Perfusion

Classify HF

1 of 4 categories (I-IV) based on physical activity limitation due to symptom burden.1 NYHA class designation changes based on worsening or improving symptoms. -This system identifies people at risk for developing HF who do not currently have heart disease (stage A). This classification encourages clinicians to actively address the patient's risk factors and treat any existing conditions to prevent further disease progression. This staging system is progressive and unidirectional. Patients advance to a higher (worse) stage as the disease progresses

interproff care for acute coronary syndrome

12-lead ECG and start continuous ECG monitoring. Position the patient in an upright position unless contraindicated and start O2 by nasal cannula to keep O2 saturation above 93%. Obtain IV access for drug administration. Give SL NTG and 162 to 325 mg of chewable aspirin if not given before arrival at the ED. Morphine is given for pain unrelieved by NTG. A high-dose statin (e.g., atorvastatin [Lipitor]) is given. -next step depends on ST elevation or depression and presence of dysrhythmias -Cardiac biomarkers are draw -Heparin to NSTEMI and UA pts

dx shock studies

ABG: resp alkalosis meta acidosis BUN INC CR INC fibrin inc, fibrinogen dec, platelet dec, PTT inc, Thrombin INC Glucose inc then dec Inc sodium then dec sodium, inc potassium then inc potassium, inc liver enzymes, dec RBC then INC RBC, inc toponin, in then dec WBC

myocardial infarction (MI)

A myocardial infarction (MI) occurs because of an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation. This causes irreversible myocardial cell death (necrosis) in the heart muscle beyond the blockage (Figs. 33.10 and 33.11). Serum cardiac biomarkers are released into the blood. Most MIs occur in the setting of preexisting CAD A STEMI, caused by an occlusive thrombus, results in ST-elevation in the ECG leads facing the area of infarction artery must be opened within 90 minutes of presentation to restore blood and O2 to the heart muscle and limit the infarct size. PCI or with thrombolytic (fibrinolytic) therapy. PCI is the first-line treatment, if available. It confirms which artery has the occlusive thrombus so it can be opened with a balloon and stent (Fig. 33.6). Thrombolytic therapy is done in hospitals that do not have a catheterization laboratory for PCI. NSTEMI patients usually undergo catheterization within 12 to 72 hours. Thrombolytic therapy is not indicated for NSTEMI. The acute MI process evolves over time, from hours to a few days. The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the heart muscle). If ischemia persists, it takes around 4 to 6 hours for the entire thickness of the heart muscle to necrose. The degree of collateral circulation influences the severity of the MI (Fig. 33.2). Not everyone develops collateral circulation. A person with a long history of CAD may develop good collateral circulation to provide the area surrounding the infarction site with an adequate blood supply

Risks

AGE hardened arteries and valves Dec contraction power/ hypertrophy of the heart muscles damage to the heart thickening less elastic

S/S Acute Decomp HF

Acute decompensated heart failure (ADHF -symptoms and signs related to pulmonary congestion and volume overload. Neurohormonal activation leads to impaired regulation of sodium excretion through the kidneys that results in sodium and fluid accumulation. The lungs become less compliant. There is increased resistance in the small airways -mild increase in the respiratory rate (RR) and a decrease in partial pressure of O2 in arterial blood (PaO2) -If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove resulting in interstitial edema (Fig. 34.1, C). Tachypnea develops, and the patient becomes symptomatic (e.g., short of breath). -worsening of the arterial blood gas values (i.e., lower PaO2, increased PaCO2, progressive respiratory acidosis) -ADHF can manifest as pulmonary edema. This is an acute, life-threatening situation, in which the lung alveoli become filled with serosanguineous fluid (Fig. 34.1, D). The most common cause of pulmonary edema is left-sided HF. -left HF, such as dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. JVD is often present and is the most sensitive and specific sign for elevated LV filling pressures. Coughing may provide an early clue to developing pulmonary edema in patients with chronic HF. The patient is usually anxious and pale and may be cyanotic. The RR is often > 30 breaths per minute. -accessory respiratory muscles. Pink, frothy sputum may be present in patients with severe disease. Auscultation of the lungs may reveal crackles and wheezes throughout. The patient's HR is often rapid, and an abnormal S3 or S4 heart sound may be heard -Hypotension indicates severe LV systolic dysfunction and the chance of cardiogenic shock. Cool extremities occur with low CO and poor perfusion. Skin pallor or mottling may be present. They result from peripheral vasoconstriction and shunting of blood to the central circulation. -1 of 4 groups based on hemodynamic and clinical status: dry-warm, dry-cold, wet-warm, and wet-cold (Table 34.4).1 The most common presentation in patients with ADHF is the wet and warm patient. A patient is "wet" due to volume overload (e.g., congestion, dyspnea) but "warm" due to adequate perfusion (warm skin, positive pulses).

dx

After a detailed health history and physical examination, a 12-lead ECG is done and compared with a previous ECG to look for changes that may indicate an ACS. Laboratory tests (e.g., cardiac biomarkers) are used to determine if the patient is experiencing an ACS. Other laboratory tests may be done (e.g., lipid profile, CRP) to identify risk factors for CAD. A chest x-ray is done to look for cardiac enlargement, aortic calcifications, and pulmonary congestion. An echocardiogram can detect resting LV wall motion abnormalities, which may suggest CAD. -stress tests

DX studies

An echocardiogram is a valuable, noninvasive diagnostic tool used in patients with HF. The echocardiogram gives information about chamber size and function, LVEF, heart valve function, wall thickness and motion, presence of effusion or thrombus, and intracardiac and pulmonary pressures. -12-lead ECG, ambulatory heart monitors, chest x-ray, 6-minute walk test, multigated acquisition (MUGA) scan, cardiopulmonary exercise stress test, cardiac MRI, and cardiac catheterization/angiogram. Polysomnography studies for obstructive sleep apnea may be done. An endomyocardial biopsy may be done as part of a heart catheterization to evaluate for infective or infiltrative disease in acutely ill patients who develop unexplained, new-onset HF unresponsive to usual care. -BNP and N-terminal prohormone of BNP (NT-proBNP) levels correlate positively with the degree of LV failure -Increases in BNP or NT-proBNP levels can be caused by conditions other than HF, including pulmonary embolism, renal failure, and acute coronary syndrome.

Biventricular failure

Biventricular failure includes both LV and RV dysfunction, the inability of both ventricles to pump effectively. Because of decreased contractility, fluid build-up and systemic venous engorgement occur. Inadequate CO results in decreased perfusion to vital organs

S/S chronic HF

Chronic HF is a progressive syndrome characterized by reduced CO and increased venous pressure, associated with underlying molecular changes that result in the death of cardiac muscle cells. Fatigue following usual daily activities can be an early symptom of chronic HF. As the falling CO cannot sustain activities, fatigue eventually limits activities. Anemia, common in HF, is another potential cause of fatigue. Dyspnea is the most common manifestation of chronic HF. It is caused by increased pulmonary pressures from interstitial and alveolar edema. Dyspnea can occur early in the HF disease process with mild exertion. As HF progresses, dyspnea develops with less exertion until dyspnea occurs at rest. Orthopnea, or dyspnea in the recumbent position, suggests HF. Orthopnea occurs due to redistribution of fluid from the lower extremities into the lungs while in a supine position. The dyspnea is usually relieved with sitting up -Paroxysmal nocturnal dyspnea (PND) is episodic, sudden dyspnea that wakes a patient at night. PND is caused by fluid accumulation in the lungs entering the alveoli while the patient is supine. The patient can awaken in a panic with feelings of suffocation and a strong desire to sit or stand to aid breathing. COUGH: chronic, nonproductive cough that is worse in the recumbent position is often associated with pulmonary congestion and can be a sign of HF. Tachycardia is an early sign of HF. One of the body's first responses to compensate for a reduced CO is to increase the HR via activation of the SNS. Palpitations, or an irregular heartbeat, can occur due to dysrhythmias that occur with chronic HF. Atrial fibrillation (AF) is the most common of these dysrhythmias. Patients may report a fast or irregular heartbeat, a fluttering sensation, or "skipped beats" that may be intermittent Edema is a common sign of HF. It may occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion). Urine output may be decreased because of decreased renal perfusion. HF patients often develop resistance to diuretics, which can result in a drop in urinary output. Nocturia is the tendency to urinate excessively during the night due to increased renal perfusion in the supine position. A low CO can result in decreased perfusion to the skin of the extremities resulting in mottling, a blue or gray coloring. A coolness or clammy feeling to touch can occur with poor perfusion -DUSKY -Dizziness, lightheadedness, near syncope, or syncope can occur due to reduced CO and hypoperfusion to the brain or dysrhythmias that often occur with chronic HF. Hypotension secondary to HF medications and hypovolemia are common causes of neurologic symptoms in chronic HF Cerebral hypoperfusion may occur because of hypoxia to the brain from decreased CO. The patient or caregiver may report confusion, forgetfulness, inattentiveness, and restlessness Snoring and daytime sleepiness can indicate sleep apnea, a common confounding condition with chronic HF. Sleep apnea screening questions include those about daytime sleepiness and falling asleep, feeling rested in the morning, frequent nighttime awakenings, and history and results of a sleep study. Chest pain or angina can be the result of the reduced CO associated with HF compounded with CAD. Chest pain in HF can also occur due to myocardial stretch from volume overload. Many factors contribute to weight changes. Progressive weight gain in the patient with chronic HF may indicate fluid retention. Renal failure may contribute to fluid retention. Abdominal fullness from ascites and hepatomegaly often causes anorexia and nausea. -cardiac cachexia with muscle wasting and fat loss.

RISK FACTORS

age, gender high in man or women over 55, ethnicity in white, family hx serum lipids high, high BP/ HTN, diabetes, sedentary lifestyle, tobacco, obesity, depression, substance abuse -Nonmodifiable risk factors are age, gender, ethnicity, family history, and genetics. Modifiable risk factors include high serum lipids, high BP, tobacco use, physical inactivity, obesity, diabetes, metabolic syndrome, psychologic states, and high homocysteine level. The risk for CAD is associated with a total serum cholesterol level greater than 200 mg/dL (5.2 mmol/L), an LDL greater than 130 mg/dL (3.4 mmol/L), a high-density lipoprotein (HDL) level less than 40 mg/dL (1.0 mmol/L) in men and less than 50 mg/dL (1.3 mmol/L) in women, and/or a fasting triglyceride level greater than 150 mg/dL (1.7 mmol/L). HDLs contain more protein by weight and fewer lipids than any other lipoprotein. HDLs carry lipids away from arteries to the liver for metabolism. This process of HDL transport prevents lipid accumulation within the arterial walls.7 Therefore high serum HDL levels are desirable and lower the risk for CAD -lipoprotein is the way that lipids travel in blood attached to protein so HDL contains more protein and less lipids -Thus HDL high is good! LDLs contain more cholesterol than any of the lipoproteins and have an attraction for arterial walls. High LDL levels correlate closely with an increased incidence of atherosclerosis and CAD Triglycerides are the most common type of fat in the blood. A certain amount of triglycerides is needed for bodily function, but high triglyceride levels may increase the risk for CAD. HTN According to the most recent published hypertension guidelines, a normal BP is defined as < 120 mm Hg/< 80 mm Hg. BP is classified as elevated (BP 120-129 mm Hg/< 80 mm Hg); stage 1 hypertension (BP 130-139 mmHg/80-89 mm Hg); or stage 2 hypertension (BP >140 mm Hg/ > 90 mm Hg The shearing stress of an elevated BP causes endothelial injury that increases the rate of atherosclerosis. Atherosclerosis, in turn, causes narrowed, thickened arterial walls and decreases the distensibility and elasticity of vessels. More force is needed to pump blood through diseased arteries. This increased force is reflected in a higher BP. This added workload results in left ventricular (LV) hypertrophy and decreased stroke volume with each contraction Tobacco smoke is related to an increase in LDL level, a decrease in HDL level, and release of toxic O2 radicals. All of these add to vessel inflammation and thrombosis. Physically active people have increased HDL levels. Exercise improves thrombolytic activity, thus reducing the risk for clot formation. Exercise may help with the development of collateral circulation in the heart. The death rate from CAD is higher in obese persons. Obesity is defined as a body mass index (BMI) of greater than 30 kg/m2 and a waist circumference more than 40 inches for men and more than 35 inches for women. We calculate BMI by dividing a person's weight (in kilograms) by the square of the height in meters (see Fig. 40.6). The incidence of CAD is 2 to 4 times greater among people who have diabetes, Metabolic syndrome refers to a cluster of risk factors for CAD whose underlying pathophysiology may be related to insulin resistance. SUBSTANCE USE MAJOR RISK DUH

