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P Wave

• Represents atrial contraction (depolarization)
• Represents the time it takes the electrical impulse to travel from the SA node to the ventricle
• Suggests problems usually with the AV node, bundle of HIS, or bundle branches but can also be from the atria

QRS complex

• QRS complex represents ventricular contraction (depolarization)
• Problems are usually from bundle branches or in the ventricles

ST segment

• ST segment indicates the period of time between the end of ventricular contraction (depolarization) and the start of ventricular relaxation (repolarization)
• ST is usually on baseline ( should be no electrical activity)

T wave

• T wave is ventricular relaxation (repolarization)
• Problems are usually from electrolyte imbalances, ischemia, or infarction

QT interval

• Represents the total time for ventricular contraction
• Problems are usually from something affecting repolarization (i.e. Drugs, electrolyte imbalances changes in HR)

The heart composed of three layers

endocardium- a thin inner lining
myocardium-a layer of muscle
epicardium- the outer layer

Conduction System

specialized nerve tissue responsible for creating and transporting the electrical impulse or, action potential.

Sinoatrial (SA) Node

The pacemaker of the heart.

Absolute refractory period

period in which cardiac muscle does not respond to any stimuli.

Depolarization

triggers machanical activity.

Systole

contraction of the myocardium, results in the ejection of blood from the ventricles.

Diastole

allows for filling from the ventricles.

Cardiac Output (CO)

amount of blood pumped by each ventricle one minute.

Preload

The volume of blood in the ventricles at the end of diastole, before the next contraction.

Afterload

the peripheral resistance against which the left ventricle must pump.

Arterial Blood Pressure (BP)

a measure of the pressure exerted by blood against the walls of the arterial system.

Systolic Blood Pressure (SBP)

the peak pressure exerted against the arteries when the heart contracts.

Diastolic Blood Pressure (DBP)

the residual pressure in the arterial system during ventricular relaxation (or filling).

Pulse Pressure

the difference betwenn SBP and DBP.

Mean Arterial Pressure (MAP)

refers to the average pressure within the arterial system that is felt by the organs in the body.

A pt with a trisuspid disorder will have impaired blood flow between the..

right atrium and right ventricle.

A pt has a severe blockage in his rightcoronary artery. Which cardiac structure is most likely to be affected by this?

AV node

If the Purkinjie system is damaged, conduction of the electrical impulse is impaired through..

ventricles

The portion of the vascular system responsible for hemostasis is the..

endothelial layer of the arteries

The auscultatory area in the left midclavicular line at the level of the fifth ICS is the..

mitral area.

Blood flows from

an area of higher pressure to an area of lower pressure (pressure gradient).

Atrioventricular (AV) valves:

separate the atria from the ventricles, The tricuspid valve separates the RA from the RV. The mitral (bicuspid) valve separates the LA from the LV. During ventricular diastole, these valves act as funnels and help move blood from the atria to the ventricles. During systole, the valves close to prevent backflow (regurgitation) of blood into the atria.

Semilunar valves

are the pulmonic valve and the aortic valve that prevent blood from flowing back into the ventricles during diastole.
The pulmonic valve separates the right ventricle from the pulmonary artery.The aortic valve separates the left ventricle from the aorta.

The left main artery divides into two branches

the left anterior descending (LAD) branch and the left circumflex (LCX) branch.

right coronary artery (RCA) originates from

the right sinus of Valsalva, encircles the heart, and descends toward the apex of the right ventricle.

To maintain adequate blood flow through the coronary arteries

mean arterial pressure (MAP) must be at least 60 mmHg.

electrophysiologic properties of heart muscle are responsible for

regulating heart rate (HR) and rhythm.

Diastole

consists of relaxation and filling of the atria and ventricles.

Systole

consists of the contraction and emptying of the atria and ventricles.

Myocardial contraction results from

the release of large numbers of calcium ions from the sarcoplasmic reticulum and from the blood.

