Cardiovascular System

Nursing 1120By: Diana Blum RN MSN

Metropolitan Community College

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Coronary Arteries

• Two major coronary arteries– arise from the aorta beyond the aortic

valve. – Blood flows to the coronary arteries

during diastole• Left main, LAD, Circumflex feeds most of

Left side of the heart• Right feeds SA node, AV node, RA, RL

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Collateral circulation is a network of tiny blood vessels, and, under normal conditions, not open. When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge and become active. This allows blood to flow around the blocked artery to another artery nearby or to the same artery past the blockage, protecting the heart tissue from injury.

Conduction Continued

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Cardiac Cycle

• Contraction and relaxation of the heart: • Diastole:• Systole:

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• Video Mysterious Heart Volume 2 chapter 3

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Cardiac Output

• the volume of blood ejected by the heart each minute and is determined by stroke volume and the heart rate.

• Normal stroke volume is 60-100 ml• Normal cardiac output is 4 to 8 L / min• (CO = HR X SV)

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Factors affecting Stroke Volume• Preload: the amount of blood remaining in

the ventricles at the end of diastole or the pressure generated at the end of diastole

• Contractility: is the ability of the cardiac muscle fibers to shorten and produce a muscle contraction. (Inotropic, + or -)

• Afterload: amount of pressure the Ventricle must overcome to eject blood volume out

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Heart Rate

• SA node : pacemaker of heart 60-100 bpm

• AV node : 40 -60 bpm• Heart is innervated by sympathetic and

parasympathetic nervous system– Sympathetic: speeds HR, and increases force

of contraction– Parasympathetic: slows HR and force

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Heart Tones• Murmur: Produced by turbulent sounds across

valves– Rub: inflamed pericardium-best heard along left

sternal border– S3 murmur: sounds like “Kentucky”– S4 murmur: sounds like “Mississippi”

http://www.blaufuss.org/ http://www.med.ucla.edu/wilkes/Rubintro.htm

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Health History

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Present Illness

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Past Medical History

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Family History:

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Review of systems• weight gain• fatigue• dyspnea• cough• orthopnea• palpitations• chest pain• fainting• concentrated urine• edema

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Functional assessment• effects of illness on ADLs and rest patterns• smoker• diet• stress• coping

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Physical Assessment

• General:• VS: orthostatic bp in both arms, apical rate

and rhythm, respiratory rate and effort• peripheral pulses:• Skin: color hair distribution, cap refill, temp• Thorax: heart sounds, lung sounds, sputum• Extremities: pulses, color, temp, edema

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Age Related Changes

• Heart less able to adapt to changing needs related to activity

• Valves thicken and stiffen• # of pacemaker cells decrease• Nerve fibers decrease• Frequent dysrhythmias

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Diagnostic Tests

• EKG: rate, rhythm, ischemia (T-inverted), injury (ST segment elevation), arrhythmias, strain, infarction (q wave)

• Echocardiogram: (TEE) sound wave test detects size of chambers, valve integrity, flow, wall motion, Cardiac Output

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Diagnostic Tests ContinuedBiomarkers: Troponin will show elevation 3-4 hr after injury

<0.10 is negative0.10-0.60 is intermediate and may indicate

injury>0.60 is positive evidence of MI

Myoglobin increases 1-4 hours after MI CPK-MB will show increase 4 hrs after MIBNP can be elevated 48 hrs after MI which

indicates heart failure

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Diagnostic Tests Continued• CBC: anemia • CMP: screening K+, etc• PT, INR• PTT• Lipid profile: see next 2 slides

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Total cholesterol

Below 200 mg/dL Desirable

200-239 mg/dL Borderline high

240 mg/dL and above

High

LDL cholesterol

Below 70 mg/dL Optimal for people at very high risk of heart disease

Below 100 mg/dL Optimal for people at risk of heart disease

100-129 mg/dL Near optimal

130-159 mg/dL Borderline high

160-189 mg/dL High

190 mg/dL and above

Very high25

HDL cholesterol

Below 40 mg/dL Poor

40-59 mg/dL Better

60 mg/dL and above

Best

Triglycerides

Below 150 mg/dL

Desirable

150-199 mg/dL

Borderline high

200-499 mg/dL

High

500 or above Very high26

Diagnostic Tests Continued• ABG: assess acid/base levels• Pulse Oximetry: generally >92%• Holter monitoring: 24+ hr of EKG + events• Stress test: treadmill or pharmacological• Cardiac Catheterization: invasive, NPO 6-8h,

consent. Visualizes chambers, valves, arteries, pressures, CO

• Heart-CT scan: assesses CAD, MRI• Nuclear scans: assess heart muscle viability• EPS: NPO, consent, IV, assess electrical activity

