Cardiac study guide PDF

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Summary

A Final review study guide of the cardiovascular system...

Description

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Cardiovascular system : Anatomy & Physiology

Function of circulation:

Blood flow of the heart

Delivers 02, nutrients, hormones and antibodies to organs, tissues and cells. Removes the end product of cellular metabolism.

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Function of the heart Pumps oxygenated blood into the arterial system to supply capillaries and tissue. Pumps oxygen poor blood from the venous system through the lungs to be reoxygenated.

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Anatomy of the heart

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Cone shaped organ located in the mediastinal space. The pericardial sac encases the heart and protects it, lubricates and holds 5-20 ml of pericardial fluid. This has two layers. ❖ the parietal pericardium which is the outer membrane. ❖ the visceral pericardium is the inner membrane attached to the heart.

Consists of 3 layers ❖ ❖

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Epicardium : outermost layer of the heart. Myocardium: middle layer of the heart, the contracting muscle. Endocardium: innermost layer of the heart, lines the inner chambers and the valves.

4 chambers ❖

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Right atrium: carries deoxygenated blood from the body via superior and inferior vena cava. Right ventricle: carries blood from the right atrium and pumps it into the lungs through the pulmonary artery. Left atrium: carries oxygenated blood from the pulmonary veins. Left ventricle: carries oxygenated blood from the left atrium and pumps it into the systemic circuit through the aorta.

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4 valves Two atrioventricular valves that close at the beginning of ventricular contraction. They prevent blood from flowing back into the atria. ❖ ❖

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Tricuspid valve : on the right side of the heart. Bicuspid valve: on the left side of the heart.

Two semilunar valves that prevent blood from flowing back into the ventricles during relaxation. ❖ Pulmonic semilunar valve: between the right ventricle and pulmonary artery. ❖ Aortic semilunar valve: between the ventricle and the aorta.

Electrical conduction: ❖

SA node: pacemaker of the heart and initiates contraction at 60- 100 BPM.

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AV : receives impulses from the SA node initiates and sustains impulses at 40-60 BPM.

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Bundle of His: continuation of the AV node and branches into the the bundle branches which terminate in the purkinje fibers.

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Purkinje fibers: network of conducting strands beneath the ventricular endocardium. They can act as a pacemaker when the SA and AV fail as pace makers. They can sustain at 20-40 BPM.

Coronary arteries ❖

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Right main coronary artery: supplies the right atrium and ventricle, the inferior left ventricle, posterior septal wall, SA and AV nodes. Left main coronary artery: consists of two main branches left anterior descending which supplies blood to the left ventricle and the ventricular septum and circumflex arteries which supply blood to the left atrium and the lateral/posterior aspects of the left ventricle.

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From the superior and inferior vena cava, oxygen poor blood goes to the right atria through the tricuspid valve. Right ventricle to the pulmonary valve. To the pulmonary trunk and arteries into the lungs CO2 is lost and 02 is gained in the pulmonary capillaries. O2 rich blood enters the pulmonary veins to the left atrium. Blood travels through the bicuspid valve and enters the left ventricle. Blood moves through the aortic valve and travels through the aorta to the systemic circuit.

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Hypertension What am I? An elevation in blood pressure above normal range. ❖ Prehypertension: 120-139/80-90 mmhg ❖ Stage1: 140-159/ 90-99 mmhg ❖ Stage 2: > 160/99 mmhg Major risk factor for diseases such as: ❖ Coronary, ❖ Cerebral, ❖ Renal, and ❖ PVD.

Assessment: CNS: Visual changes, dizziness, tinnitus,headache. HEART : Increased HR, flushed face. RESP : Chest pain. MISC.: Epistaxis. ❖ ❖ ❖ ❖

Teaching:

H: Headaches E: Epistaxis A: Asymptomatic R: Really bad chest pain T : Tinnitus

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cardiac diet: Physiology: Hypertension is a chronic elevation of blood pressure that, in the long-term, causes end-organ damage and results in increased morbidity and mortality. Blood pressure is the product of cardiac output and systemic vascular resistance.

Causes: Primary HTN (no known cause): aging, family history, African American race, obesity, smoking, stress, alcohol, hyperlipidemia, excess salt intake, low potassium intake. Secondary HTN: caused by precipitating disorders such as: ❖ Cardiovascular disorders ❖ Renal disorders ❖ Endocrine disorders ❖ Pregnancy ❖ Meds ( glucocorticoids, mineralocorticoids, estrogens)

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Low in sodium, and Low saturated fat, trans fat and cholesterol. The client should read labels to identify heart-healthy foods.