Cardiac muscle relaxes when

calcium ions are pumped back into the sarcoplasmic reticulum.

cardiac output (CO)

the amount of blood pumped from the left ventricle each minute. Cardiac Output = Heart rate x Stroke volume

Stoke volume (SV)

is the amount of blood ejected by the left ventricle during each contraction.

parasympathetic (vagus nerve) system

slows the HR

sympathetic stimulation

increases heart rate.

Preload refers

to the degree of myocardial fiber stretch at the end of diastole and just before contraction.

Afterload is

the pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels.

vascular system serves several purposes:

Provides a route for blood to travel from the heart to nourish the various tissues of the body. Carries cellular wastes to the excretory organs. Allows lymphatic flow to drain tissue fluid back into the circulation. Returns blood to the heart for recirculation.

Arterial system:

blood moves from the larger arteries to a network of smaller blood vessels, called arterioles, which meet the capillary bed.

Venous system:

blood travels from the capillaries to the venules and to the larger system of veins, eventually returning in the vena cava to the heart for recirculation.

Nutrients are exchanged across capillary membranes by

osmosis, filtration, and diffusion.

Blood pressure (BP)

is the force of blood exerted against the vessel walls.
Three mechanisms mediate and regulate BP:
1. The autonomic nervous system (ANS)
2. The kidneys
3. The endocrine system

Veins have

the ability to accommodate large shifts in volume with minimal changes in venous pressure.Veins have valves to help prevent backflow while muscles in the extremities help push the venous blood forward.

Major symptoms usually identified by patients with cardiovascular disease (CVD)

include chest pain or discomfort, dyspnea, fatigue, palpitations, weight gain, syncope, and extremity pain. When assessing for symptoms, ask the patient if he/she has "discomfort," "pressure," and "indigestion."

dyspnea on exertion (DOE)

This is usually an early symptom of heart failure and may be the only symptom experienced by women.

orthopnea

dyspnea that appears when he/she lies flat.

Paroxysmal nocturnal dyspnea (PND)

develops after the patient has been lying down for several hours. In this position, blood from the lower extremities is redistributed to the venous system, which increases venous return to the heart. A diseased heart cannot compensate for the increased volume and is ineffective in pumping the additional fluid.

Palpations

(fluttering in the chest) that occur during or after strenuous physical activity may indicate overexertion or possible heart disease.

Syncope

refers to a brief loss of consciousness. Conditions such as cardiac rhythm disturbances, especially ventricular dysrhythmias, and valvular disorders, such as aortic stenosis, may trigger this symptom.

Extremity pain may be caused by two conditions:

ischemia from atherosclerosis and venous insufficiency of the peripheral blood vessels.Patients who report a moderate-severe cramping sensation in their legs or buttocks associated with an activity such as walking have intermittent claudication related to decreased arterial tissue perfusion.

Late signs of severe right-sided heart failure

are ascites, jaundice, and anasarca (generalized edema) as a result of prolonged congestion of the liver. Heart failure may also cause fluid retention.

Rubor

(dusky redness) that replaces pallor in a dependent foot suggests arterial insufficiency.

paresthesia

muscle fatigue and discomfort, numbness, pain, coolness, and loss of hair distribution from a reduced blood supply.

Clubbing

nail straightens out to an angle of 180° and base of nail becomes spongy. Caused by chronic oxygen deprivation in body tissues, common in patients with advanced chronic pulmonary disease, congenital heart defects, and cor pulmonale (right-sided heart failure).

Peripheral edema is a common finding in patients with cardiovascular problems.

Bilateral edema of the legs - heart failure or chronic venous insufficiency. Abdominal and leg edema - heart disease and cirrhosis of the liver. Localized edema in one extremity - venous obstruction (thrombosis) or lymphatic blockage.
Document the location of edema as precisely as possible.

Hypertension

140/90 mmHg

hypotension

BP < 90/60 mmHg may not be adequate for providing enough oxygen and sufficient nutrients to body cells.

