma in early life have strong allergic component, while those who develop the disease late tend to be non-allergic. • Either type of asthma can be precipitated by cold, exercise and emotional stress.
- 23. Chronic ObstructivePulmonary Disease • Chronic obstructive pulmonary disease (COPD) or chronic obstructive airway disease (COAD) are commonly used clinical terms for a group of pathological conditions in which there is chronic, partial or complete, obstruction to the airflow at any level from trachea to the smallest airways resulting in functional disability of the lungs i.e. these are diffuse lung diseases. I. Chronic bronchitis II. Emphysema III. Bronchial asthma IV. Bronchiectasis V. Small airways disease (bronchiolitis)
- 24. I. Chronic bronchitisis an inflammatory condition of the lining of the bronchial tubes, which are the airways that carry air to the lungs. Chronic bronchitis causes coughing, wheezing, and shortness of breath. II. Emphysema is a condition that damages the air sacs in the lungs. These air sacs are responsible for exchanging oxygen and carbon dioxide in the bloodstream. When the air sacs are damaged, less oxygen can get into the bloodstream. Emphysema causes shortness of breath and difficulty breathing. III. Bronchial asthma is a chronic inflammatory disease of the airways that causes wheezing, shortness of breath, chest tightness, and coughing. Asthma attacks can be triggered by allergens, irritants, exercise, or emotional stress. IV. Small airways disease (bronchiolitis) is a general term for a group of conditions that cause inflammation and narrowing of the small airways in the lungs. This can cause coughing, wheezing, and shortness of breath. Bronchiolitis is most common in infants and young children.
- 25. • Renal System •ACUTE RENAL FAILURE (ARF) • Is a syndrome characterized by rapid onset of renal dysfunction, chiefly oliguria or anuria, and sudden increase in metabolic waste-products (urea and creatinine) in the blood with consequent development of uraemia. 1. Pre-renal causes • Pre-renal diseases are those which cause sudden decrease in blood flow to the nephron. Renal ischaemia ultimately results in functional dis orders or depression of GFR, or both. 2. Intra-renal causes • Intra-renal disease is characterized by disease of renal tissue itself. These include vascular disease of the arteries and arterioles within the kidney, diseases of glomeruli, acute tubular necrosis due to ischaemia, or the effect of a nephrotoxin, acute tubulointerstitial nephritis and pyelonephritis.
- 26. 3. Post-renal Causes •Post-renal disease is characteristically caused by obstruction to the flow of urine anywhere along the renal tract distal to the opening of the collecting ducts. • This may be caused by a mass within the lumen or from wall of the tract, or from external compression anywhere along the lower urinary tract ureter, bladder neck or urethra. • Symptoms/Causes • Syndrome of acute nephritis (glomerulo nephritis.) • Syndrome accompanying tubular pathology (acute tubular necrosis) • Pre-renal syndrome (hypovolaemia, hypotension, oedema)
- 27. CHRONIC RENALFAILURE (CRF) • Chronic renal failure is a syndrome characterized by progressive and irreversible deterioration of renal function due to slow destruction of renal parenchyma, eventually terminating in death when sufficient number of nephrons have been damaged. • Acidosis is the major problem in CRF with development of biochemical azotaemia and clinical uraemia syndrome. 1. Diseases causing glomerular pathology (Glomerular destruction, glomerulonephritis) 2. Diseases causing tubulointerstitial pathology (Damage to tubulointerstitial tissues results in alterations in reabsorption and secretion of important constituents leading to excretion of large volumes of dilute urine. ) i) Vascular causes ii) Infectious causes iii) Toxic causes
- 28. • Decreased renalreserve • Renal insufficiency • Renal failure(At this stage, about 90% of functional renal tissue has been destroyed.) • End-stage kidney (chronic kidney disease 5%) • Symptoms A. Primary uraemic (renal) manifestations • 1. Metabolic acidosis • 2. Hyperkalaemia • 3. Sodium and water imbalance • 4. Hyperuricaemia • 5. Azotaemia (high levels of nitrogen-containing compounds)
- 29. B. Secondary uraemic(extra-renal) manifestations 1. Anaemia 2. Integumentary system(Deposit of urinary pigment such as urochrome in the skin causes sallow- yellow colour) 3. Cardiovascular system (Fluid retention secondarily causes cardiovascular symptoms such as increased workload on the heart due to the hypervolaemia and eventually congestive heart failure.) 4. Respiratory system (Hypervolaemia and heart failure cause pulmonary congestion and pulmonary oedema due to back pressure) 5. Digestive system (ulcerations in the lining of the stomach and intestines. Subsequent bleeding can aggravate the existing anaemia. Gastrointestinal irritation may cause nausea, vomiting and diarrhoea.) 6. Skeletal system (Osteomalacia, Osteitis fibrosa )
- 30. • References 1. HarshMohan; Text book of Pathology; 6 th edition; India; Jaypee Publications; 2010. 2. Vinay Kumar, Abul K. Abas, Jon C. Aster; Robbins & Cotran Pathologic Basis of Disease; South Asia edition; India; Elsevier; 2014. 3. Guyton A, John .E Hall; Textbook of Medical Physiology; 12 th edition; WB Saunders Company; 2010.