BP norm

Blood pressure (BP) is the force exerted by the blood against the walls of the blood vessel. It must be adequate to maintain tissue perfusion during activity and rest. Systemic vascular resistance (SVR) is the force opposing the movement of blood within the blood vessels. The radius of the small arteries and arterioles is the principal factor determining SVR. As arteries narrow, resistance to blood flow increases. As arteries dilate, resistance to blood flow decreases. SNS inc BP and inc HR, inc contractility, inc constriction/ SVR- trigger of RAAS system inc BP Specialized nerve cells called baroreceptors are found in the carotid arteries and arch of the aorta. These cells sense changes in BP and send this information to the vasomotor centers in the brainstem. PNS dec CO dec HR CO X SVR=BP Baroreceptors have a vital role in maintaining BP stability during normal activities. They are sensitive to stretching and, when stimulated by an increase in BP, send inhibitory impulses to the sympathetic vasomotor center. SNS inhibition results in decreased HR, decreased force of contraction, and vasodilation in peripheral arterioles. -baroreceptors sense a fall in BP, the SNS is activated. The result is constriction of the peripheral arterioles, increased HR, and increased contractility of the heart. The endothelium can cause adhesion and aggregation of neutrophils and stimulate smooth muscle growth. The kidneys contribute to BP regulation by controlling sodium excretion and extracellular fluid (ECF) volume (see Chapter 44). Sodium retention results in water retention, which causes an increase in ECF volume. This action increases the venous return to the heart and SV. Together these increase CO and BP. The renin-angiotensin-aldosterone system (RAAS) plays an essential role in BP regulation (Fig. 32.1). The juxtaglomerular apparatus in the kidney secretes renin in response to SNS stimulation, decreased blood flow through the kidneys, or decreased serum sodium concentration. SNS stimulation results in the release of epinephrine along with a small fraction of NE by the adrenal medulla. Epinephrine increases CO by increasing HR and myocardial contractility. inc blood vol inc BP

basic vascular system

Blood vessels arteries: o2 blood away from heart veins: deo2 blood to heart capillary beds: beds of small vessels that allow for nutrients, fluids, o2, and ect to circulate to tissues arteries: thicker and control BP more Veins: more pliable, serve as reservoir less px both have endothelium on inside if this is harmed than clotting cascade begins

chronic stable angina

CAD is a chronic and progressive disease. Patients may be asymptomatic for many years but may eventually develop chronic stable chest pain. -myocaridal 02 demand exceeds the coronary artery abilities myocardial ischemia -due to narrowing arteries For ischemia to occur from an atherosclerotic plaque, the artery is usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery). Chronic stable angina refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms. It is often provoked by physical exertion, stress, or emotional upset. deny feeling pain, but describe a pressure, heaviness, or discomfort in the chest. This discomfort is often described as a squeezing, heavy, tight, or suffocating sensation. Although most angina pain occurs substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms. Many people with angina describe a feeling of indigestion or a burning sensation in the epigastric region. The pain of chronic stable angina usually lasts for only a few minutes. It often subsides when the precipitating factor is resolved- rest Pain at rest is unusual and may indicate UA. Because chronic stable angina is often predictable, drugs are timed to provide peak effects during the time of day when angina is likely to occur. Silent ischemia refers to ischemia that occurs in the absence of any subjective symptoms. Patients with diabetes have an increased prevalence of silent ischemia.

shock

Cardiogenic shock occurs when either systolic or diastolic dysfunction of the heart's pumping action results in reduced cardiac output (CO), stroke volume (SV), and BP. These changes compromise myocardial perfusion, further depress myocardial function, and decrease CO and perfusion. Causes of cardiogenic shock -leading cause of death from acute myocardial infarction (MI). -The heart's inability to pump the blood forward is called systolic dysfunction. This inability results in a low CO (less than 4 L/min) and cardiac index (less than 2.5 L/min/m2). Systolic dysfunction primarily affects the left ventricle since systolic pressure is greater on the left side of the heart. The most common cause of systolic dysfunction is acute MI. -The patient may have tachycardia and hypotension. Pulse pressure may be narrowed due to the heart's inability to pump blood forward during systole and increased volume during diastole. An increase in systemic vascular resistance (SVR) increases the workload of the heart. This increases myocardial O2 consumption. -patient is tachypneic and has crackles on auscultation of breath sounds because of pulmonary congestion. The hemodynamic profile shows an increase in the pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV), and pulmonary vascular resistance. -igns of peripheral hypoperfusion (e.g., cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill) occur. -decreased urine output. Anxiety, confusion, and agitation may develop with impaired cerebral perfusion Hypovolemic shock occurs from inadequate fluid volume in the intravascular space to support adequate perfusion (Table 66.1).2 The volume loss may be either an absolute or a relative volume loss. Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. In relative hypovolemia, fluid volume moves out of the vascular space into the extravascular space (e.g., intracavitary space). -We call this type of fluid shift third spacing. -decreased venous return to the heart, decreased preload, decreased SV, and decreased CO. -The patient's response to acute volume loss depends on several factors, including extent of injury, age, and general state of health. -SNS The decreased circulating blood volume causes decreases in SV, central venous pressure (CVP), and PAWP. -The patient may appear anxious. Urine output begins to decrease. If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is generally reversible. Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury and last up to 6 weeks. Neurogenic shock related to spinal cord injuries is generally associated with a cervical or high thoracic injury. -injury results in a massive vasodilation without compensation because of the loss of SNS vasoconstrictor tone.4 This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and impaired cellular metabolism -In addition to spinal cord injury, spinal anesthesia can block transmission of impulses from the SNS. Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) can decrease the vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock -hypotension (from the massive vasodilation) and bradycardia (from unopposed parasympathetic stimulation).4 The patient may not be able to regulate body temperature. Combined with massive vasodilation, the inability to regulate temperature promotes heat loss. At first, the patient's skin is warm due to the massive vasodilation. As the heat disperses, the patient is at risk for hypothermia. Later, the patient's skin may be cool or warm depending on the ambient temperature (poikilothermia, taking on the temperature of the environment). In either case, the skin is usually dry. -spinal shock is a transient condition that is present after an acute spinal cord injury (see Chapter 60). The patient with spinal shock has an absence of all voluntary and reflex neurologic activity below the level of the injury Anaphylactic shock is an acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom).5 The reaction quickly causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability. As capillary permeability increases, fluid leaks from the vascular space into the interstitial space. -Anaphylactic shock can lead to respiratory distress due to laryngeal edema or severe bronchospasm and circulatory failure from the massive vasodilation. The patient has a sudden onset of symptoms, including dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, and stridor. Skin changes include flushing, pruritus, urticaria, and angioedema. The patient may be anxious and confused and have a sense of impending doom -allergic rxn Sepsis is a life-threatening syndrome in response to an infection. It is characterized by a dysregulated patient response along with new organ dysfunction related to the infection -septic shock is a subset of sepsis. It has an increased mortality risk due to profound circulatory, cellular, and metabolic abnormalities. Septic shock is characterized by persistent hypotension, despite adequate fluid resuscitation, and inadequate tissue perfusion that results in tissue hypoxia

EXAM

Central: hypotension, tachycardia, SOB, diaphoresis, anxiety, edema peripheral, > 2 sec capp refill Tissue: less hair, pale skin, edema, cool skin, dec pulses, slowed cap refill, DX TESTS: Enzyme markers: C-reactive protein (CRP) is produced by the liver during acute inflammation Lipids: Serum lipids are measured to detect hyperlipidemia and include cholesterol lipoproteins (low-density lipoproteins, high-density lipoproteins, very low-density lipoproteins, and triglycerides). ECG: 12 lead Cardiac stres test: exercise, pharmacologic stim effect so f exercise Radiography: chest X ray, ultrasound indicate blood flow, arteriogram visiualize artery

CAD

Coronary artery disease (CAD) is a type of blood vessel disorder that we consider in the general category of atherosclerosis -hardening of the arteries/ fat deposits in the arteries When the atheromas (fatty deposits) form in the coronary arteries, the disease is called CAD. The terms arteriosclerotic heart disease (ASHD), cardiovascular heart disease (CVHD), ischemic heart disease (IHD), coronary heart disease (CHD), are other terms used to describe CAD. Endothelial injury and inflammation Damage to endothelium causes inflammation and more likely for fats to deposit or platelets and clots to form due to damage CRP c reactive protein- inflammatory lab The stages of development in atherosclerosis are (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion.

basic heart anatomy and phys

Diastole relax Systole contract Heart valves: 4 Bicuspid, tricuspid, aortic valve, pulmonic valve SA, AV, Purkinje Fibers EKG: P, QRS, T PQ atrial depol QRS: ventricular depol and arterial repol ST: ventricular repol CO= SV x HR The Frank-Starling law states that, to a point, the more the myocardial fibers are stretched, the greater their force of contraction The volume of blood stretching the ventricles at the end of diastole, before the next contraction, is called preload. Afterload is the peripheral resistance against which the left ventricle must pump. Eventually this results in ventricular hypertrophy, an enlargement of the heart muscle without an increase in CO or the size of chambers. The ability to respond to these demands by altering CO is termed cardiac reserve.

DX ACS acute coronary syndrome

ECG: The ECG is one of the primary tools to diagnose UA or an MI (STEMI or NSTEMI). Whenever possible, it should be compared to a previous ECG. -Both groups of patients may present with angina and have the same ECG changes. The only way to tell if the patient is experiencing an NSTEMI or UA is by drawing cardiac biomarkers. Serum Cardiac Biomarkers: Serum cardiac biomarkers are proteins released into the blood from necrotic heart muscle after an MI (see Table 31.6). These biomarkers are important in the diagnosis of MI. -Cardiac-specific troponin has 2 subtypes: cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI). These biomarkers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase MB (CK-MB). Serum levels of cTnI and cTnT increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days. Sets of serial cardiac biomarkers are drawn over 24 hours -A newer high-sensitivity troponin test is available that provides more rapid detection of cardiac necrosis at an earlier time than traditional troponin assays, allowing for a quicker diagnosis. -CK levels begin to rise about 6 hours after an MI, peak at about 18 hours, and return to normal within 24 to 36 hours. The CK enzymes are fractionated into bands. The CK-MB band is specific to heart muscle cells and helps to quantify myocardial damage. CK-MB is a less sensitive marker for myocardial injury compared to troponin.15 Therefore troponin is the best biomarker for diagnosis of acute MI -Myoglobin is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours. Although it is one of the first serum cardiac biomarkers to appear after an MI, it lacks cardiac specificity. It has a limited role in diagnosing MI. The patient with a STEMI must undergo cardiac catheterization within 90 minutes of presentation or receive thrombolytic therapy within 30 minutes in agencies without PCI capability. The goal is to open the totally occluded artery and limit the infarction size. The patient with UA or NSTEMI usually undergoes cardiac catheterization during the hospitalization to diagnose and evaluate the extent of the disease. -reasonable to do cardiac catheterization on stable but high-risk patients with UA or NSTEMI within 12 to 72 hours after presentation

stages of atherosclerosis

Fatty Streaks earliest lesion of lipid filled smooth muscle cells- yellow- by 20 yo- lower the LDL can slow this Fibrous Plaque thicken artery wall deposit fats and ldl in artery intima collagen covers the streak forming plaque- result sin narrow the vessel lumen and reduce blood flow to distal tissues Complicated Lesion MOST dangerous plaque grows and inflammation inc result in plaque instability, ulceration, or rupture - due to injured inner endothelial wall platelets gather and form thrombi further narrowing

