Cardiovascular - Summary Saunders Comprehensive Review for the Nclex-Rn Examination Cardiovascular N

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Cardiovascular - Summary Saunders Comprehensive Review for the Nclex-Rn Examination Cardiovascular Nursing

Diagnostic Tests Cardiac Markers CK-MB (creatinine kinase, myocardial muscle)

- an elevation in value indicates myocardial damage - an elevation occurs within hours and peaks at 18 hours following an acute ischemic attack Normal value male: 2-6ng/mL Normal value female: 2 to 5ng/mL

Troponin

Values are low, any rise can indicate myocardial cell damage - troponin I: rises within 3 hours and persists for up to 7-10 days (this one is especially related to myocardial injury) … less than 0.3ng/mL - troponin T less than 0.2ng/mL - serum levels of troponin T and I increase 4-6 hours after the onset of the MI, peak at 10-24 hours, and return to baseline after 10-14 days

Myoglobin

- myoglonin is an oxygen-binding protein found in cardiac and skeletal muscle - the level rises within 2 hours after cell death, with a rapid decline in the level after 7 hours - may not be cardiac specific

Complete Blood Count (CBC) Red Blood Cell Count - decreases in rheumatic heart disease and infective endocarditis - increases in conditions characterized by inadequate tissue oxygenation White Blood Cell Count - increases in infectious and inflammatory diseases of the heart - increases after an MI because large numbers of WBCs are needed to dispose of the necrotic tissue resulting from the infarction

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Hemocysteine - elevated levels may increase the risk of cardiovascular disease - normal value: 0.54 to 1.9 mg/L Highly Sensitive C-Reactive Protein - detects an inflammatory process (e.g. atherothrombosis) - less than 1mg/dL is considered low risk - greater than 3mg/dL Blood Coagulation Factors - an increase can occur during and after an MI, which places the patient at greater risk for thrombophlebitis and formation of clots in the coronary arteries Serum Lipids - the lipid profile measures serum cholesterol, triglyceride, and lipoprotein levels - lipid profile is used to assess the risk of developing coronary artery disease - lipoprotein-a or Lp(a) increases atherosclerotic plaques and increases clots…. Normal value should be less than 30mg/dl Electrolytes * electrolyte and mineral imbalances can cause cardiac electrical instability that can result in life-threatening dysrhythmias Potassium Hypokalemia - causes increased cardiac electrical instability, ventricular dysrhythmias, and increased risk of digoxin toxicity - ECG shows flattening and inversion of the T wave, the appearance of a U wave, and ST depression

Sodium

Calcium

Hyperkalemia - causes asystole and ventricular dysrhythmias - ECG shows tall, peaked T waves, widened QRS, or flat P waves - the serum sodium level decreases with the use of diuretics - the serum sodium level decreases in heart failure, indicating water excess Hypocalcaemia - can cause ventricular dysrhythmias, prolonged ST and QT intervals, and cardiac arrest Hypercalcemia - can cause atrioventricular block, tachycardia or

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bradycardia, digitalis hypersensitivity, cardiac arrest

Phosphorus

Magnesium

- should be interpreted with calcium levels because the kidneys retain or excrete one electrolyte in an inverse relationship to the other - low level can cause ventricular tachycardia and fibrillation

- ECG will show tall T waves and depressed ST segments (low level) - high level can cause muscle weakness, hypotension, and bradycardia Blood Urea Nitrogen - BUN is elevated in heart disorders that adversely affect renal circulation, such as heart failure and cardiogenic shock - range: B-type Natriuretic peptide (BNP) - BNP is released in response to atrial and ventricular stretch; it serves as a marker for heart failure - should be less than 100pg/mL… the higher the level, the more severe the heart failure

Diagnostic Procedures Chest X-Ray - done to determine anatomical changes such as size, silhouette, and position of the heart Holter Monitoring - noninvasive test where the client wears a monitor and an electrocardiographic tracing is recorded over 24 or more hours while the client performs their activities of daily living - the monitor identifies dysrhythmias and evaluates the effectiveness of anti-dysrhythmic or pacemaker therapy Echocardiography - non-invasive procedure that evaluates structural and functional changes in the heart - used to detect vulvar abnormalities, congenital heart defects, cardiac function Exercise Electrocardiography Testing (stress test) - studies the heart during activity and detects and evaluates coronary artery disease

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- treadmill testing is the most common - if the client is unable to tolerate exercise, an IV infusion of dipyridamole or dobutamine hydrochloride is given to dilate the coronary arteries and stimulate the effects of exercise (NPO for 3-6 hours before) Cardiac Catheterization - an invasive test involving the insertion of a catheter into the heart and surrounding vessels - obtains information about the structure and performance of the heart chambers and valves and the coronary circulation  Pre-procedure interventions: - obtain informed consent

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- assess for allergies to seafood, iodine, or radiopaque dyes… if allergic, pre-medicate with antihistamines and corticosteroids to prevent a reaction - withhold solid foods for 6 to 8 hours and liquids for 4 hours to prevent vomiting and aspiration - document height and weight (determines how much dye is needed) - document baseline vitals, especially peripheral pulses - inform patient that they may feel a fluttery feeling as the catheter passes through the heart - shave and cleanse the insertion site  Post-procedure interventions: - asses vitals and cardiac rhythms every 30 minutes for at least 2 hours - assess peripheral pulses - monitor chest pain - notify HCP if patient complains of numbness and tingling, cool pale or cyanotic extremities, or loss of peripheral pulses… emergency; could be a clot formation - maintain strict bed rest for 6 to 12 hours

NOTE: Metformin must be held for 24 hours before any procedure involving iodine dye because of the risk of lactic acidosis and the medication is not returned until prescribed by the HCP

Cardiac Dysrhythmias Management of Dysrhythmias 1. Vagal Maneuvers Carotid sinus massage - turn head away from the side - massage over 1 carotid artery for a few seconds to determine whether a change in cardiac rhythm occurs - the client must be on a cardiac monitor (ECG) and get a rhythm strip before, during, and after the procedure Valsalva Maneuver - HCP instructs the client to bear down or induces a gag reflex to stimulate a vagal response - monitor HR, rhythm, and BP - rhythm strip before, during, and after - provide an emesis basin if the gag reflex is stimulated - have a defibrillator and resuscitative equipment available 2. Cardioversion