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• http://preop.medselfed.com/asp/center.asp?centerId=heart&partnerId=preop&id=&cachedate=&emailId=&affId=&campId=&hideNav=

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CADVideo-mysterious heart volume 3 chapter 2

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Etiology of CAD

• CAD occurs when the intimal lining of the coronaries begin to plaque resulting in jagged edges and narrowed passageway for blood flow

• Atherosclerosis results in impaired blood flow to the heart muscle

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Risk Factors for CAD

Non-controllable-

Controllable-

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s/s of CAD

• Angina which results from a lack of 0xygen to the heart muscle– 4Es=

• Weakness, diaphoresis, SOB• N/V

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MI: Myocardial Infarction• Occlusion of a coronary artery resulting in

necrosis of the heart muscle.• Risk factors: same as for CAD• Pathophysiology: AMI-over 4-6 hrs ischemia

injury and infarction develop. Ischemia=lack of 02 to heart muscle, if not relieved=injury. After 20 min of ischemia=infarction

• Main S/S: chest pain and accompanying S/S

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• Within 24 hours after infarction, healing begins, collateral circulation begins.

• 10-14 days after MI=extension of MI may occur due to myocardial tissue vulnerability to stress

• Complete scar formation and healing takes about 6 weeks

• Video- mysterious heart volume 1 chapter 2

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Data Collection

Same as for CAD but will assess symptom of chest pain with accompanying s/s

May have EKG changes with or with-out ST-T wave changes or Q wave changes

Cardiac Bio-markers (Troponin, Myoglobin, CPK, CKMB)

May proceed with Echocardiogram to assess if wall motion sluggish

May go to cath lab

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Angina or MI• Angina without MI} often relieved with rest and NTG• Angina with MI } may be relieved with rest, NTG, 02, MS, rescue

angioplasty, etc.• Think MONA

– Morphine – Oxygen– Nitroglycerin– Aspirinhttp://www.youtube.com/watch?v=4GlQmTlP2jE&feature=related

http://www.youtube.com/watch?v=rEqw3AK-M_g

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Treatment continued…video mysterious heart volume 3 chapter 3-7

ASA:MS:Beta-blockerACE inhibitor:

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Treatment continued– May need antiarrhythmic meds

• like what???

– Stool softeners to reduce valsalva maneuver and prevent constipation r/t narcotic use and bed rest

– Treat: HTN, DM other co-morbid illnesses– Cardiac Rehab to follow

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Treatments

• Low fat low cholesterol diet• Prescribed exercise program 5-7 days a

week• Knows correct use of NTG for angina• Management of DM, HTN• Stop smoking• Medications to reduce work load or dilate

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Low salt diet (<2000mg) does not include:

• Soups:

• Snacks:

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Low fat <30% Low cholesterol <200mg• Lean meat: skinless• Dairy limited: egg beaters, skim milk• Olive oil, canola oil• Avoid: fried, fatty or heavily marbled meats,

sausage, lunch meat, spareribs, frankfurters, salt pork, canned fish in oil, yolks, duck. Cream sauces, gravy, buttered vegetables, sweet rolls, other processed foods

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Exercise

• 5-7 X week is goal to include stretches with warm-up, progressive walking program, light weights, stretches with cool down.

• Strengthens heart muscle, reduces BP, BS, weight, stress, tension, appetite, LDLs.

• Increases HDLs, energy and self esteem and improves immune system

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Principles of Exercise

• Practice on regular basis• Know how to do own pulse• Strive for target heart rate• Stop if chest pain occurs• Complications: CHF &

Dysrhythmias43

Nursing interventions for MI• Comfort measures• Freq VS, cardiac monitoring, I&O, CMS

checks, spacing activities• Heart & lung sounds, assess fluid volume

status, IV responsibilities, note BP & Pulse prior to heart meds!!