Nursing interventions: ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

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Provide a restful environment. Explain all procedures in detail. Listen to the client. Explain in detail diet restrictions. Document BP in the standing and lying positions. Encourage weight loss if the client is obese. Provide moderate salt restricted diet. Plan exercise regularly Encourage stress reduction measures.

Labs/ Diagnosis: ❖

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Urinalysis :Will detect protein, RBC, pus, and casts. Blood count/ESR Serum potassium, chloride and C02. Urinary catecholamine metabolites: To dx pheochromocytoma. Urine ketosteroids. IV pyelogram, urine cultures, radioisotope. Renal angiography : Test for renal disease. BUN and Creatinine.

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Treatments: ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

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Initially lifestyle changes Beta blockers Alpha Blockers Alpha 2 agonist Diuretics Vasodilators Calcium channel blockers ACE inhibitors ARBS

Medical treatment: ❖ ❖ ❖ ❖ ❖

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Lie down immediately if feeling faint, rise slowly. Avoid hot baths. Avoid alcohol. Avoid standing motionless. Avoid constipation, it interferes with drug metabolism and can cause hypotensive crisis. Always take meds on time and never skip. Never take a larger dose. Never suddenly d/c the drug this can cause rebound hypertension. Should hypotensive crisis occur wrap legs to promote venous return. Consult the HCP for use of OTC meds. Low sodium diet or cardiac diet.

Take clients BP and HR right before administration. Evaluate clients BP 30 mins post admin. Monitor for dizziness and hypotension. Monitor labs, especially potassium. Note interactions between NSAIDS and antihypertensive medication.

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Heart failure : Right sided Teaching:

What am I? Inability of the heart to maintain adequate cardiac output due to impaired pumping ability. Right sided heart failure develops from a diseased right ventricle that causes backflow to the right atrium. Almost always follows left side HF.

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Left sided :Backs up in the pulmonary circuit. Right sided: Backs up in the systemic circuit.

Physiology: Heart failure is the inability of the heart to maintain adequate cardiac output due to impaired pumping ability. Diminished cardiac output results in inadequate tissue perfusion. ❖ ❖

Acute: occurs suddenly Chronic: develops overtime, can be accompanied by acute episodes

Causes: ❖ ❖ ❖ ❖ ❖ ❖

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Coronary artery disease and heart attack High blood pressure (hypertension) Faulty heart valves. Damage to the heart muscle (cardiomyopathy) Myocarditis Heart defects you're born with (congenital heart defects) Abnormal heart rhythms (heart arrhythmias) Chronic diseases — such as diabetes, HIV, hyperthyroidism, hypothyroidism, or a buildup of iron (hemochromatosis) or protein (amyloidosis)

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Assessment: CNS; anxiety and fear. HEART : JVD, increased BP from fluid excess or decreased BP from pump, tachycardia, failure. Dependent edema. GI/GU : anorexia, abdominal distention, weight gain. MISC.: hepatomegaly, splenomegaly, swelling of fingers and hands. S: Swelling of fingers and hands W: Weight gain O: Organ enlargement L: Low hunger L: Large abdomen E: Edema in the periphery N: Nocturnal diuresis

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Administer cardiac glycoside Monitor vitals Record intake and output Daily weights Meticulous skin care 02 therapy Teach about disease process Provide a low sodium low calorie diet Bland foods and small frequent meals

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Treatments: ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Labs/ Diagnosis: Blood tests Chest X-ray Electrocardiogram (ECG) Echocardiogram Stress test Cardiac computerized tomography (CT) scan or magnetic resonance maging (MRI) Coronary angiogram Myocardial biopsy

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Digoxin Diuretics ACE ARB Low dose beta blockers Vasodilators: nitrates, milrinone Morphine sulfate Human B natriuretic peptide: acute episodes

Medical treatment: ❖

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Educate the client on signs of dig toxicity. Have the client identify risks of acute episodes. Educate the client on medications. Notify HCP if side effects occur. Call HCP if unable to take meds due to illness. Avoid caffeine, alcohol, tea, cocoa, soda. Educate the client on a low sodium, low fat, low cholesterol diet. Provide a list of potassium rich foods. Educate on fluid restriction. Balance rest and activity. Have them monitor daily weight. Monitor for signs of fluid retention. No isometric exercise, it can overwork the heart.

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Take clients BP and HR right before administration. Evaluate clients BP 30 mins post admin. Monitor for dizziness and hypotension. Monitor labs, especially potassium. Note interactions between NSAIDS and antihypertensive, medications. Monitor labs and look for signs of digoxin toxicity.

