CARDIOVASCULAR DISEASES

1. CARDIOVASCULAR DISEASES

2. REVIEW • How many chambers are in the heart? • How does the blood flow through the heart? • What vessels take blood AWAY from the heart? • What vessels take blood TO the heart? • What is Pulse Pressure? • What is Cardiac Output? • What is Stroke Volume?

3. Terms associated with Stroke Volume • Preload – degree of stretch of the cardiac muscle fibers at the end of diastole • Direct effect on stroke volume: more blood then causes more effective contraction • Afterload – pressure the ventricle myocardium must overcome to eject blood during systole • Systemic vascular resistance - resistance of the systemic pressure to the left ventricle ejection

4. Pulmonary vascular resistance - resistance of the pulmonary pressure to the right ventricle ejection • Ejection fraction – percentage of the end – diastole volume that is ejected with each stroke (42 – 50%) (used to assess contractility) • Contractility – the force generated by the contracting myocardium under any given condition • Increased contractility leads to increased stroke volume

5. Effects of Aging • Aging heart muscle can provide adequate CO until emotional /physiological stress • Less activity can lead to left ventricular atrophy • Decreased elasticity and widening of the aorta • Thickening & rigidity of the cardiac valves • Increased connective tissue in the SA & AV nodes • LEADS to decreased contractility, increased left ventricular ejection, & delayed conduction

6. Differences in Males & Females • WOMAN HEART • Smaller in size • Smaller coronary arteries • Occlude easier with atherosclorosis • Makes angioplasty more difficult • Higher stroke volume, ejection fraction, resting HR • Shorter SA to AV node conduction

7. Differences continued • Female hormones such as estrogen protect women from developing coronary artery disease (CAD) • Estrogen affects • cholesterol level • Reduce LDL • Increases HDL • Improve blood flow • Menopause – decreased estrogen causes women to be at equal risk for CAD with men

8. Signs & Symptoms to evaluate • Chest discomfort • Angina Pectoris • MI • SOB • Left ventricular failure; CHF • Edema/weight gain • Rt ventricular failure; CHF • Palpitations • Dysrhythmias; valvular disease; ventricular aneurysm; electrolyte imbalance • Fatigue • Associated with numerous heart conditions • Dizziness • Postural hypotension; dysrhythmias; vasovagal effect; cerebrovascular disorders

9. Activity & Exercise on Heart disease • Decreases in activity tolerance are usually gradual • Easily Fatigued after activity is an early indication of progressing disease • After activity, patients may experience chest pain, SOB, palpitations

10. Sleep & Rest • Progressing disease has symptoms when the patient is at rest • Increasing the number of pillows to sleep • Awakening due to SOB (paroxysmal noturnaldyspnea) • Awakening chest discomfort

11. Pulse Pressure • Systole – Diastole= Pulse Pressure • Normal: 30 – 50 mmHg • Increases in conditions that increase stroke volume • Anxiety • Exercise • bradycardia • Decreases in abnormal conditions • Shock • Heart failure • hypovolemia

12. Postural (orthostatic) pressure • When BP drops significantly after the patient assumes the upright position • Symptoms • Dizziness • Lightheadedness • syncope • Causes • Hypovolemia • Inadequate vasoconstrictor mechanisms • Insufficient autonomic effect on vascular constriction

13. Assessing Orthostatic hypotension • Have the patient lie supine & flat as symptoms permit for 10 minutes before taking BP & HR • Check supine before doing upright measurement • Check & compare supine, sitting, & standing pressures & HR • Wait 1 – 3 minutes after each postural change before measuring BP

14. NORMAL findings • LYING to sitting/standing • HR increases 5 – 20 beats above resting • Systole is the same or slightly decreases (w/in 10 mm Hg) • Slight increase in diastole (5 mm Hg)