• Client education r/t diet, meds, pulse taking activity, elimination, reporting chest pain and correct use of nitro products for angina

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Medications for Heart Disease

• Anti-Anginal:• Anti-Hypertensive:• Anti-Arrhythmic: l• Cardiac glycoside:

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Medication continued• Thrombolytic:• Anti-coagulant:• Anti-platelet aggregate:• Lipid-Lowering agents:• Diuretics:• Electrolyte replacement:

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Medication continued

• 02 to maintain 02 sat > 92% to reduce chance of angina/ischemia

• If Angina the nurse needs to have the client lie down, take VS then report to charge nurse ,met team, call md.

• Instruct client: If develops chest pain, sit down take 1 nitro every 3- 5 min x 3. If chest pain not relieved call 911

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•POST MI Complications

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• 90% will develop complication and 80% will demonstrate arrhythmia which is the most common cause of death in clients in the pre-hospital period. (VT>>>VF)

• CHF and severe Left ventricular failure• Papillary muscle dysfunction• Pericarditis• Thromboembolism • Ventricle rupture

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Nursing Diagnosis

• Decreased cardiac output r/t Dysrhythmias

• Acute Pain r/t lack of 02 to myocardium

• Anxiety r/t to feeling of doom, lack of understanding of medical diagnosis

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•Surgical Procedures

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• New in 1958 having purpose to restore the regular rhythm and to improve tissue perfusion and cardiac output.

• Temporary / permanent• Single chamber or double chamber• Teach client how to take 1 min pulse, s/s

to report to MD-dizzy, angina, dyspnea• Carry card and know precautions

Pacemaker

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Video- mysterious heart volume 2 chapter 4

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AICD

• Implantable defibrillator to correct a life threatening rhythm disturbance.– Has pacemaker back-up.

• check battery q2months• Instruct on how to take pulse for 1 min• s/s to report to MD: firing, s/s of dizziness,

dyspnea, weakness, carry card and wear bracelet, CPR for family. Know precautions

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• Nursing care for client with newly implanted pacemaker or AICD.– Assess cardiac monitor for capture/pacing

(pacer)– VS post-op then q 4 hours, IV, bed rest till am– Dressing dry and intact until AM then often

may remove. Increase activity progressively– Instruct client not to raise arm above shoulder

for 5days. May shower in 5 days

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Angioplasty with Stent

• Procedure done at the time of cardiac cath.

• Balloon angioplasty is accomplished to widen or open specific coronary vessel-stent is inserted to maintain patency of the vessel.

• pre-procedure Plavix given with follow up Plavix

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http://preop.medselfed.com/asp/center.asp?centerId=heart&partnerId=preop&id=&cachedate=&emailId=&affId=&campId=&hideNav=

EP with Ablation

• Mapping of myocardial tissue to determine irritable focus.

• Low voltage current delivered to ablate tissue causing SVT or VT

• 90% effective• http://video.google.com/videoplay?do

cid=5590000557631435292

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Nursing Care

• NPO prior• Coumadin stopped 4 days prior, Heparin 4

hours prior• Post – procedure same as heart cath

– Cardiac monitoring– Muscloskeletal and groin checks– VS– Ambulate prior to discharge

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Cardiac Surgery

• Coronary artery bypass• • Valve replacement or repair• Septal repair and other congenital repairs

– CCU post op, chest tubes– Pre-op teaching with post op expectations– See client teaching for CABG, Valve

repair/replacement, care of PTCA, MI

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• http://preop.medselfed.com/asp/center.asp?centerId=heart&partnerId=preop&id=&cachedate=&emailId=&affId=&campId=&hideNav=

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Congestive Heart Failure

• Video..the mysterious heart volume1 chapter 3 61

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• DEFINITION:EF < ____% or when the myocardium is no longer able to pump efficiently

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• Systolic failure= most common

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Causes of CHF

• CAD, advancing age• HTN is a major factor > CHF x 3 • DM, Smoking, Obesity• Valvular incompetency, alcohol

or other chemicals, idiopathic,(unknown)

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S/S of Left Sided CHF

• Fatigue• Angina• Tachycardia• Cool extremities• Hacking cough• Crackles• Frothy sputum• Gallop