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- cardioversion is a synchronized countershock to convert an undesirable rhythm to a desirable one - lower amount of energy used than defibrillation - can be used for stable tachydysrhythmias resistant to medical therapies or an emergent procedure for hemodynamically unstable ventricular or supraventricular tachydysrhythmias Pre-procedure: - if it is elective, ensure that informed consent is obtained - administer sedation as prescribed - if elective, hold digoxin for 48 hours - if elective for atrial fibrillation or flutter, the client should receive anticoagulant therapy for 4 to 6 week pre-procedure During procedure: - ensure skin is clean and dry in the area where the electrode pads/hands-off pads will be placed - stop oxygen during procedure to avoid fire hazard - ensure that no one is touching the bed or client when delivering the countershock Post-procedure: - priority assessment includes ability of the client to maintain the airway and breathing - resume oxygen administration - assess vitals and level of consciousness - monitor cardiac rhythm - monitor for indications of successful response, such as conversion to a normal sinus rhythm, strong peripheral pulses, adequate BP, and adequate urine output 3. Defibrillation - used for pulseless ventricular tachycardia or fibrillation - the defibrillator is charged to 360 joules for 1 countershock, then CPR is resumed immediately and continued for about 2 minutes - reassess the rhythm after 2 minutes, and if VF or VT continues, the defibrillator is charged to give a second shock NOTE: it is very important to ensure that oxygen is shut off before defibrillating and that no one is touching the bed or the client Until the defibrillator is attached and charged, the client is resuscitated with CPR. Once the defibrillator has been attached:  check the ECG to ensure the proper rhythm is there (ventricular fibrillation or pulseless ventricular tachycardia)  leads are checked for loose connections  nitroglycerin patch is removed from patient

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 patient does NOT have to be intubated Evaluation of successful defibrillation – patient is rousable, has a sinus rhythm, and a blood pressure within acceptable ranges

Pacemakers Temporary or permanent device that provides electrical stimulation and maintains the heart rate when the client’s intrinsic pacemaker fails to provide a perfusing rhythm Synchronous (demand): senses the client’s rhythm and paces only if the client’s intrinsic rate falls below the set pacemaker rate Asynchronous (fixed): paces at a pre-set rate regardless of the client’s intrinsic rhythm and is used when the client is asystolic or profoundly bradycardic Temporary Non-invasive transcutaneous pacing: used as a temporary emergency measure in the profoundly asystolic or bradycardic paitent - large electrode pads are placed on the chest and back and connected to an external pulse generator - wash skin with soap and water beforehand (no need to shave) - place the posterior electrode between the spine and left scapula behind the heart - place the anterior electrode between V2 and V5 over the heart - do not place over breast tissue, but below it - do not take pulse or BP on the left side... will not be accurate Invasive transvenous pacing - pacing lead wire is placed through the antecubital, femoral, jugular, or subclavian vein

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into the right atrium or right ventricle so that it is in direct contact with the endocardium - restrict patient movement to prevent lead wire displacement - monitor insertion site NOTE: vital signs are monitored and cardiac monitoring is done continuously for the client with a pacemaker Permanent - pulse generator is internal and surgically implanted in a subcutaneous pocket below the clavicle - may be powered by a lithium battery with an average lifespan of 10 years or nuclear powered with an average lifespan of 20 years - pacemaker function can be checked in the HCP office by a pacemaker interrogator or programmer from home, using a special telephone transmitter device Client Teaching  Signs of battery failure and when to notify the HCP  Report any fever, redness, swelling, or drainage from the insertion site  Report signs of dizziness, weakness, fatigue, swelling of the ankles and legs, chest pain, or shortness of breath  Keep a pacemaker identification card in the wallet and wear a MedicAlert bracelet  Instruct patient how to take pulse, to take the pulse daily, and to maintain a diary of daily pulse rates  Wear loose-fitting clothing over the pulse generator site  Inform airport security  Most electrical appliances can be used without any interference, however, do not operate electrical appliances directly over the site  Avoid contact sports  Avoid transmitter towers and anti-theft devices in stores  If any unusual feeling occurs when near any electrical devices, move 5 to 10 feet away and check the pulse  Use cellphones on side opposite the pacemaker

Coronary Artery Disease (CAD) The narrowing or obstruction of 1 or more coronary arteries as a result of atherosclerosis, which is an accumulation of lipid-containing plaque in the arteries. The disease causes decreased perfusion of myocardial tissue and inadequate myocardial oxygen supply, leading to: - hypertension - angina - dysrhythmias - MI - heart failure - death

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It develops over time; many years. When symptomatic, the disease process is usually well advanced; symptoms occur when the coronary artery is occluded to the point that inadequate blood supply to the muscle occurs, causing ischemia. Goal of treatment: alter the atherosclerotic progression.

Risk Factors Unmodifiable:  age  gender (men > women until 60yr)  ethnicity (African American > Caucasian)  genetic predisposition  family history of heart disease Modifiable:  increased serum lipids  hypertension  cigarette smoking  obesity  physical inactivity  diabetes mellitus  stressful lifestyle  psychosocial state  homocysteine level  metabolic syndrome Clinical Manifestations – 3 Major 1. Chronic Stable Angina 2. Acute Coronary Syndrome - unstable angina - MI 3. Sudden cardiac death Assessment  possibly normal findings during asymptomatic periods  chest pain  palpitations  dyspnea  syncope  cough or hemoptysis  excessive fatigue Interventions

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 assist the client to identify modifiable risk factors and to set goals to reduce the impact of risk factors  assists to identify barriers to compliance  instruct about low-calorie, low-sodium, low-cholesterol, low-fat diet with increased fiber  stress the importance that dietary changes are not temporary and must be maintained for life  provide community resources regarding exercise, smoking cessation, and stress reduction  encourage weight loss  drug therapy – lipid-lowering medications (questran, socor, Lipitor, pravachol) Medications  nitrates – dilate the coronary arteries and decrease preload and afterload  calcium channel blockers – dilate coronary arteries and reduce vasospasm  cholesterol lowering drugs – reduce the development of atherosclerotic plaque  beta blockers – reduce BP in those who are hypertensive  lipid lowering drugs Diagnostic Studies Electrocardiography - when blood flow is reduced and ischemia occurs: ST depression, T wave inversion, or both is noted… ST segment returns to normal when the blood flow returns Cardiac Catheterization - shows the presence of atherosclerotic lesions Blood Lipid Levels - may be elevated - cholesterol-lowering medications may be prescribed to reduce the development of atherosclerotic plaques

Angina Clinical syndrome characterized by paroxysms of pain or a feeling of pressure in the anterior chest caused by myocardial ischemia as a result of inadequate myocardial blood and oxygen supply.