15. Auscultation of the heart • Aortic area – 2ndintercostal space Rt of sternum • Pulmonic area – 2ndintercostal space LT of sternum • Erb’s point – 3rdintercostal space to LT • Right ventricular/tricuspid area – 4th & 5th IC to left @ midclavicular line • Left ventricular/apical area – 5th IC to left sternum @ midclavicular line • Epigastric area – below the xiphoid process

16. Heart Sounds • S1 – closing mitral /tricuspid valve • Heard loudest at the apex • Systole • S2 – closing aortic & pulmonic valves • Sometimes the pulmonic is slightly late causing a split S2 • Heard loudest at the base of the heart • Diastole

17. Gallop – blood filling the ventricles is impeded during diastole • Sounds like a galloping horse • During rapid ventricular filling • CHF: myocardial disease; ventricles fail to eject all blood during systole • Snaps & Clicks • Stenosis of the mitral valve • Early in diastole that is high pitched best heard at left sternal border

18. Murmurs – turbulent flow of blood\critically narrowed valve • Malfunctioning valve allowing regurgitant blood flow • Defect of the ventricular wall • Defect between the aorta & pulmonary artery • Friction Rub • Pericarditis • Grating sound heard in systole & diastole • Abrasion of the pericardial surface during cardiac cycle

19. Inspecting Extremities • Capillary Refill – slow peripheral flow rate • Vascular changes • Hematoma • Peripheral edema • Clubbing • Lower extremity ulcers – may be present in arterial and/or venous insufficiency

20. Respiratory findings related to CV disease • Tachypnea – heart failure • Cheyne – Stokes respirations – Severe Left ventricular failure • Dry, hacky cough – pulmonary congestion r/t heart failure • Crackles – heart failure • Wheezes – pulmonary edema or SE of beta blockers (heart medication)

21. Cardiac Enzymes • Are elevated during/after MI • Released from injured cells when the cell membranes rupture due to prolonged hypoxia • Isoenzymes come only from cardiac cells • CreatineKinase (CK) & CK – MB are the most specific for MI; they are the first to elevate • lactic dehydrogenase & its isoenzyme elevate 2 – 3 days later • Troponin I is a contractile protein only in cardiac muscle. Elevates within 3 – 4 hours after insult

22. Cholesterol Levels & HDL, LDL • Cholesterol should be less than 200 mg/dL • Used for what? • Where is it found? • Sources? • Contributing factors: age, gender, diet, exercise, & stress • LDL – normal is less than 130 mg/dL • Primary transporter of cholesterol into cell • HDL – normal MALE: 35 – 65 FEMALE: 35 – 85 • Transport cholesterol away from the cell to the liver for excretion

23. Electrolytes • Sodium • Fluid balance • Hyponatremia – fluid excess • Hypernatremia – fluid deficit • Magnesium – absorption of CA & maintains K+ stores; • Hypomagnesemia – lengthens QT interval • Calcium • Blood coagulability & neuromuscular activity • Hypocalcemia/hypercalcemia – causes dysrhythmia • Potassium • Affected b/ renal function • Decreased by diuretic (used to treat CHF) • Hypokalemia – cardiac irritability • Hyperkalemia /hypokalemia – lead to ventricular fibrillation or cardiac standstill

24. Coagulation studies • Formation of a thrombus is initiated by injury to a vessel wall or tissue • Partial thromboplastin time (PTT) • Measure the activity of the intrinsic pathway • Normal: 25 – 38 seconds • Prothrombin time (PT) • Measures the extrinsic pathway activity & monitored during anticoagulation therapy • Normal: less than 13 seconds • International Normalized Ratio (INR) • Provides a standard method for reporting PT • Patient receiving anticoag therapy: 2.0 – 3.0 • Heparin & Coumadin – drugs that provide anticoagulation therapy

25. ECG • Universal diagnostic tool • 12 Lead shows the activity from 12 different views • Used to diagnose dysrhythmias, conduction abnormalities, enlarged heart chambers, myocardial ischemia/infarction • Hypo/hyper calcemia; hypo/hyper kalemia