cardiac catheterization

For patients with increasing angina symptoms, a cardiac catheterization is the gold-standard test to identify and localize CAD oronary revascularization with percutaneous coronary intervention (PCI) may be recommended. PCI may be done at the same time as the cardiac catheterization. During PCI, a catheter with a deflated balloon tip is inserted into the blocked coronary artery. The deflated balloon is positioned inside the blockage and inflated. This compresses the plaque against the artery wall, resulting in vessel dilation and a larger vessel diameter. This procedure is called balloon angioplasty. -intracoronary stents are usually placed after a balloon angioplasty. A stent is an expandable mesh-like structure designed to keep the vessel open. It provides support to the arterial wall Because stents are thrombogenic, drugs are used to prevent platelet aggregation within the stent and acute stent thrombosis. Drugs commonly used during PCI are unfractionated heparin (UH) or low-molecular-weight heparin (LMWH), a direct thrombin inhibitor (e.g., bivalirudin [Angiomax]), and/or a glycoprotein IIb/IIIa inhibitor (e.g., eptifibatide [Integrilin]) Potential complications from cardiac catheterization with PCI include abrupt closure from coronary artery dissection or rupture, vascular injury at the artery access site (e.g., femoral, radial), acute MI from acute stent thrombosis or from plaque dislodging and blocking the vessel distal to the catheter, stent embolization, failure to cross the blockage with a balloon or stent, coronary spasm, dye allergy, renal compromise, bleeding (e.g., retroperitoneal bleeding when the femoral artery is used or vascular access-site bleeding), infection, stroke, and emergent coronary artery bypass graft (CABG) surgery. The risk for dysrhythmias during and after the procedure is always present, so patients should be on a cardiac monitor afterwards.

Phys activity/ nutritional therapy

Frequency (how often), Intensity (how hard), Type (isotonic), and Time (how long). Everyone should aim for at least 30 minutes of moderate physical activity on most days of the week. Dietary recommendations focus on ways to lower LDL cholesterol. They emphasize a decrease in saturated fat and cholesterol and an increase in complex carbohydrates and fiber -great monounsaturated and polyunsaturated fats. -Omega-3 fatty acids reduce triglyceride levels and can slow the progression of CAD. LIPID LOWERING DRUGS STATINS Guidelines recommend the following groups of people receive statin therapy: (1) patients with known CVD, (2) patients with primary elevations of LDL cholesterol levels of 190 mg/dL or greater (e.g., familial hypercholesterolemia), (3) patients 40 to 75 years old with diabetes and LDL cholesterol levels between 70 and 189 mg/dL, and (4) patients 40 to 75 years old with LDL cholesterol levels between 70 and 189 mg/dL and a 10-year risk for CVD of at least 7.5%. -Concurrent diet change is essential to reduce the need for drug therapy -WEIGHT LOSS AND INC PHYS ACTIVITY -assessed after 6 weeks and changed as needed

interproff care Acute Decompensated Heart Failure

Goals of therapy for the patient hospitalized with ADHF include (1) symptom relief; (2) optimizing volume status; (3) supporting oxygenation, ventilation, CO, and end organ perfusion; (4) identifying and addressing the cause of the ADHF; (5) avoiding complications; (6) providing patient teaching addressing factors that precipitated HF exacerbation; and (7) discharge planning. Assessment findings indicating fluid volume overload include edema, ascites, JVD, a positive hepatojugular reflux test, an S3 heart sound, crackles, hypoxia, and worsening renal function. Ultrafiltration, or aquapheresis, is an option for the patient with volume overload when diuretics have not been effective.1 It can rapidly remove intravascular fluid volume and excess sodium from the patient's blood while maintaining hemodynamic stability. Hemodialysis can be used for volume overload with concomitant renal failure -Implantation of CRT, a biventricular pacemaker, -mechanical cardiac assist devices are used temporarily to manage patients with worsening HF. The intraaortic balloon pump (IABP) is a device that increases coronary blood flow to the heart muscle and decreases the heart's workload through a process called counterpulsation. -IABP is useful in hemodynamically unstable patients because it can decrease pulmonary artery pressures and systemic vascular resistance (SVR), leading to improved CO. Ventricular assist devices (VADs) can help maintain the pumping action of a weakened heart. A VAD is a surgically implanted mechanical pump. pharm: Diuretics are the first line for treating patients with volume overload. They decrease sodium reabsorption at various sites within the kidneys, enhancing sodium and water loss. Decreasing intravascular volume with diuretics reduces volume returning to the LV (preload). -This allows for more efficient LV pumping, decreased pulmonary vascular pressures, and improved alveolar gas exchange. Vasodilators are used to treat ADHF in the absence of hypotension. IV nitroglycerin (NTG) is a primary venodilator that reduces circulating blood volume. It also improves coronary artery blood flow by dilating the coronary arteries. So, NTG reduces preload, slightly reduces afterload (in high doses), and increases myocardial O2 supply. -monitor BP TITRATE Sodium nitroprusside (Nitropress) is a potent IV arterial vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. Morphine dilates pulmonary and systemic blood vessels, reducing preload and afterload. It is often given in small IV boluses for the dyspnea associated with ADHF. Inotropic drugs increase myocardial contractility and are used for patients with evidence of cardiogenic shock or with low CO. Drugs include β-agonists (e.g., dopamine, dobutamine, norepinephrine [Levophed]) and phosphodiesterase inhibitors (milrinone). -In addition to increasing myocardial contractility and SVR, dopamine dilates the renal blood vessels and enhances urine output -improved CO, BP, urine output, and reduced filling pressures. -Milrinone has both inotropic and vasodilator properties. Milrinone improves myocardial contractility, increases CO, and reduces BP (decreases afterload)

ASSESSMENTS

HR, BP, orientation awake, alert, oriented x4, pulses, cap refill, temp, rhythm HX: lifestyle, diet, exercise, smoking, alcohol, drugs, meds, hx stroke/ MI Problem based: pain, SOB, edema, faint -pain, chest pain, pain in ischemic areas, leg pains DVT -Inadequate circulation of blood interferes with oxygen transport to tissues, making patients dyspneic or short of breath during activity. Sleep, lightheaded, SOB, chest pain, swelling feet and ankles, sleep propped up -Patients may report their socks leaving an indentation around their legs or edema in their feet that is worse at the end of the day. This edema reflects excessive fluid in the interstitial spaces, which indicates a fluid overload or an accumulation of fluids. Cor pulomale, kidney problems, excess fluid -Dizziness or fainting: dizzy, lightheaded, orthostatic hypotension

Heart Failure

Heart failure (HF) is a complex clinical syndrome that develops in response to myocardial insult. It results in the inability of the heart to provide sufficient blood to meet the oxygen (O2) needs of tissues and organs. The decreased cardiac output leads to decreased tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability. HF manifestations occur due to a defect in either ventricular systolic function/LV contraction (heart failure with reduced ejection fraction [HFrEF]) and/or a defect in ventricular diastolic function/filling (heart failure with preserved ejection fraction [HFpEF]) HF is associated with many cardiovascular diseases (CVDs), particularly long-standing hypertension (HTN), coronary artery disease (CAD), and myocardial infarction (MI) HTN and CAD are the primary risk factors for HF. HTN is a modifiable risk factor that should be aggressively treated and managed. Long-term treatment of HTN reduces the incidence of HF by 50%.1 Co-morbidities. such as diabetes, metabolic syndrome, advanced age, tobacco use, and vascular disease, contribute to the development of HF. Any interference with the normal mechanisms regulating cardiac output (CO) may cause HF. CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) HR. These factors affect stroke volume (SV), which is the amount of blood pumped per heartbeat. Thus the equation: CO = SV × HR. The major causes of HF are divided into 2 subgroups: (1) primary causes (Table 34.1) and (2) precipitating causes (Table 34.2). Precipitating causes often increase the workload of the heart, resulting in an acute condition and decreased heart function. -EX obesity Genetically linked remodeling of myocardial structure and function

heart transplant

Heart transplantation is the transfer of a healthy donor heart to a patient with a diseased heart. It is done to treat a variety of terminal or end-stage heart conditions Once a person meets the criteria for a transplant, an exhaustive physical examination and diagnostic workup are done. Heart function, vascular and immune systems are assessed. The patient and caregiver undergo a comprehensive psychologic evaluation that assesses coping skills, support systems, and commitment to follow a rigorous life-long regimen. The complexity of the transplant process may be overwhelming to a patient without an adequate support system and understanding of the needed lifestyle changes. Donor and recipient matching is based on body and heart size and an immunologic assessment. That assessment includes ABO blood type, antibody screen, panel of reactive antibody (PRA) level, and human leukocyte antigen typing. The transplant donor is someone who has irreversible brain injury. A surgical team goes to the hospital of the donor to remove donated organs after the declaration of brain death. The retrieved organs are transported on ice until they can be implanted. For the heart, this is optimally less than 4 hours. Often the donor heart is flown to the recipient's hospital. The donor heart is then implanted into the recipient using 1 of 2 approaches. In the biatrial approach, the recipient's damaged heart is removed -In the bicaval approach, the RA of the recipient's heart (with the SA node and atrial conduction intact) is preserved and then the donor heart is connected. After cardiac transplant, a variety of complications can occur, including a risk for SCD. Acute rejection is an immediate posttransplant complication, and immunosuppressive therapy is the key in posttransplant management. In the first year after transplantation, the major causes of death are infection and acute rejection.

s/s:

Hypertension is often called the "silent killer" because it is often asymptomatic until it becomes severe and target organ disease occurs fatigue, dizziness, palpitations, angina, and dyspnea. -hypertensive crisis (discussed later in the chapter) may have severe headaches, dyspnea, anxiety, and nosebleeds

Hypertension general risks

Hypertension, or high blood pressure (BP), is one of the most important modifiable risk factors that can lead to the development of cardiovascular disease (CVD). As BP increases so does the risk for myocardial infarction (MI), heart failure (HF), stroke, and renal disease Black, hispanic, and commonly male more at risk though women on BC at higher risk

hypertensive crisis

Hypertensive crisis is a term used to indicate either a hypertensive urgency or emergency. A hypertensive crisis occurs at systolic BP greater than 180 mm Hg and/or diastolic BP greater than 120 mm Hg. Without prompt treatment, a hypertensive emergency can produce severe problems. These include encephalopathy, intracranial or subarachnoid hemorrhage, HF, MI, renal failure, dissecting aortic aneurysm, and retinopathy. Hypertensive urgency has no clinical evidence of target organ disease. Hospitalization may not be needed to correct the BP. Hypertensive urgency is much more common than hypertensive emergency. It may be associated with chronic, stable complications such as stable angina, chronic HF, or prior MI or cerebrovascular accident with no threat of an acute event. s/s: hypertensive encephalopathy, a syndrome in which a sudden rise in BP is associated with a severe headache, nausea, vomiting, seizures, confusion, and coma. -Rapid cardiac decompensation ranging from unstable angina to MI and pulmonary edema is possible. Patients can have chest pain and dyspnea. -severe chest and back pain with reduced or absent pulses in the extremities. Hypertensive emergencies require hospitalization, IV administration of antihypertensive drugs, and intensive monitoring If the patient is clinically stable, drugs can be titrated to gradually lower BP over the next 24 hours. Lowering the BP too quickly or too much may decrease cerebral, coronary, or renal perfusion. A rapid decrease could cause a stroke, MI, or renal failure. Antihypertensive drugs given IV have a rapid (within seconds to minutes) onset of action. Assess the patient's BP and HR every 2 to 3 minutes during their initial administration Monitor the ECG for dysrhythmias and signs of ischemia or MI. Use extreme caution in treating the patient with CAD or cerebrovascular disease. Hypertensive urgencies usually do not need IV drugs but can be managed with oral agents. The patient with hypertensive urgency may not need hospitalization but will need follow-up. The initial decision for oral antihypertensive agents should be made based on the underlying cause of the hypertensive urgency, the patient characteristics, and comorbidities Not every patient with an elevated BP and no target organ disease will need emergent drug therapy or hospitalization. Allowing the patient to sit for 20 or 30 minutes in a quiet environment may significantly reduce BP.

health pormotion cvd cad

Identifying high risk persons -screen, look at risks, lifestyle, how seriously they take this concern, attitudes, genetics, s/s managing high risk persons help to control modifiable risk factors -clarify the issues and educate them of the threat -set goals

Microvascular angina

In microvascular angina, chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary artery. In these patients, chest pain is related to myocardial ischemia associated with atherosclerosis or spasm of the small distal branch vessels of the coronary microcirculation. These patients usually have positive stress test results and an inconsistent response to nitrates.22 Prevention and treatment of coronary MVD follow the same recommendations as for CAD.