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S/S of Right Sided CHF

• Jugular distention• Anorexia/nausea• Dependent edema• Distended abdomen• Weight gain• BP problems

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Assessment Findings

• C/O SOB, weakness, dry cough, fatigue, can not lie down must sit up to breath, has gained weight

• Auscultation of the heart} rapid HR, extra heart sounds

• Auscultation of the lungs} rales, wheezing• Examination of the extremities for

peripheral edema

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System Compensation

• Mediated thru Sympathetic Nervous System: as CO drops, baroreceptors alert brain

– This causes stimulation Beta 1=>>– Stimulation Beta 2=– Activate Alpha receptors

peripherally=constriction=>>

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Compensation

• Causing S/S of CHF because: • Contractility decreases• Stroke volume and CO continue to decrease• Afterload (pressure on the other side of the

aorta) increases• Preload ( pressure caused by increase

volume to heart creating an exaggerated stretch in the muscle) increases

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Renal Compensation

• CO drops initiating renin-angiotensin mechanism– Results in powerful

vasoconstrictor

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Ventricular Hypertrophy

• The heart enlarges which results in strain

• The increase in volume causes the ventricles to dilate

• Eventually remodeling will occur

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Diagnostic Tests

• H&P• Chest x-ray• EKG:• Echocardiogram:• CBC:• CMP:• Thyroid function • ABGs• BNP=B type natriuretic peptide= hormone released in

response to Ventricular stretch ( CHF peptide) • Nuclear studies to determine heart function, EF, tissue

viability• Cardiac Cath to determine exact nature of heart

function74

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CHF Management

• Directed at: Improving LV function (Contractility) by decreasing intravascular volume and decreasing vascular resistance

• Decreasing venous return (Preload)• Decreasing BP (Afterload)• Improving gas exchange and 02• Increasing the CO and reducing anxiety

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continued

• ACE inhibitors to < afterload by dilating vessels and < BP (ARBs)

• Beta blockers to < 02 demand by reducing the contractility of the heart and HR (not given in acute period)

• Diuretics <preload by reducing volume returning to the heart-Lasix & (Aldosterone Antagonists) K+ supplement

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continued

• ASA in low doses or Plavix to help prevent blood clot formation

• Anticoagulants for those with poor EFs to prevent CVA

• Antiarrhythmics to control ectopy• Biventricular pacing (CRT=cardiac

resynchronization therapy) to improve CO• Digoxin to increase contractility of

myocardial fibers and improving cardiac output. +inotropic agent 78

Treatment of CHF

• Treat underlying cause• Rest and hi Fowlers to reduce work

load and improve ventilation• 02 at 2-6 L/min with 02 sats >92% to

increase available 02 and prevent hypoxemia

• Freq VS and cardiac monitoring79

Treatment continued• I & O q shift• Daily am weights before breakfast and after

voiding. 2-3# weight gain in 1-4 days call MD• Sodium restricted diet• Medications: to decrease intravascular volume

thus reducing venous return, dilate and reduce BP and improve contractility

• http://chfsolutions.com/zip_how_aquapheresis_works.html#

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Educating the CHF Client

• Education re: heart failure– Explanation of heart failure– Expected S/S and when to call MD– Self monitoring of daily weights– Know medications and need to take them– 2000mg sodium restricted diet – Importance of low level daily exercise

program (energy conservation)– Prognosis / advanced directives

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• Telemetry Interpretation/ Dysrhythmias

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Lead Placement

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• A dysrhythmia is a disturbance of the rhythm of the heart caused by a problem in the conduction system.

• Categorized by site of origin: atrial , AV nodal, ventricular

• Blocks are interruptions in impulse conduction: 1st, 2nd type 1&2, 3rd or complete heart block

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Each small box measures 0.041 big box (5 small boxes) is equal to a HR of 3002 big boxes is hr of 1503 big boxes is hr of 1004 big boxes is hr of 755 big boxes is hr of 606 big boxes is hr of 507 big boxes is hr of 438 big boxes is hr of 38

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• P-wave = atrial electrical activity

