Cardiovascular System

1. Cardiovascular System Mr Ogundele

2. Diagnostic Studies • Chest X-ray Examination. A chest x-ray examination shows the size, position, contour, and structures of the heart. It shows heart enlargement, calcifications, and fluid around the heart. • Magnetic Resonance Imaging. A three-dimensional image of the heart is produced by magnetic resonance imaging (MRI). Patients such as those with pacemakers or metal implants, metal shavings, or shrapnel are not candidates for this test.

3. Diagnostic Studies • Electrocardiogram. The electrocardiogram (ECG) assesses the electrical activity of the heart from different views. The ECG shows abnormalities related to conduction,rate, rhythm, heart chamber enlargement, myocardial ischemia, myocardial infarction, and electrolyte imbalances • Echocardiogram. An echocardiogram is an ultrasound test that records the motion of the heart structures, including the valves, as well as the heart size, shape, and position.

4. Diagnostic Studies • Transesophageal Echocardiogram. Transesophageal echocardiogram provides a clearer picture than transthoracic echocardiography. It produces images by using a transducer on a probe that is placed in the esophagus. The images are clearer because lung and rib tissue does not have to be penetrated by the sound waves. • Positron Emission Tomography. Positron emission tomography (PET) shows myocardial perfusion and viability with three-dimensional images.

5. Diagnostic Studies • C-reactive Protein (CRP). C-reactive protein is a newer test for assessing cardiac disease risk. Elevated cardiac CRP levels can indicate low-grade inflammation in coronary vessels. • Cardiac Troponin. Cardiac muscle contains proteins called troponins, which control the muscle fibers that contract or squeeze the heart muscle. Troponin I and troponin T are highly sensitive indicators of myocardial damage, which is helpful in diagnosing MI. They are proteins found only in cardiac cells.

6. Diagnostic Studies • Cardiac Enzymes. When heart cells are damaged or die, they rupture and release enzymes into the bloodstream. Levels of these enzymes rise in the serum as a result. A common cardiac enzyme test is creatinekinase (CK), also referred to as creatinephosphokinase (CPK). It is often ordered with troponin tests. • CreatineKinase. Creatinekinase (CK) is found in three types of tissue: brain, skeletal muscle, and heart muscle. Isoenzymes of CK contained in these tissues are CK-BB (brain), CK-MM (skeletal muscle), and CK-MB (heart muscle). Levels of CK-MB rise within 4 to 6 hours after cardiac cells are damaged, peak in 12 to 24 hours, and return to normal in 48 to 72 hours.

7. Diagnostic Studies • Angiography. Arteriography and venography are the two types of angiography. Arteriography examines arteries. Venography studies veins. Angiography uses dye injected into the vascular system to visualize the vessels on radiographs. • Cardiac Catheterization. Cardiac catheterization allows the study of the heart’s anatomy and physiology. It is an invasive diagnostic procedure that measures pressures in the heart chambers, great blood vessels, and coronary arteries and provides information on cardiac output and oxygen saturation.

8. Nursing Diagnosis • Activity intolerance related to decreased perfusion • Impaired gaseous exchange related to cardiac failure • Self care deficit , bathing/hygiene, toileting, dressing related to fatigue, weakness or dyspnea • Ineffective tissue perfusion related to vascular damage

9. Pericarditis • Pericarditis is an acute or chronic inflammation of the pericardium (the sac surrounding the heart).

10. Pathophysiology • Acute pericarditis can be caused by Infections, renal, trauma, drug reactions etc. It resolves usually in less than 6 weeks but recurrence is possible.

11. Pathophysiology • Chronic constrictive pericarditis is the result of fibrous scarring of the pericardium. • The heart becomes surrounded by a thickened, stiff sac that limits the stretching ability of the heart’s chambers for filling. It results from neoplastic disease and metastasis, radiation, or tuberculosis.

12. Pathophysiology • Pericarditis can lead to an accumulation of fluid in the pericardial sac (pericardial effusion) and increased pressure on the heart, leading to cardiac tamponade. • This may also lead to thickening and decreased elasticity that restrict the heart’s ability to fill properly with blood.

13. Patho • The pericardium may become calcified, further restricting ventricular expansion during ventricular filling (diastole). • With less filling, the ventricles pump out less blood, leading to decreased cardiac output. • Restricted diastolic filling may result in increased systemic venous pressure, causing peripheral edema and hepatic failure.

14. S/S • Sharp substernal pain with radiation to the neck and shoulders and sometimes the back • Pericardial friction rub • Other symptoms depend on the cause of the pericarditis and may include dyspnea, low-grade fever, and cough. • Chronic constrictive pericarditis produces the signs and symptoms of right-sided heart failure.

15. Diagnosis • Complete blood cell count • Electrocardiogram • Echocardiogram • MRI • CT

16. Management • Analgesics and NSAIDs such as aspirin or ibuprofen • Corticosteroids eg, prednisone • Pericardiocentesis • Chronic constrictive pericarditis is treated with pericardiectomy,

17. Nursing Management • Nursing care focuses on relieving the patient’s pain and anxiety and maintaining normal cardiac function. • Encourage patient to assume a position of comfort e.g by sitting up and leaning forward. • Monitor vital signs and observing for the presence of symptoms of cardiac tamponade or heart failure.

