Cardiovascular System

ANATOMY Right coronary artery supplies the right atrium and right ventricle, inferior portion of the left ventricle, the posterior septal wall and the two nodes AV (90%) and SA node (55%) Left coronary artery- branches into the LAD and the circumflex branch The LAD supplies blood to the anterior wall of the left ventricle, the anterior septum and the Apex of the left ventricle The circumflex branch supplies the left atrium and the posterior left ventricle SA node- the pacemaker 2. AV nodeslowest conduction 3. Bundle of His branches into the Right and the Left bundle branch 4. Purkinje fibers- fastest conduction Heart sounds 1. S1- due to closure of the AV valves 2. S2- due to the closure of the semi-lunar valves 3. S3- due to increased ventricular filling 4. S4- due to forceful atrial contraction Sympathetic system INCREASES HR Parasympathetic system (Vagus) DECREASES HR Blood pressure Cardiac output X peripheral resistance Control is neural (central and peripheral) and hormonal Baroreceptors in the carotid and aorta Hormones- ADH, aldosterone, epinephrine can increase BP; ANF can decrease BP LABS Proteins and enzymes CK- MB ( creatine kinase) Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days Normal:7 U/L Lactic Dehydrogenase (LDH) Elevates in MI in 24 hours, peaks in 48-72 hours. Normally LDH1 is greater than LDH2. MIPROCEDURES Electrocardiogram (ECG) Holter Monitoring: non-invasive; client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop Echocardiogram Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound No special preparation is needed Stress Test: non-invasive; studies the heart during activity and detects and evaluates CAD Stress Test Treadmill testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath . Instruct client to avoid taking a hot shower for 10-12 hours after the test Pharmacological stress test Use of dipyridamole Maximally dilates coronary artery Side-effect: flushing of face Pre-test: 4 hours fasting, avoid alcohol, caffeine Post test: report symptoms of chest pain Troponin I and T Troponin I is usually utilized for MI Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks! Normal value for Troponin I is less than 0.6 ng/mL REMEMBER to AVOID IM injections before obtaining blood sample! Early and late diagnosis can be made Serum lipids

Cardiac catheterization: Insertion of a catheter into the heart and surrounding vessels Determines the structure and performance of the heart valves and surrounding vessels Used to diagnose CAD, assess coronary atery patency and determine extent of atherosclerosis Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses. Fast for 8-12 hours, teachings, medications to allay anxiety Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart; inform the patient that a feeling of warmth and metallic taste may occur when dye is administered Post-test: Monitor VS and cardiac rhythm Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site Maintain sandbag to the insertion site if required to maintain pressure Monitor for bleeding and hematoma formation Maintain strict bed rest for 6-12 hours Client may turn from side to side but bed should not be elevated more than 30 degrees and legs always straight Encourage fluid intake to flush out the dye Immobilize the arm if the antecubital vein is used Monitor for dye allergy CVP The CVP is the pressure within the SVC Reflects the pressure under which blood is returned to the SVC and right atrium Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O Elevated CVP indicates increase in blood volume, excessive IVF or heart/renal failure Low CVP may indicated hypovolemia, hemorrhage and severe vasodilatation Measuring CVP 1. Position the client supine with bed elevated

LDH2 greater than LDH1 (flipped LDH pattern) Normal: 70-200 IU/L Myoglobin Rises within 1-3 hours. Peaks in 4-12 hours. Returns to normal in a day. Not used alone. Muscular and renal disease can have elevated myoglobin ASSESSMENT Health History Obtain description of present illness and the chief complaint Chest pain, SOB, Edema, etc. Assess risk factors Physical examination Vital signs- BP, PP, MAP Inspection of the skin Inspection of the thorax Palpation of the PMI, pulses Auscultation of the heart sounds Laboratory and diagnostic studies CBC cardiac catheterization Lipid profile arteriography Cardiac enzymes and proteins CXR CVP EEG Holter monitoring Exercise ECG IMPLEMENTATION 1. Assess the cardio-pulmonary status VS, BP, Cardiac assessment 2. Enhance cardiac output Establish IV line to administer fluids 3. Promote gas exchange Administer O2 Position client in SEMI-Fowlers Encourage coughing and deep breathing exercises 4. Increase client activity tolerance Balance rest and activity periods Assist in daily activities 5. Promote client comfort Assess the clients description of pain and chest discomfort Administer medication as prescribed 6. Promote adequate sleep 7. Prevent infection Monitor skin integrity of lower extremities Assess skin site for edema, redness and warmth Monitor for fever Change position frequently 8. Minimize patient anxiety Encourage verbalization of feelings, fears and concerns Answer client questions. Provide information about procedures

Lipid profile measures the serum cholesterol, triglycerides and lipoprotein levels Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL. LDH- 130 mg/dL HDL- 30-70- mg/dL NPO post midnight (usually 12 hours) ANGINA PECTORIS Chest pain resulting from coronary atherosclerosis or myocardial ischemia Common Types: 1. Stable angina The typical angina that occurs during exertion, relieved by rest and drugs and the severity does not change 2. Unstable angina Occurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and drug 3. Variant angina Prinzmetal angina, results from coronary artery VASOSPASMS, may occur at rest ASSESSMENT FINDINGS 1. Chest pain- The most characteristic symptom; described as mild to severe retrosternal pain, squeezing, tightness or burning sensation Radiates to the jaw and left arm. Precipitated by Exercise, Eating heavy meals, Emotions like excitement and anxiety and Extremes of temperature Relieved by REST and Nitroglycerin 2. Diaphoresis 3. Nausea and vomiting 4. Cold clammy skin 5. Sense of apprehension and doom 6. Dizziness and syncope LABORATORY FINDINGS 1. ECG may show normal tracing if patient is pain-free. Ischemic changes may show ST depression and T wave inversion 2. Cardiac catheterization Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions

at 45 degrees 2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4th ICS 3. Instruct the client to be relaxed and avoid coughing and straining. NURSING MANAGEMENT 1. Administer prescribed medications Nitrates- to dilate the coronary arteries Aspirin- to prevent thrombus formation Betablockers- to reduce BP and HR Calciumchannel blockers- to dilate coronary artery and reduce vasospasm 2. Teach the patient management of anginal attacks Advise patient to stop all activities Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention 3. Obtain a 12-lead ECG 4. Promote myocardial perfusion Instruct patient to maintain bed rest Administer O2 @ 3 lpm Advise to avoid valsalva maneuvers Provide laxatives or high fiber diet to lessen constipation Encourage to avoid increased physical activities 5. Assist in possible treatment modalities PTCA- percutaneous transluminal coronary angioplasty To compress the plaque against the vessel wall, increasing the arterial lumen CABG- coronary artery bypass graft To improve the blood flow to the myocardial tissue 6. Provide information to family members to minimize anxiety and promote family cooperation 7. Assist client to identify risk factors that can be modified 8. Refer patient to proper agencies

and medications CAD CAD results from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous plaque in the vessel wall RISK FACTORS 1. Age above 45/55 and Sex- Males and post-menopausal females 2. Family History 3. Hypertension 4. DM 5. Smoking 6. Obesity 7. Sedentary lifestyle 8. Hyperlipedimia Most important MODIFIABLE factors: Smoking Hypertension Diabetes Cholesterol abnormalities