• QRS= ventricular electrical activity

• T wave= resting phase of ventricle

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P wave

Measures: 0.12-0.20

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Measures: 0.06-0.10

QRS WAVE

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QT Wave

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Heart rates

• NSR: heart rate is ___bpm• ST: heart rate ____ bpm• SB: heart rate ____bpm

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NSR

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Sinus rhythm

•PR interval- 0.12-0.20sec• QRS-0.06-0.10sec• QT segment 0.36-0.44

sec •Heart rate 60-100

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•Hr= 60-100 bpm•On strip it looks regular but

does not map out•PR interval= 0.12-0.20

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HR 40-60 bpm<60 bpm is acceleratedRhythm is regularPwaves not always present

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SB

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Sinus Bradycardia

• All criteria same except rate < 60bpm• S/S: dizziness, syncope, angina,

hypotension, sweating, nausea, dyspnea

• Sometimes no S/S• Treat underlying cause• IV atropine, pacemaker

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ST

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Sinus Tachycardia

• All criteria same as with NSR except rate >100• Causes: fever, dehydration, hypovolemia,

increased sympathetic nervous system stimulation, stress, exercise, AMI

• S/S: Palpations #1, angina and < CO from < V filling time

• Treatment: correct cause, eliminate caffeine, nicotine, alcohol. Beta blockers may be ordered

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Rate is usually WNLRhythm is regularPwaves are normal in size and shape The PR interval is prolonged (>0.20 sec) but constant

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www.unm.edu/~lkravitz/EKG/avblocks.html

Pwaves are normal in size and shape; Some pwaves are not followed by QRSPR interval: lengthens with each cycle until it appears without QRS Complex

then the cycle starts overQRS is usually narrow

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www.unm.edu/~lkravitz/EKG/avblocks.html

Ventricular rate is usually slowRhythm is irregularPwaves are normal in size and shape (more pwaves than QRS)PR interval is within normal limitsQRS is usually wide

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www.unm.edu/~lkravitz/EKG/avblocks.html

Ventricular rate is regular but there is no correlation between pwaves and QRSPwaves are normal in size and shapeNo true PR interval

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www.unm.edu/~lkravitz/EKG/avblocks.html

Atrial Fibrillation

Erratic wavy basePr is not measurableQRS 0.10 sec or less usuallyhttp://www.youtube.com/watch?v=VKxQgjj2yVU&feature=related

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A fib continued

• Atrial rate > 400 bpm with a varying Ventricular rate

• Overall rhythm irregular• No P waves, unable to measure PR interval• QRS=normal: Twave undeterminable• Causes: Rheumatic fever, mitral valve

stenosis, cad. HTN, MI, hyperthyroidism, COPD, CHF see pp. 604

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A fib continued

• Concern with A fib is the development of atrial thrombus and loss of atrial kick from ineffective atrial function.

• Treatment: Ca channel blockers and anti- arrhythmics to convert, beta blockers to < HR, anticoagulants to prevent embolization.

• Synchronized cardioversion

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Atrial rate of 250-450 bpm ventricular rate variesAtrial rhythm is regular ventricular rate is irregularNo identifiable p wavesP wave is not measurableQrs: 0.10 or less usually

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Pacer spike should fall before the P wave unless a dualChamber pacemaker; if it does not there could be a problem

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Extra beat Types

uniform=go the same directionmultifocal= go in different directionR on T=when the pvc fall on the preceding twavecouplet= 2 pvcs togetherbigeminy= pvc every other beattrigeminy=pvc every third beat

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Ventricular tachycardia

Monomorphic: beats are same size and shapePolymorphic: different size and shape

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This is a polymorphic VTUsually electrical imbalance in nature r/t NA+ or K+

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Ventricular Fibrillation

Rate can not be determined because of no identifiable wavesRapid chaotic rhythm with no patternNo p wavesNo PR intervalNo QRS

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Vtach/Vfib

• Both can be life threatening• VT= V HR 100-250 bpm• Causes: AMI, CAD, hypokalemia, dig toxic• S/S: palpitations, dizzy, angina, <LOC• Treatment: assess for pulse, if none, defib• VF=Rate undeterminable Cause: same• Treatment: CPR

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http://videos.reinolla.tv/winners/pe/

Hypertension

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• HTN is described as persistent elevation of arterial blood pressure greater than 140/90 on at least 2 or more readings on different dates.