- imbalance between oxygen supply and demand - causes include obstruction of coronary blood blow resulting from atherosclerosis, coronary artery spasm, or conditions increasing myocardial oxygen supply Types 1. Stable angina – aka exertional angina

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- occurs with activities that involve exertion or emotional stress - relieved with rest or nitroglycerin - usually has a stable pattern of onset, duration, severity, and relieving factors 2. Unstable angina – aka preinfarction angina - occurs with an unpredictable degree of exertion or emotion and increases in occurrence, duration, and severity over time - pain may not be relieved with nitroglycerin 3. Variant angina – aka Prinzmetal’s or vasospatic angina - results from coronary artery spam - may occur at rest - attacks may be associated with ST elevation 4. Intractable angina - chronic, incapacitating angina unresponsive to treatment 5. Preinfarction angina - associated with acute coronary insufficiency - lasts longer than 15 minutes - symptoms of worsening cardiac ischemia - characterized by chest pain that occurs days to weeks before an MI Precipitating Factors  physical activity  temperature extremes  strong emotions  consumption of heavy meal  cigarette smoking  sexual activity  stimulants  circadian rhythm patterns Assessment  pain - usually described as mild or moderate - substernal, crushing, squeezing - may radiate to the shoulders, arms, jaw, neck, or back - pain intensity is unaffected by inspiration and expiration - pain usually lasts less than 5 minutes, but can last up to 15 to 20 - pain is relieved by nitroglycerin  dyspnea  pallor

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 sweating  palpitations and tachycardia  dizziness and syncope  hypertension  digestive disturbances (indigestion) Interventions IMMEDIATE:  assess pain and institute pain relief measures  administer oxygen by nasal cannula  assess vitals and provide continuous cardiac monitoring and nitroglycerin to dilate the coronary arteries  ensure that bed rest is maintained and that patient is in semi-Fowlers  stay with the patient  obtain a 12-lead ECG Following acute episode:  assist the client to identify angina-precipitating events  instruct to stop activity and rest if chest pain occurs and to take nitroglycerin… call 911 if nitro does not relieve the pain (can take aspirin too)  assist the client to identify modifiable risk factors and to set goals to reduce the impact of risk factors  provide community resources regarding exercise, smoking cessation, and stress reduction  encourage weight loss

Diagnostic Studies Electrocardiography

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- readings are normal during rest – ST depression or T wave inversion during acute episode Stress Testing - chest pain or changes in the ECG or vital signs during testing may indicate ischemia Cardiac enzymes and troponin - findings are normal in angina Cardiac Catheterization - provides a definitive diagnosis by providing information about the patency of the coronary arteries Medications  antiplatelets (ASA) – reduces risk of MI  b-adrenergic blockers (Lopressor)  nitrates (nitrostat, isordil)  calcium channel blockers (Cardizem)  ACE Inhibitors (Capoten)  analgesics

Myocardial Infarction (MI) MI occurs as a result of sustained ischemia, causing irreversible cellular death.

Infarction does not occur instantly but evolves over several hours. Obvious physical

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changes do not occur in the heart until 6 hours after, when the infarcted area becomes blue and swollen. After 48h, the infarction turns grey with yellow streaks. By 8-10 days, granulation tissue forms.

Causes  thrombus  occlusion  coronary artery spasm  hypoxemia Risk Factors  atherosclerosis  CAD  high cholesterol  smoking  hypertension  obesity  physical inactivity  impaired glucose tolerance  stress Symptoms  severe, immobilizing chest pain not relieved by rest, position change, or nitrates  pain may occur while active, at rest, or sleeping; most common in early am  heaviness, pressure, tightness, burning, constricting, or crushing  substernal, retrosternal, or epigastric locations  radiation to neck, jaw, arms, or back  occasionally fever  pain lasts 30 minutes or longer  nausea and vomiting  diaphoresis  dyspnea  dysrhythmias  feelings of fear/anxiety/impending doom  pallor, cyanosis, grey/ashen, coolness of extremities OR…. Patient can be asymptomatic, have atypical discomfort, or diabetic clients may not feel severe pain because cardiac neuropathy Diagnostic Studies Troponin: level rises within 3 hours and remains elevated for up to 7-10 days Total CK: rises within 6 hours after the onset of chest pain and peaks within 18 hours after death of cardiac tissue CK-MB: peak elevation occurs 18 hours after the onset of chest pain and returns to

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normal 48-72h later WBC: elevated wbc count appears on the second day following the MI and lasts up to 1 week ECG: shows either ST elevation, T wave inversion, or non-ST elevation with an abnormal Q wave - hours to days afterward, the ST and T wave changes will return to normal, but Q wave changes are usually permanent

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Interventions – ACUTE 1. obtain a description of chest discomfort 2. Administer O2 and institute pain relief measures (morphine and nitroglycerin) 3. Assess vitals and cardiovascular status and maintain cardiac monitoring 4. Assess respiratory rate and breath sounds for signs of HF 5. Ensure bed rest and place in semi-Fowler’s 6. Establish IV access 7. Obtain 12-lead ECG 8. Monitor laboratory values 9. Monitor for cardiac dysrhythmias (particularly tachycardia and PVCs) 10. Administer thrombolytic therapy (within first 6 hours) and monitor for bleeding 11. Assess distal peripheral pulses and skin temperature 12. Monitor BP closely – if systolic is lower than 100 or 25mm lower than last reading, lower the head of bed and notify the HCP 13. Administer beta blockers

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14. Provide reassurance NOTE: Pain relief increases oxygen supply to the myocardium; administer morphine as a priority in managing pain in the client having an MI Interventions – After Acute Episode 1. Maintain bed rest 2. Allow the patient to stand to void 3. Provide ROM to prevent thrombus formation 4. Progress to dangling legs at the side of the bed for 30 minutes q3 5. Progress to ambulation 6. Administer cardiac meds (ACE inhibitors, calcium channel blockers) 7. Encourage patient to verbalize feelings Cardiogenic shock is a complication that can occur following an MI; it occurs with severe damage to the left ventricle.

Classic signs:  hypotension  rapid pulse that becomes weaker  decreased urine output  cool, clammy skin  increased respiratory rate NOTE: It is important that the nurse assess the patient developing cardiogenic shock after an MI for ventricular dysthymias

Heart Failure The inability of the heart to pump sufficient blood to maintain adequate cardiac output to meet the metabolic needs of the body. Diminished cardiac output = inadequate peripheral tissue perfusion. *Congestion of the lungs and periphery may occur; the client can develop acute pulmonary edema.