Postural (orthostatic) hypotension

occurs when the BP is not adequately maintained while moving from lying to a sitting or standing position.

Paradoxical blood pressure

is an exaggerated decrease in systolic pressure by more than 10 mmHg during the inspiratory phase of the respiratory cycle.

pulse pressure

The difference between the systolic and diastolic values is referred to as pulse pressure.

Hypokinetic pulse

is a weak pulse indicative of a narrow pulse pressure. Seen in patients with hypovolemia, aortic stenosis, and decreased cardiac output.

Hyperkinetic pulse

is a large "bounding" pulse caused by an increased ejection of blood. Occurs in patient with high cardiac output (exercise, sepsis, or thyrotoxicosis) and those with increased sympathetic system activity (pain, fever, or anxiety).

bruits

swishing sounds

Normal Heart Sounds.

The first heart sound (S1) is created by closure of the mitral and tricuspid valves. It is softer and longer. The second heart sound (S2) is caused mainly by the closing of the aortic and pulmonary valves.

Abnormal Heart Sounds

Abnormal splitting of S2 is referred to as paradoxical splitting and has a wider split heard on expiration.
S3 is called a ventricular gallop, and S4 is referred to as atrial gallop. Murmurs reflect turbulent blood flow through normal or abnormal valves. Pericardial friction rub originates from the pericardial sac and occurs with the movements of the heart during the cardiac cycle.

Serum Markers of Myocardial Damage

Acute myocardial infarction (MI), also known as acute coronary syndrome, can be confirmed by abnormally high levels of certain proteins or isoenzymes. These serum studies are commonly referred to as cardiac markers and include troponin, creatine kinase-MB, and myoglobin.

Serum Lipids

Elevated lipid levels are considered a risk factor for coronary artery disease (CAD). Cholesterol, triglycerides, and the protein components of high-density lipoproteins (HDLs) and low-density lipoproteins (LDLs) are evaluated to assess the risk for CAD.

Blood Counts

The erythrocyte count is usually increased in heart disease.
Decreased hematocrit and hemoglobin levels indicates anemia and can lead to angina or aggravate heart failure.
The leukocyte count is typically elevated after and MI and in various infectious and inflammatory diseases of the heart.

What is the primary cause of CAD?

Atherosclerosis
*Endothelial lining altered as result of inflammation and injury, platelets begin to stick and form a clot that block off blood flow through the artery

What causes damage to the endothelium in CAD?

Hypertension (uncontrolled)
Smoking
Hyperlipidemia
Elevated homocysteine
Diabetes

What is C-reactive protein and how does it relate to CAD?

It is a protein released by the liver that rises when systemic inflammation occurs. Chronic elevation is associated w/ unstable plaques and the oxidation of low-density LDL cholesterol (caused by CAD)
(Normal value = <1)

What would keep collateral circulation from forming and what occurs when there is no time for collateral circulation to develop?

A rapid onset of ACS or coronary vasospasm; and ischemia or infarction of the cardiac muscle occurs.

What would you teach a patient with CAD?

When atherosclerotic plaque occlusion of the coronary arteries occurs over a LONG period of time, there is a greater chance of developing collateral circulation, which enables the myocardium to receive adequate amounts of oxygenated blood. EXERCISE helps to develop healthy collateral circulation. Also, increase HDL cholesterol and decrease LDL.

What are risk factors/modifiable factors associated with CAD?

Non Modifiable
Age
Gender (M>F)
African American women & white middle-aged men
Family hx

Modifiable
Elevated serum lipids
Hypertension (>140/90)
Smoking
Obesity
Diabetes type II
Metabolic syndrome
Homocysteine level
Psychologic states (Depression/Anxiety)
Substance abuse (cocaine, alcohol, etc.)

Why is HTN a risk factor of CAD?

B/C the shearing stress of HTN causes endothelial damage & more force is needed to pump blood through a damaged artery

What are some "Healthy People" recommendations for CAD?

