Chpt 21- Cardiovascular assessment

Transesophageal echocardiography

A topical anesthetic agent and sedation are used during TEE because of the discomfort associated with the positioning of the transducer in the esophagus The high-quality imaging obtained during TEE makes this technique an important first-line diagnostic tool for evaluating patients with many types of CVD, including HF, valvular heart disease, arrhythmias, and many other conditions that place the patient at risk for atrial or ventricular thrombi. Pharmacologic stress testing using dobutamine and TEE can also be performed. It is frequently used during cardiac surgery to continuously monitor the response of the heart to the surgical procedure (e.g., valve replacement or coronary artery bypass). Complications are uncommon during TEE; however, if they do occur, they are serious. These complications are caused by sedation and impaired swallowing resulting from the topical anesthesia (respiratory depression and aspiration) and by insertion and manipulation of the transducer into the esophagus and stomach (vasovagal response or esophageal perforation). The patient must be assessed before TEE for a history of dysphagia or radiation therapy to the chest, which increases the likelihood of complications The nurse provides preprocedure education and ensures that the patient has a clear understanding of what the test entails and why it is being performed, instructs the patient not to eat or drink anything for 6 hours prior to the study, and checks to make sure that informed consent has been obtained. The nurse also inserts an IV line or assesses an existing IV for patency and suitability and asks the patient to remove full or partial dentures. During the test, the nurse provides emotional support and monitors level of consciousness, BP, ECG, respiration, and oxygen saturation (SpO2). During the recovery period, the patient must maintain bed rest with the head of the bed elevated to 45 degrees. Following the procedural sedation policy of the agency, the nurse monitors the patient for dyspnea and assesses vital signs, SpO2, level of consciousness, and gag reflex as recommended. Food and oral fluids are withheld until the patient is fully alert and the effects of the topical anesthetic agent are reversed, usually 2 hours after the procedure; if the gag reflex is intact, the nurse begins feeding with sips of water, then advances to the preprocedure diet. Patients are informed that a sore throat may be present for the next 24 hours; they are instructed to report the presence of a persistent sore throat, shortness of breath, or difficulty swallowing to the medical staff. If the procedure is performed in an outpatient setting, a family member or friend must be available to transport the patient home from the test site.

Common labs and test

Blood urea nitrogen (BUN): 8-20 mg/dL BUN and creatinine are end products of protein metabolism excreted by the kidneys. Elevated BUN reflects reduced renal perfusion from decreased cardiac output or intravascular fluid volume deficit as a result of diuretic therapy or dehydration. Calcium (Ca++): 8.8-10.4 mg/dL Calcium is necessary for blood coagulability, neuromuscular activity, and automaticity of the nodal cells (sinus and atrioventricular nodes). Hypocalcemia: Decreased calcium levels slow nodal function and impair myocardial contractility. The latter effect increases the risk for heart failure. Hypercalcemia: Increased calcium levels can occur with the administration of thiazide diuretics because these medications reduce renal excretion of calcium. Hypercalcemia potentiates digitalis toxicity, causes increased myocardial contractility, and increases the risk for varying degrees of heart block and sudden death from ventricular fibrillation. Creatinine Male: 0.6-1.2 mg/dL Female: 0.4-1.0 mg/dL Both BUN and creatinine are used to assess renal function, although creatinine is a more sensitive measure. Renal impairment is detected by an increase in both BUN and creatinine. A normal creatinine level and an elevated BUN suggest an intravascular fluid volume deficit. Magnesium (Mg++): 1.8-2.6 mg/dL Magnesium is necessary for the absorption of calcium, maintenance of potassium stores, and metabolism of adenosine triphosphate. It plays a major role in protein and carbohydrate synthesis and muscular contraction. Hypomagnesemia: Decreased magnesium levels are due to enhanced renal excretion of magnesium from the use of diuretic or digitalis therapy. Low magnesium levels predispose patients to atrial or ventricular tachycardias. Hypermagnesemia: Increased magnesium levels are commonly caused by the use of cathartics or antacids containing magnesium. Increased magnesium levels depress contractility and excitability of the myocardium, causing heart block and, if severe, asystole. Potassium (K+): 3.5-5 mEq/L Potassium has a major role in cardiac electrophysiologic function. Hypokalemia: Decreased potassium levels due to administration of potassium-excreting diuretics can cause many forms of arrhythmias, including life-threatening ventricular tachycardia or ventricular fibrillation, and predispose patients taking digitalis preparations to digitalis toxicity. Hyperkalemia: Increased potassium levels can result from an increased intake of potassium (e.g., foods high in potassium or potassium supplements), decreased renal excretion of potassium, the use of potassium-sparing diuretics (e.g., spironolactone), or the use of angiotensin-converting enzyme inhibitors that inhibit aldosterone function. Serious consequences of hyperkalemia include heart block, asystole, and life-threatening ventricular arrhythmias. Sodium (Na+): 135-145 mEq/L Low or high serum sodium levels do not directly affect cardiac function. Hyponatremia: Decreased sodium levels indicate fluid excess and can be caused by heart failure or administration of thiazide diuretics. Hypernatremia: Increased sodium levels indicate fluid deficits and can result from decreased water intake or loss of water through excessive sweating or diarrhea. Coagulation Studies Injury to a vessel wall or tissue initiates the formation of a thrombus. This injury activates the coagulation cascade, the complex interactions among phospholipids, calcium, and clotting factors that convert prothrombin to thrombin. The coagulation cascade has two pathways: the intrinsic and extrinsic pathways. Coagulation studies are routinely performed before invasive procedures, such as cardiac catheterization, electrophysiology testing, and cardiac surgery. Activated partial thromboplastin time (aPTT) Lower limit of normal: 21-35 s aPTT measures the activity of the intrinsic pathway and is used to assess the effects of unfractionated heparin. A therapeutic range is 1.5-2.5 times baseline values. Adjustment of heparin dose is required for aPTT <50 s (↑ dose) or >100 s (↓ dose). Prothrombin time (PT) Lower limit of normal: 11-13 s PT measures the extrinsic pathway activity and is used to monitor the level of anticoagulation with warfarin. International normalized ratio (INR): 0.8-1.2 The INR, reported with the PT, provides a standard method for reporting PT levels and eliminates the variation of PT results from different laboratories. The INR, rather than the PT alone, is used to monitor the effectiveness of warfarin. The therapeutic range for INR is 2-3.5, although specific ranges vary based on diagnosis. Hematologic Studies Complete blood count (CBC) The CBC identifies the total number of white and red blood cells and platelets, and measures hemoglobin and hematocrit. The CBC is carefully monitored in patients with cardiovascular disease. Hematocrit Male: 42-52% Female: 36-48% Hemoglobin Male: 14-17.4 g/dL Female: 12-16 g/dL The hematocrit represents the percentage of red blood cells found in 100 mL of whole blood. The red blood cells contain hemoglobin, which transports oxygen to the cells. Low hemoglobin and hematocrit levels have serious consequences for patients with cardiovascular disease, such as more frequent angina episodes or acute myocardial infarction. Platelets: 140,000-400,000/mm3 Platelets are the first line of protection against bleeding. Once activated by blood vessel wall injury or rupture of atherosclerotic plaque, platelets undergo chemical changes that form a thrombus. Several medications inhibit platelet function, including aspirin, clopidogrel, and intravenous glycoprotein IIb/IIIa inhibitors (abciximab, eptifibatide, and tirofiban). When these medications are given, it is essential to monitor for thrombocytopenia (low platelet counts). White blood cell (WBC) count: 4500-11,000/mm3 WBC counts are monitored in patients who are immunocompromised, including patients with heart transplants or in situations where there is concern for infection (e.g., after invasive procedures or surgery).

Abdominal

Abdominal distention: A protuberant abdomen with bulging flanks indicates ascites. Ascites develops in patients with right ventricular or biventricular HF (both right- and left-sided HF). In the failing right heart, abnormally high chamber pressures impede the return of venous blood. As a result, the liver and spleen become engorged with excessive venous blood (hepatosplenomegaly). As pressure in the portal system rises, fluid shifts from the vascular bed into the abdominal cavity. Ascitic fluid, found in the dependent or lowest points in the abdomen, will shift with position changes. Hepatojugular reflux: This test is performed when right ventricular or biventricular HF is suspected. The patient is positioned so that the jugular venous pulse is visible in the lower part of the neck. While observing the jugular venous pulse, firm pressure is applied over the right upper quadrant of the abdomen for 30 to 60 seconds. An increase of 1 cm or more in jugular venous pressure is indicative of a positive hepatojugular reflux. This positive test aids in confirming the diagnosis of HF. Bladder distention: Urine output is an important indicator of cardiac function. Reduced urine output may indicate inadequate renal perfusion or a less serious problem such as one caused by urinary retention. When urine output is decreased, the patient must be assessed for a distended bladder or difficulty voiding. The bladder may be assessed with an ultrasound scanner or the suprapubic area palpated for an oval mass and percussed for dullness, indicative of a full bladder.

Interventions for inpatient cardiac monitor

Alarm fatigue- delays response ECG must be free of artifact- abnormal ECG pattern by muscular activity, patient movement, electrical interference, or lead cable or electrode malfunction Artifact can mimic arrhythmias and cause unnecessary false alarms Use proper skin prep before applying electrodes and changes in electrodes every 24 hrs Assess allergies to adhesive or electrode gel Rotate site Improper position of electrodes and lead connection- mimic ischemia or arrhythmias Two leads should be selected that provide tracing for arrhythmias monitoring- 2 lead and chest lead 5 Individualize ECG alarm parameters to meet monitoring needs Atrial Fib- turn or irregular HR alarm Inop monitor alarms- communicate electrode fell off, leads are loose or low battery Hospital acquired infection- transmitted via lead wire cables Electrodes should be removed one monitoring is discontinued and skin cleansed to remove excess gel Metal containing electrodes must be removed before sending patient for MRI including MR angiography

Assess chest pain

Angina Pectoris, ACS (unstable angina, MI) Angina: Uncomfortable pressure, squeezing, or fullness in substernal chest area Can radiate across chest to the medial aspect of one or both arms and hands, jaw, shoulders, upper back, or epigastrium Radiation to arms and hands, described as numbness, tingling, or aching ACS: Same as angina pectoris Pain or discomfort ranges from mild to severe Associated with shortness of breath, diaphoresis, palpitations, unusual fatigue, and nausea or vomiting Angina: 5-15 min ACS: >15 min Angina: Physical exertion, emotional upset, eating large meal, or exposure to extremes in temperature ACS: Emotional upset or unusual physical exertion occurring within 24 h of symptom onset Can occur at rest or while asleep Angina: Rest, nitroglycerin, oxygen ACS: Morphine, reperfusion of coronary artery with thrombolytic (fibrinolytic) agent or percutaneous coronary intervention Pericarditis Sharp, severe substernal or epigastric pain Can radiate to neck, arms, and back Associated symptoms include fever, malaise, dyspnea, cough, nausea, dizziness, and palpitations Intermittent Sudden onset Pain increases with inspiration, swallowing, coughing, and rotation of trunk Sitting upright, analgesia, anti-inflammatory medications Pulmonary Disorders (pneumonia, pulmonary embolism) Sharp, severe substernal or epigastric pain arising from inferior portion of pleura (referred to as pleuritic pain) Patient may be able to localize the pain ≥30 min Follows an infectious or noninfectious process (MI, cardiac surgery, cancer, immune disorders, uremia) Pleuritic pain increases with inspiration, coughing, movement, and supine positioning Occurs in conjunction with community- or hospital-acquired lung infections (pneumonia) or venous thromboembolism (pulmonary embolism) Treatment of underlying cause Esophageal Disorders (hiatal hernia, reflux esophagitis or spasm) Substernal pain described as sharp, burning, or heavy Often mimics angina Can radiate to neck, arm, or shoulders 5-60 min Recumbency, cold liquids, exercise Food or antacid Nitroglycerin Anxiety and Panic Disorders Pain described as stabbing to dull ache Associated with diaphoresis, palpitations, shortness of breath, tingling of hands or mouth, feeling of unreality, or fear of losing control >30 min Can occur at any time including during sleep Can be associated with a specific trigger Removal of stimulus, relaxation, medications to treat anxiety or underlying disorder Musculoskeletal Disorders (costochondritis) Sharp or stabbing pain localized in anterior chest Most often unilateral Can radiate across chest to epigastrium or back Hours to days Most often follows respiratory tract infection with significant coughing, vigorous exercise, or posttrauma Some cases are idiopathic. Exacerbated by deep inspiration, coughing, sneezing, and movement of upper torso or arms Rest, ice, or heat Analgesic or anti-inflammatory m

Coping with stress

Anxiety, depression and stress known to influence development and recovery from CAD and HF Depression prevalent in women and has negative impact on quality of life Risk of depression is lower if stability in life, higher education, healthy lifestyle, and absence of comorbidities Platelet abnormalities, inflammatory response, insulin resistances, diet, exercise, smoking, substance abuse, unemployment, social isolation Exhibit common s/s- feeling worthless, guilt, problems falling and staying asleep, difficulty concentrating, restlessness, recent change in appetite or weight PHQ- 0-6- patients with positive over 3 complete focused screening called PHQ 9 and referred Stress can increase levels of catecholamines and cortisol- linked to CV Nurse ask about stressors, previous coping, perception of current mood and coping Social readjustment rating scale Death of spouse, divorce, and change in work Score less of 150 has slight risk, 150-299- moderate risk, and 300 or higher is high risk Consult with psychiatric advance PN

Auscultate

Apical and progress along left sternal border to pulmonic and aortic valve S1-intensity and splitting S2- intensity and splitting Listen for extra sounds in systole Patient turn to left side and placed on apical - S3 and 4 murmur can detect Once abnormality- entire chest surface is reexamined to determine exact location of sound and radiation Reassure patient Characteristics- location on chest wall,timing, intensity, pitch, quality Interpret heart sounds- abnormalities require further treatment Nurses in these roles readily identify abnormal heart sounds, recognize the diagnostic significance of their findings, and use their assessment skills to evaluate patients' responses to medical interventions. For example, these highly skilled nurses monitor heart sounds in patients with HF to detect the resolution of an S3 after treatment with a diuretic.