Types of Heart Failure Right or left ventricular Most HF begins with left ventricular failure and progresses failure to failure of both ventricles Acute pulmonary edema, a medical emergency, results from left ventricular failure If pulmonary edema is not treated, death will occur from suffocation because the patient will literally drown in their own fluids Forward or backward Forward: inadequate output causes decreased perfusion failure to vital organs Backward: blood backs up behind the affected ventricle,

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causing increased pressure in the atrium

Low output or high output

Systolic or diastolic failure

Low: not enough cardiac output is available to meet the demands of the body

High: when a condition causes the heart to work harder to meet the demands of the body Systolic: problems with contraction and ejection of blood Diastolic: problems with the heart relaxing and filling with blood

Compensatory Mechanisms  act to restore cardiac output to near-normal levels  initially, these mechanisms increase cardiac output, but they eventually have a damaging effect on pump action  examples: - increased HR - improved stroke volume - arterial vasoconstriction - sodium and water retention - myocardial hypertrophy Left vs. Right Sided Heart Failure – Clinical Manifestations Right Sided Left Sided  dependent edema (legs and sacrum);  pulmonary congestion (e.g. crackles) usually pitting  dyspnea  swelling of fingers and hands  tachypnea  jugular venous distention  crackles in the lungs  abdominal distention  dry, hacking cough  hepatomegaly  paroxysmal nocturnal dyspnea  splenomegaly  fatigue  anorexia  anxiety  nausea  restlessness  weight gain  frothy sputum, sometimes blood tinged  nocturia  increased or decreased BP  increased or decreased BP * RED FLAG: change in behaviour, restlessness, not sure what is going on

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NOTE: signs of left ventricular failure are evident in the pulmonary system; signs of right ventricular failure are evident in the systemic circulation Pulmonary Edema Clinical Manifestations  severe dyspnea  tachycardia  tachypnea  nasal flaring or use of accessory breathing muscles  wheezing and crackles  gurgling respirations  expectoration of large amounts of blood-tinged frothy sputum  acute anxiety and restlessness  cold, clammy skin  cyanosis PRIORITY NURSING ACTIONS 1. Place the client in a high Fowler’s position.

2. Administer oxygen.

3. Assess the client quickly, including lung sounds.

4. Ensure IV access device is in place.

5. Prepare for the administration of a diuretic and morphine sulfate.

6. Insert a Foley catheter as prescribed.

7. Prepare for intubation and ventilation support.

8. Document the event, actions taken, and client’s response.  The client is immediately placed in a high Fowler’s position, with legs in a dependent position, to reduce pulmonary congestion and relieve edema. Oxygen is always prescribed, usually in high concentration, to improve gas exchange and pulmonary function.

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 furosemide, a rapid acting diuretic, will eliminate accumulated fluid  morphine sulfate reduces venous return (preload), decreases anxiety, and also reduces the work of breathing  Foley measures output accurately  weight measurement will also determine response to treatment  digoxin may increase ventricular contractility and enhance stroke volume When in CHF, UNLOAD FAST Upright Nitrates Lasix Oxygen ACE Inhibitor Digoxin Fluids decreased Afterload decreased Sodium restriction Test (digoxin, ABGs, K+) Interventions – Post Acute Episode 1. Assist the patient to identify precipitating factors and methods of eliminating them 2. Encourage to verbalize feelings about the lifestyle changes required 3. Instruct about the prescribed medication regimen (may include digoxin, diuretics, ACE inhibitors, low-dose beta blockers, and vasodilators) 4. Advise to notify HCP is side effects occur from the medication.

5. Advise to avoid OTC medications.

6. Instruct to avoid large amounts of caffeine 7. Instruct about low-sodium, low-fat, and low-cholesterol diets 8. Provide with a list of potassium rich foods (diuretics can cause hypokalemia) 9. Instruct about fluid restriction; spread the fluid out during the day… can suck on hard candy to reduce thirst 10. Balance periods of activity and rest.

11. Avoid isometric activities 12. Monitor daily weights.

13. Report signs of fluid retention, such as edema or weight gain.

Cardiogenic Shock Failure of the heart to pump adequately, thereby reducing cardiac output and compromising tissue perfusion; necrosis of more than 40% of the left ventricle occurs which usually results from occlusion of major coronary vessels.

Impaired pumping ability of the left ventricule

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↓ ↓ stroke volume ↓

↓ inadequate systolic emptying ↓

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↓ cardiac output ↓ ↓ blood pressure ↓ ↓ cellular oxygen supply ↓ ↓ tissue perfusion ↓ impaired cellular metabolism

↑ left ventricular filing pressure ↓ ↑ left atrial pressure ↓ diastolic dysfunction: ineffective filling ↓ ↑ pulmonary venous pressure ↓ ↑ pulmonary capillary pressure ↓ ↓ pulmonary interstitial intraalveolar edema edema ↓ ↓ cellular oxygen supply cellular oxygen supply

Precipitating Causes  MI  Cardiomyopathy  Blunt cardiac injury

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 severe systemic or pulmonary hypertension  cardiac tamponade  myocardial depression from metabolic problems

Early Manifestations  hypotension (lower than 90mm systolic)  tachycardia  narrowed pulse pressure  increased myocardial oxygen consumption As shock progresses  urine output lower than 30ml/hr  cold, clammy skin  poor peripheral pulses  tachypnea  pulmonary congestion  disorientation  restlessness  confusion  continuing chest discomfort

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 decreased capillary refill time Interventions 1. Administer O2 2. Administer morphine sulfate IV (decrease pulmonary congestion and relieve pain) 3. Prepare for intubation and mechanical ventilation 4. Administer diuretics and nitrates while constantly monitoring BP 5. Administer vasopressors and positive inotropes to maintain organ perfusion.

6. Prepare for insertion of an intraaortic balloon pump to improve coronary artery perfusion and cardiac output 7. Prepare for immediate reperfusion procedures such as PTCA or coronary artery bypass graft.

8. Monitor urinary output.

11. Monitor distal pulses.

Hemodynamic Monitoring Central Venous Pressure – the pressure within the superior vena cava - measured with a central venous line in the superior vena cava - normal: 3 to 8 mmHg - high: indicates an increase in blood volume (from sodium and water retention, excessive IV fluids, kidney failure) - low: decrease in circulating blood volume (from fluid imbalances, hemorrhage, severe vasodilation); may see pooling or blood in the extremities Mean Arterial Pressure – an approximation of the average pressure in the systemic circulation throughout the cardiac cycle Must be between 60 and 70 mmHg for adequate organ perfusion

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Endocarditis Inflammation of the inner lining of the heart and valves. Ports of entry for the infecting organism include the oral cavity (especially if the client had a dental procedure in the previous 6 months), infections (genitourinary, cutaneous, GI, systemic), and surgery or invasive procedures, such as IV line placement.