Coronary Surgical Revascularization

In patients with chronic stable angina, coronary revascularization with CABG surgery is recommended for patients who (1) fail medical management, (2) have left main coronary artery or 3-vessel disease, (3) are not candidates for PCI (e.g., blockages are long or difficult to access), or (4) have failed PCI and continue to have chest pain CABG surgery consists of the placement of arterial or venous grafts to provide blood from the aorta or a branch of a major artery that originates from the aorta (e.g., internal mammary artery) to the heart muscle distal to blocked coronary arteries. CABG surgery requires a sternotomy (opening of the chest cavity) and cardiopulmonary bypass (CPB). During CPB, blood is diverted from the patient's heart to a machine where it is oxygenated and returned (via a pump) to the patient. Minimally invasive direct coronary artery bypass (MIDCAB) offers patients with disease of the LAD or right coronary artery an approach to surgical treatment that does not involve a sternotomy and CPB. The technique requires several small incisions between the ribs or a mini-thoracotomy The off-pump coronary artery bypass (OPCAB) procedure uses a median sternotomy to access all coronary vessels. OPCAB is performed on a beating heart (no CPB) using mechanical stabilizers. OPCAB is associated with less blood loss, less renal dysfunction, less postoperative atrial fibrillation, and fewer neurologic complications Totally endoscopic coronary artery bypass (TECAB) uses a robotic technology to perform CABG surgery Transmyocardial laser revascularization is an indirect revascularization procedure. It is used for patients with advanced CAD who are not candidates for traditional CABG surgery and who have persistent angina despite maximum medical therapy. The procedure involves the use of a high-energy laser to create channels in the heart muscle to allow blood flow to ischemic areas

interprofessional care

Lifestyle modifications: These are (1) manage blood pressure, (2) control cholesterol, (3) reduce blood sugar, (4) get active, (5) eat better, (6) lose weight, and (7) stop smoking. -overweight have an increased incidence of hypertension and increased risk for CVD. Weight reduction has a significant effect on lowering BP in many people. -1 kg of weight lost, BP will decrease by 1 mm Hg. When a person decreases caloric intake, sodium and fat intake are usually also reduced DASH (Dietary Approaches to Stop Hypertension) eating plan stresses fruits, vegetables, fat-free or low-fat milk and milk products, whole grains, fish, poultry, beans, seeds, and nuts. Healthy adults should restrict sodium intake to 2300 mg/day or less. Blacks, people middle aged and older, and those with hypertension, diabetes, or CKD should restrict sodium to 1500 mg/day or less.7 This involves avoiding foods known to be high in sodium. The AHA calls 6 food groups that are the highest sodium sources throughout the United States the "Salty Six." They recommend not adding salt and reducing intake of foods in these groups: bread products, lunch meat and cured meats, pizza, soup, sandwiches, and poultry excess alcohol intake is strongly associated with hypertension. Drinking 3 or more alcoholic drinks a day is a risk factor for CVD and stroke. Men should limit their intake of alcohol to no more than 2 drinks per day and women and lighter weight men to no more than 1 drink per day; exercise: at least 150 minutes per week. Nicotine contained in tobacco causes vasoconstriction and increases BP, especially in people with hypertension. Smoking tobacco is a major risk factor for CVD. monitor, screen, manage risk factors

Antiplatelet therapy cvd cad

Low-dose aspirin (81 mg) is recommended for people who have CAD. For people at risk but without known CAD, low-dose aspirin is recommended for adults 50 to 59 years old who have a calculated 10-year CVD risk of 10% or more, are not at increased risk for bleeding (e.g., history of GI bleeding), have a life expectancy of at least 10 years, and are willing to take low-dose aspirin for at least 10 years. Adults who have no contraindications (e.g., history of bleeding), have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefit.

Circulator Assistive Devices

Mechanical circulatory assist devices (CADs) are used to decrease cardiac work and improve organ perfusion in patients with HF when conventional drug therapy is no longer adequate. CADs include intraaortic balloon pumps (IABPs) and left or right ventricular assist devices (VADs). The type of device used depends on the extent and nature of the heart problem. CADs provide support in 3 situations: (1) the left, right, or both ventricles require support while recovering from acute injury (e.g., postcardiotomy); (2) the patient must be stabilized before surgical repair of the heart (e.g., a ruptured septum); and (3) the heart has failed, and the patient is awaiting heart transplantation. All CADs decrease cardiac workload, increase myocardial perfusion, and augment circulation. The IABP provides temporary circulatory assistance by reducing afterload (through reducing systolic pressure) and augmenting the aortic diastolic pressure. This improves coronary blood flow. -The IABP provides temporary circulatory assistance by reducing afterload (through reducing systolic pressure) and augmenting the aortic diastolic pressure. This improves coronary blood flow. -the IABP consists of a sausage-shaped balloon, a pump that inflates and deflates the balloon, a control panel for synchronizing the balloon inflation to the cardiac cycle, and fail-safe features. The balloon is inserted percutaneously or surgically into the femoral artery. It is moved toward the heart and placed in the descending thoracic aorta just below the left subclavian artery and above the renal arteries -A pneumatic device fills the balloon with helium at the start of diastole (immediately after aortic valve closure) and deflates it just before the next systole. -IABP therapy is known as counterpulsation because the timing of balloon inflation is opposite the ventricular contraction. The IABP assist ratio is 1:1 in the acute phase of treatment, meaning that 1 IABP cycle of inflation and deflation occurs for every heartbeat. -In late diastole when the balloon is totally inflated, blood is forcibly displaced distal to the extremities and proximal to the coronary arteries and main branches of the aortic arch. Diastolic arterial pressure rises (diastolic augmentation). This increases coronary artery perfusion pressure and perfusion of vital organs. The rise in coronary artery perfusion pressure increases blood flow to the myocardium Vascular injuries, such as aortic dissection and compromised distal circulation, are common with IABP therapy. Thrombus and embolus formation add to the risk for circulatory compromise to the extremity. The action of the IABP can destroy platelets and cause thrombocytopenia. Movement of the balloon can block the left subclavian, renal, or mesenteric arteries. This can result in a weak or absent radial pulse, decreased urine output, and reduced or absent bowel sounds. Patients receiving IABP therapy are prone to infection. Mechanical complications from IABP are rare but can occur. Improper timing of balloon inflation may cause increased afterload, decreased CO, myocardial ischemia, and increased myocardial O2 demand. If the balloon develops a leak, the pump will automatically stop. The catheter needs to be promptly removed to avoid an embolus. -The patient with an IABP is relatively immobile, limited to side-lying or supine positions with the head of bed (HOB) elevated less than 45 degrees. The patient may be receiving mechanical ventilation and will likely have multiple invasive lines. A ventricular assist device (VAD) provides short- and long-term support for the failing heart and allows more mobility than the IABP. -A typical VAD shunts blood from the left atrium or ventricle to the device and then to the aorta. Some VADs provide right or biventricular support -ailure to wean from cardiopulmonary bypass (CPB) after surgery is a key indicator for VAD support. VADs can support patients with HF caused by MI and patients awaiting heart transplantation. A VAD is a temporary device that can partially or totally support circulation until the heart recovers or a donor heart is found. Appropriate patient selection for VAD therapy is critical. Indications include (1) failure to wean from CPB or postcardiotomy cardiogenic shock, (2) a bridge to recovery or heart transplantation, and (3) patients with New York Heart Association Class IV heart disease (see Table 34.3) who have failed medical therapy. Relative contraindications for VAD therapy include (1) BSA less than manufacturer's limit (e.g., 1.2 m2), (2) irreversible end-stage organ damage, and (3) co-morbidities that would limit life expectancy to less than 3 years Research on mechanical CADs has led to the development of a fully implantable artificial heart that can sustain the body's circulatory system. This device can provide a bridge to transplantation or replace the hearts of patients who are not eligible for a transplant and have no other treatment options. A major advantage of the artificial heart is that patients do not need immunosuppression therapy and thus avoid its inevitable, long-term effects. Risks include infection, thrombus, and stroke. Patients need lifelong anticoagulation and ongoing care thorough cardiovascular assessments. These include measuring hemodynamic parameters (e.g., arterial BP, CO/CI, SVR), auscultating the heart and lungs, and evaluating the ECG (e.g., rate, rhythm). Assess for adequate tissue perfusion (e.g., skin color and temperature, mental status, capillary refill, peripheral pulses, urine output, bowel sounds) at regular intervals Observe the patient for bleeding, cardiac tamponade, ventricular failure, infection, dysrhythmias, renal failure, hemolysis, and VTE. The patient with VAD may be mobile and need an activity plan.

HTN CLASS

Normal blood pressure is defined as a systolic BP (SBP) < 120 mm Hg and a diastolic BP (DBP < 80 mm Hg. Elevated blood pressure is defined as an SBP between 120 -129 mm Hg and a DBP < 80 mm Hg. Hypertension (stage 1) is defined as an SBP between 130-139 mm Hg and a DBP between 80-89 mm Hg. Hypertension (stage 2) is defined as an SBP > 140 mm Hg and a DBP > 90 mm Hg

Collateral Circulation

Normally, some arterial anastomoses or connections, called collateral circulation, exist within the coronary circulation. Two factors contribute to the growth and extent of collateral circulation: (1) inherited predisposition to develop new blood vessels (angiogenesis) and (2) presence of chronic ischemia (poor blood flow). When plaque blocks the normal flow of blood through a coronary artery and the resulting ischemia is chronic, increased collateral circulation may develop when blockages are forming such as plaques that could block off blood flow the body creates alternate routes of perfusion -extra vessels around the artery to maintain the perfusion to the target organ

assessment htn

Orthostatic hypotension occurs when a patient moves from a supine to standing position, and there is a decrease of 20 mm Hg or more in SBP, a decrease of 10 mm Hg or more in DBP, and/or an increase in the HR of 20 beats/min. Document any lightheadedness or dizziness during the procedure, which is considered an abnormal finding.15 Common causes of orthostatic hypotension include dehydration and inadequate vasoconstrictor mechanisms related to disease or drug therapy. Focus efforts on (1) controlling BP in persons already identified as having hypertension; (2) identifying and controlling BP in at-risk groups, such as blacks, obese people, and blood relatives of people with hypertension; (3) screening those with limited access to health care; and (4) connecting persons with a HCP and/or health insurance if needed.

s/s MI

PAIN -severe chest pain unlike any other pain, it is usually described as a heavy, pressure, tight, burning, constricted, or crushing feeling -substernal or epigastric area. The pain may radiate to the neck, lower jaw, and arms or to the back -indigestion feeling -often occurs in the early morning hours. It usually lasts for 20 minutes or longer and is more severe than chronic angina pain. -tooth ache SNS STIM -ischemic heart cells release catecholamines -diaphoresis, increased HR and BP, and vasoconstriction of peripheral blood vessels. On physical examination, the patient's skin may be ashen, clammy, and cool to touch CARDIOVASCULAR -BP and HR may be high initially. Later, the BP may drop because of decreased CO. If severe enough, this may result in decreased renal perfusion and urine output. Crackles, if present, may persist for several hours to several days, suggesting LV dysfunction. Jugular venous distention (JVD), hepatic engorgement, and peripheral edema may mean right ventricular dysfunction. N/V -reflex stimulation of the vomiting center by the severe pain. FEVER temperature may increase to 100.4° F (38° C) within 24 to 48 hours. The temperature elevation may last for as long as 4 to 5 days. This increase in temperature is due to a systemic inflammatory process