Past health hx, family history

Assess for understanding of personal risk factors for peripheral vascular, cerebrovascular, and CAD and measures Increase age, males, and heredity include race are not modifiable Smoking, HTPN, high cholesterol, obesity, diabetes, physical inactivity Patient who do not understand connection between risk and CAD are unwilling to recommend lifestyle changes or manage illness

Age related changes in heart

Atria ↑ Size of left atrium Thickening of the endocardium ↑ Atrial irritability Irregular heart rhythm from atrial arrhythmias Left ventricle Endocardial fibrosis Myocardial hypertrophy (thickening) Infiltration of fat into myocardium Left ventricle stiff and less compliant Progressive decline in cardiac output Fatigue ↓ Exercise tolerance Signs and symptoms of heart failure or ventricular arrhythmias ↑ Risk for ventricular arrhythmias Prolonged systole Point of maximal impulse palpated lateral to the midclavicular line ↓ Intensity S1, S2; split S2 S4 may be present Valves Thickening and rigidity of AV valves Calcification of aortic valve Abnormal blood flow across valves during cardiac cycle Murmurs may be present Thrill may be palpated if significant murmur is present Conduction system Connective tissue collects in SA node, AV node, and bundle branches ↓ Number of SA node cells ↓ Number of AV, bundle of His, and right and left bundle branch cells Slower SA node rate of impulse discharge Slowed conduction across AV node and ventricular conduction system Bradycardia Heart block ECG changes consistent with slowed conduction (↑ PR interval, widened QRS complex) Sympathetic nervous system ↓ Response to beta-adrenergic stimulation ↓ Adaptive response to exercise: contractility and heart rate slower to respond to exercise demands Heart rate takes more time to return to baseline Fatigue Diminished exercise tolerance ↓ Ability to respond to stress Aorta and arteries Stiffening of vasculature ↓ Elasticity and widening of aorta Elongation of aorta, displacing the brachiocephalic artery upward Left ventricular hypertrophy Progressive increase in systolic BP; slight ↑ in diastolic BP Widening pulse pressure Pulsation visible above right clavicle Baroreceptor response ↓ Sensitivity of baroreceptors in the carotid artery and aorta to transient episodes of hypertension and hypotension Baroreceptors unable to regulate heart rate and vascular tone, causing slow response to postural changes in body position Postural BP changes and reports of feeling dizzy, fainting when moving from lying to sitting or standing position

Brain type B natriuretic peptide, C reactive protein and homocysteine

BNP is a neurohormone that regulates BP and fluid volume Secreted from ventricles in response to increase preload with resulting elevated ventricular pressure BNP in blood increase as ventricular walls expand from increase pressure- monitor HF Elevated BNP can occur with pulmonary embolism, MI, and ventricular hypertrophy Correlates levels with abnormal physical assessment findings before definitive HF Greater than 100 pg/ml- HF C reactive protein in liver in response to systemic inflammation Thought to associated with atherosclerosis High sensitivity is used with other test to predict CVD 3 mg or higher- greatest risk Homocysteine- AA linked to atherosclerosis because it damages endothelial lining of arteries and promote thrombus formation Elevated Blood levels indicated CAD, stroke, and peripheral vascular disease Genetics- diet low in folate, vitamin B6 and B12- elevated levels 12 hours fast before blood work Less than 12 mcmol, high risk 15 or greater

Elimination

Bowel and bladder habits are identified Nocturia common in HF Fluid collected in gravity dependent tissue (extremities) during day (edema) redistributes into circulatory system once patient recumbent at night Increased circulatory volume is excreted by kidneys (increase urine production) Straining during defecation- patient bears down (Valsalva maneuver)- increase baroreceptors Triggers vagal response- HR slows and result in syncope Occur with urination Cardiac meds affect GI or bleeding, the nurse ask about bloating, diarrhea, constipation, stomach upset, heartburn, loss of appetite, N/V Screening for bloody urine or stools- antiplatelet medications (Aspirin, clopidogrel, prasugrel, ticagrelor) Platelet inhibitors(abciximab, eptifibatide, tirofiban) or anticoagulant(Low molecular weight heparin- dalteparin or enoxaparin, or oral anticoagulants such as warfarin, rivaroxaban

Central venous pressure

CVP is a measurement of the pressure in the vena cava or right atrium. The pressure in the vena cava, right atrium, and right ventricle is equal at the end of diastole; thus, the CVP also reflects the filling pressure of the right ventricle (preload). The normal CVP is 2 to 6 mm Hg. It is measured by positioning a catheter in the vena cava or right atrium and connecting it to a pressure monitoring system. The CVP is most valuable when it is monitored over time and correlated with the patient's clinical status. A CVP greater than 6 mm Hg indicates an elevated right ventricular preload. There are many problems that can cause an elevated CVP, but the most common problem is hypervolemia (excessive fluid circulating in the body) or right-sided HF. In contrast, a low CVP (less than 2 mm Hg) indicates reduced right ventricular preload, which is most often from hypovolemia. Dehydration, excessive blood loss, vomiting or diarrhea, and overdiuresis can result in hypovolemia and a low CVP. This diagnosis can be substantiated when a rapid IV infusion of fluid causes the CVP to increase. Preferred site is the subclavian vein; the femoral vein is generally avoided During this sterile procedure, the physician threads a single-lumen or multilumen catheter through the vein into the vena cava just above or within the right atrium. Once the CVP catheter is inserted, it is secured and a dry sterile dressing is applied. Position of the catheter is confirmed by a chest x-ray.

Cardiac Electrophysiology

Cardiac conduction- generates and transmits electrical impulse that stimulate contraction of myocardium Conduction system first stimulates contraction of atria and ventricles Synchronization of atrial and ventricular events allows ventricles to fill up before ventricular ejection, maximizing cardiac output Nodal cells and Purkinje cells Automaticity: ability to initiate an electrical impulse Excitability: ability to respond to an electrical impulse Conductivity: ability to transmit an electrical impulse from one cell to another provides synchronization Both SA node(primary pacemaker of heart and atrioventricular node (secondary pacemaker) composed of nodal cells SA- junction of superior VC and right atrium SA in normal resting adult heart has inherent firing of 60-100 impulses per minute-rate changes in response to metabolic demands Electrical impulses initiate by SA are conducted along myocardial cells of atria via internodal pathway Impulses causes electrical stimulation and subsequent contraction of atria Impulse then conduct to AV nodes, located in right atrial wall near tricuspid valve AV nodes coordinate incoming electrical impulses from atria after slight delay allowing atria time to contract and complete ventricular filling Relays impulse to ventricles Impulse is conducted though bundle conducting tissue- bundle of His- divides into right branch bundle(conduct impulse to right ventricle) and left bundle branch (left ventricle) Transmit impulse to left ventricle- largest chamber of heart, the left bundle branch divides into left anterior and posterior bundle branches Impulses travel though bundle branches to reach terminal point in conduction system called Purkinje fibers Rapidly conduct impulses through thick walls of ventricles- stimulates ventricular myocardial cell contraction Heart rate determined by myocardial cells with fastest inherent firing rate SA node has highest rate of 60-100 per minute AV- 40- 60 Ventricular pacemaker has lowest with 30-40 impulses per minute SA node malfunctions- AV node take over at lower rate Should both fail- the pacemaker site in ventricle wall will fire inherent bradycardia rate of 30-40

Cardiac hemodynamics

Cardiac cycle- heart from beginning of one beat to the next Number of cycles complete in one minute depends on HR Each cycle has three sequential events: Diastole, atrial systole, and ventricular systole Cause blood flow through heart due to changes in chamber pressures and valvular function during diastole and systole Diastole- all hour chambers are relaxed AV valves are open and semilunar valves are closed Pressure in all chambers are lowest during diastole which facilitates ventricular filling Venous blood returns to right atrium from superior and inferior VC then into right ventricle Left side- O2 blood returns from lungs via pulmonary veins into left atrium and ventricle End of diastole, atrial systole occurs at atrial muscle contract in response to electrical impulse of SA node Atrial systole increase the pressure in atria, ejecting blood into ventricles Augments ventricular blood volume by 15-25% and referred as atrial kick Ventricular systole begins in response to propagation of electrical impulse that began in SA node Beginning of ventricular systole, the pressure inside ventricular rapidly increase, force AV valves to close Blood ceases to flow from atria into ventricles and regurgitate into atria is prevented Rapid increase in pressure inside right and left ventricles forces pulmonic and aortic valve to open, and blood eject into pulmonary artery and aorta Pressure in ventricles and corresponding artery equalizes, the flow decreases End of systole, pressure in right and left ventricles rapidly decreases Pulmonary arterial and aortic pressure decrease, causing closure of semilunar valve Chamber pressure can be measured with special catheters Hemodynamic monitoring

Gerontologic considerations

Changes in cardiac structure and function Loss of cells through conduction system leads to slower HR Size of heart due to hypertrophy- reduces BV that chambers can hold Changes structure in myocardium, reducing strength of contraction Both negatively affect CO Valves due to stiffening close improperly Resulting in backflow of blood created heart murmur CVS takes longer to compensate from increase metabolic demands due to stress, exercise, or illness OA may be symptomatic with fatigue, SOB, palpitations and need physical exam Heart of women- tends to be smaller Coronary arteries are narrower in diameter than men Atherosclerosis- difference makes procedures such as cardiac catheterization and angioplasty difficult Develop CAD 10 years later then men and have protective mechanism due to estrogen Effects of estrogen are an increase in high-density lipoprotein (HDL) that transports cholesterol out of arteries; (2) a reduction in low-density lipoprotein (LDL) that deposits cholesterol in the artery; and (3) dilation of the blood vessels, which enhance blood flow to the heart Testerone increase and estrogen decrease, women who are postmenopausal have greater risk for CVD, CAD, and HF Hormonal therapy- not recommended in postmenopause

Exercise and rest

Changes in patient activity tolerance often gradual and go unnoticed Nurse determine present changes in comparing current levels within 6-12 months New symptoms or changes in usual symptoms during activity is finding Activities induced angina or SOB- CAD CAD related symptoms occur when myocardial ischemia is present- inadequate arterial blood supply to myocardium, increase demands (exercise, stress, anemia) Patient experiences symptoms need to seek medical attention Fatigue, associated with low left ventricular ejection fraction (less than 40%) with certain medications (beta- adrenergic- blocking agents) can result in activity intolerance Patients with fatigue- having medication adjusted Presence of architectural barriers in home (Stairs) he patient participation in cardiac rehab and current past exercise patterns- intensity, duration and frequency Worse HF-orthopnea- need to sit up Sleep upright in chairs or add pillows Sudden awakenings with SOB called paroxysmal nocturnal dyspnea Nighttime symptom- reabsorption of fluids from dependent areas of body back into circulation within hours of lying in bed Sudden fluid shift increase preload and places increase demand on heart of patient with HF, causing sudden pulmonary congestion Sleep disorder breathing- abnormal respiration due to intermittent episodes of upper airway obstruction causing apnea and hypopnea (shallow respirations) Cause intermittent hypoxemia, SNS activation, and increase intrathoracic pressure that puts mechanical stress on heart and large arterial walls SDB impacts the length and quality of sleep Short sleep less than 7 hrs and poor quality associated with HTPN, atherosclerosis and stroke Untreated SDB- HR and arrhythmias OSA- treated with CPAP, weight loss, positional therapy, mandibular advancement devices, oral appliances, or surgery Health Hx- nurse assess SDB by asking risk such as snoring, bouts from awakening of sleep, awaken with headache, experience hypersomnolence(daytime sleep) Determines used for CPAP, MAD, or oral appliances