Risk Factors  IV drug users  clients who have had valve replacements or repair of valves with prosthetic materials  other structural cardiac defects Clinical Manifestations  fever  anorexia and weight loss  cardiac murmurs  heart failure  embolic complications  petechiae  splinter hemorrhages in the nail beds  Osler’s nodes (reddish, tender lesions) on the pads of the fingers, hands, and toes  Janeway lesions (nontender hemorrhagic lesions) on the fingers, toes, nose, or earlobes  splenomegaly  clubbing of the fingers Interventions  provide adequate rest balanced with activity to prevent thrombus formation  maintain antiembolism stockings  monitor for signs of heart failure  monitor for splenic emboli (sudden abdominal pain radiating to the left shoulder and the presence of rebound abdominal tenderness on palpation)  monitor for renal emboli (flank pain radiating to the groin)  monitor for confusion, aphasia, or dysphasia (CNS emboli)

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 monitor for pulmonary emboli (dyspnea, chest pain, cough)  assess skin, mucous membranes, and conjunctiva for petechiae

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 assess nail beds for splinter hemorrhages  assess for Osler’s nodes and Janeway lesions  assess for clubbing  evaluate blood culture results  administer IV antibiotics Patient Education – Endocarditis  Maintain aseptic technique during setup and administration of IV antibiotics  Administer IV antibiotics at scheduled times to maintain the blood level  Monitor IV catheter sites for signs of infection and report any signs to the HCP immediately  Record temperature daily for up to 6 weeks; report high fever  Maintain good oral hygiene; brush with a soft toothbrush twice a day minimum and rinse well  Avoid floss or oral irrigation  Cleanse any skin lacerations thoroughly and apply topical antibiotic ointment  Inform all HCPs of history of endocarditis and request prophylactic antibiotics prior to invasive respiratory or dental procedures

Pericarditis Acute or chronic inflammation of the pericardial sac and the outer fibrous layer. It is most often idiopathic; coxsackievirus B group most common.

Other causes: - uremia - bacterial infection - acute MI - tuberculosis - neoplasm - trauma With MI client, there are 2 syndromes: Acute (48-72 hours) Dressler’s syndrome (appears 4-6 weeks later) Clinical Manifestations  pericardial friction rub – hallmark finding; heard on auscultation  progressive, severe chest pain (worse with deep inspiration and supine, relieved by sitting and leaning forward, radiates to trapezius muscle)  dyspnea  fever and chills

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 fatigue and malaise

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 elevated WBC  atrial fibrillation is common  signs of right ventricular failure in clients with chronic pericarditis Interventions  place in high Fowler’s or upright and leaning forward  administer oxygen  administer analgesics, NSAIDs, or corticosteroids for pain  auscultate for pericardial friction rub  check results of blood culture to identify causative organisms  administer antibiotics  administer diuretics and digoxin  monitor for signs of cardiac tamponade and notify HCP if it may occur Complications  pericardial effusion - accumulation of excess fluid in the pericardium - cough, dyspnea, tachypnea  cardiac tamponade  accumulation of fluid in pericardial sac

Cardiac Tamponade Accumulation of fluid in the pericardial cavity. Tamponade restricts ventricular filling, and cardiac output drops. This is a severe, life-threatening condition.

NOTE: Acute cardiac tamponade can occur when small volumes of fluid (20-50ml) accumulate rapidly in the pericardium.

Symptoms  hypotension  narrowed pulse pressure  JVD with clear lung sounds  pulsus paradoxus  muffled heart sounds  decreased cardiac output Interventions 1. Transfer to critical care unit for hemodynamic monitoring 2. Administer IV fluids to manage decreased cardiac output 3. Prepare for CXR or echocardiography 4. Prepare for pericardiocentesis to withdraw pericardial fluid; monitor for recurrence of cardiac tamponade - blood pressure should increase almost immediately after procedure

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5. If the client continues to experience recurrent tamponade, a portion or all of the pericardium may be removed to allow adequate ventricular filling and contraction.

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Rheumatic Fever Rheumatic fever: inflammatory disease that may affect connective tissues of the body.

Rheumatic heart disease: chronic condition resulting from rheumatic fever.

Acute rheumatic fever: complication that occurs as a delayed sequela (2-3 weeks) to group A streptococcal pharyngitis; found primarily in young adults Clinical Manifestations  chest pain  excessive fatigue  palpitations  thumping sensation in the chest  SOB  edema  Aschoff’s bodies  extracardiac lesions (connective tissue, joints, skin, and CNS) Assessment  malaise  anorexia  palpitations  ataxia  chest and abdominal pain  low-grade fever  subcutaneous nodules  chorea  polyarthritis Subjective data: IV drug use, dyspnea, fatigue, palpitations, angina Objective data: fever, diaphoresis, crackles, adventitious heart sounds, tachycardia, hypotension Interventions  no single diagnostic test  treatment – drug therapy and supportive measures

Valvular Heart Disease Valvular heart disease occurs when the heart valves cannot open fully (stenosis) or close completely (regurgitation).

Mitral Stenosis

Mitral

Aortic Stenosis

Aortic

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Regurgitation Majority of adult cases result from rheumatic heart

Asymptomatic for years until development of

Regurgitation Usually discovered in childhood, adolescence, or

Results in volume overload as the valve does not

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disease:  dyspnea  palpitations  fatigue  a fib  accentuated first heart sound  low-pitched, rumbling diastolic murmur  hoarseness  chest pain  seizures

some degree of left ventricular failure:  thready peripheral pulses  cool, clammy extremities  symptoms of LVF

early adulthood; those later in life often results from rheumatic fever.

Poor prognosis:  angina  syncope on exertion  dyspnea on exertion  harsh systolic murmur

close completely during diastole… can see pulmonary hypertension and right ventricular failure:  sudden manifestation of cardiovascular collapse  weakness  severe dyspnea  tachycardia  angina  hypotension  orthopnea  blowing diastolic murmur

Tricuspid Valve Stenosis  occurs almost excuslively in clients with rheumatic mitral stenosis, who are IV drug users, or those treated with a dopamine agonist Symptoms:  easily fatigued  effort intolerance  complaints of fluttering sensation in the neck  cyanosis  signs of RVF (ascites, hepatomegaly, peripheral edema, JVD) Pulmonic Valve Stenosis  almost always congenital  results in backward flow of blood into the right ventricle  causes right ventricle hypertension and hypertrophy Symptoms:  fatigue  loud midyastolic murmur  signs of RVF (ascites, hepatomegaly, peripheral edema, JVD) Valve Replacement Procedures Mechanical Prosthetic Valves: durable -risk of thromboembolism and lifetime anticoagulation therapy is required* Bioprosthetic Valves: xenografts (grafts from other species)

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- porcine valves (pig), bovine valves (cow), or hemografts (human cadavers) - the risk of clot formation is small; therefore, long-term anticoagulation therapy may not be indicated

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Post Operative Interventions - monitor closely for signs of bleeding - monitor cardiac output and for signs of heart failure - administer digoxin as prescribed to maintain cardiac output and prevent atrial fibrillation - client education Client Education Following Valve Replacement  Fatigue is common, rest is important  Anticoagulant therapy is necessary if a mechanical prosthetic valve has been inserted  Teach hazards of anticoagulation therapy and to notify HCP if bleeding or excessive bruising occurs  Importance of good oral hygiene to reduce the risk of infective endocarditis  Brush teeth twice daily with a soft toothbrush followed by oral rinses – avoid irrigation devices, electric toothbrushes, and flossing (these activities can cause the gums to bleed, allowing bacteria to enter the mucous membranes and enter the blood stream)  Monitor incision and report drainage or redness  Avoid any dental procedures for 6 months  Heavy lifting is to be avoided  If a prosthetic valve was inserted, a soft clicking sounds may be audible  Importance of prophylactic antibiotics before any invasive procedure  Inform all HCP about the valve replacement  Obtain and wear a MedicAlert bracelet

Cardiomyopathy A group of diseases that directly affect the structural or functional ability of the myocardium; can be primary or secondary. Treatment is palliative, not curative, and the client needs to deal with numerous lifestyle changes and a shortened lifespan.