Electrocardiography and other studies

PQRST 60-100 QRS: vent depol and atrial repol ST: vent repol PQ: atrial depol exercise, stress testing, 6 min walk, hemodynamic monitoring, chest X ray, echocardiography (ultrasound) ((1) valvular structures and motion, (2) heart chamber size and contents, (3) ventricular and septal motion and thickness, (4) pericardial sac, and (5) ascending aorta. The ejection fraction (EF), or the percentage of end-diastolic blood volume that is ejected during systole, can be measured.) cardiac CT: Cardiac CT is a heart-imaging test that uses CT technology with or without IV contrast (dye) to see the heart anatomy, coronary circulation, and great blood vessels (e.g., aorta, pulmonary veins, artery). Cardiovascular MRI It is sensitive enough to find even small MIs that are not apparent with single-photon emission computed tomography (SPECT). Nuclear cardiology: This procedure is used to diagnose CAD, make a prognosis in existing CAD, distinguish viable heart muscle from scar tissue, and determine the potential for success of various interventions (e.g., coronary artery bypass surgery, percutaneous coronary intervention) Positron emission tomography (PET) stress testing is increasingly being used due to its high sensitivity for revealing myocardial ischemia and viability invasive studies catheterization -n cardiac catheterization (often called cardiac cath), your doctor puts a very small, flexible, hollow tube (called a catheter) into a blood vessel in the groin, arm, or neck. Then he or she threads it through the blood vessel into the aorta and into the heart. Once the catheter is in place, several tests may be done. Your doctor can place the tip of the catheter into various parts of the heart to measure the pressures within the heart chambers or take blood samples to measure oxygen levels. Your doctor can guide the catheter into the coronary arteries and inject contrast dye to check blood flow through them. (The coronary arteries are the vessels that carry blood to the heart muscle.) This is called coronary angiography. Intravascular ultrasound (IVUS), or intracoronary ultrasound (ICUS), is an invasive procedure done in the catheterization laboratory with coronary angiography. The 2-D or 3-D US images provide a cross-sectional view of the arterial walls of the coronary arteries. The electrophysiology study (EPS) records and manipulates the heart's electrical activity using electrodes placed inside the heart chambers. It provides information on SA node, AV node, and ventricular conduction. It is particularly helpful in determining the source and treatment of dysrhythmias.

Emergency PCI

Percutaneous Coronary Intervention -Emergent PCI is the first line of treatment for patients with confirmed STEMI (i.e., ST-elevation on the ECG and positive cardiac biomarkers). The goal is to open the blocked artery within 90 minutes of arrival to an agency that has an interventional cardiac catheterization laboratory to limit the infarction size. patient undergoes a cardiac catheterization to locate and assess the severity of the blockage(s), determine the presence of collateral circulation, and evaluate LV function. The advantages of PCI (compared to CABG surgery) include (1) it allows for faster reperfusion to limit infarction size; (2) it provides an alternative to surgical intervention; (3) it is performed with local anesthesia; (4) the patient is ambulatory shortly after the procedure; (5) the length of hospital stay is about 3 to 4 days after MI compared with the 4 to 6 days with CABG surgery, thus reducing hospital costs; and (6) the patient can return to work several weeks sooner after PCI, compared with a 6- to 8-week convalescence after CABG.

Complications of heart failure

Pleural effusion, fluid between the 2 tissue layers (pleura) that cover the lung and line the chest wall, is a common complication in HF. Increased capillary hydrostatic pressure in the systemic or pulmonary circulation from HF causes fluid leakage into the pleural space. Pleural effusions may result in symptoms of dyspnea, cough, and chest pain Both atrial and ventricular dysrhythmias are common in HF. Structural changes, including myocardial stretch, fibrosis, and chamber dilatation, alter the electrical paths of the heart. Early and delayed depolarizations, both common in HF, can trigger dysrhythmias. AF is quite common in patients with HF, and the prevalence increases as the severity of HF increases. AF occurs when numerous sites in the atria fire spontaneously and rapidly, and organized atrial depolarization (contraction) no longer occurs. Loss of "atrial kick" during systole may contribute to decreased CO and worsening HF symptoms. -Thrombus risk -An enlarged LV and very low LVEF also increase the risk for thrombus formation in the LV. Anticoagulant therapy may be considered for patients with these problems. Patients with HF are at risk for dangerous ventricular dysrhythmias (e.g., ventricular tachycardia [VT], ventricular fibrillation [VF]). SCD (sudden loss of cardiac function due to a fatal ventricular tachyarrhythmia), is a major cause of death in the HF population. -Cardiac resynchronization therapy (CRT) in the form of implantable cardiac devices can significantly improve morbidity and mortality for these patients. Many HF patients receive a combination ICD and CRT device HF can lead to severe hepatomegaly. The liver becomes congested with venous blood from right HF or ADHF. The hepatic congestion can lead to impaired liver function. Eventually liver cells die, fibrosis occurs, and cirrhosis can develop Reduction in CO results in decreased renal perfusion, decreased glomerular filtration rate, and increased serum creatinine. -Impaired renal function with HF is an independent risk factor for HF morbidity and mortality The primary cause of anemia in chronic HF is chronic kidney insufficiency due to the renal vasoconstriction that often occurs with HF. This vasoconstriction results in reduced erythropoietin production in the kidney, leading to anemia.

Risk Factors

Populations at greatest risk of impaired perfusion are middle-age and older adults, especially among males and African Americans. Also at risk are infants with congenital heart defects. -impaired perfusion as a result of trauma; this leads to central perfusion failure attributable to blood loss. Adults in middle and old age are commonly affected by atherosclerosis involving the heart and peripheral vessels, myocardial disease, and other chronic conditions that negatively impact the cardiovascular system Unmodifiable: age, gender, genetics Modifiable: smoking, lipids, sedentary lifestyle, obesity, diabetes, hypertension

HTN etiology

Primary hypertension (essential or idiopathic) is elevated BP without an identified cause. -Although the exact reason for primary hypertension is unknown, there are multiple contributing factors -diabetes, obesity, alcohol, ethinicity -BP rises with any increase in CO or SVR. As hypertension progresses from elevated to stage 1, increases in both blood volume and CO are often present, leading to an increase in SVR -genetics links shoudl be screened- even children- urged to adopt a healthy lifestyle Excess sodium intake is linked to the development of hypertension. Although most people consume a high-sodium diet, only 1 in 3 will develop hypertension. Secondary hypertension is elevated BP with a specific cause that often can be identified and corrected -sudden -PREGNANCY INDUCED, SLEEP APNEA, ENDOCRINE OR HORMONE DISORDERS The effect of sodium on BP has a strong genetic component. The effect of sodium is more significant in blacks and middle-aged and older adults. Primary risk factors: Age, alcohol, diabetes, inc lipids, ethnicity, excess sodium, fam hx, gender, obesity, sedentary lifestyle, SES, stress, tobacco use

Prinzmetal's Angina (variant angina)

Prinzmetal's angina (variant angina) is a rare form of angina that often occurs at rest and not with increased physical demand. It is sometimes seen in patients with a history of migraine headaches, Raynaud's phenomenon, and heavy smoking. It is usually due to spasm of a major coronary artery. Strong contraction (spasm) of smooth muscle in the coronary artery results from increased intracellular calcium.21 The spasm may occur in the presence or absence of CAD. cocaine causes coronary artery spasms and could feel like MI The pain may be relieved by moderate exercise, with SL NTG, or it may disappear spontaneously Calcium channel blockers and/or nitrates are an option. Stopping the use of any offending substances is recommended.

adpie HF

Review the patient's dietary habits to identify issues related to an exacerbation of HF. Explore the patient's chronic health problems as they may exacerbate HF, affecting the plan of care and the timing and choice of therapies. -meds -chronic conditions he overall goals for the patient with HF include (1) decrease in symptoms (e.g., shortness of breath, fatigue); (2) decrease in peripheral edema; (3) increase in exercise tolerance; (4) adherence with the treatment plan, including appropriate evidence-based medication and device therapies; and (5) no complications related to HF. Communication and joint decision making among the patient, caregiver, and interprofessional team are integral to high-quality, patient-centered care. -emphasis is on aggressively identifying and treating risk factors in the patient with stage A HF to prevent or slow the progression to symptomatic HF -. Recommended lifestyle modifications begin with weight management, diet, and regular exercise. Often, medications are needed. Many persons with HF have 1 or more episodes of ADHF. Common precipitating factors to HF hospitalization include respiratory infections, dysrhythmias, acute coronary syndrome, uncontrolled HTN, and nonadherence to medications and/or diet. Goals of ambulatory HF care include symptom management, QOL maintenance, morbidity and mortality benefit from therapy, identifying and mitigating factors precipitating ADHF and hospitalization, and closely monitoring responses to and potential side effects of therapies. Therapeutic options for stage D HF patients include: (1) chronic inotropic therapy, (2) mechanical circulatory support (MCS) devices, (3) palliative care and hospice that may or may not include ICD deactivation, and (4) heart transplant -Long-term MCS devices include LV assist devices (VADs), including percutaneous devices (PVAD) and transplanted devices (LAVDs, BiVADs) Palliative care may be appropriate earlier in the course of the illness in conjunction with other therapies intended to prolong life. Palliative nursing care of the HF patient emphasizes (1) unifying the patient, family, and health care team in formulating a plan of care; (2) aggressive symptom management; (3) avoiding therapies that are no longer appropriate or effective and may prolong suffering; (4) integrating emotional and spiritual support for patient and family; and (5) determining when a patient may be ready to consider hospice care. Patients with advanced CVD are eligible for hospice when (1) an HCP certifies that a life expectancy of 6 months or less is expected assuming the disease takes its normal course, (2) the patient has received optimal medical treatment and is not a candidate for further invasive procedures, and (3) the patient is assessed at NYHA Class IV. End-stage HF patients who meet hospice criteria are often referred late or not at all. Challenges in referring these patients to hospice include (1) difficulties with accurate life expectancy prediction, (2) reluctance to accept a DNR order due to multiple resuscitation survivals and implantable devices, and (3) a lack of patient and family understanding as to the chronic and terminal nature of HF

Right sided Heart Failure

Right-sided HF occurs when the right ventricle (RV) does not pump effectively. When the RV fails, fluid backs up into the venous system This causes movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention [JVD]). The most common cause of right-sided HF is left-sided HF. As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. The RV must work harder to push blood to the pulmonary system. Over time, this increased workload weakens the RV and gradually it fails. -RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease)

regulation cardiovascular

SNS inc HR BP Contraction Beta 1 PNS slow HR, BP Baroreceptors: in aortic arch and carotid sinus sensitive to stretch and pressure Dec HR, vasodilation, DEC BP or inc as needed

sudden cardiac death

Sudden cardiac death (SCD) is a sudden, unexpected death resulting from a variety of cardiac causes SCD is defined as sudden unexpected death occurring within 1 hour of symptom onset. In SCD, a sudden disruption in heart function from a life-threatening dysrhythmia produces an abrupt loss of CO and cerebral blood flow. Acute ventricular dysrhythmias (e.g., ventricular tachycardia, ventricular fibrillation) cause most cases of SCD. -defibrilators have dec affect of VT and VF Besides patients with CAD, patients with LV dysfunction and structural heart disease are at risk for SCD. Structural heart disease includes LV hypertrophy, myocarditis, and hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a risk factor for SCD, especially in young, athletic people. Some people have symptoms within 1 hour of an SCD event, such as angina, palpitations, dizziness, or lightheadedness. People who experience SCD because of CAD fall into 2 groups: (1) those who had a prior (old) MI and (2) those who had an acute MI. SCD is more common in people who had a prior (old) MI interproff care: People who survive an SCD event need a diagnostic workup to determine whether they had an acute MI. Serial analysis of cardiac biomarkers and ECGs are done to rule out ACS. Because some people with SCD have undiagnosed CAD, cardiac catheterization is done to identify if significant CAD (e.g., greater than 70% stenosis in multiple coronary arteries) was the cause of the SCD event. ICD: implanted defib -The most common approach to preventing a recurrence of SCD is the use of an ICD Rapid cardiopulmonary resuscitation (CPR) and defibrillation with an automatic external defibrillator (AED), combined with early advanced cardiac life support, has improved long-term survival rates for a witnessed arrest due to ventricular dysrhythmias.