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Heart failure : Left sided What am I? Inability of the heart to maintain adequate cardiac output due to impaired pumping ability. Left sided HF: a result of left ventricular dysfunction which causes blood to backup into the left atrium and into the pulmonary veins. Left = Lung ❖

Types ❖ ❖

Left sided : backs up in the pulmonary circuit. Right sided : backs up in the systemic circuit.

Physiology: Inability of the heart to maintain adequate cardiac output due to impaired pumping ability. Diminished cardiac output results in inadequate tissue perfusion. Acute: occurs suddenly. Chronic: develops overtime, can be accompanied by acute episodes.

Causes: ❖ ❖ ❖ ❖ ❖ ❖

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Coronary artery disease and heart attack. High blood pressure (hypertension) Faulty heart valves Damage to the heart muscle (cardiomyopathy) Myocarditis Heart defects you're born with (congenital heart defects) Abnormal heart rhythms (heart arrhythmias) Chronic diseases — such as diabetes, HIV, hyperthyroidism, hypothyroidism, or a buildup of iron (hemochromatosis) or protein (amyloidosis)

Assessment: CNS: Anxiety and fear, cerebral anoxia, fatigue. HEART: Decreased cardiac output, s3 gallop, increased BNP. RESP: Dyspnea, orthopnea, cheyne stokes, pleural effusion , pulmonary edema cough, cardiac asthma. MISC.: Decreased renal function, muscular weakness, microalbuminuria.

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E: Edema (pleural) P: Pleural effusion I: Increased BNP C: Cardiac asthma

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F: Fatigue A: Anxiety I: Inability to breath (dyspnea, orthopnea) L: Listen for S3 gallop

Nursing interventions: ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Administer cardiac glycoside Monitor vitals Record intake and output Daily weights Meticulous skin care 02 therapy Teach about disease process Provide a low sodium low calorie diet Bland foods and small frequent meals

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Treatments: ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖

Labs/ Diagnosis: ❖ ❖ ❖ ❖ ❖ ❖ ❖

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Blood tests BNP Chest X-ray Electrocardiogram (ECG) Echocardiogram Stress test Cardiac computerized tomography (CT) scan or magnetic resonance imaging (MRI) Coronary angiogram Myocardial biopsy

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Educate the client to maintain aseptic technique. Instruct the client on how to administer IV antibiotics. Have the client record temp daily for six weeks. Encourage oral hygeine for six weeks with a soft bristle toothbrush 2x daily. Have the client clean any skin lacerations and apply antibiotic ointment. Client should inform all HCP’s of hx of endocarditis. Client should use prophylactic antibiotics for oral procedures. Tech the client the signs and symptoms of emoli and HF. Digoxin Diuretics ACE ARB Low dose beta blockers Vasodilators: nitrates, milrinone Morphine sulfate Human B natriuretic peptide: acute episodes

Medical treatment: ❖ ❖ ❖ ❖ ❖

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Take clients BP and HR right before administration. Evaluate clients BP 30 mins post admin. Monitor for dizziness and hypotension. Monitor labs, especially potassium. Note interactions between NSAIDS and antihypertensive, medications. Monitor dig labs and look for signs sx of dig toxicity.

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Coronary Artery Disease

What AM I ?

Surgical Procedures

Narrowing or obstruction of one or more coronary arteries as a result of atherosclerosis.

Physiology: Atherosclerotic buildup will cause decreased perfusion to the myocardial tissue leading to inadequate myocardial oxygenation thus causing hypertension, angina, dysrhythmias, MI, HF or death. Symptoms occur when the coronary artery is occluded 50-75%. Goal of treatment to decrease atheroscleroic progression.

Causes: Modifiable risks ❖ F: family history ❖ A: age ❖ T: thrombus ❖ ❖ ❖ ❖ ❖

H: high cholesterol E: ethnicity A: alcohol abuse R: release of stress hormones T: tobacco use

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Assessment: HEART: Chest pain, palpitations RESP: Dyspnea MISC.: Fatigue RESP: Cough, hemoptysis CNS: Syncope L: Low energy I: Irritating cough, hemoptysis P: Palpitations I: Intense chest pain D: Dyspnea S: Syncope

Nursing interventions: ❖ ❖

Labs/ Diagnosis: ❖ ❖

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ECG: to monitor for ST elevation indicative of MI. Cardiac Cath: to look for extent of atherosclerotic buildup. Blood lipids: monitors cholesterol levels such as HDL. LDL and triglycerides.