MYOCARDIAL INFARCTION Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood supply ETIOLOGY and Risk factors 1. CAD 2. Coronary vasospasm 3. Coronary artery occlusion by embolus and thrombus 4. Conditions that decrease perfusionhemorrhage, shock Risk factors 1. Hypercholesterolemia 2. Smoking 3. Hypertension 4. Obesity 5. Stress 6. Sedentary lifestyle PATHOPHYSIOLOGY Interrupted coronary blood flow myocardial ischemia anaerobic myocardial metabolism for several hours myocardial death depressed cardiac function triggers autonomic nervous system response further imbalance of myocardial O2 demand and supply Assessment findings 1. CHEST PAIN Chest pain is described as severe, persistent, crushing substernal discomfort Radiates to the neck, arm, jaw and back .Occurs without cause, primarily early morning NOT relieved by rest or nitroglycerin Lasts 30 minutes or longer 2. Dyspnea 3. Diaphoresis 4. Cold clammy skin 5. N/V 6. restlessness, sense of doom 7. tachycardia or bradycardia 8. hypotension 9. S3 and dysrhythmias Laboratory findings 1. ECG- the ST segment is ELEVATED. T wave inversion, presence of Q wave 2. Myocardial enzymes- elevated CK- MB, LDH and Troponin levels 3. CBC- may show elevated WBC count 4. Test after the acute stage- Exercise

Nursing Interventions 1. Provide Oxygen at 2L, Semi-fowlers 2. Administer medications Morphine to relieve pain nitrates, thrombolytics, aspirin and anticoagulants Stool softener and hypolipidemics 3. Minimize patient anxiety Provide information as to procedures and drug therapy 4. Provide adequate rest periods 5. Minimize metabolic demands Provide soft diet Provide a low-sodium, low cholesterol and low fat diet 6. Minimize anxiety Reassure client and provide information as needed 7. Assist in treatment modalities such as PTCA and CABG 8. Monitor for complications of MIespecially dysrhythmias, since ventricular tachycardia can happen in the first few hours after MI 9. Provide client teaching Medical Management 1. ANALGESIC The choice is MORPHINE It reduces pain and anxiety Relaxes bronchioles to enhance oxygenation 2. ACE Prevents formation of angiotensin II Limits the area of infarction 3. Thrombolytics Streptokinase, Alteplase Dissolve clots in the coronary artery allowing blood to flow NURSING INTERVENTIONS AFTER ACUTE EPISODE 1. 1. Maintain bed rest for the first 3 days 2. Provide passive ROM exercises 3. Progress with dangling of the feet at side of bed 4. Proceed with sitting out of bed, on the chair for 30 minutes TID 5. Proceed with ambulation in the room toilet hallway TID Cardiac rehabilitation To extend and

CARDIOMYOPATHIES Heart muscle disease associated with cardiac dysfunction ASSOCIATED FACTORS 1. Heavy alcohol intake 2. Pregnancy 3. Viral infection 4. Idiopathic PATHOPHYSIOLOGY Diminished contractile proteins poor contraction decreased blood ejection increased blood remaining in the ventricle ventricular stretching and dilatation. SYSTOLIC DYSFUNCTION HYPERTROPHIC CARDIOMYOPATHY Associated factors: 1. Genetic 2. Idiopathic Pathophysiology Increased size of myocardium reduced ventricular volume increased resistance to ventricular filling diastolic dysfunction RESTRICTIVE CARDIOMYOPATHY Associated factors 1. Infiltrative diseases like AMYLOIDOSIS 2. Idiopathic Pathophysiology Rigid ventricular wall impaired stretch and diastolic filling decreased output Diastolic dysfunction Assessment findings 1. PND 2. Orthopnea 3. Edema 4. Chest pain 5. Palpitations 6. Dizziness 7. Syncope with exertion Laboratory Findings 1. CXR- may reveal cardiomegaly 2. ECHOCARDIOGRAM 3. ECG 4. Myocardial Biopsy Medical Management 1. Surgery 2. Pacemaker insertion 3. Pharmacological drugs for symptom relief Nursing Management 1 .Improve cardiac output Adequate rest Oxygen therapy Low sodium diet 2. Increase patient tolerance Schedule activities with rest periods in between 3. Reduce patient anxiety Support Offer information about transplantations Support family in anticipatory grieving

tolerance test, thallium scans, cardiac catheterization

improve quality of life Physical conditioning Patients who are able to walk 3-4 mph are usually ready to resume sexual activities

INFECTIVE ENDOCARDITIS Infection of the heart valves and the endothelial surface of the heart Can be acute or chronic Etiologic factors 1. Bacteria- Organism depends on several factors 2. Fungi Risk factors 1. Prosthetic valves 2. Congenital malformation 3. Cardiomyopathy 4. IV drug users 5. Valvular dysfunctions Pathophysiology Direct invasion of microbes microbes adhere to damaged valve surface and proliferate damage attracts platelets causing clot formation erosion of valvular leaflets and vegetation can embolize Assessment findings 1. Intermittent HIGH fever 2. anorexia, weight loss 3. cough, back pain and joint pain 4. splinter hemorrhages under nails 5. Oslers nodes- painful nodules on fingerpads 6. Roths spots- pale hemorrhages in the retina 7. Heart murmurs 8. Heart failure Prevention Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc. LABORATORY EXAM Blood Cultures to determine the exact organism Nursing management 1. regular monitoring of temperature, heart sounds 2. manage infection 3. long-term antibiotic therapy Medical management 1. Pharmacotherapy IV antibiotic for 2-6 weeks Antifungal agents are given

CHF A syndrome of congestion of both pulmonary and systemic circulation caused by inadequate cardiac function and inadequate cardiac output to meet the metabolic demands of tissues Inability of the heart to pump sufficiently The heart is unable to maintain adequate circulation to meet the metabolic needs of the body Classified according to the major ventricular dysfunction- Left or Right Etiology 1. CAD 2. Valvular heart diseases 3. Hypertension 4. MI 5. Cardiomyopathy 6. Lung diseases 7. Post-partum 8. Pericarditis and cardiac tamponade PATHOPHYSIOLOGY LEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion ventricular failure decreased cardiac output decreased perfusion to the brain, kidney and other tissues oliguria, dizziness PATHOPHYSIOLOGY RIGHT ventricular failure blood pooling in the venous circulation increased hydrostatic pressure peripheral edema; ventricular failure blood pooling venous congestion in the kidney, liver and GIT LEFT SIDED CHF ASSESSMENT FINDINGS 1. Dyspnea on exertion 2. PND 3. Orthopnea 4. Pulmonary crackles/rales 5. cough with Pinkish, frothy sputum 6. Tachycardia 7. Cool extremities 8. Cyanosis