Non-obstructed  dyspnea  angina  fatigue  syncope  palpitations  S4 gallop  ventricular dysrhythmias  sudden death common

Symptoms Obstructed Same as non-obstructed, but with mitral regurgitation murmur and atrial fibrillation Treatment  symptomatic  beta blockers  conversion of a fib

Restrictive  dyspnea  fatigue  right sided HF  S3 and S4 gallops  heart block  emboli Treatment  supportive

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Treatment  symptomatic  beta blockers  vasodilators  heart transplant

 digoxin, nitrates, and other vasodilators contraindicated

 treatment of hypertension  conversion from dysrhythmias  exercise restrictions  emergency treatment of acute pulmonary edema

Vascular Disorders Venous Thrombosis Thrombus can be associated with an inflammatory process. When a thrombus develops, inflammation occurs, thickening the vein wall and leading to emolization.

Types Thrombophlebitis: thrombus associated with inflammation Phlebothrombosis: thrombus without inflammation Phlebitis: vein inflammation associated with invasive procedures, such as IV lines Deep vein thrombophlebitis: more serious than superficial; risk of pulmonary embolism Risk Factors – Thrombus Formation  venous stasis from varicose veins, HF, immobility  hypercoagulability disorders  injury to venous wall from IV injections; administration of vessel irritants (e.g. chemotherapy)  orthopedic and abdominal surgery  pregnancy  ulcerative colitis  oral contraceptives  certain malignancies  fractures or other injuries of the pelvis or lower extremities Phlebitis  red, warm area radiating up the vein and extremity  pain and swelling  apply warm, moist soaks to dilate the vein and promote circulation  assess for signs of complications such as tissue necrosis, infection, or PE Deep Vein Thrombophlebitis Assessment  calf or groin tenderness or pain with or without swelling  positive Homans’ sign; can have false-positives so not a reliable assessment

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 warm skin that is tender to touch Interventions  provide bed rest

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 elevate the affected extremity above the level of the heart  avoid the use of pillow under knee  provide anti-embolism stockings  administer intermittent or continuous warm, moist compresses  palpate the site gently, monitoring for warmth and edema  measure and record the circumferences of the thigh and calves  monitor for SOB or chest pain, which can indicate pulmonary emboli  administer thrombolytic therapy  administer heparin therapy  monitor PTT during heparin therapy  administer warfarin following heparin therapy when symptoms have subsided  monitor prothrombin and INR during warfarin therapy Patient Education  hazards of anticoagulation therapy  signs and symptoms of bleeding  avoid prolonged sitting or standing, constrictive clothing, or crossing the legs when seated  elevate the legs for 10 to 20 minutes every few hours  plan a progressive walking program  inspect the legs for edema, measure circumference of the legs  wear antiembolism stockings  avoid smoking  avoid medications unless prescribed by HCP  obtain and wear a MedicAlert bracelet

Venous Insufficiency Results from prolonged venous hypertension, which stretches the veins and damages the valves. The resultant edema and venous stasis cause venous stasis ulcers, swelling, and cellulitis. Treatment focuses on decreasing edema and promoting venous return from the affected extremity. Treatment for venous stasis ulcers focuses on healing the ulcer and preventing stasis and ulcer recurrence.

Assessment  stasis dermatitis or brown discoloration along the ankles, extending up to the calf  edema  ulcer formation: edges are uneven, ulcer bed is pink, and granulation is present; usually located on the lateral malleolus Interventions NOTE: for venous insufficiency, leg elevation is usually prescribed to assist with the return of blood to the heart

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 compression stockings during the day and evening (on awakening before getting out of bed); may be lifelong

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 instruct to avoid prolonged sitting or standing, constrictive clothing, or crossing the legs when seated  elevate the legs above the level of the heart for 10 to 20 minutes every few hours each day  instruct in the use of an intermittent sequential pneumatic compression system (used twice daily for 1 hour in the morning and evening) Wound Care  assess the patient’s ability to care for the wound and initiate home care resources as necessary  if an Unna boot (dressing constructed of gauze with zinc oxide) is prescribed, the HCP will change it weekly  the wound is cleansed with normal saline before application of the Unna boot (iodine and hydrogen peroxide are not used because they destroy granulation tissue)  the Unna boot is covered with an elastic wrap that hardens to promote venous return and prevent stasis  monitor for signs of arterial occlusion from the Unna boot being too tight  keep tape OFF the client’s skin  occlusive dressings such as polyethylene film or a hydrocolloid dressing may be used to cover the ulcer Medications  apply topical agents to the wound as prescribed to debride the ulcer, eliminate necrotic tissue, and promote healing  when applying topical agents, apply an oil-based agent such as petroleum jelly on surrounding skin, because debriding agents can injure healthy tissue  administer antibiotics if infection of cellulitis occurs

Varicose Veins Distended, protruding veins that appear darkened and tortuous.

Assessment  pain in the legs with dull aching after standing  vein walls weaken and dilate, and valves become incompetent Trendelenburg Test  place the patient in a supine position with the legs elevated  when the client sits up, if varicosities are present, veins fill from the proximal end; veins normally fill from the distal end Interventions  emphasize the importance of antiembolism stockings as prescribed

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 instruct to elevate the legs as much as possible  instruct to avoid constrictive clothing and pressure on the legs  prepare for sclerotherapy or vein stripping as prescribe

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Sclerotherapy  a solution is injected into the vein, followed by the application of a pressure dressing  incision and drainage od the trapped blood in the sclerosed vein is performed 14 to 21 days after the injection, followed by the application of a pressure dressing for 12 to 18 hours Laser therapy – a laser fiber is used to heat and close the main vessel contributing to the varicosity Vein stripping – varicose veins may be removed if they are larger than 4mm in diameter or if they are in clusters (other treatments are usually attempted before this)

Arterial Disorders Peripheral Artery Disease (PAD) Conditions affecting the arteries in the neck, abdomen, and extremities. Tissue damage occurs below the level of the arterial occlusion. Atherosclerosis is the most common cause of PAD. Assessment  intermittent claudication (pain in the muscles resulting from an inadequate blood supply) – classic symptom  rest pain, characterized by numbness, burning, or aching in the distal portion of the lower extremities - this awakens the patient at night, but is relieved by placing the extremity in the dependent position (dangling)  lower back or buttock discomfort  loss of hair and dry scaly skin on the lower extremities  thickened toenails  cold and gray-blue colour of skin in the lower extremities  decreased or absent peripheral pulses  elevation pallor and dependent rubor in lower extremities  signs of arterial ulcer formation occurring on or between the toes or on the upper aspect of the foot that are characterized as painful  BP measurements at the thighs, calf, and ankle are lower than the brachial pressure (normally these readings are higher than those in upper extremities)  in males, may have some degree of sexual dysfunction NOTE: Because swelling in the extremities prevents arterial blood flow, the client with PAD is instructed to elevate the feet at rest but to refrain from elevating them above the level of the heart, because extreme elevation slows arterial blood flow to the feet. In severe cases, clients with edema may sleep with the affected limb hanging from the bed

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or they may sit upright in a chair for comfort.