healing from MI

The dead heart cells release enzymes that are important diagnostic indicators of MI (see serum cardiac biomarkers By 6 weeks after MI, scar tissue has replaced necrotic tissue and the injured area is considered healed. Often the scarred area is less compliant than the surrounding area. This condition may be manifested by abnormal wall motion on an echocardiogram or nuclear imaging (e.g., hypokinesis, akinesis), LV dysfunction, altered conduction patterns, dysrhythmias, or HF. The scarred area may become an irritable focus for life-threatening dysrhythmias causing sudden cardiac death (SCD) years late These changes in the infarcted heart muscle also cause changes in the unaffected areas. To try to compensate for the damaged muscle, the normal myocardium hypertrophies and dilates. -ventricular remodeling.

care for angina

The goal of treatment for a patient admitted with angina is to decrease O2 demand and/or increase O2 supply. Nursing care focuses on the priority problems of managing acute pain and anxiety while increasing O2 delivery to the myocardium. The overall goals for a patient who presents with angina include (1) relief of pain, (2) immediate and appropriate treatment, (3) preservation of heart muscle if an MI is suspected, (4) effective coping with illness-associated anxiety, (5) participation in a rehabilitation plan, and (6) reduction of risk factors. (1) position patient upright unless contraindicated and apply supplemental O2, (2) assess vital signs, (3) place patient on continuous ECG monitor, (4) obtain a 12-lead ECG, (5) provide prompt pain relief, first with NTG, followed by an IV opioid analgesic, if needed, (6) obtain cardiac biomarkers, (7) assess heart and breath sounds, and (8) obtain a chest x-ray. The patient may be anxious and may have pale, cool, clammy skin. The BP and HR may be high. Auscultation of the heart may reveal an atrial (S4) or a ventricular (S3) gallop education is key Emphasize the importance of risk factor modification to slow the progression of CAD educate how to manage and what to avoid -Help the patient to identify personal risk factors for CAD and ways to reduce modifiable risk factors The most common medications to optimize myocardial perfusion in chronic stable angina include nitrates, angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and calcium channel blockers

interproff care Chronic Heart Failure

The goals of chronic HF therapies include (1) optimal symptom management, (2) mortality and morbidity benefit, (3) minimizing side effects, and (4) monitoring responses to therapies. Specifically, these therapies treat the underlying cause and contributing factors, maximize CO, improve ventricular function, improve quality of life (QOL), and preserve target organ function. The use of supplemental O2 improves saturation and helps meet tissue O2 needs -A structured exercise program, such as cardiac rehabilitation, should be considered for all patients with chronic HF. -The result of neurohormonal blockade is decreased plasma aldosterone levels, decreased SNS activity, vasodilation, and sodium and water excretion. ACE inhibitors are first-line drugs for chronic HFrEF. They decrease mortality, morbidity, hospitalizations, and symptoms in patients with HFrEF. ARBs promote afterload reduction and vasodilation. The side effects are similar to those of ACE inhibitors except that ARBs do not typically cause a cough. Angioedema is less common. Sacubitril/valsartan (Entresto) is a combination of a neprilysin inhibitor (sacubitril) and an ARB (valsartan). -his results in decreased SVR, afterload, and CVP and increased natriuresis and diuresis. Spironolactone (Aldactone) and eplerenone (Inspra) are potassium-sparing diuretics that inhibit aldosterone activation. These drugs work by binding to receptors at the aldosterone-dependent sodium-potassium exchange site in the distal renal tubule, where they have a mild diuretic effect. β-Blockers directly block the negative effects of the SNS (e.g., increased HR) on the failing heart. Three β-blockers decrease mortality in patients with HFrEF: metoprolol succinate (Toprol XL), bisoprolol (Zebeta), and carvedilol (Coreg). Ivabradine selectively inhibits a particular sodium/potassium current in the SA node, resulting in a decreased HR. This drug is a fixed combination of the vasodilator hydralazine and isosorbide dinitrate. It can significantly reduce mortality and improve LVEF and exercise tolerance by reducing afterload through blood vessel vasodilation. Digitalis (digoxin), a weak positive inotrope, acts primarily as a neurohormonal modulator that reduces the effects of the SNS and suppresses renin secretion from the kidneys. Low-dose digitalis decreases HF hospitalizations and symptoms in patients who are still symptomatic despite standard HF therapies Diuretics reduce symptoms of fluid overload and congestion in both HFrEF and HFpEF. Diuretics reduce edema, pulmonary venous pressure, and preload Patients with HFrEF may benefit from implantable cardiac devices. HF patients must be on appropriate therapies before becoming a candidate for device therapy. -With CRT, an extra pacing lead is placed through the coronary sinus to a coronary vein of the LV. This lead coordinates right and left ventricular contractions nutritional therapy: Poor adherence to a low-sodium diet and failure to take prescribed medications as directed are the most common reasons for readmissions of HF patients to the hospital -HF guidelines vary with regard to sodium restriction in HF management. There is agreement that excess sodium may worsen HF symptoms and facilitate an exacerbation. -2g sodium per day -To monitor fluid status, tell patients to weigh themselves at the same time each day. To ensure valid trending, this should be before breakfast, using the same scale, and wearing the same type of clothing.

ADPIE ACS

The immediate goals for a patient with ACS include (1) relief of pain, (2) quick and appropriate treatment, and (3) preservation of heart muscle. During the hospitalization, the overall goals include: (1) effective coping with illness-associated anxiety, (2) participation in a rehabilitation plan, and (3) reduction of risk factors. When the patient is admitted to the intensive care or telemetry unit, monitor vital signs and pulse oximetry frequently (e.g., every hour) during the first few hours Obtain serial 12-lead ECGs, and draw serial cardiac biomarkers Maintain bed rest and limit activity for 12 to 24 hours, with a gradual increase in activity unless contraindicated. further depends on NSTEMI UA Vs STEMI pain: Provide NTG, morphine, and supplemental O2 as needed to eliminate or reduce chest pain monitor: Maintain continuous ECG monitoring while the patient is in the ED and ICU and after transfer to a step-down unit. Treat life-threatening dysrhythmias quickly. During the initial period after MI, ventricular fibrillation is the most common lethal dysrhythmia. -Perform a physical assessment to detect changes from the patient's baseline findings. Assess heart and breath sounds and for signs of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins). -monitor intake output -monitor oxygenation status -It is important to promote rest and comfort for the patient with any degree of heart damage. Bed rest may be ordered for the first few days after a large MI. -A degree of anxiety is present in all patients with ACS. Your role is to identify the source of anxiety and assist the patient in reducing it. education: Tell the patient that more complete teaching will begin once the patient is feeling stronger -educate using simple bried terms, assess when best to educate, and help anticipate rehab or treatments what happens from here? assess support of the patient, visitors, and any additional support needed Physical activity, an integral part of rehabilitation, is necessary for optimal physiologic functioning and psychologic well-being. It has a direct, positive effect on maximal O2 uptake, increasing CO, decreasing blood lipids, decreasing BP, increasing blood flow through the coronary arteries, increasing muscle mass and flexibility, improving the psychologic state, and assisting in weight loss and control. -Teach patients that 30 to 60 minutes of moderate-intensity aerobic activity (e.g., brisk walking) at least 5 days a week is recommended by the AHA -monitor HR, O2, BP ECT during activity

Comp mechanisms

The main compensatory mechanisms include (1) neurohormonal responses: renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS); (2) ventricular dilation; and (3) ventricular hypertrophy. RAAS: INC BP The renin-angiotensin-aldosterone system (RAAS) is a regulatory system that works to maintain normal homeostasis. The goal of RAAS activation is augmentation of preload and ventricular contractility to maintain CO. RAAS activation promotes retention of fluid and sodium. -Chronic activation of the RAAS can cause harmful effects, such as cardiac myocyte apoptosis (programmed cell death), hypertrophy, and fibrosis. These cause the burdensome signs and symptoms that develop with HF SNS: Baroreceptors sense low arterial pressure, stimulating the SNS to try to maintain CO. Catecholamines (epinephrine and norepinephrine) are released. -increases HR (chronotropy) and ventricular contractility (inotropy). Ultimately, chronic SNS stimulation increases myocardial O2 demand on the already weakened heart. -these factors further increase in the heart's workload, intensify ventricular dysfunction, and force ventricular remodeling. Peptides and cytokines: Endothel in, a vasoconstrictor peptide made by the vascular endothelial cells, is stimulated by hypoxia, ischemia, neurohormones, and inflammatory cytokines. -Proinflammatory cytokines are released by myocytes in response to heart injury (e.g., MI, HF). Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress heart function by exerting a negative inotropic effect, causing myocyte hypertrophy and apoptosis. -Systemic inflammation -increase in the heart's workload, progressive LV dysfunction, myocyte hypertrophy, and ventricular remodeling. Vent adaptations: -Dilation Dilation is an enlargement of the heart chambers -It occurs when pressure in the heart chambers (usually the LV) is elevated over time. The heart muscle fibers stretch in response to the volume of blood in the heart at the end of diastole. -Dilation starts as an adaptive mechanism to cope with increasing blood volume. However, excessive preload exhausts the Frank-Starling mechanism, cardiac muscle fibers are overstretched, and further increases in preload no longer increase CO -BIG FLOPPY VENTRICLES CANNOT DO ANYTHING Hypertrophy: Hypertrophy is an adaptive increase in the muscle mass and heart wall thickness as a slow response to overwork and strain -Initially, the increased contractile power of the muscle fibers leads to an increase in CO and maintains tissue perfusion. Over time, hypertrophic heart muscle has poor contractility, needs more O2 to perform work, has poor coronary artery circulation (tissue becomes ischemic more easily), and is prone to dysrhythmias Remodeling: - altered shape of the ventricles eventually leads to increased ventricular mass, increased wall tension, increased O2 consumption, and impaired contractility. The actual shape of the heart becomes less elliptical and more spherical. Although the ventricles become larger, they become less effective pumps. -Ventricular remodeling is a risk factor for life-threatening dysrhythmias and sudden cardiac death (SCD). Beneficial: -Natriuretic peptides (atrial natriuretic peptide [ANP] and brain [b-type] natriuretic peptide [BNP]) are hormones made by the heart muscle. ANP is released from the atria and BNP is released from the ventricles in response to increased blood volume and ventricular wall stretching -Renal effects include: (1) increased glomerular filtration rate and diuresis and (2) excretion of sodium (natriuresis). Cardiovascular effects include vasodilation and decreased BP. Hormonal effects include (1) inhibition of aldosterone and renin secretion and (2) interference with ADH release. The combined effects of ANP and BNP help to counter the adverse effects of the SNS and RAAS. -High serum BNP corresponds proportionately with fluid retention and is a predictor of mortality in HF. -NO and prostaglandin work to relax the arterial smooth muscle, resulting in vasodilation and decreased afterload. Compensated HF occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion. Decompensated HF occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.