RIGHT SIDED CHF ASSESSMENT FINDINGS 1. Peripheral dependent, pitting edema 2. Weight gain 3. Distended neck vein 4. hepatomegaly 5. Ascites 6. Body weakness 7. Anorexia, nausea 8. Pulsus alternans LABORATORY FINDINGS 1. CXR may reveal cardiomegaly 2. ECG may identify Cardiac hypertrophy 3. Echocardiogram may show hypokinetic heart 4. ABG and Pulse oximetry may show decreased O2 saturation 5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF NURSING INTERVENTIONS 1. Assess patient's cardio- pulmonary status 2. Assess VS, CVP and PCWP. Weigh patient daily to monitor fluid retention 3. Administer medications- usually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators and hypolipidemics are prescribed 4. Provide a LOW sodium diet. Limit fluid intake as necessary 5. Provide adequate rest periods to prevent fatigue 6. Position on semi-fowlers to fowlers for adequate chest expansion 7. Prevent complications of immobility NURSING INTERVENTION AFTER THE ACUTE STAGE 1. Provide opportunities for verbalization of feelings 2. Instruct the patient about the medication regimen- digitalis, vasodilators and diuretics 3. Instruct to avoid OTC drugs, Stimulants, smoking and alcohol 4. Provide a LOW fat and LOW sodium diet

amphotericin B 2. Surgery Valvular replacement

9. decreased peripheral pulses 10. Fatigue 11. Oliguria 12. signs of cerebral anoxia CARDIAC TAMPONADE A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion) This condition restricts ventricular filling resulting to decreased cardiac output Acute tamponade may happen when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac Causative factors 1. Cardiac trauma 2. Complication of Myocardial infarction 3. Pericarditis 4. Cancer metastasis ASSESSMENT FINDINGS 1. BECKs Triad- Jugular vein distention, hypotension and distant/muffled heart sound 2. Pulsus paradoxus 3. Increased CVP 4. decreased cardiac output 5. Syncope 6. anxiety 7. dyspnea 8. Percussion- Flatness across the anterior chest

CARDIOGENIC SHOCK Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion ETIOLOGY 1. Massive MI 2. Severe CHF 3. Cardiomyopathy 4. Cardiac trauma 5. Cardiac tamponade ASSESSMENT FINDINGS 1. HYPOTENSION 2. oliguria (less than 30 ml/hour) 3. tachycardia 4. narrow pulse pressure 5. weak peripheral pulses 6. cold clammy skin 7. changes in sensorium/LOC 8. pulmonary congestion LABORATORY FINDINGS Increased CVP Normal is 4-10 cmH2O NURSING INTERVENTIONS 1. Place patient in a modified Trendelenburg (shock ) position 2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE 3. Administer O2 4. Morphine is administered to decreased pulmonary congestion and to relieve pain 5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz cath and IABP 6. Monitor urinary output, BP and pulses 7. Cautiously administer diuretics and nitrates HYPERTENSION A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over a sustained period, based on two or more BP measurements. Types of Hypertension 1. Primary or ESSENTIAL Most common type 2. Secondary Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushings, Conns , SIADH PATHOPHYSIOLOGY Multi-factorial

5. Provide potassium supplements 6. Instruct about fluid restriction 7. Provide adequate rest periods and schedule activities 8. Monitor daily weight and report signs of fluid retention Laboratory FINDINGS 1. Echocardiogram 2. Chest X-ray NURSING INTERVENTIONS 1. Assist in PERICARDIOCENTESIS 2. Administer IVF 3. Monitor ECG, urine output and BP 4. Monitor for recurrence of tamponade Pericardiocentesis Patient is monitored by ECG Maintain emergency equipments Elevate head of bed 45-60 degrees Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration and myocardial trauma

ASSESSMENT FINDINGS 1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V Risk factors for Cardiovascular Problems in Hypertensive patients Major Risk factors 1. Smoking 2. Hyperlipidemia 3. DM 4. Age older than 60 5. Gender- Male and post menopausal W 6. Family History DIAGNOSTIC STUDIES 1. Health history and PE 2. Routine laboratory- urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS 3.

NURSING INTERVENTIONS 1. Provide health teaching to patient Teach about the disease process Elaborate on lifestyle changes Assist in meal planning to lose weight 1. Provide health teaching to the patient Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day Limit alcohol intake to 30 ml/day Regular aerobic exercise Advise to completely Stop smoking 2. Provide information about antihypertensive drugs Instruct proper

etiology BP= CO (SV X HR) x TPR Any increase in the above parameters will increase BP 1. Increased sympathetic activity 2. Increased absorption of Sodium, and water in the kidney 3. Increased activity of the RAAS 4. Increased vasoconstriction of the peripheral vessels 5. insulin resistance VASCULAR DISEASES ANEURYSM Dilation involving an artery formed at a weak point in the vessel wall Saccular= when one side of the vessel is affected Fusiform= when the entire segment becomes dilated RISK FACTORS Atherosclerosis Infection= syphilis Connective tissue disorder Genetic disorder= Marfans Syndrome ASSESSMENT Asymptomatic Pulsatile sensation on the abdomen Palpable bruit LABORATORY: CT scan Ultrasound X-ray Aortography Medical Management: Antihypertensives Synthetic graft Nursing Management: Administer medications Emphasize the need to avoid increased abdominal pressure No deep abdominal palpation Remind patient the need for serial ultrasound to detect diameter changes RAYNAUDS DISEASE A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain and pallor of the fingertips or toes Cause : UNKNOWN Most commonly affects WOMEN, 16- 40 years old ASSESSMENT FINDINGS 1. Raynauds phenomenon A localized episode of vasoconstriction of the small

Other lab- CXR, creatinine clearance, 24-huour urine protein MEDICAL MANAGEMENT 1. Lifestyle modification 2. Drug therapy 3. Diet therapy Drug therapy Diuretics Beta blockers Calcium channel blockers ACE inhibitors A2 Receptor blockers Vasodilators

compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition Instruct to avoid over-the-counter drugs that may interfere with the current medication 3. Promote Home care management Instruct regular monitoring of BP Involve family members in care Instruct regular follow-up 4. Manage hypertensive emergency and urgency properly BUERGERS DISEASE Thromboangiitis obliterans A disease characterized by recurring inflammation of the medium and small arteries and veins of the lower extremities Occurs in MEN ages 20-35 RISK FACTOR: SMOKING! PATHOPHYSIOLOGY Cause is UNKNOWN Probably an Autoimmune disease Inflammation of the arteries thrombus formation occlusion of the vessels ASSESSMENT FINDINGS 1. Leg PAIN Foot cramps in the arch (instep claudication) after exercise Relieved by rest Aggravated by smoking, emotional disturbance and cold chilling 2. Digital rest pain not changed by activity or rest 3. Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances 4. Paresthesia Diagnostic Studies 1. Duplex ultrasonography 2. Contrast angiography Nursing Interventions 1. Assist in the medical and surgical management Bypass graft amputation 2. Strongly advise to AVOID smoking 3. Manage complications appropriately Medical Management 1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles Cilostazol (Pletaal) inhibits platelet aggregation and increases