Maintain a healthy weight
Reduce sodium intake
Increase physical activity
Avoid tobacco (especially smoking)
Limit daily alcohol
Diet of low cholesterol & sat. fat and HIGH in fruits and veggies

What medications are used to tx CAD?

Antiplatelets (Aspirin, Plavix)

What is Stable Angina?

Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms caused by reversible myocardial ischemia (caused by narrowing of coronary arteries).

What are the clinical manifestations of Stable Angina?

Pain lasting usually 3 to 5 minutes (subsides when precipitating factor is relieved)
Pain at rest is UNUSUAL
ST segment depression

Patient Describes
constrictive, squeezing, heavy, suffocating
Pain is substernal and may radiate to neck, jaw, shoulders, L arm, or between shoulder blades.

What product of anaerobic metabolism causes the "pain" sensation of Stable Angina?

Myocardium becomes hypoxic and LACTIC ACID accumulates from anaerobic metabolism. The lactic acid irritates nerve fibers and pain travels to cardiac nerve roots and thoracic posterior nerve roots.

What are the 5 types of stable angina and what happens w/ each?

1) Silent Ischemia--asymptomatic, associated with DM

2) Nocturnal angina--occurs only at night but not necessarily during sleep or recumbant position

3) Angina Decubitus--occurs only when recumbant and is relieved by standing/ sitting

4) Prinzmetal's (variant) Angina--occurs at rest in response to spasm of coronary artery (hx of migraine, cocaine, Raynauds); may be relieved by moderate exercise

5) Microvascular Angina (MVD)--affects distal branches of CA, pain triggered by ADLs vs. physical exercise; may feel fatigued or anxious

What would you teach a patient about taking Nitroglycerin?

*4mg sublingual (do NOT chew or swallow/ do not inhale spray form); Relieves pain in 3 min
*Repeat q 5 min x3; if still not affective, call 911
*Don't take if systolic <90
*Don't combine w/ drugs for erectile dysfunction
*Teach about Orthostatic Hypotension (sit down before taking)
*Always take med w/ you, keep in closed/dark bottle, good for 6 mos after opening.
*May cause tingling/burning under tongue
*HR may increase and may develop pounding headache
*For prophylaxis: take 5-10 min before activity

What diagnostic studies determine the presence of Stable Angina?

*Health hx/physical exam
*Lab studies
*12-lead EKG
*Chest x-ray
*Echocardiogram
*Exercise stress test or Pharmacological stress test
*PCI (percutaneous coronary intervention)
*Cardiac catheterization
*Angiogram (to view)

What occurs with Acute Coronary Syndrome (ACS)?

A once stable atherosclerotic plaque deteriorates and ruptures, exposing intima to blood. (stimulates platelet aggregation and local vasoconstriction)
*May cause partial or total occlusion of CA (can result in myocardial damage)

What are the three types of ACS?

1) Unstable angina (UA)
2) Non-ST segment elevation MI (Non-STEMI)
3) ST-segment elevation (STEMI)

What are the clinical manifestations of Unstable Angina ACS?

*Unpredictable!
*Chest pain has new qualities
*Occurs at rest or sleep, increasing frequency, easily provoked by minimal or no exertion
*pain gets worse and changes in pain pattern
*doesn't have to have hx of chest pain
MEDICAL EMERGENCY
*Women present with SOB, FATIGUE, indigestion, & anxiety

What is a Non-STEMI?

Partial occlusion of artery w/ damage to the endocardium (ST wave depression or normal ST in EKG)

What is a STEMI?

Complete occlusion of artery w/ damage to myocardium (ST wave elevation in EKG)

What are the clinical manifestations of ACS Myocardial Infarction?