Interventions

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1. Assess pain 2. Monitor the extremities for color, motion and sensation, and pulses.

3. Obtain BP. 4. Assess for signs of ulcer formation or gangrene 5. Assist with developing an individualized exercise program, which in initiated gradually and increased slowly, will improve arterial flow 6. Instruct to walk to the point of claudication, stop and rest, then walk a little further 7. Avoid crossing the legs (interferes with blood flow) 8. Avoid exposure to cold (causes vasoconstriction) to the extremities and to wear socks or insulated shoes for warmth at all times 9. NEVER apply direct heat to the limb (e.g. heating pad or hot water) because the decreases sensitivity in the limb can cause burning 10. Inspect skin daily and report signs of breakdown 11. Avoid tobacco and caffeine.

Procedures to Improve Arterial Blood Flow 1. Percutaneous transluminal angioplasty 2. Laser-assisted angioplasty 3. Atherectomy 4. Bypass surgery

Raynaud’s Disease Episodic vasospastic disorder of small cutaneous arteries, most frequently fingers and toes. Vasospasm causes constriction of the cutaneous vessels. Attacks are intermittent and occur with exposure to cold or stress. Cause is unknown. Characterized by vasospasm-induced colour changes to the fingers, toes, ears, and nose (blue, white, or red).

Assessment  blanching of extremity, followed by cyanosis during constriction  reddened tissue when the vasospasm is relieved  numbness, tingling, swelling, and a cold temperate at the affected site Interventions  monitor pulses  administer vasodilators  medication therapy  avoid cold and stress  avoid smoking  wear warm clothing, socks, and gloves in cold weather  avoid injuries to fingers and hands

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Buerger’s Disease

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Occlusive disease of the median and small arteries and veins. The distal upper and lower limbs are affected most commonly.

Assessment  intermittent claudication  ischemic pain occurs in the digits while at rest  aching pain that is more severe at night  cool, numb, or tingling sensation  diminished pulses  extremities that are cool and red in the dependent condition  development of ulcerations in the extremities Interventions  monitor pulses  administer vasodilators  medication therapy  avoid cold and stress  avoid smoking  wear warm clothing, socks, and gloves in cold weather  avoid injuries to fingers and hands

Aortic Aneurysms Abdominal dilation of the arterial wall caused by localized weakness and stretching in the medial layer or wall of the aorta. The aneurysm can be located anywhere along the abdominal aorta. The goal of treatment is to limit the progression of the disease by modifying risk factors, controlling BP, recognizing symptoms early, and preventing rupture. Occurs in men more often than women and incidence increases with age. Male gender and smoking are stronger risk factors than hypertension and diabetes. Most common cause = atherosclerosis.

Thoracic

Types of Aneurysms  pain extending to neck, shoulders, lower back, or abdomen  syncope  dyspnea  increased pulse  cyanosis  hoarseness  difficulty swallowing

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Abdominal

 prominent, pulsating mass in abdomen, at or above the umbilicus  bruit may be auscultated over the aorta  tenderness on deep palpation  abdominal or lower back pain

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Rupturing

 may cause mottling of feet/toes with presence of palpable pedal pulses *can also be detected when patient is examined for an unrelated problem (e.g. CT scan, abdominal x-ray) SERIOUS complication of an untreated aneurysm  severe abdominal or back pain  lumbar pain radiating to the flank and groin  hypotension  tachycardia  signs of shock  hematoma at flank area  massive hemorrhage (if anterior)

Diagnostic Testing Done to confirm the presence, size, and location of the aneurysm:  abdominal ultrasound  CT  arteriography  MRI  ECG – to rule out an MI  chest x-ray – to see mediastinal silhouette and any abnormal widening of thoracic aorta Interventions Goal: prevent aneurysm from rupturing Early detection and treatment imperative Small aneurysm: conservative treatment Greater than 5.5cm is the threshold for repair  monitor vital signs  assess for back or abdominal pain  assess for the sensation of pulsation in the abdomen  check peripheral circulation – pulses, temperature, colour  observe for signs of rupture  note any tenderness over the abdomen  monitor for abdominal distention  administer antihypertensives to maintain the BP within normal limits and to prevent strain on the aneurysm  if ruptured, emergent surgical intervention is required (33-94% mortality)

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NOTE: it is crucial to instruct the client with an aortic aneurysm to report immediately the occurrence of chest or back pain, shortness of breath, difficulty swallowing, or hoarseness.

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Aortic Dissection Not a type of aneurysm, occurs most commonly in the thoracic aorta. Acute and lifethreatening; mortality rate of 90% if not surgically repaired. A tear in intimal lining allows blood to track between intima and media, so as the heart contracts, each systolic pulsation increases pressure on the damaged area, further increasing dissection. May occlude major branches of the aorta, cutting off blood supply to the brain, abdominal organs, kidneys, spinal cord, and extremities.

Clinical Manifestations Pain - characterized as sudden, severe pain in the anterior part of the chest - may also be intrascapular pain radiating down the spine to the abdomen - described as tearing or ripping - may mimic that of an MI - as dissection progresses, pain is felt above and below diaphragm Cardiovascular, neurological, and respiratory symptoms - if aortic arch is involved, patient will have neurological deficiencies Complications Cardiac Tamponade - severe life-threatnening complication that occurs when blood escapes from dissection into the pericardial sac - symptoms include: hypotension, narrowed pulse pressure, distended neck veins, muffled heart sounds, pulsus paradoxus Abdominal Aortic Aneurysm Resection Surgical resection or excision of the aneurysm; the excised section is replaced with a graft that is sewn end to end.