18. MGT • Teaching the patient about pericarditis and its treatment relieves anxiety and allows a feeling of control by allowing the patient to make knowledgeable health-care decisions. • Provide psychological support

19. Cardiac tamponade • Pericardial/cardiac tamponade is an acute condition in which fluid in the pericardial sac causes impaired ventricular filling. Causes • The commonest cause of tamponade is malignancy. It may occur with other causes of pericarditis and effusion and also as a post-traumatic or post procedure complication

20. Cardiac tamponade • The pericardium is a non-distensible bag around the heart. • Once the space between the pericardium and the heart becomes full of fluid the ventricles are prevented from filling properly during diastole thus reducing the cardiac output.

21. Clinical features • Hypotension with sinus tachycardia and a raised JVP, • The pulse is of low volume and reduced on inspiration (pulsus paradoxus). • Oliguria or anuria develops • shock. Investigations • Echocardiogram • X ray • ECG

22. Management • If there is compromise of the cardiac output, needle aspiration of the pericardium should be performed via the xiphisternal route, preferably under radiographic guidance. • The relief following pericardiocentesis is often temporary, so a fine catheter should be inserted for continuous drainage until the underlying condition is corrected.

23. Cardiomyopathy • Cardiomyopathy is an enlargement of the heart muscle. • There are three types of cardiac structure and function abnormalities in cardiomyopathy: (1) dilated, (2) hypertrophic, and (3) restrictive • A consequence of all types of cardiomyopathy can be heart failure, myocardial ischemia, and myocardial infarction due to reduced cardiac output.

24. Patho Dilated Cardiomyopathy • The size of the ventricular cavity enlarges with reduced cardiac output. • Contractile function decreases as the myocardial tissue is destroyed. • Blood moves more slowly through the left ventricle, which often results in blood clot formation. • This may lead to Left ventricular failure while in the long run an elevated end-diastolic pressure with resultant increase in pressure within the pulmonary circulation and eventually right-sided heart failure.

25. Patho Hypertrophic Cardiomyopathy • Hypertrophic cardiomyopathy is enlargement of the cardiac muscle wall, often of the septum and left ventricle. • This may result in obstruction to the outflow of the left ventricle and this is known as obstructive hypertrophic cardiomyopathy • Hypertrophic cardiomyopathy causes the ventricular wall to be rigid, which decreases ventricular filling.

26. Patho Restrictive Cardiomyopathy • Restrictive cardiomyopathy impairs ventricular stretch and limits ventricular filling. • Cardiac muscle stiffness is present with no ventricular dilation, although systolic emptying of the ventricle remains normal.

27. S/S • Manifestation of cardiomyopathy depends on the type of abnormality. Most patients show varying degrees of signs and symptoms of heart failure • Chest pain • Arrhythmias • Dyspnea • Fatigue • Syncope

28. Diagnostic Evaluation • Cardiomegaly is seen on a chest x-ray examination. • Echocardiography shows muscle thickness and chamber size to differentiate between the types of cardiomyopathy. • ECG will display dysrhythmias • Cardiac catheterization is sometimes used to rule out coronary artery disease as a causative factor

29. Management Hypertrophic • β-blockade is the mainstay of treatment as this lowers the pressures within the left ventricle. • Surgical treatment: Occasionally resection of the hypertrophied septal wall (myotomy/myectomy) is indicated. It is usually reserved for severely symptomatic patients.

30. Management Restrictive • No specific treatment. • Low-dose diuretics and vasodilators may provide some relief from symptoms.

31. Management Dilated • General measures include bed rest, fluid restriction and quitting alcohol. • Treatment focuses on the symptoms of heart failure seen. Angiotensin-converting enzyme (ACE) inhibitors, beta blockers, diuretics, and digoxinmay be given to increase cardiac output. • Anticoagulants are given to prevent emboli formation in patients with atrial fibrillation

32. Nursing Management • Obtain patient history • Conduct physical assessment, noting vital signs and any signs or symptoms of heart failure. • Careful monitor the patient to detect complications, such as heart failure, emboli, or dysrhythmias • Maintain normal cardiac function by monitoring vital signs and symptoms of heart failure. • Increasing activity tolerance by planning rest periods, scheduling activities in small amounts, avoiding tiring activities, and providing small meals that require less energy to digest than large meals.

33. Nsg Mgt • Patients are taught to avoid alcohol because it decreases cardiac function • Reduce anxiety by providing explanations for procedures, as well as educating the patient about the disease and its treatment • Provide psychological support.

34. Infective endocarditis • An infection of the endocardium (endothelial lining of the heart and valves). • Males develop IE more often than females. There is a higher incidence of IE in the older adult.

35. Patho • Infective endocarditis may occur on normal endocardium but it is more common on a congenital or acquired cardiac abnormality • The bacteria proliferate on the endocardium, causing the development of friable vegetations containing bacteria, fibrin and platelets. • Damage to valve leaflets occurs as the vegetations grow. As blood flows through the heart, these vegetations may break off and become emboli.