PAIN is hallmark:
*Severe, immobilizing chest pain NOT relieved by rest, position change, or nitrate administration
*Described as heaviness, constriction, tightness, burning, pressure, or crushing
*May occur while pt is at rest, asleep, or awake
*Substernal, retrosternal, epigastric & may radiate to neck, jaw, arms, back

*Women: SOB & Fatigue
*Older adults: confusion, PE, dizziness, dysrhythmias

Sympathetic NS Stimulation d/t epinephrine and norepinephrine (catecholamine) release:
*diaphoresis: sweating/wet skin
*vasoconstriction
*Skin: ashen, pale, and/or cool to touch

Cardiovascular Symptoms:
*Increased HR & BP
*Crackles in lungs
*JVD
*Abnormal heart sounds (S1 and S2 are NORMAL)
*Murmur

*N/V
*Fever within first 24 hours

Describe the healing process of an MI?

1) Within 24 hours, leukocytes infiltrate the are of necrosis
2) Enzymes are released from dead cardiac cells
3) Neutrophils and Macrophages remove necrotic tissue
4) Development of collateral circulation improves areas of poor perfusion
5) Serum glucose may be elevated from glycogenolysis and lypolysis
6) Necrotic zone identifiable by EKG changes
7) 10-14 days after MI, scar tissue is still weak and vulnerable to stress
8) By 6 weeks after MI, scar tissue has replaced necrotic tissue but is less compliant than normal tissue which may lead to CHF
9) Ventricular remodeling (myocardium may hypertrophy and dilate to compensate--may cause heart failure)

What are the complications of an MI?

*Dysrhythmias (most common cause of cell death pre-hospital)
*Heart Failure presenting w/ dyspnea, restlessness, agitation, tachycardia, pulmonary congestion (crackles), S3 or S4 heart sounds, and respiratory distress
*Cardiogenic Shock (occurs when inadequate oxygen and nutrients are supplied to heart's tissues because of severe LV failure.)
*Papillary muscle dysfunction (causing mitral valve regurgitation and murmur)
*Ventricular aneurysm
*Acute Pericarditis "Dressler's Syndrome" (inflammation of pericardium; may have fever & friction rub may be heard)

What are the Serum cardiac markers, what are the levels, and what do they mean?

*Draw these within 10 minutes of ER arrival*
1) Myoglobin-earliest indicator, 99-100% sensitive to heart if measured w/in 12 hours of MI event

2)Troponin I and T- most specific for MI
*Normal Troponin T =<0.1 ng/mL
*Normal Troponin I =<0.4 ng/mL so >2.3=MI

3) CK-MB- specific for MI; level correlates w/ size of infarction. (>5% = MI); Rise 3-12 hours after MI and peak in 24 hours; return to normal in 2-3 days

What is the MONA protocol?

Depending on agency protocol:
1) Administer morphine 5-10mg as ordered
2) Administer oxygen at 4L per N/C as ordered
3) Continue nitrate therapy as ordered
4) Administer 81-325mg Aspirin (ASA) as ordered

What is the acute nursing management of an anginal attack?

1) Administration of supplemental oxygen
2) 12-lead EKG as ordered
3) Prompt pain relief first w/ nitrate followed by an opioid analgesic if needed (vasodilation)
4) Auscultation of heart sounds
5) comfortable positioning of patient
6) For anxiety give Benzodiazepine

What is the etiology of Sudden Cardiac Death?

Most are caused by ventricular dysrhythmias (V-tach, V-fib); caused less commonly as result of LV outflow obstruction (aortic stenosis)

What are the primary risk factors of SCD?

*Left ventricular dysfunction: look @ ejection fraction (REMEMBER: normal EF is 50-70%
*Male gender (esp. African American)
*Family hx of premature atherosclerosis
*Smoking
*DM
*Hypercholesterolemia
*HTN
*Cardiomyopathy

What are the characteristics of a Normal Sinus Rhythm?

*Rate is normal (43 and 93 beats/min in men and 52 and 94 beats/min for women; 110 to 150 beats/min in infants)
*P waves are present on an ECG
*Rhythm is regular

What is considered normal P-wave morphology?