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis. Usually found in males age 50 and above The legs are most often affected Risk factors: Non-Modifiable 1. Age 2. gender 3. family predisposition Modifiable 1. Smoking 2. HPN 3. Obesity 4. Sedentary lifestyle 5. DM 6. Stress ASSESSMENT FINDINGS 1. INTERMITTENT CLAUDICATION- the hallmark of PAOD This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of exercise or activity. the hallmark of PAOD This pain is RELIEVED by REST This commonly affects the muscle group below the arterial occlusion 2. Progressive pain on the extremity as the disease advances 3. Sensation of cold and numbness of the extremities 4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position 5. Muscle atrophy, leg ulceration and gangrene Diagnostic Findings 1. Unequal pulses between the extremities 2. Duplex ultrasonography 3. Doppler flow studies Medical Management 1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles

arteries of the hands and feet that causes color and temperature changes.W-B-R Pallor- due to vasoconstriction, then Blue- due to pooling of Deoxygenated blood Red- due to exaggerated reflow/hyperemia 2. tingling sensation 3. Burning pain on the hands and feet Medical management Drug therapy with the use of CALCIUM channel blockers To prevent vasospasms Nursing Interventions 1. instruct patient to avoid stressful situations 2. instruct to avoid exposure to cold and remain indoors when the climate is cold 3. instruct to avoid all kinds of nicotine 4. instruct about safety. Careful handling of sharp objects VENOUS DISEASES VARICOSE VEINS Dilated veins usually in the lower extremities Predisposing Factors Pregnancy Prolonged standing or sitting Constipation (for hemorrhoids) Incompetent venous valves Pathophysiology Factors venous stasis increased hydrostatic pressure edema

Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation 2. Surgery- Bypass graft and anastomoses Nursing Interventions 1. Maintain Circulation to the extremity Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time Administer post-operative care to patient who underwent surgery 2. Monitor and manage complications Note for bleeding, hematoma, decreased urine output Elevate the legs to diminish edema Encourage exercise of the extremity while on bed Teach patient to avoid leg-crossing 3. Promote Home management Encourage lifestyle changes Instruct to AVOID smoking Instruct to avoid leg crossing Assessment findings Tortuous superficial veins on the legs Leg pain and Heaviness Dependent edema Laboratory findings Venography Duplex scan pletysmography Medical management Pharmacological therapy Leg vein stripping Anti-embolic stockings

vasodilatation 2. Surgery- Bypass graft and anastomoses Nursing Interventions Post-operative care: after amputation Elevate stump for the FIRST 24 HOURS to minimize edema and promote venous return Place patient on PRONE position after 24 hours Assess skin for bleeding and hematoma Wrap the extremity with elastic bandage

Nursing management 1. Advise patient to elevate the legs 2. Caution patient to avoid prolonged standing or sitting 3. Provide high-fiber foods to prevent constipation 4. Teach simple exercise to promote venous return 5. Caution patient to avoid knee-length stockings and constrictive clothings 6. Apply anti-embolic stockings as directed 7. Avoid massage on the affected area

HEMATOLOGIC SYSTEM ANEMIA A condition in which the hemoglobin concentration is lower than normal Three broad categories 1. Loss of RBC- occurs with bleeding 2. Decreased RBC production 3. Increased RBC destruction

HYPOPROLIFERATIVE / IRON DEFICIENCY ANEMIA Results when the dietary intake of iron is inadequate to produce hemoglobin Etiologic Factors 1. Bleeding- the most common cause 2. Mal-absorption 3. Malnutrition 4. Alcoholism Pathophysiology The body stores of iron

MEGALOBLASTIC ANEMIAS Anemias characterized by abnormally large RBC secondary to impaired DNA synthesis due to deficiency of Folic acid and/or vitamin B12 Folic acid deficiency Causative factors 1. Alcoholism 2. Mal-absorption 3. Diet deficient in uncooked vegetables Pathophysiology of Folic acid deficiency.

APLASTIC ANEMIA Acondition characterized by decreased number of RBC as well as WBC and platelets CAUSATIVE FACTORS 1. Environmental toxins- pesticides, benzene 2. Certain drugsChemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides 3. Heavy metals 4. Radiation Pathophysiology Toxins cause a direct bone marrow depression acellualr bone marrow decreased production of blood elements ASSESSMENT FINDINGS 1. fatigue 2. pallor 3. dyspnea 4. bruising 5. splenomegaly 6. retinal hemorrhages LABORATORY FINDINGS 1. CBCdecreased blood cell numbers 2. Bone marrow aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats Medical Management 1. Bone marrow transplantation 2. Immunosupressant drugs 3. Rarely, steroids 4. Blood transfusion Nursing management 1. Assess for signs of bleeding and infection 2. Instruct to avoid exposure to offending agents

decrease, leading to depletion of hemoglobin synthesis The oxygen carrying capacity of hemoglobin is reduced tissue hypoxia Assessment Findings 1. Pallor of the skin and mucous membrane 2. Weakness and fatigue 3. General malaise 4. Pica 5. Brittle nails 6. Smooth and sore tongue 7. Angular cheilosis Laboratory findings 1. CBC- Low levels of Hct, Hgb and RBC count 2. low serum iron, low ferritin 3. Bone marrow aspiration- MOST definitive Medical management 1. Hematinics 2. Blood transfusion Nursing Management 1. Provide iron richfoods Organ meats (liver) Beans Leafy green vegetables Raisins and molasses 2. Administer iron. Oral preparations tablets- Fe fumarate, sulfate and gluconate. Advise to take iron ONE hour before meals. Take it with vitamin C. Continue taking it for several months Liquid It stains teeth. Drink it with a straw. Stool may turn blackish- dark in color. Advise to eat high-fiber diet to counteract constipation IM preparation Administer DEEP IM using the Z- track method. Avoid vigorous rubbing. Can cause local pain and staining

Decreased folic acid impaired DNA synthesis in the bone marrow impaired RBC development, impaired nuclear maturation but CYTOplasmic maturation continues large size Vitamin B12 deficiency Causative factors 1. Strict vegetarian diet 2. Gastrointestinal malabsorption 3. Crohn's disease 4. gastrectomy Vitamin B12 deficiency Pernicious Anemia Due to the absence of intrinsic factor secreted by the parietal cells Intrinsic factor binds with Vit. B12 to promote absorption Megaloblastic Anemias Assessment findings 1. weakness 2. fatigue 3. listless 4. neurologic manifestations are present only in Vit. B12 deficiency Megaloblastic Anemias Assessment findings Pernicious Anemia Beefy, red, swollen tongue Mild diarrhea Extreme pallor Paresthesias in the extremities Laboratory findings 1. Peripheral blood smearshows giant RBCs, WBCs with giant hypersegmented nuclei 2. Very high MCV 3. Schillings test 4. Intrinsic factor antibody test Medical Management 1. Vitamin supplementation Folic acid 1 mg daily 2. Diet supplementation Vegetarians should have vitamin intake 3. Lifetime monthly injection of IM Vit B12 Nursing Management 1. Monitor patient 2. Provide assistance in ambulation 3. Oral care for tongue sore 4. Explain the need for lifetime IM injection of vit B12

HEMOLYTIC ANEMIA: SICKLE CELL A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene. Causative factor Genetic inheritance of the sickle gene- HbS gene Pathophysiology Decreased O2, Cold, Vasoconstriction can precipitate sickling process Factors cause defective hemoglobin to acquire a rigid, crystal-like C-shaped configuration Sickled RBCs will adhere to endothelium pile up and plug the vessels ischemia results pain, swelling and fever Assessment Findings 1. jaundice 2. enlarged skull and facial bones 3. tachycardia, murmurs and cardiomegaly Primary sites of thrombotic occlusion:

POLYCYTHEMIA VERA Refers to an INCREASE volume of RBCs The hematocrit is ELEVATED to more than 55% Clasified as Primary or Secondary Primary Polycythemia A proliferative disorder in which the myeloid stem cells become uncontrolled Causative factor unknown Pathophysiology The stem cells grow uncontrollably The bone marrow becomes HYPERcellular and all the blood cells are increased in number The spleen resumes its function of hematopoiesis and enlarges Blood becomes thick and viscous causing sluggish circulation Overtime, the bone marrow becomes fibrotic Assessment findings 1. Skin is ruddy 2. Splenomegaly 3. headache 4. dizziness, blurred vision 5. Angina, dyspnea and thrombophlebitis