Left Sided Heart Failure

The most common form of HF, left-sided HF, results either from the inability of the LV to (1) empty adequately during systole or (2) fill adequately during diastole HFrEF results from an inability of the heart to pump blood effectively. -Patients with HFrEF generally have an LVEF < 40%. It can be as low as 5% to 10%. HFrEF is caused by impaired contractile function (e.g., MI), increased afterload (e.g., HTN), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disorders). -loses the ability to generate enough pressure to eject blood forward through the aorta -The weakened heart muscle cannot generate adequate SV, which impairs CO. Because the LV cannot effectively push blood forward, end diastolic volumes and pressures in the LV increase -When the LV fails, blood backs up into the left atrium (LA). This causes fluid accumulation in the lungs. The increased pulmonary hydrostatic pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This results in pulmonary congestion and edema HFpEF results from the inability of the ventricles to relax and fill during diastole. -HTN is the primary cause of HFpEF -older age, female gender, diabetes, and obesity -LV is generally stiff and noncompliant, resulting in high filling pressures. Decreased filling of the ventricles results in decreased SV -DEC FILLING CANNOT STRETCH DEC CONTRACTION/ SV -CO leading to fluid congestion -(1) signs and symptoms of HF, (2) normal LVEF, and (3) evidence of LV diastolic dysfunction by echocardiography or cardiac catheterization.

age and htn

The prevalence of hypertension increases with age (1) loss of elasticity in large arteries from atherosclerosis, (2) increased collagen content and stiffness of the myocardium, (3) increased peripheral vascular resistance, (4) decreased adrenergic receptor sensitivity, (5) blunting of baroreceptor reflexes, (6) decreased renal function, and (7) decreased renin response to sodium and water depletion.

Preload, afterload, SVR, heart rate ect.

The two variables that contribute to cardiac output are stroke volume (the amount of blood ejected with each contraction) and heart rate. Preload refers to the end diastolic volume in the heart (the amount of blood in the ventricles at the end of diastole) and is influenced by the stretch capacity of myocardial fibers and the amount of blood returned to the heart from the systemic circulation. Another factor that affects cardiac output is systemic vascular resistance (SVR) or the amount of resistance within the vasculature the heart pumps against (also referred to as afterload). SVR is moderated by the diameter of the blood vessels and blood volume. Preload: helps you out- helps stretch the cardiac muscle/ aids in filling Afterload: the resistance the heart must contract against to get blood to the body SVR: systemic vascular resistance: how dilated or narrow the veins and arteries are inc or dec blood pressure contraction/ stroke volume: how hard/ the amount of blood the heart contracts to pump blood CO: the amount of blood pumped in 1 min

post op care

These include (1) hemodynamic monitoring (e.g., CO), (2) an arterial line for continuous BP monitoring, (3) pleural and mediastinal chest tubes for chest drainage, (4) continuous ECG monitoring, (5) an endotracheal tube connected to mechanical ventilation, (6) epicardial pacing wires for emergency pacing of the heart, (7) a urinary catheter to monitor urine output, and (8) a nasogastric tube for gastric decompression. Major complications of CPB are systemic inflammation, bleeding and anemia from damage to red blood cells and platelets, fluid and electrolyte imbalances, infections, and hypothermia (because blood is cooled as it passes through the CPB machine). Focus your care on assessing the patient for bleeding (e.g., chest tube drainage, incision sites), monitoring hemodynamics, checking fluid status, replacing blood and electrolytes as needed, and restoring temperature (e.g., warming blankets). wound care -Other nursing interventions include strategies to manage pain and prevent venous thromboembolism (e.g., early ambulation, sequential compression device) and respiratory complications (e.g., incentive spirometry, splinting during coughing and deep-breathing exercises).

thrombolytic therapy

Thrombolytic (fibrinolytic) therapy is indicated only for patients with a STEMI. Advantages include availability and rapid administration in agencies that do not have an interventional cardiac catheterization laboratory or when one is too far away to transfer the patient quickly. Treatment of STEMI with thrombolytic therapy aims to limit the infarction size by dissolving the thrombus in the coronary artery to reperfuse the heart muscle. The goal is to give the thrombolytic within 30 minutes of the patient's arrival to the ED Because thrombolytics lyse the pathologic clot, they may also lyse other clots (e.g., a postoperative site). Inclusion criteria for thrombolytic therapy are (1) chest pain less than 12 hours with 12-lead ECG findings consistent with acute STEMI and (2) no absolute contraindications (Table 33.15). Patients with chest pain lasting 12 to 24 hours with ECG changes supporting STEMI may be considered for thrombolytic therapy Each hospital has a protocol for giving thrombolytic therapy, but 2 steps should be completed before thrombolytic therapy is started: (1) draw blood to obtain baseline laboratory values and (2) start 2 or 3 lines for IV therapy. Perform all other invasive procedures before giving the thrombolytic agent to reduce the risk for bleeding. Assess heart rhythm, vital signs, and pulse oximetry. Assess the heart and lungs often to evaluate the patient's response to therapy. Regularly assess for changes in neurologic status that may indicate cerebral bleeding. When reperfusion occurs (e.g., a blocked coronary artery is opened and blood flow is restored to the heart muscle), several clinical signs can be seen. The most reliable sign is the return of the ST segment to baseline on the ECG. Other signs include resolution of chest pain and an early, rapid rise of the serum cardiac biomarkers within 3 hours of therapy, peaking within 12 hours. -The major complication with thrombolytic therapy is bleeding. Ongoing nursing assessment is essential. Minor bleeding (e.g., surface bleeding from IV sites or gingival bleeding) is expected and controlled by applying manual pressure followed by a pressure dressing or ice packs

unstable Angina

Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or less effort than the patient's chronic stable angina pattern. The pain usually lasts 10 minutes or more. chronic stable can turn into unstable unpredictable and must be treated immediately.

DX cardiovascular

When cells are injured, they release their contents, including enzymes and other proteins, into the circulation. These biomarkers are useful in the diagnosis of acute coronary syndrome (ACS) Cardiac-specific troponin is a heart muscle protein released into circulation after injury or infarction. Two subtypes, cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI), are specific to heart muscle. -Copeptin, a substitute marker for arginine vasopressin (AVP), can be detected immediately in patients with an acute MI -Creatine kinase (CK) enzymes are found in a variety of organs and tissues and occur as 3 isoenzymes. These isoenzymes are specific to skeletal muscle (CK-MM), brain and nervous tissue (CK-BB), and the heart (CK-MB). ECG 12 lead, 6 min walk test, stress test, chest x ray, CT, MRI,, MRA, PET, Echo C-reactive protein (CRP) is made by the liver during periods of acute inflammation. Homocysteine (Hcy) is an amino acid made during protein catabolism There are 3 natriuretic peptides: (1) atrial natriuretic peptide (ANP) from the atrium, (2) b-type natriuretic peptide (BNP) from the ventricles, and (3) c-type natriuretic peptide from endothelial and renal epithelial cells. BNP is the marker of choice for distinguishing between a cardiac or respiratory cause of dyspnea. These lipoproteins circulate in the blood bound to protein. A lipid panel usually measures cholesterol, triglyceride, low-density lipoprotein (LDL), and high-density lipoprotein (HDL).

Primary, secondary, tertiary prevention

primary: promote health and prevent disease- lifestyle changes secondary: screen for BP HTN, Lipid screening Tertiary/ collaboration: Nutritional therapy, activity, exercise, positioning, smoking cessation, pharm Vasodilators, vasopressor, diuretic, antidysrythmIc, cardioglycosides, anticoagulants, antiplatelet, thrombolytics, lipid lowering agents SURGICAL: pacemaker, electrical cardioversion, intra-aortic balloon pump (A pneumatic device fills the balloon with helium at the start of diastole and deflates it just before the next systole.), heart valve surgery, heart transplant, coronary artery bypass graft, peripheral artery revascularization, stent placement angioplasty, Endarterectomy is a surgical procedure in which the artery is opened to remove obstructing plaque that is impairing perfusion

meds for angina

short acting nitrate -Dilating peripheral blood vessels: This results in decreased SVR, venous pooling, and decreased venous blood return to the heart (preload). Therefore myocardial O2 demand is decreased because of the reduced cardiac workload. Dilating coronary arteries and collateral vessels: This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is hard to achieve sublingual nitroglycerin -SL NTG tablets or translingual spray (Nitrolingual) usually relieves pain in about 5 minutes and lasts about 30 to 40 minutes. The recommended dose of NTG is 1 tablet taken sublingually (SL) or 1 to 2 metered sprays on or under the tongue for symptoms of angina. If symptoms are unchanged or worse after 5 minutes, the patient should repeat NTG every 5 minutes for a maximum of 3 doses -contact the emergency response system (e.g., 911) if symptoms have not resolved completely after 3 doses -if tablet tingles it is still good -change positions slowly it dilates vessels and can cause drop BP -Patients can use NTG prophylactically before starting an activity that is known to cause angina (e.g., emotionally stressful situation, sexual intercourse) long acting nitrate -isosorbide dinitrate (e.g., Isordil) and isosorbide mononitrate, are longer acting than SL or translingual NTG. They are used to reduce the frequency of angina attacks and to treat Prinzmetal's angina. The main side effect is headache from the dilation of cerebral blood vessels. Tell patients to take acetaminophen (Tylenol) to relieve the headache -Orthostatic hypotension is a complication of all nitrate Nitropaste is a 2% NTG topical ointment dosed by the inch. It is placed on the upper body or arm, over a flat muscular area that is free of hair and scars. Once absorbed, it prevents angina for 3 to 6 hours. The ointment should be wiped off each evening to allow for a 10- to 14-hour nitrate-free interval to prevent nitrate tolerance. Currently 2 systems are available for transdermal NTG drug delivery: silicone gel and polymer matrix. These systems allow timed release of NTG over a 24-hour period. These preparations may be removed in the evening to allow for a 10- to 14-hour nitrate-free interval to reduce the risk for NTG tolerance. ACE inhibitor- lisinopril- cough Patients with chronic stable angina and a normal EF, diabetes, and 1 other CAD risk factor should also take an ACE inhibitor to decrease the risk for MI, stroke, and death. These drugs result in vasodilation and reduced blood volume. Most important, they can prevent or reverse ventricular remodeling in patients who have had an MI beta blockers These drugs decrease myocardial contractility, HR, SVR, and BP, all of which reduce the myocardial O2 demand and relieve angina symptoms. -These include bradycardia, hypotension, wheezing from bronchospasm, and GI effects. Many patients report weight gain, depression, fatigue, and sexual dysfunction. -DO NOT GIVE WITH BRADYCARDIA Ca channel blockers Their main effects are: (1) systemic vasodilation with decreased SVR, (2) decreased myocardial contractility, (3) coronary vasodilation, and (4) decreased HR. They are used to treat Prinzmetal's angina. -Side effects include fatigue, headache, dizziness, flushing and peripheral edema. Ranolazine (Ranexa), a sodium current inhibitor, is used to treat chronic angina in patients who have not had an adequate response with other antianginal medications

Consequences of impaired perfusion

central: occlusion to coronary arteries no blood to myocardial tissue= myocardial infarction altered conduction through the heart inadequate pumping heart valve stenosis or insuff impairs blodo flow through heart shock heart cannot pump cardiogenic, fluid lost hemorrhagic, vasodilation anaphylactic, neurogenic, septic TISSUE: Impairment of tissue perfusion is associated with occlusion, constriction, or dilation of arteries or veins. -atherosclerosis/ thrombi occlude, vasoconstriction, vasodilation, ischemia -Ischemia is reversible cellular injury that occurs when the demand for oxygen exceeds the supply because of a reduction or cessation of blood flow. -Destruction of tissues releases enzymes such as creatine kinase (CK); measurement of these enzymes after a myocardial infarction indicates the degree of damage to the heart muscle

Primary Causes

primary causes: -Cardiomyopathy -Congenital heart defects -CAD -HTN -Hyperthyroidism -Myocarditis -Pulm HTN -Rheumatic Heart Dx -Valc disorders

BP

arterial blood pressure is a measure of the pressure exerted by blood against the walls of the arterial system. The systolic blood pressure (SBP) is the peak pressure exerted against the arteries when the heart contracts. The diastolic blood pressure (DBP) is the residual pressure in the arterial system during ventricular relaxation (or filling). BP= CO x SVR Pulse pressure is the difference between the SBP and DBP. It is normally about one third of the SBP. If the BP is 120/80 mm Hg, the pulse pressure is 40 mm Hg. An increased pulse pressure due to an increased SBP may occur during exercise or in people with atherosclerosis of the larger arteries. related to BP is mean arterial pressure (MAP). The MAP refers to the average pressure within the arterial system that is felt by organs in the body.