Common assessment findings

Clubbing of the fingers or toes (thickening of the skin under the fingers or toes) Chronic hemoglobin desaturation most often due to congenital heart disease, advanced pulmonary diseases Cool/cold skin and diaphoresis Low cardiac output (e.g., cardiogenic shock, acute myocardial infarction) causing sympathetic nervous system stimulation with resultant vasoconstriction Cold, pain, pallor of the fingertips or toes Intermittent arteriolar vasoconstriction (Raynaud disease). Skin may change in color from white, blue, and red accompanied by numbness, tingling, and burning pain Cyanosis, central (a bluish tinge observed in the tongue and buccal mucosa) Serious cardiac disorders (pulmonary edema, cardiogenic shock, congenital heart disease) result in venous blood passing through the pulmonary circulation without being oxygenated Cyanosis, peripheral (a bluish tinge, most often of the nails and skin of the nose, lips, earlobes, and extremities) Peripheral vasoconstriction, allowing more time for the hemoglobin molecules to become desaturated. It can be caused by exposure to cold environment, anxiety, or ↓ cardiac output Ecchymosis or bruising (a purplish-blue color fading to green, yellow, or brown) Blood leaking outside of the blood vessels Excessive bruising is a risk for patients on anticoagulants or platelet-inhibiting medications Edema, lower extremities (collection of fluid in the interstitial spaces of the tissues) Heart failure and vascular problems (PAD, chronic venous insufficiency, deep vein thrombosis, thrombophlebitis) Hematoma (localized collection of clotted blood in the tissue) Bleeding after catheter removal/tissue injury in patients on anticoagulant/antithrombotic agents Pallor (↓ skin color in fingernails, lips, oral mucosa, and lower extremities) Anemia or ↓ arterial perfusion. Suspect PAD if feet develop pallor after elevating legs 60 degrees from a supine position Rubor (a reddish-blue discoloration of the legs, seen within 20 s to 2 min after placing in a dependent position) Filling of dilated capillaries with deoxygenated blood, indicative of PAD Ulcers, feet and ankles: Superficial, irregular ulcers at medial malleolus. Red to yellow granulation tissue Rupture of small skin capillaries from chronic venous insufficiency Ulcers, feet and ankles: Painful, deep, round ulcers on feet or from exposure to pressure. Pale to black wound base Prolonged ischemia to tissues due to PAD. Can lead to gangrene Thinning of skin around a cardiac implantable electronic device Erosion of the device through the skin Xanthelasma (yellowish, raised plaques observed along nasal portion of eyelids) Elevated cholesterol levels (hypercholesterolemia)

Self perception Roles and relationship

Cognitive and emotional processes that people use to formulate their beliefs and feelings Key determinants to adherence of self care and recovery after acute cardiac event People have misconception about health consequences of illness and risk for nonadherence Questioning can guide nurse for planning interventions to ensure management of illness Patients with CVD are managing complex medical regimens and CVD or cardioverter defibrillations and left ventricular assist devices Hospital stays for cardiac disorders have shortened Cardiac catheterization are used in ambulatory setting Support from family Social support helps with depression and CVD outcomes Sexual dysfunction affected twice in those with CVD Depression, anxiety erectile dysfunction, and major cardiac events such as MI are common reports decreased sexual activity Patients and partners are concerned about physical exertion to heart and activity can cause another heart attack, sudden death, or angina, dyspnea, or palpitations Couples often lack adequate information about physical demands related to sexual activity- LI exercise Initiate discussion of sexuality and encourage them to discuss problems Reproductive childbearing history Plans for pregnancies, previous, contraceptive use, menopause, and use of HT History of preeclampsia during pregnancy, preterm labor, or giving birth to infant for gestational age have higher risk for developing CVD

Pharmacologic

Cognitively impaired and unable to follow direction or physical disabled will not achieve target HR by exercising on treadmill Vasodilation like dipyridamole, adenosine, or regadenoson given IV infusion are used to mimic the effects of exercise by maximally dilating normal coronary arteries and identify stenotic arteries that can not dilate S/E- chest pain, headache, flush, nause, heart block and dyspnea Reverse with IV aminophylline Adenosine has short half life Vasodilate meds used with radionuclide imaging techniques Patients must avoid xanthine derivatives including theophylline, aminophylline, and caffeine as they block effects of vasodilating Dobutamine is another option- synthetic sympathomimetic agent that increase HR, myocardial contractility, and BP- increase metabolic demand for heart Agent of choice when ECG is used is effect on altering myocardial wall motion (enhance contractility) Patients with bronchospasms or pulmonary disease and can not tolerate having doses of theophylline withheld Not eat for at least 3 hrs before Avoid chocolate and caffeine Transient sensation during infusion of vasodilating agent such as flushing or nause

Medication

Collaborate with healthcare providers, pharmacist, and obtain patient medical include dose and frequency Vitamins, herbals, and OTC medications What are the names and doses of your medications? What is the purpose of each of these medications? How and when are these medications taken? Do you ever skip a dose or forget to take them? Are there any special precautions associated with any of these medications? •What symptoms or problems do you need to report to your primary provider? Patients recovering from ACS including coronary stent replacement or CA bypass graft are prescribed antiplatelet therapy- 2 antiplatelet drugs are prescribed for patient Aspirin- OTC, second is P2Y12 inhibitor- Clopidogrel, prasugrel)- depends on symptoms, diagnosis Reinforce adherence to medication regimen

Ambulatory ECG

Continuous at or intermittent at home Longer term Monitor etiology of chest pain, syncope, or palpitation caused by arrhythmias, detect episodes of myocardial ischemia, evaluated effectiveness of treatment of HF and arrhythmias and function of ICD and pacemakers Continuous monitor or Holter monitors- small portable recorders connected to chest electrode to record all ECG activity using two or more leads on digital memory Patient to note date and time of symptoms and activities Adherence to wear monitor ECG patch monitor- eliminate need of multiple ECG electrodes, wires, and recorders Intermittent monitors- capture arrhythmias when experiencing symptoms such as palpitation, dizzy, or lightheadedness Transmitted wireless Patient activates symptom event monitor by pressing button Loop recorder- can record and store short periods of ECG activity Under skin or wrist band Detect bradycardia, tachycardia, and irregular rhythms More monitoring capabilities Cardiac implanted electronic device- pacemaker and ICD Reveal LINQ- SubQ Triggers when arrhythmia is detected Eliminate need to change electrodes

Stress test

Coronary arteries dilate four times their usual diameter in response to increase metabolic demands for oxygen and nutrients Affected by atherosclerosis dilate less compromising blood flow to myocardium and causing ischemia Abnormalities in CVF- detected during increase oxygen demands Cardiac stress test- exercise, pharmacologic, and radionucleotides imaging- evaluate myocardial ischemia and higher myocardial oxygen Cardiac imaging at performed during rest state and immediate after stress test Results can identify specific coronary artery lesions and ischemia areas of heart Since complications of stress can be dangerous (MI, cardiac arrest, HF, and bradycardia) have advance life support

Hemodynamic monitor

Critically ill patients require continuous assessment of their cardiovascular system to diagnose and manage their complex medical conditions. This type of assessment is achieved by the use of direct pressure monitoring systems, referred to as hemodynamic monitoring. Common forms include CVP, pulmonary artery pressure, and intra-arterial BP monitoring. Patients requiring hemodynamic monitoring are cared for in critical care units. Some progressive care units also admit stable patients with CVP, pulmonary artery catheters, or intra-arterial BP monitoring. To perform hemodynamic monitoring, a CVP, pulmonary artery, or arterial catheter is introduced into the appropriate blood vessel or heart chamber. It is connected to a pressure monitoring system that has several components, including: A disposable flush system, composed of IV normal saline solution, tubing, stopcocks, and a flush device, which provides continuous and manual flushing of the system. A pressure bag placed around the flush solution that is maintained at 300 mm Hg of pressure. The pressurized flush system delivers 3 to 5 mL of solution per hour through the catheter to prevent clotting and backflow of blood into the pressure monitoring system. A transducer to convert the pressure coming from the artery or heart chamber into an electrical signal. •An amplifier or monitor, which increases the size of the electrical signal for display on an oscilloscope. Ensuring that the system is set up and maintained properly. For example, the pressure monitoring system must be kept patent and free of air bubbles. Checking that the stopcock of the transducer is positioned at the level of the atrium before the system is used to obtain pressure measurements. This landmark is referred to as the phlebostatic axis Establishing the zero reference point in order to ensure that the system is properly functioning at atmospheric pressure. This process is accomplished by placing the stopcock of the transducer at the phlebostatic axis, opening the transducer to air, and activating the zero function key on the bedside monitor. Measurements of CVP, BP, and pulmonary artery pressures can be made with the head of the bed elevated up to 60 degrees; however, the system must be repositioned to the phlebostatic axis to ensure an accurate reading Complications from the use of hemodynamic monitoring systems are uncommon and can include pneumothorax, infection, and air embolism. The nurse observes for signs of pneumothorax during the insertion of catheters using a central venous approach (CVP and pulmonary artery catheters). The longer any of these catheters are left in place (after 72 to 96 hours), the greater the risk of infection. Air emboli can be introduced into the vascular system if the stopcocks attached to the pressure transducers are mishandled during blood drawing, administration of medications, or other procedures that require opening the system to air. Therefore, nurses handling this equipment must demonstrate competence prior to caring independently for a patient requiring hemodynamic monitoring. Catheter-related bloodstream infections are the most common preventable complication associated with hemodynamic monitoring systems

Gerontologic

Decreased elasticity of arteries and loss of adjacent CT- palpable peripheral pulses Palpation of precordium in OA is affected by changes in shape of chest Cardiac impulse may be not palpable in patient with COPD- increase anterior posterior chest diameter Kyphoscoliosis- spinal deformity that occurs in OA move towards cardiac apex downward so palpation of apical impulse is obscured Hypertension- age and race Isolated systolic hypertension concern for over 55- stiffness of vasculature and decrease in vascular elasticity due to aging Orthostatic hypotension- impaired baroreceptors function to regulate BP Orthostatic risk- prolonged bed rest, dehydrations, and CV medications- beta blockers, ACE inhibitors, angiotensin receptor blockers, diuretics, nitrates S4- associated with HPTN in OA Decrease in compliance on left ventricle S2 split Soft systolic ejection murmur resulting from sclerotic changes in aortic leaflets

Stroke volume

Determined by preload, afterload and contractility Preload- degree of strethin ventricular cardiac muscle fibers at end of diastole End of diastole is period of filling volume in highest and degree of stretch on muscle fibers is greatest Volume of blood within ventricle at end of diastole determines preload which affects stroke volume AKA- left ventricular end diastole pressure Volume of bloor returning, the muscle fibers stretch increase preload, resulting in stronger contractions and greater stroke volume Frank Starling law of the heart is maintained until the physiologic limit of muscle is reached Starling- the greater the initial length or stretch of sarcomeres (cardiac muscle cells), the greater the degree of shortening Result occurs due to increase interaction between thick and thin filaments in cardiac muscle Preload is decreased reductions in volume of blood returning to ventricles Diuresis- venodilating (nitrates), excessive blood loss, or dehydration reduce preload It increase by increasing the returning circulation of blood volume to ventricles Controlling loss of blood or body fluids and replacing fluids (blood transfusion and IV) help increase Afterload- Resistance of ejection of blood from ventricles is second determinant of stroke volume Resistance of systemic BP to left ventricular ejection is systemic vascular resistance Resistance of pulmonary BP to right ventricular ejection is pulmonary vascular resistance The inverse relationship between afterload and stroke volume Afterload is increased by arterial vasoconstriction- decrease SV Opposite of vasodilation- afterload is reduced because there is less resistance to eject- SV increase

Chest pain

Differentiate cause of pain, the nurse ask scale pain, location and quality Nurse assess radiation of pain to other areas and determine associated S/S- nausea or diaphoresis Identify the events that precipitate onset of symptoms, duration, and measure aggravation or relieve The location of chest symptoms is not well correlated with the cause of the pain. For example, substernal chest pain can result from a number of causes as outlined in The severity or duration of chest pain or discomfort does not predict the seriousness of its cause. For example, when asked to rate pain using a 0 to 10 scale, patients experiencing esophageal spasm may rate their chest pain as a 10. In contrast, patients having an acute MI, which is a potentially life-threatening event, may report having moderate pain rated as a 4 to 6 on the pain scale. More than one clinical cardiac condition may occur simultaneously. During an MI, patients may report chest pain from myocardial ischemia, shortness of breath from HF, and palpitations from arrhythmias. Both HF and arrhythmias can be complications of an acute MI.