*Upright in leads I, II and usually aVF
*Inverted in aVR
*Upright, biphasic or inverted in III and aVL
*The right to left activation results in P waves that are upright or biphasic in V1 and V2, and upright in V3 through V6

What ECG changes can be noted with LEFT atrial enlargement?

*The P wave is WIDE in lead II (≥0.12 sec) and is usually NOTCHED in I and II.
*The P duration/PR segment is greater than 1.6.
*The terminal P wave in lead V1 is deep and delayed with the negative deflection being greater than 40 m sec in duration and/or ≥0.1 mV in height.

What ECG changes can be noted with RIGHT atrial enlargement?

*Prominent P waves (0.2 mV in height) in the limb leads, particularly II and aVF, and in an anterior lead such as V1.
*The initial P force in lead V1 is often ≥60 mV-msec.
*The P wave duration is 0.11 sec or less with an axis of 65º or more.

What is the purpose of the SA node?

The heart's natural "pace-maker"; sets the pace for the heart.

What is characteristic of a normal PR interval?

*0.12 seconds-0.2 seconds
*PR intervals shorten as heart rate increases
NOTE: PR interval may be prolonged by intraatrial, AV nodal, and infranodal conduction abnormalities.

What are the two types of sinus arrhythmias?

1) Respiratory type (phasic)
2) Non-respiratory type (non-phasic)

What is characteristic of a Respiratory or phasic arrhythmia?

*Common, normal, decreases in age
*Results from changes in autonomic tone during the respiratory cycle .
*Inspiration reflexively inhibits vagal tone, thereby increasing the heart rate. With expiration, vagal tone rises to its previous state, and the rate declines again.
*This type of sinus arrhythmia disappears with breath holding.

What is characteristic of a Non-respiratory or non-phasic arrhythmia?

*The acceleration and deceleration of the SA node is not related to the respiratory cycle.
*This form of arrhythmia can occur in the normal heart, diseased heart, or after digitalis intoxication.

What are the signs and symptoms of dysrhythmias?

*Palpitations, dizziness, lightheadedness, syncope, chest discomfort, neck discomfort, dyspnea, weakness, and anxiety
*Secondary consequences of arrhythmias, often due to underlying heart disease, are an additional source of symptoms (e.g., congestive heart failure, ischemia, and thromboemboli.)
*Arrhythmias such as ventricular fibrillation and asystole can cause cardiac arrest.

What are the goals of therapy in arrhythmia patients?

*Improve symptoms
*Decrease anxiety
*Identify the causal mechanism of the arrhythmia
*Tailor a plan of care for the patient
*Educate the patient on s/s of an acute cardiac event
*Prevent a potentially serious cardiac event

What are the risk factors associated with A-fib?

*Age (greater than 65)
*Left atrial enlargement shown to precede and predispose AF
*Hypertensive heart disease
*Coronary artery disease
*Valvular disease/history of rheumatic fever
*Obesity
*Diabetes
*Chronic Kidney disease
*Hyperthyroidism
*COPD
*Sleep Apnea
*Alcohol
*Caffeine

What meds are used for A-fib?

1) Amiodarone: when no other meds have worked; used to slow heart rate down
2) Anticoagulants (warfarin): r/t risk of thrombus formation

What are potential complications of cardioversion?

*Transient Ischemic Attack (TIA)
*Stroke can occur if a blood clot forms in the left atrium because of sluggish blood flow and a piece of the clot breaks off. Embolus may also travel to kidney, eye, extremities

What is Infective Endocarditis?

An infection of the endocardial layer (contiguous w/ valves) of the heart

What are the classifications/types of Infective Endocarditis?

1) Acute: individuals w/ healthy valves and manifests as a rapidly progressive illness (healthy but drug abuser)
2) Subacute: individuals with preexisting valve disease and the clinical course of the infection may extend over months (often chronic)

*NOTE: also classified by cause (IVDA or fungal) and Site involvement (prosthetic valve endocarditis-PVE)

What are predisposing conditoins that increase the risk of Infective Endocarditis?