Preoperative  assess all peripheral pulses as a baseline for comparison postoperatively  assess neurological status for comparison  teach deep breathing and coughing exercises Postoperative  monitor vitals  monitor peripheral pulses distal to the graft site  monitor for signs of graft occlusion – changes in pulses, cool extremities below the graft, white or blue extremities or flanks, severe pain, abdominal distention  limit elevation of the head of the bed to 45 degrees to prevent flexion of the graft  monitor for hypovolemia and kidney failure resulting from severe blood loss during surgery  monitor urine output hourly, report urine output less than 30-50ml/hr

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 monitor serum creatinine and BUN daily  monitor respiratory status and auscultate lung sounds

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 encourage turning, coughing, and deep breathing while splinting the incision  ambulate as prescribed  do not lift objects heavier than 15 to 20 pounds for 6 to 12 weeks  avoid activities requiring pushing, pulling, or straining  do not drive a vehicle until indicated by HCP Thoracic Aneurysm Repair A thoracotomy approach is used to enter the thoracic cavity and excise the aneurysm; a graft or prosthesis is sewn into the aorta.

Postoperative  monitor vitals, renal, and neurological status  monitor for signs of hemorrhage – e.g. drop in BP and increase in HR an respirations  monitor chest tube for an increase in chest drainage, which may indicate bleeding or separation at the graft site  assess sensation and motion of all extremities and notify the HCP immediately if deficits are noted, which can occur because of a lack of blood supply to the spinal cord during surgery  monitor respiratory status  do not lift objects heavier than 15 to 20 pounds for 6 to 12 weeks  avoid activities requiring pushing, pulling, or straining  do not drive a vehicle until indicated by HCP Embolectomy The removal of an embolus from an artery with the use of a catheter.

Preoperative  obtain baseline vascular assessment  administer anticoagulants and thrombolytics  place a bed cradle on the bed  avoid bumping the bed  place the extremity in a slightly dependent position Postoperative  monitor affected extremity for colour, temperature, and a pulse  assess sensory and motor function of the affected extremity  monitor for signs of a new thrombi or emboli  administer oxygen  monitor pulse oximetry  monitor for edema, pain on passive movement, poor capillary refill, numbness – signs of swollen skeletal muscles  avoid prolonged standing or sitting and elevate the legs when sitting  wear antiembolism stockings

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 ambulate daily  hazards of anticoagulation therapy

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CRITICAL THINKING Q. A hospitalized client with a diagnosis of abdominal aortic aneurysm suddenly complains of severe back pain and shortness of breath. What should the nurse do?

A. The nurse should suspect a rupture, which is a surgical emergency, and immediately contact the HCP. The nurse should also obtain information about the back pain, stay with the client, monitor vital signs and neurological status, and provide support. Other signs of rupture include severe abdominal pain or fullness, soreness over the umbilicus, and a sudden development of discolouration in the extremities.

Hypertension Prehypertension – systolic: 120-139mmHg, diastolic: 80-89mmHg Stage 1 – systolic: 140-159mmHg, diastolic: 90-99mmHg Stage 2 – systolic equal to or greater than 160mmHg, diastolic greater than or equal to 100mmHg Hypertension is a major risk factor for coronary, cerebral, renal, and peripheral vascular disease. It is usually asymptomatic initially; since it goes unnoticed, it goes on for longer periods of time and can ultimately cause damage to target organs. Prevalence increasese with age, in less educated patients, men > female until age 55, then women > men.

Primary Hypertension Elevated BP without an identifying cause; accounts for 90 to 95% of all cases.

Contributing Factors:  increases SNS activity  aging  family history  African American race  obesity  smoking  greater than ideal body weight  diabetes  excessive alcohol intake  increase intake of salt and caffeine Clinical Manifestations  called the “silent killer” as it is asymptomatic until it becomes severe and target organ disease has occurred  fatigue

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 reduced activity tolerance  dizziness  palpitations

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 angina  dyspnea  flushed face  epistaxis  visual disturbances Secondary Hypertension Elevated BP with a specific cause that often can be identifies and corrected; 5 to 10% in adults and 80% in children.

Contributing Factors – usually secondary causes  hypokalemia  narrowing of the aorta  renal disease  endocrine disorders  pregnancy  brain tumours  head injury  PIH  medications (e.g. estrogens, glucocorticoids, mineralocorticoids) Treatment is directed at eliminating the underlying cause. Secondary hypertension is a contributing cause to hypertensive crisis.

Interventions  obtain BP 2 or more times on both arms, supine and standing  compare BP with prior documentation  identify current medication therapy  obtain weight  evaluate nietary patterns and sodium intake  assess for visual changes or retinal damage  assess for cardiovascular changes such as JVD or dysrhythmias  periodic monitoring of BP; every 3-6 months once it is stable Nonpharmacological Interventions  weight reduction if necessary  dietary sodium restriction to 2g daily  moderate to reduced intake of alcohol and caffeine  exercise  smoking cessation  relaxation techniques  biofeedback therapy  elimination of unnecessary medications that may contribute

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Client Education  Importance of compliance

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 Disease process (esp. that symptoms usually do not develop until organs have suffered damage)  Regular exercise program; avoid heavy weight lifting  Express feelings about daily stress and identify ways to reduce stress  Relaxation techniques  Teach the technique for monitoring BP  Maintain a diary of daily BP readings  Emphasise the importance of lifelong medication  Dietary restrictions – sodium, fat, calories, cholesterol  How to shop for and prepare low-sodium meals  Provide with a lsit of products containing sodium  Read labels to determine sodium content – sodium, NaCl, or MSG (monosodium glutamate)  Bake, roast, or boil foods; avoid salt in preparation of meals  Fresh foods are the best to consume; avoid canned  Actions, side effects, and scheduling of medications  Avoid OTC medications  Stress the importance of follow-up care

Hypertensive Crisis A severe and abrupt elevation in blood pressure (diastolic greater than 120-130). Acute and life-threatening condition requiring immediate emergency treatment because target organ damage can occur quickly (brain, heart, kidneys, eyes [retina]).

Clinical Manifestations  headache  nausea and vomiting  drowsiness and confusion  seizures  blurred vision  stupor  changes in neurological status  tachycardia and tachypnea  diaphoresis  transient blindness  renal impairment  chest pain  dyspnea  back pain  cyanosis * may be mistaken for a stroke patient, but unlike with a stroke, the patient does NOT present with unilateral or focal signs Interventions

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1. Maintain a patent airway.

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2. Administer antihypertensive medications intravenously.

- must monitor BP every 2-3 minutes or continuously as IV drugs have a rapid onset - important to prevent hypotension - be cautious as lowering BP too much can cause decreased cerebral perfusion and result in a stroke 3. Maintain bed rest, with head of bed elevated 45 degrees.

4. Assess for hypotension.

5. Have emergency medications and resuscitation equipment readily available.

6. Monitor IV therapy, assessing for fluid overload.

7. Insert a Foley catheter.

8. Monitor strict intake an output.

- if oliguria or anuria occurs, notify the HCP 9. Assess neuro vitals.

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