Electrophysiological test

EPS may be indicated for patients with syncope, palpitations, or both, and for survivors of cardiac arrest from ventricular fibrillation (sudden cardiac death) EPS is used to distinguish atrial from ventricular tachycardias when the determination cannot be made from the 12-lead ECG; to evaluate how readily a life-threatening arrhythmia (e.g., ventricular tachycardia, ventricular fibrillation) can be induced; to evaluate AV node function; to evaluate the effectiveness of antiarrhythmic medications in suppressing the arrhythmia; or to determine the need for other therapeutic interventions, such as a cardiac implantable electronic device, or radiofrequency ablation.

Ventricular function and wall motion CT

Equilibrium radionuclide angiocardiography (ERNA), also known as multiple-gated acquisition (MUGA) scanning Used conventional scintillation camera interfaced with computer Sequential viewing of heart The sequential images are analyzed to evaluate left ventricular function, wall motion, and ejection fraction. Cardiac CT- form of cardiac imaging that uses x-rays to provide accurate cross-sectional "virtual" slices of specific areas of the heart and surrounding structures. Two types of cardiac CT scanning include coronary CT angiography and electron beam CT (EBCT) (for coronary calcium scoring). Coronary CT angiography requires the use of an IV contrast agent to enhance the x-rays and improve visualization of cardiac structures. This test is used to evaluate coronary arteries for stenosis, the aorta for aneurysms or dissections, graft patency after coronary artery bypass grafting, pulmonary veins in patients with atrial fibrillation, and cardiac structures for congenital anomalies. Patients may receive beta-blockers prior to the scan to control heart rate and rhythm and reduce artifact. Another way to minimize artifact is to have patients hold their breath periodically throughout the scan. Coronary CT angiography is used with caution in patients with renal insufficiency. The contrast agent used during the CT scan is excreted through the kidneys; therefore, renal function should be assessed prior to the scan. It may be necessary to administer IV hydration before and after the scan to minimize the effect of the contrast on renal function. Patients will require premedication with corticosteroids and antihistamines if they experienced a reaction to a contrast agent in the past EBCT is used to calculate a coronary artery calcium score that is based on the amount of calcium deposits in the coronary arteries. This score is used to predict the likelihood of cardiac events, such as MI, or the need for a revascularization procedure in the future. Coronary artery calcium scoring is used for the evaluation of individuals without known CAD and offers limited incremental prognostic value for individuals with known CAD, such as those with stents and bypass grafts. Currently, EBCT is thought to be a reasonable test to consider in patients with low to intermediate risk for future CAD-related events. Results of the test may help to reclassify them to higher risk and thus intensify primary prevention measures Patients need to be prepared to hold their breath at certain times during the procedure, so it is important for the nurse to practice with the patient before going for CT scan. The patient is positioned on a table, and the scanner rotates around the table during the test. The procedure is noninvasive and painless. However, to obtain adequate images, the patient must lie completely still during the scanning process. An IV is necessary if contrast is to be used to enhance the images. The patient should be told to expect transient flushing, metallic taste, nausea, or bradycardia during the contrast infusion.

Arterial pulse

Evaluate pulse rate, rhythm, amplitude, contour obstruction to BV Pulse rate- low 50 bmp in healthy athletics young adults to 100 after exercise or excitement Anxiety can raise pulse rate during physical Rate is higher than expected- reassess near end of physical when relaxed Rhythm- Minor variation with respiration Pulse rate can increase during inhalation and slow during exhalation Sinus arrhythmias- children and young adults If pulse is irregular, the HR should be counted by auscultating apical, located in PMI, for full minute while palpating Any issue between contractions heard and pulse should be noted Disturbances of rhythm or arrhythmias can result in pulse deficit- difference between apical and radial pulse rate Pulse deficit in atrial fibrillation, atrial flutter, and premature ventricular contraction Arrhythmias stimulate the ventricle to contact prematurely before diastole is finished Early ventricular contractions produced smaller SV which can be heard during auscultation but not pulse Amplitude- assess peripheral arterial circulation Nurse assess pulse amplitude, bilaterally and describes and record amplitude of each artery Absent, diminished or normal or bounding 0: Not palpable or absent +1: Diminished—weak, thready pulse; difficult to palpate; obliterated with pressure +2: Normal—cannot be obliterated +3: Moderately increased—easy to palpate, full pulse; cannot be obliterated +4: Markedly increased—strong, bounding pulse; may be abnormal Subjective- specify location of artery and scale range Pulse is absent or difficult to palpate, the nurse can use continuous wave Doppler Portable ultrasound device has transducer that is placed over artery Transducer emits and receives ultrasound beams Rhythmic changes are heard as blood cells flow whereas obstruction is evidence by no changes is sound Contour- Patient with stenosis of aortic valve, valve opening is narrowed, reducing amount of blood ejected into aorta Pulse pressure is narrow and pulse is felt Aortic insufficiency the aortic valve does not completely close, allowing blood to flow back from aorta into left ventricle Rise of pulse wave is strone, and fall is precipitous Collapse pulse True contour is felter over palpating over carotid artery rather than distal radial Palpitations of arterial pulse- nurse located and evaluate all arterial pulses Palpated at points where arteries are near skin surface and easily compressed against bone or firm musculature Pulses detected over right and left temporal, common carotid, brachial, femoral, popliteal, dorsalis pedis, and posterior tibial arteries Light palpitation- fingers can obliterate temporal, dorsalis, pedis, and posterior tibial pulse Jugular venous pulse- Right side heart- reflects central venous pressure Right atria or ventricle at end of diastole Internal jugular pulsations are difficult to see, pulsations over external Sternocleidomastoid muscle Patients with euvolemia(normal BV), the jugular veins are visible suping with HOB elevated to 30 degrees Distension with 45 to 90 degrees- abnormal increase in CVP Observed with right side failure, due to hypovolemia, pulmonary hypertension, pulmonary stenosis,

Nutrition

Exercise, weight loss, and careful monitoring for CVD risk: hyperlipidemia, HTPN< and diabetes Diets restricted in NA, fat, cholesterol, or calories The patient's current height and weight (to determine body mass index [BMI]); waist measurement; BP; and any laboratory test results such as blood glucose, glycosylated hemoglobin (diabetes), total blood cholesterol, HDL and LDL levels, and triglyceride levels (hyperlipidemia) How often the patient self-monitors BP, blood glucose, and weight as appropriate to the medical diagnoses The patient's level of awareness regarding their target goals for each of the risk factors and any problems achieving or maintaining these goals What the patient normally eats and drinks in a typical day and any food preferences (including cultural or ethnic preferences) Eating habits (canned or commercially prepared foods vs. fresh foods, restaurant meals vs. home cooking, assessing for high-sodium foods, dietary intake of fats) •Who shops for groceries and prepares meals

Common symptoms

Experienced with CVD related to arrhythmias and conduction issues Structural, infectious, and inflammatory disorders, complications of CAD such as HF and cardiogenic shock Chest pain or discomfort (angina pectoris, ACS, arrhythmias, valvular heart disease) Pain or discomfort in other areas of upper body, including one or both arms, back, neck, jaw, or stomach (ACS) Shortness of breath or dyspnea (ACS, cardiogenic shock, HF, valvular heart disease) Peripheral edema, weight gain, abdominal distention due to enlarged spleen and liver or ascites (HF) Palpitations (tachycardia from a variety of causes, including ACS, caffeine or other stimulants, electrolyte imbalances, stress, valvular heart disease, ventricular aneurysms) Unusual fatigue, sometimes referred to as vital exhaustion (an early warning symptom of ACS, HF, or valvular heart disease, characterized by feeling unusually tired or fatigued, irritable, and dejected) Dizziness, syncope, or changes in level of consciousness (cardiogenic shock, cerebrovascular disorders, arrhythmias, hypotension, orthostatic hypotension, vasovagal episode) Symptoms vary between men and women Chest pain and discomfort related to ACS occur in both Women experience more atypical and nonspecific symptoms related to chest pain at rest, pain in jaw, arm, neck, middle back, or epigastric, N/V, syncope, sweating, anxiety

Myocardium

Middle muscular layer Myocytes- interconnected network of muscle fibers Encircle heart forming spiral from top of base to bottom of apex Contraction- muscular configuration facilitates twisting and compressive movement of heart that begins in atria and moves to ventricles Sequential and rhythmic contraction followed by relaxation of muscle fibers maximize volume of blood ejected with each contraction Cyclical pattern of myocardial contraction controlled by conduction

Opening and snaps and systolic clicks

No sound produced when valves open Diseases valve leaflets create abnormal sounds as opening during diastole or systole Opening snaps- abnormal diastolic sounds heard during opening of AV Mitral stenosis can cause opening snap- high pitched sound very early in diastole High pressure in left atrium that displaces snap open a rigid valve leaflet Occurs too long after S2 and can be mistaken for split and too early for diastole mistake for S3 Murmur or turbulent blood flow is expected following opening of snap Open best heard during diaphragm use Stenosis of one semilunar valve creates short high pitch sound in early systole, immediately after S1 Systolic click-opening of rigid and calcified aortic or pulmonic valve during ventricular contraction Mid to late systolic clicks can be heard with mitral or tricuspid valve prolapse as malfunctioning valve leaflet is displaced into atrium during ventricular systole Murmurs- heard over abnormal systolic sound

Contractility

Force generated by contracting myocardium Enhance catecholamines, sympathetic neuronal activity, and certain medication( digoxin, dopamine, and dobutamine) Increase contractility results in increase SV Depressed by hypoxemia, acidosis, and certain medications- (beta-adrenergic- blocking agents like metoprolol) Heart can achieve increase in SV during exercise if preload increase through venous return If contractility increase through SNS discharge, and afterload is decreased through peripheral vasodilation with decrease aortic pressure Percentage of end diastolic BV that is ejected with each heartbeat is ejection fraction Left ventricle- 55-65% Right ventricle is measured rarely Used to measure myocardial contractility Ejection fraction of less than 40% indicates patient decrease ventricular function and requires treatment of HF

Heart valves

Four valves in uni-direction Thin leaflets of fibrous tissue open and close in response to movement of blood and pressure changes within chamber Atrioventricular valve- Tricuspid- separates right ventricular and atrium Mitral or biscuspid- left Diastole- tricuspid and mitral open allowing blood in atria to flow freely into relaxed ventricular Ventricular systole begins- ventricular contract and blow flows upward into cusps of tricuspid and mitral valves, causing them to close Pressure against these valve increase, two additional structures, the papillary muscles and chordae tendineae, maintain valve closure Papillary muscle located on ventricular walls are connected to valve leaflets by chordae tendineae, which are thin fibrous bands During ventricular systole, contraction of papillary muscle cause chordae tendineae to become taut, keeping valve leaflet approximated and closed Prevents backflow of blood into atria- regurgitation Semilunar valve- Two composed of three leaflets Valve between right ventricle and pulmonary artery is called pulmonic valve Valve between left ventricle and aorta- aortic valve Semilunar valve are closed during diastole Pressure in pulmonary artery and aorta decrease, causing blood flow back towards semilunar valves Action fills cusps with blood and closes valves Forces open during ventricular systole as blood ejects from right and left ventricles into pulmonary aorta and artery

Orthostatic BP changes

Gravitational redistribution of 500 ml of blood in lower extremities upon standing Venous pooling reduces blood return to heart, compromising preload that reduces SV and CO ANS is activated- SNS increase HR and enhances peripheral vasoconstrictions- PNS- vagus nerve decrease Stabilization in 1 minute Normal postural response occurs when person moves from lying to standing A heart rate increase of 5 to 20 bpm above the resting rate; (2) an unchanged systolic pressure, or a slight decrease of up to 10 mm Hg; and (3) a slight increase of 5 mm Hg in diastolic pressure. Orthostatic hypotension- decrease of 20 mm Hg in systolic and BP of 10 mm Hg in diastolic within 3 minutes if lying or sitting or standing Accompanied by dizzy, lightheadedness, or syncope Increase with age and risk for fall CVD- significant reduction in preload, which compromises CO Reduced preload- reflective of intravascular volume depletion is caused by dehydration from overdiuresis, bleeding due to antiplatelet or anticoagulation medication or post intravascular procedures or medication that dilate BV (nitrates and antispasmodic) Mechanism to maintain CO (increase HR and peripheral vasoconstriction) can not compensate for loss in intravascular BP drops and HR increase with lying, sitting, or upright Supine: BP 120/70 mm Hg, heart rate 70 bpm Sitting: BP 100/55 mm Hg, heart rate 90 bpm Standing: BP 98/52 mm Hg, heart rate 94 bpm Position the patient supine for 10 minutes before taking the initial blood pressure (BP) and heart rate measurements. •Reposition the patient to a sitting position with legs in the dependent position, wait 2 minutes, then reassess both BP and heart rate measurements. •If the patient is symptom free or has no significant decreases in systolic or diastolic BP, assist the patient into a standing position, obtain measurements immediately, and recheck in 2 minutes; continue measurements every 2 minutes for a total of 10 minutes to rule out orthostatic hypotension. •Return the patient to a supine position if orthostatic hypotension is detected or if the patient becomes symptomatic. •Document heart rate and BP measured in each position (e.g., supine, sitting, standing) and any signs or symptoms that accompany the postural changes.