Laboratory findings 1. CBC- shows elevated RBC mass 2. Normal oxygen saturation 3 Elevated WBC and Platelets Complications 1. Increased risk for thrombophlebitis, CVA and MI 2. Bleeding due to dysfunctional blood cells Medical Management 1. To reduce the high blood cell mass- PHLEBOTOMY 2. Allopurinol 3. Dipyridamole 4. Chemotherapy to suppress bone marrow Nursing Management 1. Primary role of the nurse is EDUCATOR 2. Regularly asses for the development of complications 3. Assist in weekly phlebotomy 4. Advise to avoid alcohol and aspirin 5. Advise tepid sponge bath or cool water to manage pruritus

spleen, lungs and CNS Chest pain, dyspnea 1. Sickle cell crises Results from tissue hypoxia and necrosis 2. Acute chest syndrome Manifested by a rapidly falling hemoglobin level, tachycardia, fever and chest infiltrates in the CXR Medical Management 1. Bone marrow transplant 2. Hydroxyurea Increases the HbF 3. Long term RBC transfusion Nursing Management 1. manage the pain Support and elevate acutely inflamed joint Relaxation techniques analgesics 2. Prevent and manage infection Monitor status of patient Initiate prompt antibiotic therapy 3. Promote coping skills Provide accurate information Allow patient to verbalize her concerns about medication, prognosis and future pregnancy 4. Monitor and prevent potential complications Provide always adequate hydration Avoid cold, temperature that may cause vasoconstriction. Leg ulcer Aseptic technique .Priapism Sudden painful erection Instruct patient to empty bladder, then take a warm bath

LEUKEMIA Malignant disorders of blood forming cells characterized by UNCONTROLLED proliferation of WHITE BLOOD CELLS in the bone marrowreplacing marrow elements . The WBC can also proliferate in the liver, spleen and lymph nodes. The leukemias are named after the specific lines of blood cells afffected primarily Myeloid Lymphoid Monocytic The leukemias are named also according to the maturation of cells ACUTE The cells are primarily immature CHRONIC The cells are primarily mature or diferentiated ETIOLOGIC FACTORS UNKNOWN Probably exposure to radiation Chemical agents Infectious agents Genetic PATHOPHYSIOLOGY of ACUTE Leukemia Uncontrolled proliferation of immature cells suppresses bone marrow function severe anemia, thrombocytopenia and granulocytopenia PATHOPHYSIOLOGY of CHRONIC Leukemia Uncontrolled proliferation of DIFFERENTIATED cells slow suppression of bone marrow function milder symptoms

ASSESSMENT FINDINGS ACUTE LEUKEMIA Pallor Fatigue Dyspnea Hemorrhages Organomegaly Headache vomiting ASSESSMENT FINDINGS CHRONIC LEUKEMIA Less severe symptoms organomegaly LABORATORY FINDINGS Peripheral WBC count varies widely Bone marrow aspiration biopsy reveals a large percentage of immature cells- BLASTS. Erythrocytes and platelets are decreased Medical Management 1. Chemotherapy 2. Bone marrow transplantation Nursing Management 1. Manage AND prevent infection Monitor temperature Assess for signs of infection Be alert if the neutrophil count drops below 1,000 cells/mm3 2. Maintain skin integrity 3. Provide pain relief 4. Provide information as to therapychemo and bone marrow transplantation

Cardiovascular Drugs
Antihypertensive drugs: The Drugs employed to control hypertension can be classified as: Diuretics Beta-blockers Alpha adrenergic blockers Calcium channel blockers Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers Peripheral vasodilators Evaluating the effectiveness of these drugs is simply to monitor the BP if it becomes NORMAL THE PRILS: ANGIOTENSION CONVERTING Pharmacodynamics: The mechanism of Clinical indications of the ACE ENZYME INHIBITORS action of the ACE inhibitors These agents inhibitors Hypertension, either alone or in BLOCK the conversion of AI to AII in prevent the conversion of angiotensin I to combination with other agents. Congestive the LUNGS. angiotensin II by inhibiting the enzyme in the heart failure, left ventricular dysfunction These agents alter one of the lungs- the angiotensin converting enzyme. Diabetes mechanisms of blood pressure control- The action leads to decreased AII and decreased Contraindications and Precautions in

the RAAS or renin- angiotensinaldosterone system. Angiotensin II is a very powerful vasoconstrictor and stimulus for the release of aldosterone. The Prils Benazepril Captoprilprototype Enalapril Enalaprilat Fosinopril Lisinopril Moexipril Quinapril Ramipril Trandorapril THE OLOL THE BETA-BLOCKERS S (B1) These agents are antagonist of the beta- receptors of the sympathetic nervous system. They reduce cardiac output by diminishing the sympathetic nervous system response and sympathetic tone. The olols The Beta-Blockers Vascular resistance and heart rate decrease causing reduced blood pressure. Beta-blockers can either block the beta- receptor, beta 2 receptor or BOTH. The selective betablockers (B1) are specific to one type of receptor only. Common beta-blockers- the -OLOL Non-selective (B1 and B2) Propranolol Carteolol Nadolol Penbutolol Pindolol Timolol Selective and Specific (B1) Acebutolol Atenolol Betaxolol Bisoprolol Metoprolol Pharmacodynamics: These agents block the betaadrenergic receptors in the body, thereby decreasing the heart rate and in turn, the blood pressure. The non-selective agents block both Beta 1 and 2 receptors causing bronchial constriction. The onset of action is 30 minutes and the duration may range from 6-12 hours. Clinical Indications Hypertension Angina pectoris Myocardial infarction

aldosterone level leading to a decrease in blood pressure. The effect of lowering the blood pressure is attributed to the decrease in cardiac workload and decrease peripheral resistance and blood volume.

Contraindications and precautions These agents are not given to patients with: Heart blocks Bradycardia Congestive heart failure Chronic obstructive pulmonary disease Diabetes Side effects and adverse effects CVS- Bradycardia, Hypotension, rebound hypertension when abruptly stopped RespiBronchoconstriction, bronchospasms Othersinsomnia, depression, nightmares, constipation Impaired ability of the liver to convert glycogen to glucose causing HYPOGLYCEMIA! Implementation Monitor patients vital signs. Take the heart rate before giving the drug Instruct the patient to take the drug as prescribed. Warn not to abruptly stop the medication Suggest to avoid over-the-counter medications Give health teaching as to name of drug, dosages and side effects. Remind client NOT to change position abruptly as to avoid orthostatic Hypotension Alert diabetic clients of the possible hypoglycemic effect Inform that this can cause sexual dysfunction Advise client to utilize other means to control blood pressure such as diet modification, exercise, lifestyle changes, etc Advise to eat high fiber foods to counteract constipation