• The Joint National Committee, Detection, Evaluation, and Treatment of High Blood Pressure defines normal: – BP as S < 120 mm Hg and D < 80 mm

Hg– PreHTN: SBP 120-139 DBP 80-89– Stage 1: SBP 140-159 DBP 90-99– Stage 2: SBP >160 DBP >100

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Types of Hypertension

• Essential HTN: (Primary) which is the most common 90-95% of population

• Secondary HTN: is a result of another disease, kidney, pregnancy.

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Factors that determine arterial pressure

• Cardiac output which is the volume of blood pumped by the heart in 1 minute

• Peripheral vascular resistance which is the force in the peripheral blood vessels that the left ventricular must overcome to eject blood out of the heart

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Possible Causes of PVR

• Narrowing of blood vessels, PVD, CAD, kidney disease: > renin/angiotensin =vasoconstriction

• Release of catecholamine (epinephrine and adrenalin) = vasoconstriction

• > blood volume= more work to pump• > Blood viscosity=harder to pump• Ability of blood vessel to stretch

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Causative Factors of HTN

• Hyperlipidemia Obesity• Atherosclerosis Sedentary• DM Family Hx• Cigarette smoking• Age > 60• Men• Post menapausal women

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S/S

• Often none• Occipital headache more severe

on rising• Lightheadedness• Epistaxis• Known as the ‘Silent Killer’

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Complications

• Damage to blood vessels of the eyes, heart, kidney, brain resulting in:

• Stroke• CHF• AMI• Renal failure • Blindness

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Lifestyle Change Education

• Exercise, dash diet, stop smoking, weight management and control, stress reduction, medications and recording BP frequently

• Avoid OTC meds• Instruct on how to do postural BPs

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Valvular Disorders

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• STENOSIS:

• INSUFFICIENCY:

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Stenosis

• Narrowing of the opening of the valves. Limits the amount of blood which is ejected from one chamber to the next.

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Mitral Stenosis

• Mitral valve leaflets become thickened and fibrotic. Affect women age 20-40

• CHF may develop• TX if failure develops: Digoxin, Lasix, beta

blockers, and anti arrhythmics, lo Na diet, etc• Will monitor with yearly echocardiogram• Surgery if worsens• Prophylactic antibiotics prior to invasive

procedure or dental work

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Insufficiency

• The inability of the valves to close completely.

• Allows the blood to backflow. • Mitral valve is the most commonly

affected

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Cardiac insufficiency can be caused by many factors – by a swelling of the heart muscle (1), an enlargement of the hollow chambers in the heart (2), a heart attack (3) or a blood clot (4).

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Mitral Insufficiency

• Often accompanies mitral stenosis as a result of rheumatic fever.

• Valve leaflet become rigid and shorten, prevents closure of valve.

• Hypertrophy of Left Atrium and Ventricle = L sided heart failure occurs

• Murmur heard. F/U with echocardiogram• TX: vasodilators, same as for stenosis

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Mitral Valve Prolapse

• When the Left ventricle leaflets become enlarged, and protrude into the left atrium during systole.

• Benign but may progress to Mitral insufficiency

• More common in women age 20-55

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S/S of mitral prolapse• Often none• Others experience chest pain, palpitations,

dizziness, syncope, dysrhythmias• Monitor with echocardiogram• May do heart catherization• Manage stress, beta blockers if

tachycardia

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Aortic Stenosis• Occurs when valve cusps become

fibrotic and calcify. • Most commonly caused by aging and

atherosclerosis. • Occurs most predominantly in men• Untreated will lead to Left sided CHF

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Aortic Insufficiency

• Caused primarily by rheumatic fever• May also be caused by chronic HTN• Predominantly in men• Hypertrophy of the Left ventricle and

eventually to left sided CHF• Blood may eventually back up into the

pulmonary system and lead to Right Ventricle failure

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S/S and Treatment

• Aortic murmur, tachycardia, palpitations, CHF with fatigue, SOB, ascites

• Monitored with echocardiogram assessing L ventricular dilatation

• Chest X-ray-enlargement of heart• May do cardiac cath• May need valve repair or replacement

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•Inflammatory Diseases of the Heart

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• Inflammation of the heart most often results from systemic infections and may include any layer of the heart:What are they???