Interventions

Hand hygiene Wash hands with soap and water or use alcohol-based hand rubs before and after contact with the catheter for any reason. Dressing Wear clean or sterile gloves when changing the dressing. Cleanse the skin during dressing changes with a >0.5% chlorhexidine preparation with alcohol. Use a chlorhexidine-impregnated dressing at the catheter insertion site. Do not use topical antibiotic ointment or creams on insertion sites. Dress the site with sterile gauze or sterile, transparent, semipermeable dressing to cover the catheter site. If the patient is diaphoretic or if the site is bleeding or oozing, use a gauze dressing until it is resolved. Change gauze dressings every 2 d or transparent dressings at least every 7 d and whenever dressings become damp, loosened, or visibly soiled. Catheter site Assess the site regularly—visually when changing the dressing or by palpation through an intact dressing. Remove the dressing for a thorough assessment if the patient has tenderness at the insertion site, fever without obvious source, or other signs of local or bloodstream infection. Needleless catheter systems Change needleless connectors, administration sets, and pressure tubing per institutional policy, usually every 96 h. Scrub ports, connectors, and hubs with alcohol, chlorhexidine/alcohol, or povidone-iodine before and after access. Apply alcohol-impregnated caps to needless connectors between uses. Bathing Clean the skin daily with a 2% chlorhexidine wash. Do not submerge the catheter or catheter site in water. Showering is permitted if the catheter and related tubing are placed in an impermeable cover. Patient education Ask patients to report any new discomforts from the catheter site.

Hardwire, telemetry, lead system

Hardwire monitor- continuously observe heart for arrhythmias and conduction disorders using one or two ECG leads Additional components to continuously monitor hemodynamic parameters (noninvasive BP, arterial pressure, pulmonary artery pressure) Respiratory parameters (RR, oxygen saturation) ST segments of myocardial ischemia Telemetry- transmission of radio waves from battery operated transmitter to central bank of monitors Primary benefit of using telemetry- wireless- ambulate while one or two ECG leads are monitor Lead system- number of electrodes needed is dictated by lead system 3-5 lead systems Type determines number of lead options of monitor 5-seven different lead selections Two ECG leads are continuous ECG monitor- leads 2, and 5 2-best visualization of atrial depolarization (p wave) 5- ventricular depolarization and useful to monitor for certain arrhythmias(premature ventricular contractions tachycardias, bundle block branch) The monitoring system requires an adequate electrical signal to analyze the patient's cardiac rhythm. Proper use of this technology includes the correct application of electrodes to reduce false alarms on the cardiac monitor. When applying electrodes, the recommendations below should be followed to optimize skin adherence and conduction of the heart's electrical current: •Débride the skin surface of dead cells with soap and water; dry well using a wash cloth or gauze. •Clip (do not shave) hair from around the electrode site, if needed. •Connect the electrodes to the lead wires prior to placing them on the chest (connecting lead wires when electrodes are in place may be uncomfortable for some patients). •Peel the backing off the electrode, and check to make sure the center is moist with electrode gel. •Locate the appropriate lead placement, and apply the electrode to the skin, securing it in place with light pressure. •Change the electrodes every 24 hours, examine the skin for irritation, and apply the electrodes to different locations. •If the patient is sensitive to the electrodes, use hypoallergenic electrodes.

Anatomy of the heart

Heart is hollow muscular organ located in thorax- space between lungs (mediastinum) and rest on diaphragm Influence weight and size by age, body weight, extent of exercise, and heart disease Heart pumps blood to tissue and supplies with O2 Inner layer- endocardium- consist of endothelial tissue and lines inside of heart and values Middle- myocardium- muscle fibers and responsible for pumping Exterior- epicardium Heart encased in thin fibrous sac called pericardium- 2 layers Adhering to epicardium is visceral pericardium Enveloped in visceral is parietal pericardium- tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral column and supports heart in mediastinum Space between two layers or pericardial space is filled with 20 ml fluids- lubricates surface of heart and reduces friction during systole

Measuring apical

Heart is inspected, palpation, and auscultate of precordium or anterior chest wall Aortic area—second intercostal space to the right of the sternum. To determine the correct intercostal space, the nurse first finds the angle of Louis by locating the bony ridge near the top of the sternum, at the junction of the sternum and the manubrium. From this angle, the second intercostal space is located by sliding one finger to the left or right of the sternum. Subsequent intercostal spaces are located from this reference point by palpating down the rib cage. 2.Pulmonic area—second intercostal space to the left of the sternum 3.Erb point—third intercostal space to the left of the sternum 4.Tricuspid area—fourth and fifth intercostal spaces to the left of the sternum 5.Mitral (apical) area—left fifth intercostal space at the midclavicular line 6.Epigastric area—below the xiphoid process Apical is felt as light with 1-2 cm diameter Felt in onset of first heart and last for only half of ventricular systole Nurse uses palm of hand to locate apical impulse initially and finger pads to assess size and quality Palpation of apical can be facilitated by repositioning patient to left lateral- puts heart closer to chest wall Apical is palatable in one intercostal space Two or more adjacent intercostal space indicates left ventricular enlargement Apical below fifth intercostal space or lateral to midclavicular line denotates left ventricular enlargement from left HF Apical is palpated in two distinct separate areas and pulsation movements are paradoxical (not simultaneous), ventricular aneurysm Forceful apical impulse- left ventricular heave or lift- lift from hand from chest wall Vibration or purring- turbulent blood flow Detect with palm of hand Vibration known as thrill- loud murmur Location- serious valvular heart disease, atrial or ventricular septal defect (abnormal opening) or stenosis of large artery

Murmur

Heart murmurs are described in terms of location, timing, intensity, pitch, quality, and radiation. These characteristics provide information needed to determine the cause of the murmur and its clinical significance. Location Pinpointing the location of the murmur helps to determine the underlying structures that are involved in generating the abnormal sounds. The description should include the exact location from which the sound emanates, such as the location of the intercostal space and other important landmarks (right or left sternal border; midsternal, midclavicular, anterior axillary, or midaxillary lines). For example, a ventricular septal defect can be located at the left sternal border in the third and fourth intercostal spaces. Timing A murmur is described in terms of when it occurs during the cardiac cycle (systole or diastole). Murmurs are further differentiated by identifying exactly when during systole or diastole they are heard. A skilled clinician can detect that the murmur is occurring during early, mid, or late systole or diastole. Some murmurs have sounds that occur in both systole and diastole. Intensity A grading system is used to describe the intensity or loudness of a murmur. Grade 1: Very faint and difficult for the inexperienced clinician to hear Grade 2: Quiet but readily perceived by the experienced primary provider Grade 3: Moderately loud Grade 4: Loud and may be associated with a thrill Grade 5: Very loud; heard when stethoscope is partially off the chest; associated with a thrill Grade 6: Extremely loud; detected with the stethoscope off the chest; associated with a thrill Pitch Pitch describes the sound frequency, identified as high, medium, or low pitched. High-pitched murmurs are heard best with the stethoscope's diaphragm, whereas low-pitched sounds are detected using the bell of the stethoscope placed lightly on the chest wall. Quality Quality describes the sound that the murmur resembles. Murmurs can produce a rumbling, blowing, whistling, harsh, or musical sound. For example, murmurs caused by mitral or tricuspid regurgitation have a blowing quality, whereas mitral stenosis generates a rumbling sound. Radiation Radiation refers to the transmission of the murmur from the point of maximal intensity to other areas in the upper chest. The examiner determines if radiation is present by listening carefully to areas of the heart adjacent to the point where the murmur is the loudest. If radiation is present, the exact location is described. A murmur associated with aortic stenosis, for example, can radiate into the neck, down the left sternal border, and into the apical area.

Lungs

Hemoptysis: Pink, frothy sputum is indicative of acute pulmonary edema. Cough: A dry, hacking cough from irritation of small airways is common in patients with pulmonary congestion from HF. Crackles: HF or atelectasis associated with bed rest, splinting from ischemic pain, or the effects of analgesic, sedative, or anesthetic agents often results in the development of crackles. Typically, crackles are first noted at the bases (because of gravity's effect on fluid accumulation and decreased ventilation of basilar tissue), but they may progress to all portions of the lung fields. Wheezes: Compression of the small airways by interstitial pulmonary edema may cause wheezing. Beta-adrenergic-blocking agents (beta-blockers), particularly noncardioselective beta-adrenergic-blocking agents such as propranolol, may cause airway narrowing, especially in patients with underlying pulmonary disease.

Cardiac Action Potential

Nodal and Purkinje cells (electrical cells) generate and transmit impulse across heart, stimulating cardiac myocytes (working cells) to contract Due to exchange of electrically charged particle-ions, across channels located in cell membrane Channels regulate movement and speed of specific ions such as Na, K, and Ca Na enters into channels, Ca- enter through slow channels Resting or polarized state- NA is primary extracellular ion, K- intracellular Difference in ion concentration means inside cell is negative compared with positive on the outside When Na or Ca cross membrane into cell and K ions exits into exit into extracellular Exchange of ions create positive intracellular space and negative extracellular space- depolarization Once depolarization is complete, the exchange of ions revert to resting state- repolarization Repeated cycle of depolarize and repolarize- cardiac AP

Self management of cardiac catheter

If the artery in your wrist artery was used: Return to normal activities tomorrow. Strenuous activities of the wrist such as manual labor, tennis, or driving may be restricted for a few days per your provider's orders. •If the artery in your groin was used: For the next 24 hours, do not bend at the waist, strain, or lift heavy objects. •Do not submerge the puncture site in water. Avoid tub baths, but shower as desired. •Talk with your primary provider about when you may return to work, drive, or resume strenuous activities. •If bleeding occurs, sit (arm or wrist approach) or lie down (groin approach) and apply firm pressure to the puncture site for 10 minutes. Notify your primary provider as soon as possible and follow instructions. If there is a large amount of bleeding, call 911. Do not drive to the hospital. •Call your primary provider if any of the following occur: swelling, new bruising or pain from your procedure puncture site, temperature of 101°F or more. •If test results show that you have coronary artery disease, talk with your primary provider about options for treatment, including cardiac rehabilitation programs in your community. •Talk with your primary provider about lifestyle changes to reduce your risk for further or future heart problems, such as quitting smoking, lowering your cholesterol level, initiating dietary changes, beginning an exercise program, cardiac rehabilitation, or losing weight. •Your primary provider may prescribe one or more new medications depending on your risk factors (medications to lower your blood pressure or cholesterol; aspirin or clopidogrel to prevent blood clots). Take all of your medications as instructed. If you feel that any of them are causing side effects, call your primary provider immediately. Do not stop taking any medications before talking to your primary provider.

Nursing interventions for catheterization

Instructing the patient to fast, usually for 8 to 12 hours, before the procedure. Informing the patient that if catheterization is to be performed as an outpatient procedure, a friend, family member, or other responsible person must transport the patient home. Informing the patient about the expected duration of the procedure and advising that it will involve lying on a hard table for less than 2 hours. Reassuring the patient that IV medications are given to maintain comfort. Informing the patient about sensations that will be experienced during the catheterization. Knowing what to expect can help the patient cope with the experience. The nurse explains that an occasional pounding sensation (palpitation) may be felt in the chest because of extra heartbeats that almost always occur, particularly when the catheter tip touches the endocardium. The patient may be asked to cough and to breathe deeply, especially after the injection of the contrast agent. Coughing may help disrupt an arrhythmia and clear the contrast agent from the arteries. Breathing deeply and holding the breath help lower the diaphragm for better visualization of heart structures. The injection of a contrast agent into either side of the heart may produce a flushed feeling throughout the body and a sensation similar to the need to void, which subsides in 1 minute or less. •Encouraging the patient to express fears and anxieties. The nurse provides education and reassurance to reduce apprehension. Observing the catheter access site for bleeding or hematoma formation and assessing peripheral pulses in the affected extremity (dorsalis pedis and posterior tibial pulses in the lower extremity, radial pulse in the upper extremity) every 15 minutes for 1 hour, every 30 minutes for 1 hour, and hourly for 4 hours or until discharge. BP and heart rate are also assessed during these same time intervals. Evaluating temperature, color, and capillary refill of the affected extremity during these same time intervals. The patient is assessed for affected extremity pain, numbness, or tingling sensations that may indicate arterial insufficiency. The best technique to use is to compare the examination findings between the affected and unaffected extremities. Any changes are reported promptly. Screening carefully for arrhythmias by observing the cardiac monitor or by assessing the apical and peripheral pulses for changes in rate and rhythm. A vasovagal reaction, consisting of bradycardia, hypotension, and nausea, can be precipitated by a distended bladder or by discomfort from manual pressure that is applied during removal of an arterial or venous catheter. The vasovagal response is reversed by promptly elevating the lower extremities above the level of the heart, infusing a bolus of IV fluid, and administering IV atropine to treat the bradycardia. Maintaining activity restrictions for 2 to 6 hours after the procedure. The determination of bed rest, chair activity, and time to commence ambulation is dependent upon location of arterial approach, size of the catheter used during the procedure, medications administered, and method used to maintain hemostasis. If manual pressure or a mechanical device was used during a femoral artery approach, the patient remains on bed rest for up to 6 hours with the affected leg straight and the head of the bed elevated no greater than 30 degrees. For comfort, the patient may be turned from side to side with the affected extremity straight. If a percutaneous vascular closure device or patch was deployed, the nurse checks local nursing care standards and anticipates that the patient will have fewer activity restrictions. If the radial closure device was used, the patient can sit up in a chair until the effects of sedation have dissipated, and early ambulation is encouraged. After the vascular closure device removal, a dressing is applied over the catheter access site. Patients can return to normal activities the day after the procedure but must avoid strenuous wrist activities for several days (Mason et al., 2018). Analgesic medication is given as prescribed for discomfort. Instructing the patient to report chest pain and bleeding or sudden discomfort from the catheter insertion sites promptly. Monitoring the patient for CIN by observing for elevations in serum creatinine levels. IV hydration is used to increase urinary output and flush the contrast agent from the urinary tract; accurate oral and IV intake and urinary output are recorded. •Ensuring patient safety by instructing the patient to ask for help when getting out of bed the first time after the procedure. The patient is monitored for bleeding from the catheter access site and for orthostatic hypotension, indicated by complaints of dizziness or lightheadedness.