the Use of ACE inhibitors Presence of allergy is a clear contraindication. The ACE inhibitors are NOT given to patients with renal dysfunction because these drugs may cause further decrease in renal blood flow. If given to pregnant women, the drugs cross the placenta and produce renal abnormalities in the fetus. Adverse effects CVS- reflex tachycardia, chest pain, angina, cardiac arrhythmias CNSdizziness, drowsiness, and lightheadedness GIT- GI irritation, nausea, vomiting, peptic ulcer, constipation and liver damage Renalrenal insufficiency, proteinuria Others- rash, photosensitivity, dermatitis and alopecia, sodium excretion and potassium retention, fatal pancytopenia. COUGH- this cough is really unrelenting and bothersome. Implementation The nurse should encourage the patient to implement lifestyle changes such as weight reduction, smoking cessation, decreased intake of alcohol, dietary restriction of salt/fats and increased exercise. Give the drug on an empty stomach, either 1 hour before or 2 hours after meals to ensure proper drug absorption Monitor the patient who is at risk of developing fluid volume alteration Provide comfort measures like safety Precaution, environmental control, skin care, oral care and symptomatic relief of cough. Provide patient teaching including the name of drug, dosage, measure to handle adverse effects and the warning signs to report. Stress the importance of NOT abruptly stopping the medication if symptoms are improving. Caution the patient to change position slowly and to avoid hazardous or delicate tasks and driving if drowsiness is a problem

THE SARTANS THE ANGIOTENSIN II RECEPTOR BLOCKERS These are SELECTIVE agents that specifically bind to the angiotensin II receptors in the blood vessels and adrenal cortex to prevent the release of aldosterone and to prevent vasoconstriction. Pharmacodynamics- The mechanism of action of the A-R-B These agents work by attaching to the Angiotensin II receptors in the vascular smooth muscles and in the adrenal gland. The action results in VASODILATION because AII action (constriction) is inhibited and BLOCKAGE of aldosterone release CALCIUM CHANNEL BLOCKERS These agents prevent the movement of calcium into the cardiac and smooth muscle cells when the cells are stimulated. This blocking of calcium will interfere with the muscle cell's ability to contract, leading to a loss of smooth muscle tone, vasodilation, and a decrease in peripheral resistance. These effects will decrease blood pressure, cardiac workload, and myocardial oxygen consumption. Calcium channel blockers are very effective in the treatment of angina because they decrease the cardiac workload. Pharmacodynamics: Mechanism of action Calcium channel blockers inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction. This effect will depress myocardial contractility, slow cardiac impulse formation in the conductive tissues, and relax and dilate arteries, causing a fall in blood pressure and a decrease in venous

Prototype: Losartan Candesartan Irbesartan Losartan Telmisartan Valsartan Clinical Use of the A-R-B Hypertension, either alone or in combination. These agents are also used if the patient cannot tolerate the unrelenting cough associated with ACE inhibitors. Contraindications and precautions These agents are contraindicated in the presence of allergy. It is NOT GIVEN to pregnant mothers because of the associated FETAL DEATH and severe fetal abnormalities. Lactating women should also avoid these drugs because they can affect the neonate.

CONTRAINDICATION and PRECAUTIONS These drugs are contraindicated in the presence of allergy to any of these drugs With heart block or sick sinus syndrome because these could be exacerbated by the conduction-slowing effects of these drugs With renal and hepatic dysfunction, which could alter the metabolism and excretion of these drugs; and with pregnancy and lactation because of the potential for adverse effects on the fetus and neonate. ADVERSE EFFECTS The adverse effects are related to their effects on cardiac output and on smooth muscle. CNS effects include dizziness, lightheadedness, headache, and fatigue. GI problems can include nausea and hepatic injury related to direct toxic effects hepatic cells. Cardiovascular effects include hypotension, bradycardia, peripheral edema, and heart block. Skin flushing and rash may also occur The main use is the treatment of angina. Also in hypertension. Also in vascular spasm= Raynauds IMPLEMENTATION Monitor blood pressure carefully while patient is on therapy because of increased hypotensive episodes If possible, obtain serial ECG tracing

Adverse effects CNS- headache, dizziness, weakness, syncope and orthostatic Hypotension GIT- Diarrhea, abdominal pain, nausea, dry mouth and tooth pain Respiratory- mild cough Skin- rash, dry skin and alopecia. Implementation Encourage the patient to implement lifestyle changes, including weight loss, smoking cessation, decrease in alcohol and salt in the diet, and increased exercise, to increase the effectiveness of anti-hypertensive therapy. Administer without regard to meals; give with food to decrease GI distress if needed. Alert the surgeon and mark the patient's chart prominently if the patient is to undergo surgery to alert medical personnel that the blockage of compensatory angiotensin II could result in hypotension following surgery that needs to be reversed with volume expansion. Ensure that the patient is not pregnant before beginning therapy and suggest the use of barrier contraceptives while on this drug to avert potential fetal death or abnormalities that have been associated the these drugs. Find an alternative method of feeding the baby if patient is nursing to prevent the potentially danger- block of the reninangiotensin system in the neonate. Monitor the patient carefully in any situation that might lead to a drop in fluid volume (e. g., excessive eating, and vomiting diarrhea, dehydration) to detect treat excessive hypotension that may occur. Provide comfort measures to help the patient tolerate drug effects (e.g., small, frequent meals; access to bathroom facilities; safety precautions if CNS effects occur environmental control; appropriate skin care needed; analgesics as needed).

return. The calcium channel blockers that are used in the treatment of hypertension include the following: The -dipine and others Diltiazem (Cardizem, Tiamate) Verapamil Amlodipine (Norvasc) Felodipine (Plendil) Isredipine (DynaCirc) Nicardipine(Cardene) Nifedipine (CALCIBLOC, Procardia XL)- prototype! Nisoldipine (Sular) THE VASODILATORS Vasodilators produce relaxation of the vascular smooth muscle, decreasing peripheral resistance and reducing blood pressure. They cause the reflex tachycardia that occurs when blood pressure drops The vasodilators are used to treat severe hypertension Diazoxide (Hyperstat) Hydralazine (Apresoline) Minoxidil (Loniten) Sodium Nitroprusside (Nitropress) Tolazoline (Priscoline) Pharmacodynamics: The vasodilators act directly on vascular smooth muscle to cause muscle relaxation, leading to vasodilation and drop in blood pressure. They are indicated for the treatment of severe hypertension that has not responded to other therapy. Contraindications and Precautions The vasodilators are contraindicated in the presence of known allergy to the drug; with pregnancy and lactation because of the potential for adverse effects on the fetus and neonate; and with any condition that could be exacerbated by

Provide comfort measures to help patient tolerate drug effects- includes serving small frequent feedings and safety precaution due to hypotension and dizziness Provide health teaching as to drug name, dosage, administration, side effects and warning manifestations to report

IMPLEMENTATION Encourage the patient to implement lifestyle changes, including weight loss, smoking cessation, decrease in alcohol and salt in the diet, and increased exercise, to increase the effectiveness of antihypertensive therapy. Monitor blood pressure closely during administration to evaluate for effectiveness and to ensure quick response if blood pressure falls rapidly or too much. Monitor blood glucose and serum electrolytes to avoid potentially serious adverse effects. Monitor the patient carefully in any situation that might lead to a drop in fluid volume (e.g., excessive sweating, vomiting, diarrhea, dehydration) to detect and treat excessive hypotension that may occur. Provide comfort measures to help the patient tolerate drug effects (e.g., small, frequent meals, access to bathroom facilities safety precaution if CNS effects occur, environmental control, appropriate skin care as needed, analgesic as needed). Provide thorough patient teaching Offer support and encouragement to deal with the diagnosis drug regimen.