36. Patho • This may result in destruction of valve leaflets, perforation and hence disturbance of function. The disease process predisposes to the formation of thrombus with the potential for emboli. • Cytokine generation causes fever. There is a vasculitis and the formation of immune complexes. • With bacteremia, bacteria attach mainly to the valves of the heart, although any heart endothelial surface can be infected. Heart failure may result from valve damage, especially of the aortic valve.

37. Causes Portals of entry for organisms into the bloodstream result from intravenous (IV) drug use, surgery, dental or invasive procedures, and infections of the skin and gastrointestinal or genitourinary tract. Risk factors include the following: • IV drug use • Compromised immune system • Congenital or valvular heart disease (e.g., mitral valve prolapse with regurgitation, valvularreplacement surgery, or rheumatic carditis) • Gingival gum disease

38. Signs and Symptoms • Fever • Murmur • Night sweats • Fatigue • Weight loss • Weakness • Pain in abdomen, joints, muscles, back • Nailbed splinter hemorrhages • Petechiae Diagnostic Test • Blood cultures • Echocardiography is used to visualise vegetations and to assess the degree of valvular dysfunction • WBC count with differential

39. Management • IV antimicrobial medications such as penicillin, vancomycin, amphotericin B (to cure infection) • Antipyretics (to reduce fever) • Rest (to decrease cardiac workload) • Surgical valve replacement (to restore normal valve function) • Recovery from the disease can be greatly improved with surgery. Antimicrobial therapy continues after surgery.

40. Hypertension Hypertension can be defined as persistent high blood pressure (BP). • Normal :A systolic BP <120 mmHg or a diastolic BP < 80 mmHg. • Prehypertension :A systolic BP between 120-139 mmHg or a diastolic BP between 80-89 mmHg. • Grade 1 (mild): A systolic BP of ≥140 mmHg or a diastolic BP of ≥90 mmHg • Grade 2 (moderate): A systolic BP of ≥160 mmHg or a diastolic BP of ≥100 mmHg • Grade 3 (severe): A systolic BP of ≥180 mmHg or a diastolic BP of ≥110 mmHg

41. Aetiology • It can either be a primary (essential) and secondary hypertension: Essential hypertension (>90%) • is the chronic elevation of blood pressure from an unknown cause. Risk factors include • Non-modifiable: Genetic (racial and familial), gender (males higher). • Modifiable: Obesity, alcohol intake, diet (especially high salt intake).

42. HTN • Secondary hypertension (<10%) • Renal (80%): Most commonly glomerulonephritis, and polycystic kidneys. • Endocrine causes: Acromegaly, Cushing’s syndrome, • Pregnancy (pre-eclampsia). • Drugs: Oral contraceptives, NSAIDs, steroids.

43. Patho • Blood pressure equals the amount of blood pumped out by the heart (cardiac output) multiplied by the peripheral vascular resistance. • If the caliber of blood vessel becomes smaller because of atherosclerosis or vasoconstriction, blood pressure increases in an effort to force the blood through the small opening. • Factors that impair normal regulation of blood pressure may lead to hypertension. Many of these factors are not well understood.

44. Patho • Some of this factors are • Sympathetic nervous system overstimulation, which causes vasoconstriction, can contribute to hypertension. • Alterations in baroreceptors and chemoreceptors may also influence the development of hypertension. • Increase in hormones that cause sodium retention, such as aldosterone, lead to increased fluid retention. • Changes in kidney function that alter the excretion of fluid also result in an increase in overall body fluid that may contribute to hypertension

45. Patho • Blood pressure can be raised via sympathetic nervous system (by causing peripheral vasoconstriction and increased heart rate) In response to either physical or emotional activities that require more oxygen for the organs and tissue. • In some instances, kidney can secrete excess renin, renin acts on a substance called angiotensinogen, coverts it to angiotensin I, angiotensin I is converted to angiotensin II by ACE.

46. Patho. • Angiotensin II acts directly on the blood vessels causing them to constrict and stimulate the adrenal gland to release aldosterone. • Aldosterone, secreted by the adrenal cortex, increases the reabsorption of sodium ions by the kidneys

47. Patho. • Water follows the sodium back to the blood; this increases blood volume & B/P • The whole process leads to sodium and water retention causing increased cardiac output and elevation of blood pressure

48. Malignant Hypertension • Is used to describe rapidly progressive moderate to severe hypertension that is difficult to control. Diastolic pressure ranges from 140 to 170 mmHg and unless effective intervention is found, pt may suffer brain, kidney and heart damage

49. Signs and Symptoms • HTN is a silent disease and signs may only appear in the later stage when damage has already been done to major organ ( e.g renal ischemia, aortic aneurysm, left ventricular hypertrophy etc). Some Symptoms that patients may complained of are: • Headache • Dizziness • Blurred vision • Blackouts • Fatigue • Nervousness

50. Diagnostic test • ECG, blood glucose, hematocrit, serum potassium, calcium, lipoprotein profile, high-density • low-density lipoprotein cholesterol (HDL-C and LDLC, respectively), and triglyceride levels