Intra arterial blood pressure monitoring

Intra-arterial BP monitoring is used to obtain direct and continuous BP measurements in critically ill patients who have severe hypertension or hypotension. Arterial catheters are also useful when arterial blood gas measurements and blood samples need to be obtained frequently. The radial artery is the usual site selected. However, placement of a catheter into the radial artery can further impede perfusion to an area that has poor circulation. As a result, the tissue distal to the cannulated artery can become ischemic or necrotic. Patients with diabetes, peripheral vascular disease, or hypotension, receiving IV vasopressors, or having had previous surgery are at highest risk for this complication. Before arterial line insertion, two tests may be considered to assess circulation; namely, a Doppler ultrasound or a modified Allen's test. A Doppler ultrasound assesses blood flow of the artery. The modified Allen's test assesses collateral circulation. To perform the Allen's test, the patient's hand is elevated and the patient is asked to make a fist. The nurse compresses the radial and ulnar arteries simultaneously, causing the hand to blanch. After the patient opens the fist, the nurse releases the pressure on the ulnar artery. If blood flow is restored (hand turns pink) within 7 seconds, the circulation to the hand may be adequate enough to tolerate placement of a radial artery catheter Site preparation and care are the same as for CVP catheters. The catheter flush solution is normal saline, which is the same as for CVP and pulmonary artery catheters. A transducer is attached, and pressures are measured in millimeters of mercury (mm Hg). The nurse monitors the patient for complications, which include local obstruction with distal ischemia, external hemorrhage, massive ecchymosis, dissection, air embolism, blood loss, pain, arteriospasm, and infection.

Assessment

Severity of symptoms, presence of risk factors, practice setting ED nurse performs assessment focused on acute coronary syndrome, s/s caused by ruptured atheromatous plaque is disease coronary artery ECG

Coronary arteries

Left and right and branch supply arterial blood to heart Arteries originate from aorta above aortic valve leaflets Perfused with diastole Normal rate of 60-80 bpm,- ample time for diastole for myocardial perfusion HR increase- diastole shortens- not allowing time for myocardial perfusion Patient at risk for myocardial ischemia During tachycardia Left coronary artery has 3 branches Artery point of origin to first branch- left main coronary artery Two branches arise from left main coronary artery: left anterior descending artery, which course down anterior wall of heart, and circumflex artery, which circles around lateral left wall Right side- travels to inferior wall of heart Posterior wall of heart receives blood supply from additional branch from right coronary artery called posterior descending artery Superficial to coronary artery are coronary veins Venous blood from veins returns to heart through coronary sinus

Cholesterol levels

Lipid required for hormone synthesis and cell membrane formation Large quantities in brain and nerve tissue Diet from animals and liver- synthesized Variations in cholesterol- age, gender, diet, exercise, genetics, menopause, and stress Total cholesterol level is calculated by adding HDL and LDL, and 20% triglyceride High cholesterol increase risk for CVD regardless of age Statins- cholesterol reducing meds Other non statins- reduce cholesterol- ezetimibe, bile acid sequestrants, PCSK9 inhibitors LDL- primary transported of cholesterol and triglycerides into cell HDL has protective action because of transports cholesterol away from tissue and cells of arterial wall to liver for excretion Triglycerides- Free fatty acids and glycerol Adipose tissue and source of energy Increase after meal and affected by stress Diabetes, alcohol use, obesity can elevate Direct correlation with LDL and inverse with HDL

Magnetic Resonance Angiography

MRA is a noninvasive, painless technique that is used to examine both the physiologic and anatomic properties of the heart. MRA uses a powerful magnetic field and computer-generated pictures to image the heart and great vessels. It is valuable in diagnosing diseases of the aorta, heart muscle, and pericardium, as well as congenital heart lesions. The application of this technique to the evaluation of coronary artery anatomy is limited because the quality of the images is distorted by respirations, the beating heart, and certain implanted devices (stents and surgical clips). In addition, this technique cannot adequately visualize the small distal coronary arteries as accurately as conventional angiography performed during a cardiac catheterization. MRA cannot be performed on patients who have metal plates, prosthetic joints, or other metallic implants that can become dislodged if exposed to MRA. Patients are instructed to remove any jewelry, watches, or other metal items (e.g., ECG leads). Transdermal patches that contain a heat-conducting aluminized layer (e.g., nitroglycerin, clonidine, fentanyl) must be removed before MRA to prevent burning of the skin. During MRA, the patient is positioned supine on a table that is placed into an enclosed imager or tube containing the magnetic field. A patient who is claustrophobic may need to receive a mild sedative before undergoing an MRA. An intermittent clanking or thumping that can be annoying is generated by the magnetic coils, so the patient may be offered a headset to listen to music. The scanner is equipped with a microphone so that the patient can communicate with the staff. The patient is instructed to remain motionless during the scan.

Invasive CO monitor

Monitoring cardiac output using the pulmonary artery catheter has been the standard of practice in critical care since its inception over 50 years ago. Its use has diminished recently with the availability of new, less invasive devices. Several types of devices are commercially available. Selection of a specific device for clinical use is determined by availability, provider preferences, and the patient's clinical condition Pulse pressure analysis uses an arterial pressure waveform to continuously estimate the patient's stroke volume. One such device, the Edwards Lifesciences Vigileo monitoring system, is connected to an existing radial or femoral arterial line via its FloTrac transducer. Using age, gender, body surface area, and BP of the patient, this device calculates continuous cardiac output and other parameters used in the management of critically ill patients. The major drawback to this device is that in order for it to capture accurate data, it must first capture optimal arterial waveforms. Therefore, this type of device has limited usefulness in patients with poor waveform signals, some arrhythmias, hemodynamic instability, and those who may be concomitantly using an intra-aortic balloon pump Esophageal Doppler probes are used to noninvasively estimate cardiac output. The esophageal probe measures blood flow velocity within a cross-sectional area of the descending aorta to calculate cardiac output. The use of this device in the perioperative setting has been shown to improve patient outcomes, including decreased lengths of hospital stay and an overall decrease in rates of complications The Fick method, which uses carbon dioxide (CO2) measures, is an additional method used to estimate cardiac output. To obtain cardiac output using this method, a rebreathing loop is attached to the ventilator along with an infrared CO2 sensor, an airflow sensor, and pulse oximeter. Continuous readings of cardiac output may be updated every 3 minutes with the use of this device. As an alternative, a Fick calculation may be done that uses the patient's body surface area and oxygen consumption (arterial and venous saturations and hemoglobin) to determine cardiac output.

Murmurs and friction rub

Murmurs- turbulent blood flow in heart Cause turbulent- narrow valve, malfunctioning valve that allows regurgitant blood flow, congenital defect of ventricular, defect between aorta and pulmonary artery or increase flow of blood through normal structure (fever, pregnancy, hyperthyroidism) Timing cardiac cycle, location in chest wall, intensity, pitch, quality Friction rub- Systole and diastole Abrasion of inflamed pericardial surface from pericarditis Confused with murmur- identify sound and distinguish in systole and diastole Diaphragm- sitting up and leaning Identidfy

Refractory

Myocardial cell must repolarize before depolarizing Repolarization- cells are in pause Effective or absolute refractory and relative refractory Effective- cells are unresponsive to electrical stimulus and incapable of initiating an early depolarization Corresponds with time in phase o to middle of phase 3 of AP Relative refractory- corresponds to short time at end of phase 3 Electrical stimulus is stronger, the cell can depolarize prematurely Early depolarization of atrium or ventricle cause premature contraction, placing patient at risk for arrhythmias Premature ventricular contractions in certain situations such as presence of myocardial ischemia- early ventricular depolarization can trigger life threatening arrhythmias- ventricular tachycardia or ventricular fibrillation

Radionuclide imaging

Noninvasive test that use radioisotopes to evaluate coronary artery perfusion, detect myocardial ischemia and infarction or assess left ventricular function Radioisotopes are unstable atoms that give of small amounts of energy in gamma ray form Detected with gamma scintillation camera Myocardial perfusion imaging- single photon emission CT or PET- after acute MI to determine if arterial perfusion to heart is compromised during activity to evaluate the extent of myocardial damage Compare with stress test with relax heart Differentiate ischemic myocardium from infarct related myocardium Fixed defect- does not change in size before and after stress- indicates no perfusion in area of myocardium Detects that are larger after stress- reduced perfusion to area of heart- reversible defect Cardiac catheterization is recommended after positive test results to determine severity of obstruction to blood flow Myocardial perfusion imaging with stress test should be prepared for type of stressors to be used Imaging is performed in two stages- resting and IV inserted into radioisotope and electrodes on chest to monitor HR

Echocardiography Transthoracic echo

Noninvasive ultrasound test that is used to measure the ejection fraction and examine the size, shape, and motion of cardiac structures. It is particularly useful for diagnosing pericardial effusions; determining chamber size and the etiology of heart murmurs; evaluating the function of heart valves, including prosthetic heart valves; and evaluating ventricular wall motion. The ultrasound is generated by a handheld transducer applied to the front of the chest. The transducer picks up the echoes and converts them to electrical impulses that are recorded and displayed on a monitor. It creates sophisticated, spatially correct images of the heart. An ECG is recorded simultaneously to assist in interpretation of the echocardiogram. With the use of Doppler techniques, an echocardiogram can also show the direction and velocity of the blood flow through the heart. These techniques are used to assess for "leaking valves," conditions referred to as valvular regurgitation, and will also detect abnormal blood flow between the septum of the left and right heart. Echocardiography may be performed with an exercise or pharmacologic stress test. Images are obtained at rest and then immediately after the target heart rate is reached. Myocardial ischemia from decreased perfusion during stress causes abnormalities in ventricular wall motion and is easily detected by echocardiography. A stress test using echocardiography is considered positive if abnormalities in ventricular wall motion are detected during stress but not during rest. These findings are highly suggestive of CAD and require further evaluation, such as a cardiac catheterization. Is performed while a transducer that emits sound waves is moved over the surface of the chest wall. Gel applied to the skin helps transmit the sound waves. Periodically, the patient is asked to turn onto the left side or hold a breath. The test takes about 30 to 45 minutes. If the patient is to undergo an exercise or pharmacologic stress test with echocardiography, information on stress testing is also reviewed with the patient.