Those predisposed by:
1) Cardiac conditions (prosthetic valves, RHD, Pacemakers, Marfan's syndrome, etc.)
2) Non-cardiac conditions (hospital-acquired bacteria, IV drug abuse)
3) Procedure-associated risks (IV devices, oral procedures, respiratory procedures, GU/GI procedures)

What are some causative agents of Infective Endocarditis?

bacteria, viruses, fungus

*NOTE: contributing factors include: Aging, IVDA, prosthetic valves, & intravascular devices

How does Infective Endocarditis occur?

Blood flow turbulence within the heart allows causative organisms to infect previously damaged valves or other endothelial structures

How is Infective Endocarditis treated?

*Penicillin has greatly improved the prognosis of the disease

What situations warrant prophylaxis for IE?

*GU/GI or respiratory procedures ONLY if pt is in high risk category (valve replacement, IVDA, etc.)
*Oral procedures involving perforation of oral mucosa, dental extractions/implantations, teeth cleaning w/ anticipated bleeding
*Biopsy
*T&A
*Presence of wound infection
*Presence of UTI

What are vegetations associated with IE?

Consist of fibrin, leukocytes, platelets, and microbes that adhere to the valve surface or endocardium (may result in embolization)

What happens w/ left-sided vegetations?

Emboli can progress to various organs (brain, kidneys, and spleen) & Limb infarction (tissue death) may occur

What happens w/ right-sided vegetations?

The lesions progress to the lungs and result in pulmonary embolism (PE)

What are the clinical manifestations of IE?

Chills, weakness, malaise, fatigue, anorexia, arthralgias, back pain, abdominal discomfort, weight loss, headache, clubbing of fingers, osler's nodes (bumps on fingers/toes), Roth's spots (spots on retina), low grade fever

How is Infective Endocarditis diagnosed?

Two blood cultures are drawn from two different sites. (Negative cultures should be kept for 3 weeks if clinical diagnosis remains endocarditis b/c of possibility of slow growing organisms)

What are the treatment goals of IE?

1) Normal or baseline cardiac function
2) Performance of ADLs w/o fatigue
3) Knowledge of therapeutic program to prevent recurrence of endocarditis

What are some nursing diagnoses for IE?

1) Decreased CO r/t altered rhythm, valvular insufficiency, and fluid overload
2) Activity intolerance r/t generalized weakness and alteration in oxygen transport secondary to valvular dysfunction
3) Hyperthermia related to infection of cardiac tissue (inflammatory response/fever)

What should be expected upon evaluation of treatment of IE?

*Vital signs WNL
*Absence of fever, chills, diaphoresis, HA
*Completion of ADLs w/o fatigue, SOB, or physiologic distress
*Increased understanding of disease process and self-care
*Ability to recognize s/s of infection
*Knowledge of pre-procedure ABX, report valve problems to all health care providers

What assessment/physical symptoms would be noted in someone with Pericarditis?

*Progressive, severe chest pain that is sharp
*Pt may exhibit shallow breathing
*Pain worse with deep inspiration and lying supine
*Relieved by sitting up and leaning forward
*Dyspnea
*Pain may radiate (often to trapezius)

Assessment:
*HALLMARK: Pericardial friction rub (scratching, high-pitched)

What are the types of valvular disorders?

Regurgitant and Stenosis (Mitral, Aortic, Tricuspid)

What happens in Valvular regurgitation?

*Valves do not close completely
*Allows back flow through the valve in the area just to the left of that valve
*Can result from deformity or erosion of valve cusps
*Caused by: bacteria (acquired) or congenital

What happens in Valvular stenosis?

*valve leaflets fuse together and cannot fully open or close
*the opening narrows and becomes rigid
*Impeded forward flow
*Caused by: bacteria (acquired) or congenital

What is Mitral Stenosis?