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Endocarditis

• Inner layer: tends to affect the valves (Mitral=L). Organisms (Bacterial or fungal) present in blood stream and collect (colonize) on the valves: Rheumatic heart disease, congenital defects or mitral valve prolapse

• IV drug users or invasive procedures

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• Clients with known valvular disease need to be treated with prophylactic antibiotics prior to any invasive procedure including dental. Immunosuppression and any source of contamination places clients at risk

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Pathophysiology

• Bacteria may enter blood stream:• Bacteria collect on valves and

vegetate• Complications: Ventricular septal

defect, CHF(#1 cause of death) and embolization

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S/S• Fever- (99-105)• Chills and night sweats may accompany• Malaise, fatigue and weight loss• Appearance of petechiae in the mouth,

conjunctiva and legs• Chest and abdominal pain indicating

embolization

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Treatment and Diagnostics

• H&P and Lab testsCBC with diff with leukocytosis, > sed rate, blood cultures

• May have heart murmur Echocardiogram to visualize valves and vegetation

• Chest x-ray: CHF• Long term antibiotics, rest, limited activity,

prophylactic anticoagulants, valve replacement after inflammation treated

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Nursing Assessment

• Frequent VS and assess for fever• Assess for heart murmur• Note cough• Assess peripheral edema• Rest with limited activity, administer

meds in a timely manner

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Nursing Diagnosis

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• myocarditis

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• Muscle layer: Local or diffuse inflammation of the myocardium. May be viral or bacterial, an autoimmune process or drug toxicity.

• May result in cardiomyopathy=

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Pathophysiology• Characterized by degeneration and

necrosis of myocardial tissue that is different of that caused by MI

• Tissue next to necrosed area hypertrophies, loses elasticity, results in CHF and arrhythmias

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S/S

• Asymptomatic• May have fever, fatigue, sore

throat, dyspnea, muscle aches• Lymph nodes may be enlarged• Chest pain 7-10 days after virus• CHF S/S

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Diagnosis• Based on Hx, S/S, and testing-enzymes> • May hear friction rub, rales• Jugular vein distention• Chest x-ray, echocardiogram=hypertrophy• EKG=arrhythmias• Biopsy (RV) shows lymphatic infiltration

and cell necrosis

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Treatment

• Bed rest• 02• Meds: cardiac glycoside-Lanoxin,

anticoagulants, antiarrhythmic, antibiotics, steroids

• Cardiac monitoring• NI same as for endocarditis • ND same as for endocarditis

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• Pericarditis

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• Outer-surrounds heart• Inflammation of the pericardium. • Primary or secondary• Acute or chronic• Acute: virus, bacteria, fungi,

chemotherapy, MI• Chronic: TB, radiation or metastases

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Pathophysiology

• Inflammation causes an increase in the amount of pericardial fluid and inflammation of surrounding tissues.

• Fluid accumulates in the pericardial space• Adhesions may occur which causes loss of

elasticity which causes constriction and prevents adequate filling of ventricles.

• May lead to tamponade==pericardiocentesis

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Tamponade

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S/S

• Chest pain is hallmark• Most severe on inspiration, sharp,

stabbing, or dull and burning.• Pain is relieved by sitting up or

leaning forward• Dyspnea, chills and fever

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Diagnosis • WBC elevated• Serial EKG show that ST segment increases

and resolves in several weeks. A fib may occur

• Echocardiogram to see pericardial thickening and effusion

• Enzymes can be increased• Blood cultures to ID organism

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Treatment

• Analgesics• Antipyretics• Anti-inflammatory agents• Antibiotics• May need OR to create a pericardial

window to allow for drainage of fluid• NI and ND same as for endocarditis

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• Nursing the Heart Client

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Assessment

• Heart rate and rhythm, color, temperature, cognition

• Circulation: peripheral CMS checks• Vital signs to include 02 saturations

and telemetry interpretation• Subjective: c/o chest pain, SOB,

fatigue, lightheadedness, dizziness

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Nursing Diagnosis

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Ekg practice

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•www.mirule.com retrieved on 4/8/07.•Images found at www.aol.com.

Retrieved on 4/8/07.• Aehlert, B. RN BSPA (2006). EKGs

Made Easy. Mosby (3rd ed). St Louis.

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•The End

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