Heart auscultation

Normal heart sounds S1 and S2- closure of a AV valves and semilunar Corresponds with ventricular systole Systole is shorter than period between S1 and S2 (diastole) S1- tricuspid and mitral valve closure creates first heart sound Lub Loudest at apical area Identifiable and serves as point of reference for remainder cardiac cycle Intensity of S1 increase during tachycardia or mitral stenosis AV valves are wide during ventricular contraction Accentuated S1 occurs as AV valves close with greater force than normal Arrhythmias can vary intensity of S1 from beat to beat due to lack of synchronization atrial and ventricular contraction S2- Closure of pulmonary and aortic valves Dub Aortic- loudest over Pulmonic is softer sound Pulmonic valve lags behind aortic Split S2- inspiration and and disappears Inspiration- decrease in intrathoracic pressure and increase in venous return to right atrium and ventricle Right ventricle takes longer to eject, which causes pulmonic valve to close later Splitting of S2- remains constant during inspiration and expiration is abnormal finding Abnormal splitting of second heart sound can be disease state (valvular heart disease, septal defect, bundle branch block) Heard over pulmonic Abnormal- Systole and diastole when structural and functional problems S3 and S4- opening snaps, gallops, systolic clicks and murmurs Gallops- diastole Sounds create vibration of ventricle and surrounding structure as blood meets resistance during ventricular filling Low frequency and heard over with bell S3- DUB diastole with rapid ventricular filling as blood flows from atrium into non compliant ventricle Represents normal in children and adults 35-40 OA- HF Right ventricle involved - right side S3 is heard over tricuspid are with patient supine Left side- apical area with patient left lateral S4- LUB late diastole Before S1 during atrial contraction as blood forcefully enters ventricle Resistance to Blood flow during ventricular hypertrophy caused by hypertension, CAD, cardiomyopathies, aortic stenosis, and numerous other conditions Produced in left ventricle auscultated with bell over apical with patient in left lateral position A right side S4- tricuspid area supine S3 and 4 present- quadruple rhythm During tachycardia-combines loud summation glalop

Physical assessments

Obtain health Hx, establish patient current or baseline conditions, response to treatment Frequency of assessment determined by purpose encounter and condition Focused cardiac- outpatient Acute care- more extensive assessment ever 8 hours The heart as a pump (reduced pulse pressure, displaced PMI from fifth intercostal space midclavicular line, gallop sounds, murmurs) Atrial and ventricular filling volumes and pressures (elevated jugular venous distention, peripheral edema, ascites, crackles, postural changes in BP) Cardiac output (reduced pulse pressure, hypotension, tachycardia, reduced urine output, lethargy, or disorientation) Compensatory mechanisms (peripheral vasoconstriction, tachycardia) Patients LOC (alert, lethargic, comatose) and mental status (orientation) Changes in LOC and mental status can be inadequate perfusion of brain from compromised cardiac output or thrombotic event (Stroke) Observe signs for distress, include pain or discomfort, SOB Notes size of patient Height and weight- BMI and waist circumference Obesity greater than 30 and abdominal fat (males- greater than 40 and females greater than 35 are at risk Examine skin- head and finish with lower extremities Skin color, temp, and texture, assess for acute and chronic problems with arterial or venous circulation Signs and symptoms of acute obstruction of arterial blood flow in the extremities, referred to as the six Ps, are pain, pallor, pulselessness, paresthesia, poikilothermia (coldness), and paralysis. During the first few hours after invasive cardiac procedures (e.g., cardiac catheterization, percutaneous coronary intervention [PCI], or cardiac electrophysiology testing), affected extremities should be assessed frequently for these acute vascular changes. Major blood vessels of the arms and legs may be used for catheter insertion. During these procedures, systemic anticoagulation with heparin is necessary, and bruising or small hematomas may occur at the catheter access site. However, large hematomas are a serious complication that can compromise circulating blood volume and cardiac output. Patients who have undergone these procedures must have catheter access sites frequently observed until hemostasis is adequately achieved. Edema of the feet, ankles, or legs is called peripheral edema. Edema can be observed in the sacral area of patients on bed rest. The nurse assesses the patient for edema by using the thumb to place firm pressure over the dorsum of each foot, behind each medial malleolus, over the shins or sacral area for 5 seconds. Pitting edema is the term used to describe an indentation in the skin created by this pressure The degree of pitting edema relies on the clinician's judgment of depth of edema and time the indentation remains after release of pressure. Pitting edema is graded as absent (0) or as present on a scale from trace (1+ ≤0.25 inch) to severe (4+ ≥1 inch) It is important that clinicians use a consistent scale in order to ensure reliable clinical measurements and management. Peripheral edema is a common finding in patients with HF and peripheral vascular diseases, such as deep vein thrombosis or chronic venous insufficiency. Prolonged capillary refill time indicates inadequate arterial perfusion to the extremities. To test capillary refill time, the nurse compresses the nail bed briefly to occlude perfusion and the nail bed blanches. Then, the nurse releases pressure and determines the time it takes to restore perfusion. Normally, reperfusion occurs within 2 seconds, as evidenced by the return of color to the nail bed. Prolonged capillary refill time indicates compromised arterial perfusion, a problem associated with cardiogenic shock and HF. Clubbing of the fingers and toes indicates chronic hemoglobin desaturation and is associated with congenital heart disease. •Hair loss, brittle nails, dry or scaling skin, atrophy of the skin, skin color changes, and ulcerations are indicative of chronically reduced oxygen and nutrient supply to the skin observed in patients with arterial or venous insufficiency (see Chapter 26 for a complete description of these conditions)

Action potential

Phase 0: Cellular depolarization is initiated as positive ions influx into the cell. During this phase, the atrial and ventricular myocytes rapidly depolarize as sodium moves into the cells through sodium-fast channels. The myocytes have a fast-response action potential. In contrast, the cells of the SA and AV node depolarize when calcium enters these cells through calcium-slow channels. These cells have a slow-response action potential. Phase 1: Early cellular repolarization begins during this phase as potassium exits the intracellular space. Phase 2: This phase is called the plateau phase because the rate of repolarization slows. Calcium ions enter the intracellular space. Phase 3: This phase marks the completion of repolarization and return of the cell to its resting state. Phase 4: This phase is considered the resting phase before the next depolarization.

Right heart catheterization and Left heart catheterization

Precedes left heart catheterization. It is performed to assess the function of the right ventricle and tricuspid and pulmonary valves. The procedure involves the passage of a catheter from a brachial, internal jugular, or femoral vein into the right atrium, right ventricle, pulmonary artery, and pulmonary arterioles. Pressures and oxygen saturations from each of these areas are obtained and recorded. The pulmonary artery pressures are used to diagnose pulmonary hypertension. A biopsy of a small piece of myocardial tissue can also be obtained during a right heart catheterization. The results of the biopsy are used to diagnose the etiology of a cardiomyopathy (abnormality of myocardium) or heart transplant rejection. At the completion of the procedure, the venous catheter is removed and hemostasis of the affected vein is achieved using manual pressure. Although right heart catheterization is considered relatively safe, potential complications include arrhythmias (from contact of the catheter with the endocardium), venous spasm, infection at the insertion site, and right heart perforation. Prior to left heart catheterization, patients who have previously experienced a reaction to a contrast agent are premedicated with antihistamines (e.g., diphenhydramine) and corticosteroids (e.g., prednisone). Patients at risk for CIN receive pre- and postprocedure preventive strategies. IV saline hydration increases vascular volume, facilitates removal of contrast from the kidneys, and reduces the risk of CIN Left heart catheterization is performed to evaluate the aortic arch and its major branches, patency of the coronary arteries, and the function of the left ventricle and mitral and aortic valves. Left heart catheterization is performed by retrograde catheterization of the left ventricle. In this approach, the interventional cardiologist usually inserts the catheter into the right radial or a femoral artery and advances it into the aorta and left ventricle. Potential complications include arrhythmias, MI, perforation of the left heart or great vessels, and systemic embolization. During a left heart catheterization, angiography is performed. Angiography is an imaging technique that involves the injection of the contrast agent into the arterial catheter. The contrast agent is filmed as it passes through the chambers of the left heart, aortic arch, and its major arteries. Coronary angiography is another technique used to observe the coronary artery anatomy and evaluate the degree of stenosis from atherosclerosis. To perform this test, a catheter is positioned into one of the coronary arteries. Once in position, the contrast agent is injected directly into the artery and images are obtained. The procedure is then repeated using the opposite coronary artery. Ventriculography is also performed to evaluate the size and function of the left ventricle. For this test, a catheter is positioned in the left ventricle and a large amount of contrast agent (30 mL) is rapidly injected into the ventricle. The manipulation of catheters in the coronary arteries and left ventricle as well as injection of the contrast agent can cause intermittent myocardial ischemia. Vigilant monitoring throughout left heart catheterization is needed to detect myocardial ischemia, which can trigger chest pain and life-threatening arrhythmias. Once the procedure is completed, the arterial catheter is withdrawn. There are several options available to achieve arterial hemostasis, including applying manual pressure and hemostatic devices available from numerous vendors. For the radial artery, a compression device, such as the Terumo TR Band®, is positioned over the artery. It has a mechanism that is inflated with air to put pressure against the artery. It remains in place for about 2 hours. A radial approach and a compression device are both common practices and are associated with lower risks for bleeding and vascular complications, as well as a shorter time to ambulation post procedure For the femoral approach, manual pressure may be used alone or in combination with mechanical compression devices such as the FemoStop™. Many types of percutaneously deployed vascular closure devices are also available. These devices are positioned at the femoral arterial puncture site after completion of the procedure. They deploy a saline-soaked gelatin sponge (QUICKSEAL), collagen (VasoSeal), sutures (Perclose ProGlide™), or a combination of both collagen and sutures (Angio-Seal). Other products that expedite arterial hemostasis include external patches (Syvek Patch, Clo-Sur P.A.D.). These products are placed over the puncture site as the catheter is removed and manual pressure is applied for 4 to 10 minutes. Once hemostasis is achieved, the patch is covered with a dressing that remains in place for 24 hours. The interventional cardiologist determines which closure device, if any, will be deployed based on the artery used to insert the catheter, patient's condition, device availability, and personal preference. Major benefits of the vascular closure devices include reliable, immediate hemostasis and a shorter time on bed rest without a significant increase in bleeding or other complications. Rare complications associated with these devices include bleeding around the closure device, infection, and arterial obstruction.

Pulmonary artery pressure monitoring

Pulmonary artery pressure monitoring is used in critical care for assessing left ventricular function, diagnosing the etiology of shock, and evaluating the patient's response to medical interventions (e.g., fluid administration, vasoactive medications). A pulmonary artery catheter and a pressure monitoring system are used. A variety of catheters are available for cardiac pacing, oximetry, cardiac output measurement, or a combination of functions. Pulmonary artery catheters are balloon-tipped, flow-directed catheters that have distal and proximal lumens The distal lumen has a port that opens into the pulmonary artery. Once connected by its hub to the pressure monitoring system, it is used only to continuously measure pulmonary artery pressures. The proximal lumen has a port that opens into the right atrium. It is used to administer IV medications and fluids or to monitor right atrial pressures (i.e., CVP). Each catheter has a balloon inflation hub and valve. A syringe is connected to the hub, which is used to inflate or deflate the balloon with air (maximum 1.5-mL capacity). The valve opens and closes the balloon inflation lumen. A pulmonary artery catheter with specialized capabilities has additional components. For example, the thermodilution catheter has three additional features that enable it to measure cardiac output: a thermistor connector attached to the cardiac output computer of the bedside monitor, a proximal injectate port used for injecting fluids when obtaining the cardiac output, and a thermistor (positioned near the distal port) The pulmonary artery catheter, covered with a sterile sleeve, is inserted into a large vein, preferably the subclavian, through a sheath. As noted previously, the femoral vein is avoided; insertion techniques and protocols mirror those used for inserting a CVP catheter The sheath is equipped with a side port for infusing IV fluids and medications. The catheter is then passed into the vena cava and right atrium. In the right atrium, the balloon tip is inflated, and the catheter is carried rapidly by the flow of blood through the tricuspid valve into the right ventricle, through the pulmonic valve, and into a branch of the pulmonary artery. When the catheter reaches the pulmonary artery, the balloon is deflated and the catheter is secured with sutures Fluoroscopy may be used during insertion to visualize the progression of the catheter through the right heart chambers to the pulmonary artery. This procedure can be performed in the operating room, in the cardiac catheterization laboratory, or at the bedside in the critical care unit. During insertion of the pulmonary artery catheter, the bedside monitor is observed for pressure and waveform changes, as well as arrhythmias, as the catheter progresses through the right heart to the pulmonary artery. Once the catheter is in position, the following are measured: right atrial, pulmonary artery systolic, pulmonary artery diastolic, mean pulmonary artery, and pulmonary artery wedge pressures Monitoring of the pulmonary artery diastolic and pulmonary artery wedge pressures is particularly important in critically ill patients because they are used to evaluate left ventricular filling pressures (i.e., left ventricular preload). It is important to note that the pulmonary artery wedge pressure is achieved by inflating the balloon tip for a maximum of 15 seconds, which causes it to float more distally into a smaller portion of the pulmonary artery until it is wedged into position. This is an occlusive maneuver that impedes blood flow through that segment of the pulmonary artery. Therefore, the wedge pressure is measured immediately and the balloon deflated promptly to restore blood flow.