Stenosis that has narrowed the mitral valve obstructing backflow from the L atrium into the L ventricle during diastole (relaxation)

What is Mitral Stenosis caused by?

*Usually as a result of acute or chronic RHD of bacterial endocarditis
*Rarely from congenital heart defects

What are clinical manifestations of Mitral Stenosis?

*Most common is dyspnea on exertion
*Cough
*hemoptysis r/t back flow (coughing up blood)
*Frequent pulmonary infectoins (bronchitis/pneumonia)
*Paroxysmal nocturnal dyspnea
*Orthopnea
*Weakness
*Fatigue
*Palpitations

SEVERE:
*Right-sided HF manifestations (JVD, hepatomegaly, ascites, peripheral edema, basilar crackles, & severe/late cyanosis of the face and/or extremities

What would the nurse find upon assessment of Mitral Stenosis?

*Loud S1
*Split S2
*Murmur
*Mitral snap (r/t atrial pressure)

What happens to cardiac output as it relates to mitral valvular disease?

1. Normal balance of oxygen supply/demand is upset
2. Heart begins to fail
3. Increased muscle mass/size = increased myocardial oxygen consumption
4. Size and workload of heart exceeds blood supply
**Which causes ischemia followed by dyspnea and pain, losing functional muscle
**Contractile force, SV, and CO decrease d/t loss of functional muscle, leading to increased pressure on the left side of the heart reflected backward into the pulmonary system causing pulmonary edema and HTN and right-sided ventricular failure.

What is Mitral Regurgitation?

Mitral valvular insufficiency that allows the blood to flow back into the Left Atrium during systole b/c the valve does not fully close.

What is a common cause of Mitral Regurgitation?

*RHD (rheumatic heart disease)
*Congenital defects may also cause Mitral regurg.

What are the manifestations of Mitral Regurgitation?

*Fatigue
*Weakness
*Dyspnea on exertion
*Orthopnea

SEVERE or ACUTE:
*manifestations of left-sided heart failure: pulmonary congestion, pulmonary edema, and increase in high pulmonary pressure which may lead to Rt side complications

What is Aortic Stenosis?

An obstruction of blood flow from the L ventricle into the aorta during systole (contraction)

What happens in Aortic Stenosis?

*Valvular annulus decreases in size, increasing the work of the L ventricle to eject volume through the narrowed opening into the aorta
*The ventricle hypertrophies (to compensate and maintain adequate SV and CO)
*Workload increases myocardial oxygen consumption (may precipitate myocardial ischemia)
*Coronary blood flow may decrease
*L ventricular end-diastolic pressure increases r/t reduced SV
*L atrial pressure increases (pulmonary vascular congestion and pulmonary edema may result)

What is cardiomyopathy and how is it classified?

Constitutes a group of diseases that directly affect the functional ability of the myocardium

CLASSIFIED"
1) Primary: etiology is unknown
2) Secondary: result of another disease

Does cardiomyopathy affect function and conduction?

YES

What are the 3 types of cardiomyopathy?

1) Dilated
2) Hypertrophic
3) Restrictive

What is Dilated cardiomyopathy?

*Left Ventricle is dilated and has thinned; therefore increasing chamber size and volume.

*Characterized by diffuse inflammation and rapid degeneration of myocardial fibers

RESULTING IN:
*Impairment of systolic function (contractility)
*Atrial enlargement
*Blood stasis in L ventricle

What are the goals of therapy in Dilated cardiomyopathy?

* Interventions focus on controlling HF by enhancing myocardial contractility and decreasing afterload.

MEDS:
*Nitrates/loop diuretics to decrease preload
*ACE inhibitors (decrease afterload)
*Beta blockers (control neurohormonal stimulation)
*Antidysrhythmics

OTHER INTERVENTIONS:
*Drug and nutritional therapy
*Alcohol abstinence
*Ventricular assistive device (VAD) to allow heart to rest and recover from acute HF

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