DRUGS FOR THE TREATMENT OF CONGESTIVE HEART FAILURE Vasodilators- Nitrates that act to directly relax vascular muscle tone and cause decrease in blood pressure with pooling of blood in the veins. The preload and afterload will be decreased ACE inhibitors- are agents that block the conversion of angiotensin I to angiotensin II. The result is blockage of the vasoconstriction and decreased blood volume. The afterload will be decreased. Diuretics are employed to decrease the blood volume, which decreases the venous return and the blood pressure. The results are decreased preload and decreased afterload. Beta stimulators will stimulate the beta receptors in the sympathetic nervous system, increasing the myocardial contraction- called positive inotropic effect. Cardiotonic drugs- these agents affect the INTRACELLULAR calcium levels in the heart muscles leading to increased contractility . The result is increased cardiac output, increased renal blood flow, increased perfusion and increased urine formation. The cardiotonic drugs are: the cardiac glycosides and the phosphodiesterase inhibitors.

a sudden fall in blood pressure, such as cerebral insufficiency. ADVERSE EFFECTS CNS- dizziness, anxiety, headache CVS- reflex tachycardia, CHF, chest pain, edema; skin rash, lesions (abnormal hair growth with minoxidil), hypotension GI upset, nausea, and vomiting Cyanide toxicity (dyspnea, headache, vomiting, dizziness, ataxia, loss of consciousness, imperceptible pulse, absent reflexes, dilated pupils, pink color, distant heart sounds, shallow breathing) may occur with nitroprusside, which is metabolized to cyanide and which also suppresses iodine uptake and can cause hypothyroidism.

THE ANTIANGINAL DRUGS In the treatment of angina, three agents are commonly employed- Organic nitrates Beta-blockers and Calcium-channel blockers. The benefits of the drugs lie in their different mode of action. The nitrates can cause vasodilatation of the veins and to some extent, coronary artery Beta-blockers will decrease the heart rate Calcium-channel blockers will decrease force of contraction leading to a decreased myocardial workload and demand. They can also produce vasodilation Anti anginal drugs are effective if the chest pain is relieved

THE CARDIAC GLYCOSIDES These are agents extracted from the foxglove plant. They are available in oral and parenteral preparations. The following are the cardiac glycosides: Digoxin (Lanoxin) Digitoxin (Crystodigin) Ouabain Pharmacodynamics: the Mechanism of action They increase the level of CALCIUM inside the cell by inhibiting the Sodium- Potassium pump. More calcium will accumulate inside the cell during cellular depolarization. Positive inotropic Effect- the myocardium will contract forcefully Increased cardiac output Increased blood flow to the body organs like the kidney and liver Negative chronotropic effect- the heart rate is slowed due to decreased rate of cellular repolarization Bradycardia Decreased conduction

Drug-Drug Interactions If taken with Verapamil, Amniodarone, quinidine, quinine, erythromycin and tetracyclines- can increase the risk of INCREASED effects of digitalis. If taken with potassium-losing diuretics like furosemide- can INCREASE the risk of toxicity and arrhythmias. Potassium replacement must be given. If given with cholestyramine, charcoal and colestipol- can cause impaired absorption of digitalis Implementation Administer the initial rapid digitalization and loading dose as ordered intravenously Monitor the APICAL pulse rate for ONE full minute before administering the drug. Withhold the drug if Less than 60 in adults Less than 90 in infants More than 110 in adults Retake pulse in one hour, if pulses remain abnormal, refer! Check the spelling of the drug- DIGOXIN is different from DIGITOXIN!

DRUGS FOR SHOCK DOPAMINE This is a sympathomimetic drug often used to treat Hypotension in shock states that are not caused by Hypovolemia. This drug is an immediate precursor of nor-epinephrine, occurs naturally in the CNS basal ganglia where it functions as a neurotransmitter. Pharmacodynamics: It can activate the alpha and beta adrenergic receptor depending upon the concentration. It stimulates receptors to cause cardiac stimulation and renal vasodilation. The dose range is 1-20 micrograms/kg/min Pharmacokinetics: Dopamine is administered IV, excreted in the urine. At low dose (1-2 micrograms), dopamine DILATES the renal and mesenteric blood vessels producing an increase output (dopaminergic effect) At moderate dose of 2-10 micrograms, dopamine enhance cardiac output by increasing heart rate (beta 1-adrenergic

velocity through the AV node Clinical Use of the cardiac glycosides Treatment of congestive heart failure Treatment of dysrhythmias like atrial flutter, atrial fibrillation and paroxysmal atrial tachycardia Contraindications and Precautions Contraindicated in the presence of allergy to any cardiac glycoside. They are NOT given to patients with ventricular dysrhythmias, heart block or sick sinus syndrome, aortic stenosis, acute MI, electrolyte imbalances (HYPOKALEMIA, HYPOMAGNESEMIA and HYPERCALCEMIA) and renal failure (may cause accumulation of drug) Adverse Effects of the Cardiac glycosides CNS- Headache, weakness , seizures and drowsiness CVS- arrhythmias If digitalis toxicity is developing- the nurse must assess the following adverse effects: Anorexia, nausea and vomiting, visual changes- YELLOW halo around an object, and palpitations or very slow heart rate

Check the dosage preparation and the level of digitalis in the blood. (Therapeutic level is 0.5 to 2.0 nanograms/mL) Administer intravenous drug VERY slow IV over 5 minutes to avoid arrhythmias. Do NOT administer intramuscularly because it can cause severe pain Administer the drug without food if possible to avoid delayed absorption. Weight patient daily to determine fluid retention Maintain emergency equipment and drugs= Potassium salts, Lidocaine for arrhythmias, phenytoin for seizures, atropine for bradycardia. Provide comfort measures- small, frequent meals, adequate lighting, comfortable position, rest periods and safety precautions Provide health teaching- drug name, action, dosage and side effects. Advise the patient to report any of the following: Visual changes, rapid weight gain, unusually low heart rate, persistent nausea, vomiting and anorexia Monitor serum potassium level Evaluation Evaluate effectiveness of the drug: Increased urine output Normal heart rate in arrhythmia

effect) and elevates blood pressure through peripheral vasoconstriction (alpha adrenergic effect) At higher doses of more than 10 micrograms- vasoconstriction of all vessels will predominate that can lead to diminished tissue perfusion Dopamine is indicated to treat Hypotension, to increase heart rate and to increase urine output (given less than 5 mg/kg/min) The nurse typically prepares the dopamine drip- dopamine (at a concentration of 400-800 mg) is mixed in 250 mL D5W and administered as drip via an infusion pump for precise dosage administration. Sodium bicarbonate will inactivate the dopamine Side effects- Tachycardia hypertension ectopic beats, angina dysrhythmias, myocardial ischemia, nausea and vomiting. Nursing consideration Check the IV site hourly for signs of drug infiltration of dopamine, which can cause severe tissue necrosis. Phentolamine should be infiltrated in multiple areas to reduce tissue damage. Drug is effective if Urine output is increased and BP is increased

THE ORGANIC NITRATES These agents are simple nitric and nitrous acid esters of alcohols. Being alcohol, they differ in their volatility. The following are the nitrates commonly used: Nitroglycerin- A moderately volatile nitrate Isosorbide Dinitrate (Isordil) or mononitrate Amyl nitrate- an extremely volatile nitrate Nitroglycerin This agent is supplied in oral, spray, transdermal and ointment preparations. Pharmacodynamics: the mechanism of action Nitroglycerin relaxes the smooth muscles in the vascular system

Implementation Monitor vital signs, especially watchful for hypotensive episodes Advise patient to remain supine or sit on a chair when taking the nitroglycerin for the first time. Emphasize that he should change his position slowly or rise from bed slowly to avoid orthostatic Hypotension Offer sips of water before giving sublingual nitroglycerin because dryness may inhibit drug absorption Apply nitroglycerin ointment to the designated mark on paper. The nurse should remove any excess ointment on the skin from the previous dose.