Age

babies have inc hr dec BP as we grow inc BP dec HR and the heart is able to pump effectively OLD: Atherosclerosis inc BP, orthostatic hypotension, dec CO

Central Perfusion and Tissue Perfusion

central: Central perfusion is generated by cardiac output—the amount of blood pumped by the heart each minute -This central perfusion propels blood to all organs and their tissues from patent arteries through capillaries and returns the blood to the heart through patent veins. -SA- AV- Purkinje -RA, Tricuspid, RV, Pulm artery, Pulm Vein, LA, Bicuspid, LV, Aorta, Sup and inf vena cava Tissue Perfusion: Tissue perfusion refers to the volume of blood that flows through target tissues. This perfusion is supplied by blood flowing from arteries to capillaries. - HIGH PX Arteries, arterioles, capillary beds, venules, veins LOW PX capillary hydrostatic pressure, that pushes blood through capillaries into the interstitial spaces allowing delivery of oxygen, fluid, and nutrients to cells. Osmotic pressure: Oncotic pressure: albumin and other proteins pull water and other products back inot the capillary beds to remain in the vascular system Hydrostatic pressure pushed/ blood pressure pushed fluids, o2, nutrients, ect out into the interstitial space for absorption by the tissues ex edema venules are more flexible and expandable- reservoir for blood- dec workload of heart Arterioles: maintain blood pressure by constricting or dilating in response to stimuli

complications

common complications of hypertension are target organ diseases occurring in the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vessels (peripheral vascular disease), kidneys (nephrosclerosis), and eyes (retinal damage) CAD: development of atherosclerosis Left Vent Hypertrophy: left V must work harder against the lead pipes to pump blood this inc size of muscles, dec ventricle size, harms the heart-increases myocardial work and O2 demand HF: shortness of breath on exertion, paroxysmal nocturnal dyspnea, and fatigue affects begin base don side of heart that is failing PVD: inc atherosclerosis peripheral vascular disease (PVD), aortic aneurysm, and aortic dissection Nephrosclerosis: Hypertension is one of the leading causes of chronic kidney disease (CKD), especially among blacks - ischemia of renal blood vessels -This leads to atrophy of the tubules, destruction of the glomeruli, and eventual death of nephrons. Initially intact nephrons can compensate, but these changes may eventually lead to renal failure - high creatinine or BUN Damage to the retinal vessels indicates related vessel damage in the heart, brain, and kidneys. Manifestations of severe retinal damage include blurring of vision, retinal hemorrhage, and vision loss.

acute coronary syndrome

ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) may develop. ACS includes the spectrum of non-ST elevation acute coronary syndrome (UA and non-ST-segment-elevation myocardial infarction [NSTEMI]), and ST-segment-elevation myocardial infarction (STEMI) -ST elevation represents myocardial injury that is potentially reversible, but, if not treated, will likely evolve to permanent necrosis (tissue death) of the myocardium heart muscle becomes hypoxic within the first 10 seconds of a total coronary occlusion heart muscle becomes hypoxic within the first 10 seconds of a total coronary occlusion ACS is caused by the decline of a once-stable atherosclerotic plaque. The previously stable plaque ruptures, releasing the lipid core into the vessel. This causes platelet aggregation and thrombus formation. The vessel may be partially blocked by a thrombus (manifesting as UA or NSTEMI) or totally blocked by a thrombus (manifesting as STEMI). We are not sure what causes the plaque to suddenly become unstable. Systemic inflammation (described earlier) may play a role.

MI complications

most common complication after MI are Dysrhythmias Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most common cause of death in patients in the prehospital period. -bradycardias (e.g., complete heart block) develop when key areas of the conduction system are destroyed (e.g., infarction involves the sinus or atrioventricular node). VT or VF most often occurs within the first 4 hours after the onset of pain. Premature ventricular contractions (PVCs) may precede VT and VF. Life-threatening ventricular dysrhythmias must be treated immediately. Heart failure (HF) is a complication that occurs when the right or left ventricle's pumping action is reduced. Depending on the severity and extent of the injury, left-sided HF occurs initially with subtle signs, such as mild dyspnea, restlessness, agitation, or slight tachycardia. Other signs indicating the onset of left-sided HF include pulmonary congestion on chest x-ray, S3 or S4 heart sounds, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea. Signs of right-sided HF include JVD, hepatic congestion, or lower extremity edema Cardiogenic shock occurs when O2 and nutrients supplied to the tissues are inadequate because of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction. Papillary muscle rupture is a rare and life-threatening complication. It causes acute and massive mitral valve regurgitation with no time for the heart to compensate. Dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium. This condition aggravates an already damaged LV by reducing CO even further. The patient undergoes rapid clinical decline. Treatment includes afterload reduction with nitroprusside (Nipride) and/or IABP therapy and immediate cardiac surgery with mitral valve repair or replacement Left ventricular aneurysm results when the infarcted heart wall is thin and bulges out during contraction. This can develop within a few days, weeks, or months. It is more common with anterior MIs. -Besides ventricular rupture, which is usually fatal, ventricular aneurysms can hide thrombi that can lead to an embolic stroke. Anticoagulation therapy is recommended for these patients unless contraindicated A new loud systolic murmur heard in patients with acute MI may signal ventricular septal wall rupture. Depending on the size of the defect and degree of right and LV dysfunction, HF and cardiogenic shock may occur. The patient must undergo emergency repair, either surgically or percutaneously. The defect can quickly expand and lead to hemodynamic compromise. -LV free wall rupture is an emergent clinical situation. Rapid hemodynamic compromise and death ensues if not treated immediately. Although this is a rare complication, death rates are high Acute pericarditis, an inflammation of the visceral and/or parietal pericardium, may occur 2 or 3 days after an acute MI. Pericarditis is characterized by mild to severe chest pain that increases with inspiration, coughing, and movement of the upper body. Sitting in a forward position often relieves the pain. The pain is usually different from pain associated with an MI. Assess the patient with suspected pericarditis for the presence of a friction rub over the pericardium. -Fever may be present. The patient may have hypotension and/or a narrow pulse pressure if it is accompanied by significant pericardial effusion or cardiac tamponade. Asymptomatic pericardial effusions are common after STEMI. -This reflects the inflammation of the pericardium. Treatment includes pain relief with high doses of aspirin -Nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids are avoided in the first 4 weeks after MI because they can interfere with myocardial scar formation Dressler syndrome is pericarditis and fever that develop 1 to 8 weeks after MI. Although the cause is unclear, it may be an autoimmune reaction to the necrotic heart muscle. The patient has chest pain, fever, malaise, a pericardial friction rub, and arthralgia. A pericardial effusion may be present. Laboratory findings include a high white blood cell count and sedimentation rate. High-dose aspirin is the treatment of choice.

drug therapy

nitrates: persistent chest pain IV NTG is used in the initial treatment of the patient with ACS. SL NTG can be used until the IV NTG is prepared. The goal of therapy is to reduce angina pain and improve coronary blood flow. IV NTG decreases preload and afterload while increasing the myocardial O2 supply. -Because hypotension is a common side effect, closely monitor BP. Patients who become hypotensive may be volume depleted and may benefit from an IV fluid bolus Morphine is the drug of choice for chest pain that is unrelieved by NTG. As a vasodilator, it decreases cardiac workload by lowering myocardial O2 consumption, reducing contractility, and decreasing BP and HR. In addition, morphine can help reduce anxiety and fear - monitor resp depression β-blockers decrease myocardial O2 demand by reducing HR, BP, and contractility. ACE inhibitors should be started within the first 24 hours if the BP is stable and there are no contraindications Dysrhythmias are the most common complications after an MI. In general, they are self-limiting and not treated aggressively unless they are life threatening (e.g., sustained ventricular tachycardia). A lipid panel is done on all patients with ACS. Patients with ACS or CAD should receive lipid-lowering drugs indefinitely, unless contraindicated After an MI, the patient may be predisposed to constipation because of bed rest and opioid drugs. Stool softeners (e.g., docusate sodium [Colace]) prevent straining and the resultant vagal stimulation from the Valsalva maneuver. Initially, patients may be NPO (nothing by mouth) except for water until stable (e.g., pain free, nausea resolved). Advance the diet as tolerated to a low-salt, low-saturated-fat, and low-cholesterol diet

CVD/ CAD overview

often a symptomatic or Angina chest pain stable and may become unstable or an MI (ACS acute coronary syndrome ) CAD dec hearts ability to pump and effectively perfuse

Interrelated concepts and examples

pain, cognition, elimination, gas exchange, mobility, nutrition, patient education, inflammation, clotting A fib heart failure hyperlipidemia HTN MI Peripheral artery dx ventricular septal defect

assessment of cardiovascular

past health history medications present illness surgeries lifestyle/ health problems nutrition elimination sleep/rest activity exercise cognitive gender, race, age sexuality stress values PHYS exam vital signs Peripheral vascular: skin color, hair, venous patterns, clubbing, edema, neck veins, ulcers from venous stasis Palpation: palpate lower extremities, edema, pulses, moisture- edema from 1+ to 4+ and pulses 0 to 3+ Thorax: palpate and listen to the heart, carotid pulses, S1 OR S2, murmurs, pericardial friction rubs look for pallor, cyanosis, clubbing, longer than 3 second capp refill

perfusion

perfusion refers to the flow of blood through arteries and capillaries delivering nutrients and oxygen to cells. When blood supply is available but decreased, the term ischemia is used. The scope of perfusion ranges from optimal perfusion to no perfusion Optimal perfusion Impaired perfusion No perfusion (necrosis tissue death)

impaired perfusion

when central perfusion is impaired, clinical manifestations are systemic; in other words, the entire body is affected. Significant reduction of central perfusion results in shock, which occurs when blood supply to tissues is impaired because of inadequate cardiac output, significant blood loss, or vasodilation throughout the body. Inadequate tissue perfusion can result from poor central perfusion or from a mechanism within the organ itself, such as a blocked blood vessel leading to or from the tissue or from excessive edema within the tissue interfering with the cellular oxygen exchange or increased pressure and associated constriction or collapse of arterioles.

DX studies

• History and physical examination, including an ophthalmic examination • Fasting blood glucose • Routine urinalysis • Basic metabolic panel with eGFR • Complete blood count • Serum lipid profile (total lipids, triglycerides, HDL and LDL cholesterol, total-to-HDL cholesterol ratio) • Serum uric acid, calcium, and magnesium • 12-Lead ECG

drug therapy

• In patients 65 years or older with an average SBP of more than 130 mm Hg who are ambulatory and living in a community setting, rather than living in a care facility, treatment goals should be to obtain an SBP < 130 mmHg. • In patients 65 years or older with an average SBP of more than 130 mm Hg who live in a care facility, and/or have multiple comorbidities or limited life expectancy, treatment should be based on patient preference, clinical experiences, and team input. • In patients over 18 years old with hypertension, known CVD or other risk factors, a BP of 130/80 mm Hg is the goal of treatment. • In all other patients without CVD or other risk factors, a BP of less than 130/80 mm Hg may be reasonable. Drugs currently available for treating hypertension have 2 primary actions: (1) decrease the volume of circulating blood and (2) reduce SVR • Adrenergic-inhibiting agents act by decreasing the SNS effects that increase BP. Adrenergic inhibitors include drugs that work centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels. • Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II and reduce angiotensin II (A-II)-mediated vasoconstriction and sodium and water retention. • A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in the walls of the blood vessels. • Calcium channel blockers (CCB) increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells. • Direct vasodilators decrease the BP by relaxing the vascular smooth muscle and reducing SVR. • Diuretics promote sodium and water excretion, reduce plasma volume, and reduce the vascular response to catecholamines. The 3 preferred 3 first-line drugs are a thiazide diuretic, a calcium channel blocker, and an ACE inhibitor or ARB. For most patients, a diuretic should be the first drug ordered A common side effect of several of the antihypertensive drugs is orthostatic hypotension.