PTCA: Compresses the plaque against the walls of the arteries and dilates vessels. Laser angioplasty: Vaporizes the plaque. Atherectomy : Removes plaque from the artery. Vascular stent: Prevent the artery from closing and restenosis. Coronary artery bypass graft: Improves blood flow to the myocardium decreasing the risk for ischemia and infarction.

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Educate on the risk factors of CAD. Assist in goal setting for smoking, alcohol and substance abuse cessation. Educate the client on proper diet, low sodium, low calorie, low fat, increased fiber. Lifestyle changes are not temporary. Provide resources for cessation of smoking and substance abuse. Explain the importance of exercise.

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Nitrates: dilate the coronary arteries and decrease preload and afterload. Calcium channel blockers: dilate coronary arteries and reduce vasospasm. Cholesterol lowering meds : HMG-COA reductase inhibitors, reduce the development of plaques. Beta Blockers: reduce BP for clients who are hypertensive.

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Coronary Artery Disease: Angina What am I?

Teaching:

Chest pain resulting from myocardial ischemia resulting from inadequate blood and 02 supply.

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Stable angina : occurs during active periods and subsides when resting or after taking Nitroglycerin. Unstable angina : occurs with unpredictable amounts of exertion and does not subside with rest or nitroglycerin, lasts longer than 15 minutes. Variant angina : results from coronary artery spasm, can happen during rest.

Physiology: Angina pectoris is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand. It is a common presenting symptom (typically, chest pain) among patients with coronary artery disease (CAD).

Causes: Modifiable risks ❖ Smoking ❖ High fat intake ❖ Sedentary lifestyle ❖ Diabetes ❖ Obesity ❖ Chronic stress ❖ Depression ❖ Birth control ❖ Substance abuse ❖ Non modifiable risks ❖ Age ❖ Family history ❖ Gender ( males) ❖ Race ( african american)

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Assessment: HEART: Chest pain can be crushing, substernal, squeezing, and radiate to shoulders arms and jaw pain palpitations, tachycardia, HTN. RESP: Dyspnea MISC.: Fatigue, pallor, sweating. GI: Dgestive disturbances. CNS: Syncope, dizziness. C: chest pain H: hypertension E: elevated HR S: substernal pain T: tiredness P: pallor A: lot of sweating I: intense squeezing pain N: non normal respirations

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ECG: ST depression or t wave inversion during pain. Stress Test: changes in EKG or vitals could indicate ischemia. Cardiac enzyme levels: findings are normal in angina. Cardiac catheterization: provides a definite dx by monitoring patency of coronary arteries.

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Labs/ Diagnosis:

Identify precipitating events. If chest pain occurs take nitroglycerine as ordered no more than 3x 5 min. Apart. If chest pain is not relieved call 911. Provide diet restrictions. Identify modifiable risk factors. Assist in goal setting. Provide community resources.

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Assess pain and institute relief measures. Administer 02. Assess vitals provide continuous cardiac monitoring. Administer nitroglycerine as prescribed. Ensure bed rest is maintained in semi-fow Obtain 12 lead EKG. Establish IV access.

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Nitrates : Dilate the coronary arteries and decrease preload and afterload. Calcium channel blockers: Dilate coronary arteries and reduce vasospasm. Cholesterol lowering meds : HMG- COA reductase inhibitors, reduce the development of plaques. Beta Blockers: Reduce BP for clients who are hypertensive. Antiplatelet meds: To inhibit platelet aggregation and decrease the risk of MI.

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Peripheral vascular disease: Venous Assessment:

What am I? Refers to diseases of blood vessels outside the heart and brain. A narrowing of vessels that carry blood to the legs, arms, stomach or kidneys. There are two types of PVD: • Functional PVDs don’t involve defects in blood vessels’ structure. (The blood vessels aren’t physically damaged.) These diseases often have symptoms related to “spasm” that may come and go. • Organic PVDs are caused by structural changes in the blood vessels. Examples could include inflammation and tissue damage.

Physiology: There is a decrease in efficiency of returning blood to the heart related to incompetent valves and inadequate pumping action of the muscles surrounding the veins.

HEART : Normal or decreased pulses. DERM: cool brown skin, edema, ulcers, pain redness and induration along the vein, limb may be warmer. MISC.: deep muscle tenderness, risk for PE. P: pain in the affected limb. A: alteration in limb temp. I: induration and redness. N : normal or decreased pulse.

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❖ Thrombophlebitis Venous stasis Hypercoagulability Inju...