DO NOT give more than 3 tablets!!! If chest pain persists for more than 15 minutes, hospital consult should be done immediately. Instruct the client to avoid alcohol while taking nitroglycerin to avoid potentiating the hypotensive effect of the medication If beta blockers and calcium-channel blockers are given, instruct the patients to consult the physician before discontinuing the medication Other components of health teaching for home self-administration: If taking Sublingual Nitroglycerin, the patient should be instructed to place the tablet under the

by its conversion to nitric oxide, a chemical mediator in the body that relaxes smooth muscles. Administered nitrates Increased nitrates in the blood increased formation of nitric oxide increased cGMP formation increased dephosphorylation of myosin Vascular smooth muscle relaxation vasodilatation Pharmacokinetics- absorption to excretion It can be given orally, parenterally and topically. The onset of action of nitroglycerin is more than 1 hour. Because significant first-pass hepatic effect, Nitroglycerin is given SUBLINGUALY. Side effects and adverse effects HEADACHE is the most common effect of nitroglycerin. CVS- postural Hypotension, facial flushing, tachycardia TOLERANCE- the tolerance to the actions of nitrates develop rapidly. This can be managed by providing a day of abstinence.

She should NEVER USE her bare fingers because the drug can be absorbed, utilize gloves or tongue blades instead. Apply nitroglycerin patch to an area with few hairs. Never touch the medication portion. The patch and the ointment should NOT be applied near the area for defibrillation because explosion and skin burns may result Emphasize that tolerance to the nitroglycerin can occur. If the medication cannot relieve the pain, report to the hospital immediately. Provide client health teaching- the sublingual nitroglycerin tablet is USED if chest pain occurs The dose may be repeated if pain is unrelieved within 5 minutes. Repeat the medication administration if the pain has not yet subsided.

tongue for quick absorption. A burning sensation/biting/stinging sensation may indicate that the tablet is FRESH! Store the tablet in a dark container, keep it away from heat and direct sunlight to avoid lessening the potency Other components of health teaching for home self-administration: HEADACHES are common in the initial period of nitroglycerin therapy. Advise patient to take PARACETAMOL for relief The nitroglycerin patch is applied once a day, usually in the morning. The sites should be rotated, in the chest, arms and thighs avoiding hairy areas. Other components of health teaching for home self-administration: Position supine with elevated legs to manage Hypotension. Nitroglycerin tablet can be taken prophylactically in situations where chest pain is anticipated- Sex, exercise, etc.. If patient is taking beta blockers, instruct how to obtain heart rate in a minute

ANTI-ARRHYTHMIAS Arrhythmias (sometimes called Dysrhythmias) are conduction dysfunctions caused by abnormalities in impulse generation or impaired transmission of the impulses. They are simply deviations from the normal rate or pattern of the heartbeat. Four things may happen during arrhythmias: The heart will beat too FAST (tachycardia, either the atrium or the ventricle) The heart will beat too slow (bradycardia) The heart will respond to other impulses generated by the cardiac cells (other than the SA node) The heat will respond to impulses traveling along extra

Class 2 agents- are BETA blockers that affect the depolarization. They decrease the conduction velocity, automaticity and recovery time. Examples are: Propranolol, Metoprolol, pindolol, acebutol and esmolol Class 3 agents- are POTASSIUM channel blockers that diminish the outward potassium current during repolarization of cardiac cells. They increase the refractory period and prolong the action potential. Examples are: sotalol, bretylium, amniodarone Class 4 agents- are calcium channel blockers that decrease the calcium influx into the specialized cardiac muscle cells causing slowed conduction. They increase the refractory period

Planning The client will no longer experience abnormal cardiac rhythm The client will comply with the drug regimen Implementation Monitor Vital signs especially BP and HR. Patient can develop Hypotension Administer the parenteral drugs slow IV for a period of 2-3 minutes Monitor ECG for abnormal patterns and report findings. Instruct to report palpitations and abnormal cardiac rate Maintain life support equipment on standby to treat severe adverse reactions that might occur

pathways Anti-arrhythmic agents are given to modify impulse generation and conduction. The desired action of these antidysrhythmics is to restore the cardiac rhythm to normal. They affect the action potential of the cardiac cells, altering their automaticity, conductivity, or BOTH Because the anti-arrhythmic drugs affect the conduction system, they also can produce ARRHYTHMIAS! They are also Pro-Arrhythmics! The classes of anti-arrhythmic agents: Class 1 agents - are fast SODIUM channel blockers that affects the depolarization phase. Class 2 agents- are BETA blockers that affect the depolarization. Class 3 agents- are POTASSIUM channel blockers that diminish the outward potassium current during repolarization of cardiac cells. Class 4 agents- are calcium channel blockers that decrease the calcium influx into the specialized cardiac muscle cells causing slowed conduction Class 1 agents - Class 1 AQuinidine, Procainamide, Disopyramide, Moricizine Class 1 BLidocaine, Mexiletine, Tocainide Class 1 C- Encainide, Flecainide, propafenone

of the AV node, which decreases the ventricular response. The examples of calcium channel blockers are diltiazem and verapamil Miscellaneous- digoxin and adenosine General Nursing Process for Antiarrhythmics Assessment Patient Historythe nurse obtains health and drug histories. She should elicit symptoms of shortness of breath, heart palpitations, coughing, chest pain, previous angina or dysrhythmias, and the current medications. Physical Examinationthe nurse performs assessment and baseline monitoring Laboratory exams- the nurse obtains ECG results and cardiac markers- CK-MB, AST and LDH) Nursing Diagnoses Alteration on perfusion: decreased cardiac output Alteration in thought processes and sensoryperceptual alteration Anxiety related to irregular heartbeat Risk for activity intolerance Risk for injury related to CNS effects Knowledge deficit regarding drug therapy

Implementation Establish safety precautions- side rails, lighting, and noise control. Provide client teaching. Instruct the client to take the prescribed drug as ordered. Emphasize the client to avoid alcohol, caffeine and tobacco. Alcohol can intensify the hypotensive effects, caffeine increases the cathecolamine levels and tobacco can promote vasoconstriction. Instruct the client to report side effects including dizziness, faintness, and nausea and vomiting. Evaluation Evaluate the effectiveness of the prescribed anti-dysrhythmic by comparing heart rates with baseline heart rate. Assess the clients response to the drug. Monitor for adverse effect- sedation, Hypotension, cardiac arrhythmias, respiratory depression, CNS effect. Evaluate the effectiveness of the teaching plan. Monitor the effectiveness of comfort measures and compliance to regimen.