26. Reading EKG’s • Waveform represents the functions of the heart’s conduction activity • Printed on graph paper • Time & rate measured on horizontal axis • Amplitude or voltage is measured on vertical axis • Represented by P Q R S T

27. P wave – is the electrical impulse from the SA node through the atria (atrial depolarization) • Normal: 2.5 mm or less in height and .11 second duration • QRS Complex – ventricular muscle depolarization; less than .12 seconds in duration • Depression after P wave is the Q wave that is .04 seconds • Positive deflection after P wave is R wave • Negative deflection after R is the S wave

28. T wave – represents ventricular muscle repolarization (resting state); after QRS wave & usually in the same direction of the QRS complex • U wave – represents the repolarization of Purkinje fibers; may be seen in hypokalemia or HTN • PR interval – beginning of P wave to beginning of QRS complex. • Time for SA node stimulation, atrial depolarization, & conduction through the AV node • Normal .12 - .20 seconds

29. ST segment – early ventricular repolarization; lasts for end of QRS to beginning of T wave • Beginning of ST segment is identified by a change in the thickness of the terminal portion of the complex • QT interval – total time for ventricular depolarization & repolarization ; beginning of QRS to end of T wave • .32 - .40 seconds

30. Interpreting EKG • 1 minute strip has 300 large squares & 1500 small squares • 15 large boxes in 3 seconds; 5 lg boxes/1 sec • Calculate the HR: count the R peaks in 6 seconds & multiply by 10 • If the R peaks are equal distance apart, then the rate is regular

31. Dysrhythmia disorders • Formation of new electrical activity or alteration in the electrical activity • Review of normal conduction • What are the structures & the steps to electrical activity?

32. Sinus Bradycardia • SA node fires at a slower than normal rate • Slower metabolic needs, vagal stimulation, medications, increased ICP, MI (inferior wall) • Sinus Tachycardia • Faster than normal rate • Blood loss, anemia, shock, hypervolemia, hypovolemia, CHF, pain, fever, exercise

33. Sinus Arrhythmia • SA nodes creates an irregular rhythm; increases during inspiration & decreases during expiration • Causes: heart disease, valvular disease

34. Atrialdysrhythmia • Atrial Flutter • Atrium beats 250 – 400 times/minute • Too fast for the AV node to send all to ventricles • Atrial Fibrillation

35. Inflammatory Disorders • Endocarditis – inflammation of endocardium • Bacterial – leaflets of the mitral valve erode due to bacteria • Libman – Sacks – found in patients with lupus • Myocarditis – inflammation of the muscle • Acute (usually caused by a virus) • Chronic • Pericarditis – inflammation of the sac/outer layer • Acute • Chronic

36. Valvular Disease • Mitral Valve Prolapse • Usually benign • Causes • Calium degeneration • Inflammatory endocarditis • MI • Complications • Arrhythmia • Cardiomyopathy • Heart failure

37. Mitral Valve Stenosis • Hardening of the mitral valve caused by calcification/fibrosis • Narrowing of the valve opening • Dialation of the left atrium • S & S • Dyspnea on exertion • Paroxysmal nocturnal dyspnea/orthopnea • Fatigue/weakness • Right sided heart failure • crackles

38. Aortic Stenosis • Congenital aortic valve defect • Due to rheumatic fever • Treatment • Digoxin Nitroglycerine • Diuretics • S & S • Exertionaldyspnea • Syncope • Angina, palpitations • Left sided failure

39. Hypertension • Essential – progressive • 90% cases • Could be from mechanisms that: • Control cardiac output • Systemic vascular resistance • Blood volume • Secondary • Caused by another disorder • Less than 10% cases