Heart chambers

Pumping action is accomplished via rhythmic relaxation and contraction of muscular wall of two top chambers (atria) and two bottom (ventricles) Relaxation- diastole- all four chambers relax which allows ventricle to fill in preparation of contraction Period of ventricular filling Systole- contraction of atria and ventricles Atrial and ventricular strokes are not simultaneous events Atrial systole first just at end of diastole followed be ventricular stroke Synchronization allows ventricular filling completely prior to ejection of blood from chambers Right side- distributes venous or Deoxygenated blood to lungs via pulmonary artery (pulmonary circulation for oxygenation Pulmonary artery is only artery that carries deoxygenated blood Right atrium receives venous blood returning to heart from superior vena cava (head, neck, upper extremities), inferior vena cava (trunk and lower extremities) and coronary sinus (coronary circulation) Left side- distributes O2 blood to body via aorta (systemic circulation) Left atrium O2 blood from pulmonary circulation via pulmonary veins Varying thickness of atrial and ventricular walls due to workload required by each chamber Myocardial layer of both atria is thinner than ventricles because of little resistance of blood flow out atria and into ventricular during diastole Ventricular walls are thicker- overcome resistance to blood flow from pulmonary and systemic circulation Left ventricle is more muscular than right- overcome aortic and arterial pressure- right ventricle contracts against low pressure system within pulmonary arteries and capillaries Right ventricles lies anteriorly beneath sternum, and left posterior Pulsation created during normal ventricular contraction- apical impulse (point of maximal impulse) PMI- intersection of midclavicular line of left chest wall and fifth intercostal space

Health history

Recognize cardiac symptoms and known what to do for self care management Ethnic and SES can lead to delay for treatment Women AA- MI delay treatment SES-poverty, health care cost, lack of insurance, transportation, and proximity to health care Lack of knowledge of symptoms of ACS or experience denial, fear, or uncertainty about chest pain Women have misperception that the risk of cardiac disease is only linked to weight Individualized care can include family member support

cardiac ouput

Refers to total amount of blood ejects by one ventricle in liters per minute 4-6 L in adults but varies depending on metabolic needs Multiple stroke volume by HR Stroke volume- blood ejected from one ventricle per heartbeat- 60-130ml Responds to metabolic demands of tissue associated with stress, exercise, and illness Compensate- enhance by increase SV and HR Changes in HR due to inhibition or stimulation of SA nodes mediated between PNS and SNS of autonomic Branches of PNS- travel to SA nodes by vagus nerve Stimulation of vagus slow hearts SNS- increase through innervation of beta 1 receptor sites within SA nodes HR- increase through in catecholamines secreted by adrenal glands and excess thyroid hormones HR controlled by CNS and baroreceptors Baroreceptors are specialized nerve cells located in aortic arch and in both internal carotid arteries (point of bifurcation from common carotid arteries Baroreceptor sensitive to changes in BP HPTN- cell rate increase discharge, transmit impulse to cerebral medulla Action initiates PNS and inhibits SNS, lowering HR and BP Decrease baroreceptors simulation during hypotension decrease in PNS and increase SNS Compensatory mechanism elevation in BP through vasoconstriction and increase HR

Diagnostics

Sample blood for To screen for risk factors associated with CAD To establish baseline values before initiating other diagnostic tests, procedures, or therapeutic interventions To monitor response to therapeutic interventions •To assess for abnormalities in the blood that affect prognosis Cardiac biomarker- diagnosis of MI evaluates hx and physical examination 12 lead ECG Serum cardiac biomarkers Myocardial cells become necrotic from prolonged ischemia or trauma related specific enzymes (creatinine kinase), CK isoenzymes, and protein (myoglobin, troponin T, and troponin I) Leak into interstitial spaces of myocardium and carried by lymphatic system into circulation Abnormal high levels of substances can be detected in blood

CVD disorders

Several cardiovascular disorders are associated with genetic abnormalities. Some examples are: •Arrhythmogenic right ventricular dysplasia (ARVD) •Brugada syndrome •Familial hypercholesterolemia •Hypertrophic cardiomyopathy •Long QT syndrome •Jervell and Lange-Nielsen syndrome (autosomal recessive form) •Romano-Ward syndrome (autosomal dominant form) •Genetic connective tissue disorders that impact the cardiovascular system: •Ehlers-Danlos syndrome •Loeys-Dietz syndrome •Marfan syndrome Genetic blood disorders that can impair the function of the cardiovascular system: •Factor V Leiden •Hemochromatosis •Sickle cell disease Family History Assessment Specific to Cardiovascular Disorders •Assess all patients with cardiovascular symptoms for coronary artery disease, regardless of age. •Inquire about a family history of sudden death or unexplained death. •Ask about other family members with biochemical or neuromuscular conditions (e.g., hemochromatosis or muscular dystrophy). Patient Assessment Specific to Cardiovascular Disorders •Assess for signs and symptoms of hyperlipidemias (xanthomas, corneal arcus, or abdominal pain of unexplained origin). •Obtain an electrocardiogram and an echocardiogram. •Assess for muscular weakness. •Assess for episodes of shortness of breath, dizziness, or palpitations. •Review laboratory data for abnormal values. •Gather dietary history. •Assess for secondary risk factors (e.g., diet, smoking, overweight, high stress, alcohol use).

SPECT and PET

Single Protons Emission CT- inject nuclear medicine radionucleotide The nurse's primary role is to prepare the patient for SPECT and insert an IV catheter or assess an existing IV for patency and suitability. The IV is used to inject the tracer. The patient may be concerned about receiving a radioactive substance and needs to be reassured that these tracers are safe—the radiation exposure is similar to that of other diagnostic x-ray studies. No postprocedure radiation precautions are necessary. During PET, tracers are given by injection; one compound is used to determine blood flow in the myocardium, and another determines the metabolic function. The PET camera provides detailed three-dimensional images of the distributed compounds. The viability of the myocardium is determined by comparing the extent of glucose metabolism in the myocardium to the degree of blood flow. For example, ischemic but viable tissue will show decreased blood flow and elevated metabolism. For a patient with this finding, revascularization through surgery or angioplasty will probably be indicated to improve heart function. Restrictions of food intake before the test vary among institutions, but because PET evaluates glucose metabolism, the patient's blood glucose level should be within the normal range before testing. Refrain from alcohol and caffeine- simulate HR Diabetics- discuss insulin and food restrictions Assess claustrophobia The nurse inserts an IV or assesses the existing IV catheter for patency and suitability, and then describes the procedure to the patient. The patient is positioned on a table with hands above the head. The table then slides into a donut-shaped scanner. While in the scanner, the patient must lie still so that clear images of the heart can be obtained. A baseline scan is performed, which takes about 30 minutes. Then a tracer is injected into the IV and the scan is repeated. The patient's glucose level is monitored throughout the procedure. The scan takes from 1 to 3 hours to complete.

Chest x ray

Size, contour and position of heart Cardiac and pericardial calcification and demonstrates physiologic alterations in pulmonary circulation Help diagnose complications (HF) Correct placement of pacemaker and pulmonary artery catheters confirmed Fluoroscopy- x ray imaging that allows visualization of heart on screen Shows cardiac and vascular pulsations and cardiac contour ECG- electrical currents in heart Leads- different recordings of electrode combinations 12 lead Diagnose arrhythmias, conduction, and chamber enlargement, myocardial ischemia, injury, or infarction Suggest cardiac effects of electrolyte disturbances (high or low CA and K) and effect of antiarrhythmic meds) 15 lead- three additional across chest across right precordium and used for diagnosis of right ventricular and left posterior (ventricular) infarction 18- lead ECG adds three posterior leads to 15 lead ECG and useful for early detection of myocardial ischemia and injury Patient age, gender, BP, height, weight, and symptoms, and medications Continuous ECG- high risk for arrhythmias Cardiac monitoring detects abnormalities in heart rate and rhythm ST segments- presence of myocardial ischemia or injury Two type of continuous ECG used- hardwire cardiac monitor and telemetry Monitor more than one ECG lead simultaneously. Monitor ST segments (ST-segment depression is a marker of myocardial ischemia; ST-segment elevation provides evidence of an evolving MI). Provide graded visual and audible alarms (based on priority, asystole merits the highest grade of alarm). Interpret and store alarms. •Trend data over time. Print a copy of rhythms from one or more specific ECG leads over a set time (called a rhythm strip). •Save electronic copies of cardiac rhythms into the electronic health record (EHR).

BP and PP

Systemic arterial BP is pressure exerted on walls of arteries during ventricular systole and diastole Affected by factors such as cardiac output, distention of arteries, and volume, velocity, and viscosity of blood Less than 120 and less than 80 is normal HTPN- two stages and based Stage 1- systolic between 130-139 mm Hg or diastolic between 80-89 Stage 2- Over 140 and over 90 Hypotension- abnormally low systolic and diastolic that result in fainting Difference in systolic and diastolic is PP Normal is 40 mm hg Narrow pulse BP of 92/74 and pulse of 18 occurs when vasoconstriction that is compensating for low SV and ejection velocity (shock, HF, hypovolemia, mitral regurgitation or obstruction to blood flow during systole (mitral or aortic stenosis) Compensates allows for adequate organ perfusion Wide pulse pressure (88/38 and pp 50)- elevated SV (Anxiety, exercise, bradycardia) or vasodilation (fever, septic shock) Abnormal pulse pressure- further test

cardiac catheterization (CC)

This procedure involves the percutaneous insertion of radiopaque catheters into a large vein and an artery. Fluoroscopy is used to guide the advancement of the catheters through the right and left heart, referred to as right and left heart catheterizations, respectively. In most situations, patients undergo both right and left heart catheterizations. However, right heart catheterization is performed without a left heart catheterization when patients only need myocardial biopsies or measurement of pulmonary artery pressures. Of note, left heart catheterization involves the use of a contrast agent. These agents are necessary to visualize patency of the coronary arteries and evaluate left ventricular function. In preparation for the procedure, patients have blood tests performed to evaluate metabolic function (electrolytes and glucose) and renal function (blood urea nitrogen and creatinine level). Baseline coagulation studies (activated partial thromboplastin time [aPTT], international normalized ratio [INR], and prothrombin time [PT]) are obtained to guide dosing of anticoagulation during the procedure. Because bleeding and hematoma formation are procedural risks, a complete blood cell count (CBC; includes the hematocrit, hemoglobin, and platelets) is necessary to establish baseline values. Later these results are compared with postprocedure results to monitor for blood loss. A health history is obtained to assess for previous reactions to a contrast agent and determine if the patient has any risk factors for contrast-induced nephropathy (CIN). This uncommon complication is a form of acute kidney injury that is usually reversible. Patients with chronic kidney disease or renal insufficiency, diabetes, HF, hypotension, dehydration, use of nephrotoxic medications, and advanced age are at risk for CIN. CIN is defined as an increase in the baseline serum creatinine by 25% or more or an absolute increase of 0.5 mg/dL within 48 to 72 hours after the administration of contrast During a cardiac catheterization, the patient has one or more IV catheters for administration of fluids, sedatives, heparin, and other medications. The patient is continuously monitored for chest pain or dyspnea and for changes in BP and ECG, which are indicative of myocardial ischemia, hemodynamic instability, or arrhythmias. Resuscitation equipment must be readily available, and staff must be prepared to provide advanced cardiac life support measures as necessary. Postprocedure, patients remain on bed rest for 2 to 6 hours before they are permitted to ambulate. Variations in time to ambulation are related to the size of the catheters used during the procedure, the site of catheter insertion (femoral or radial artery), the patient's anticoagulation status, and other factors (e.g., advanced age, obesity, bleeding disorder). The use of a radial access site and smaller (4- or 6-Fr) arterial catheters are associated with shorter bed rest restrictions. Cardiac catheterization may be performed in the ambulatory setting. Unless the results demonstrate the need for immediate treatment, patients are discharged home. Hospitalized patients undergoing cardiac catheterization for diagnostic and interventional purposes (PCI, valvuloplasty) are returned to their hospital rooms for recovery

Exercise

Treadmill or bike Monitor two or more ECG leads for HR, rhythm, ischemic change, BP, temp, physical appearance, perceived exertion, chest pain, dyspnea, dizziness, leg cramp, and fatigue HR achieved or signs of myocardial ischemia- test stops Abnormal- chest pain, ventricular arrhythmias, ST segment depression, and lack of HR or BP elevations Preparation of exercise stress, fast before test to avoid stimulants like smoke or coffee Medications taken with sips of water Hold beta blockers, calcium channel blockers, and digitalis for 48 hrs The nurse prepares the patient for the stress test by describing how the stress test is performed, the type of monitoring equipment used, the rationale for insertion of an IV catheter, and what symptoms to report. The exercise method is reviewed, and patients are asked to put forth their best exercise effort. If the test is to be performed with echocardiography or radionuclide imaging (described in the next section), this information is reviewed as well. After the test, the patient is monitored for 10 to 15 minutes until vital signs and assessment findings return to normal. Once stable, patients may resume their usual activities.

Chemistry, blood, and coagulation

ipid, brain (B-type) natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine measurements Lipid Cholesterol, triglycerides, and lipoproteins used for developing CAD risk Family Hx of premature heart disease, or lipoprotein abnormality Cholesterol and triglycerides transported into blood by combining plasma proteins to form lipoprotein called LDL and HDL