40. Silent Killer • Affects other organs in the body • Brain • Narrowed blood vessels will have clotted blood & cause strokes • Weakened blood vessel walls can lead to hemorrhage • Eyes • Increased BP cause hemorrhage in retina • Swelling of optic disc leads to blindness • Kidneys • Arterioles harden & restrict O2 to glomeruli

41. Different Drugs for HTN • Diuretics • Beta Blockers • ACE Inhibitors

42. Thiazide Diuretics • Generic: Hydrochlorothiazide • Effective & most cost-efficient • Usually tried first • Increases excretion of water, sodium, chloride, & potassium • Treats: edema, uncomplicated HTN, prophylaxis of kidney stones, electrolyte imbalance • SE: Hypokalemia, hypochloremia, muscle weakness, postural hypotention, vertigo, HA, fatigue, lethargy, hyperglycemia, elevated uric acid • CI: diabetes, gout, severe renal disease, impaired liver function • Interactions: NSAIDS, corticosteroids, digitalis

43. Beta-Adrenergic Blocker • Inderal (propranolol) & Tenormin (atenolol) • Used in patients with angina, postmyocardial infarction • SE: hypotension, vertigo, syncope, bradycardia, irritability, confusion, insomnia, N & V, Brochospams (in asthma), hypoglycemia, • CI: Major surgery, diabetes, renal or liver impairment, bradycardia, asthma, COPD • Interactions: Antidepressants • Potentiate the hypotensive effects in: • Diuretics • Tranquilizers • Tagamet • Other cardiac drugs • alcohol

44. Calcium – Channel blockers • Cardizem (diltiazem) & Procardia (nifedipine) • Used in patients with diabetes or high coronary risk • Suppress the Calcium in muscle contraction; reducing excitability & dilates coronary arteries • SE: hypotension, HA, vertigo, bradycardia, edema, N, constipation, & abdominal discomfort • CI: heart block, heart failure, pregnancy, children • Interaction: lithium, diuretics, barbiturates

45. ACE Inhibitors • Angiotensin – converting enzyme inhibitors • Catopril & enalapril • Decreases vasoconstriction (no change in CO or HR) • Usually used with diuretic therapy • Used in patients with heart disease, diabetes, renal disease • SE: rash, loss of taste perception, severe hypotension, chronic dry cough, nasal congestion, hyperkalemia • CI: Lupus, heart failure, angioedema, pregnancy • I: diuretics, vasodilators, K+ sparing diuretics, NSAIDS

46. Heart Failure • Myocardium can’t pump effectively enough to meet the body’s needs • Possible Causes • Increased pressure/volume resulting myocardial function • Left ventricular remodeling • Altered hemodynamics to maintain CO • Hormonal changes that accelerate HR & increase EF

47. Classifications • Right or Left sided • Right – result of ineffective Rt ventricular contraction due to infarction, PE, back flow due to Lt side failure • Left – ineffective Lt ventricular contraction leading to pulmonary congestion & decreased CO • Systolic or diastolic • Systolic – LT ventricle can’t pump to body • Diastolic – left ventricle can’t relax & fill appropriately leading to decreased SV • Acute or chronic • Acute – the compensatory mechanisms kick in; fluid status is normal • Chronic – S & S present for some time, compensatory mechanisms kicked in & fluid overload is present

48. Signs & Symptoms Left RIGHT Edema Jugular vein distention Hepatomegaly Generalized weight gain • Dyspnea • Cough • Tachycardia • Fatigue • Muscle weakness • Edema • Weight gain • Crackles

49. Cardiomyopathy • Refers to the disease of the heart muscle fibers • 3 classes • Dilated - affects systolic function • Hypertrophic – primarily affects diastolic function • Restrictive – stiffness of the ventricle caused by left ventricular hypertrophy or endocardial fibrosis

50. CAD (Coronary Artery Disease) • Progressive buildup of atherosclerotic plaque in the coronary arteries • Risk factors • High LDL’s • Uncontrolled HTN • Sex (Men are more prone) • Smoking • Heredity