4. cardiovascular delfin

CARDIO VASCULAR SYSTEM

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CARDIOVASCULAR SYSTEM

Consists: heart, arteries, veins, capillaries

Functions: 1. circulation of blood

2. delivery of oxygen and other nutrients to tissues of the body 3. removal of carbon dioxide and other products of cellular metabolism

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CARDIOVASCULAR CARDIOVASCULAR SYSTEM

HEART ANATOMY and PHYSIOLOGY:

A. Heart wall1. pericardium

a. fibrous pericardium

b. serous pericardium

2. epicardium3. myocardium4. endocardium

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B. Chambers1. Atria a. right

b. left2. Ventricles a. right

b. leftC. Valves

1. Atrioventricular valvesa. Mitral valveb. Tricuspid valve

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c. Function:- permit unidirectional flow of blood

from specific atrium to specific ventricle during ventricular diastole

- prevent reflux during ventricular systole

- valve leaflets open during ventricular diastole and close during ventricular systole; valve closure produces the first heart sounds (S1)

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2. Semilunar valvesa. Pulmonary valveb. Aortic valvec. Function:

- permit unidirectional flow of blood from specific ventricle to arterial vessel during ventricular systole

- prevent reflux during ventricular diastole- valves open when ventricles contract

and close during ventricular diastole; valve closure produces the second heart sound (S2)04/11/2304/11/23 sdelfin2010sdelfin2010

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D. Conduction System1. Sinoatrial (SA) node2. Internodal Tracts3. Atrioventricular (AV) node4. Bundle of His

- right bundle branch- left bundle branch

5. Purkinje fibers* Electrical activity of heart can be visualized by ECG

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CONDUCTION SYSTEMCONDUCTION SYSTEM

DIASTOLE-DIASTOLE- consist of relaxation and consist of relaxation and filling of the atria and ventricles.filling of the atria and ventricles.

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

SA NODE- SA NODE- main regulator of HRmain regulator of HR

- transmit impulse to the surrounding - transmit impulse to the surrounding atrial muscle.atrial muscle.

AV NODE- AV NODE- transmit impulses to the transmit impulses to the surrounding ventricular muscle.surrounding ventricular muscle.

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CONDUCTION SYSTEMCONDUCTION SYSTEM

BUNDLE OF HIS- BUNDLE OF HIS- continuation of AV continuation of AV Node and has a left and right Node and has a left and right bundles and fuse with purkinje bundles and fuse with purkinje fibers.fibers.

PURKINJE FIBERS- PURKINJE FIBERS- terminal terminal branches of the conduction system branches of the conduction system and are responsible for carrying the and are responsible for carrying the wave of depolarization to both wave of depolarization to both ventricular walls.ventricular walls.

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E. Coronary Circulation1. Arteries

a. right coronary arteryb. left coronary artery

2. Veinsa. coronary sinus veinsb. thebesian veins

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VASCULAR SYSTEMFunction: a. supply tissues with bloodb. remove wastesc. carry unoxygenated blood back to the heart

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TYPES OF BLOOD VESSELSA. ArteriesB. ArteriolesC. Capillaries: the following exchanges occur:

- oxygen and carbon dioxide- solutes between the blood and tissues- fluid volume transfer between the

plasma and interstitial spacesD. VenulesE. Veins

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CARDIAC OUTPUT CARDIAC OUTPUT CO= SV x HRCO= SV x HR

CARDIAC OUTPUT- CARDIAC OUTPUT- is the volume of is the volume of blood (in liters) ejected by the heart blood (in liters) ejected by the heart each minute. CO ranges from 4L to each minute. CO ranges from 4L to 7L/ min.7L/ min.

STROKE VOLUMESTROKE VOLUME-is the amount of -is the amount of blood ejected by the left ventricle. SV blood ejected by the left ventricle. SV ranges from 60-100 ml/min.ranges from 60-100 ml/min.

Example: Example: HR 80 bpm X SV 80 ml/min =6400ml or 6.4 LHR 80 bpm X SV 80 ml/min =6400ml or 6.4 L04/11/2304/11/23 sdelfin2010sdelfin2010

PRELOAD-PRELOAD- the filing of the the filing of the ventricles at the end of diastole. ventricles at the end of diastole. The more ventricles fill, the more The more ventricles fill, the more the cardiac muscles are the cardiac muscles are stretched, the greater the force of stretched, the greater the force of the contraction during systole the contraction during systole ( Starling’s law). If there is a ( Starling’s law). If there is a decrease in the preload, then decrease in the preload, then there is a decrease in contractility there is a decrease in contractility and in cardiac output.and in cardiac output.

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AFTER LOAD- AFTER LOAD- the pressure in the the pressure in the aorta that the ventricle must aorta that the ventricle must overcome to pump blood into the overcome to pump blood into the systemic circulation. A decrease in systemic circulation. A decrease in the afterload causes a decrease in the afterload causes a decrease in the workload of the ventricles; this the workload of the ventricles; this in turn will assist to increase the in turn will assist to increase the stroke volume and the cardiac stroke volume and the cardiac output.output.

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ASSESSMENT HEALTH HISTORYA. Presenting problem

1. Nonspecific symptoms may include- fatigue - shortness of breath- cough - palpitations- headache - weight loss/gain- syncope - difficulty sleeping- dizziness - anorexia

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2. Specific signs and symptomsa. chest painb. dyspnea (shortness of breath)c. orthopnea / paroxysmal nocturnal dyspnead. palpitations: precipitating factorse. edemaf. cyanosis

B. Lifestyle: occupation, hobbies, financial status, stressors, exercise, smoking, living conditions

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C. Use of medications: OTC drugs, contraceptives, cardiac drugs

D. Nutrition: dietary habits, cholesterol, salt intake, alcohol consumption

E. Past Medical History ( RHD, MI, HPN, STD, CVA)

F. Family history: heart disease (congenital, acute, chronic); risk factors (DM, hypertension, obesity)

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PHYSICAL EXAMINATIONA. Skin and mucous membranes: - color/texture, temperature, hair distribution

on extremities, atrophy or edema, petechiaeB. Peripheral pulses: - palpate and rate all arterial pulses

(temporal, carotid, brachial, radial, femoral, popliteal, dorsalis pedis and posterior tibial) on scale of: 0=absent, 1=palpable, 2=normal, 3=full, 4=full and bounding

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C. Assess for arterial insufficiency and venous impairment

D. Measure and record blood pressureE. Inspect and palpate the neck vessels:

a. jugular veins: note location, characteristics, jugular venous pressureb. carotid arteries: location and characteristics

F. Auscultate heartsounds - normal (S1, S2)- abnormal (S3, S4)

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AREAS FOR AREAS FOR AUSCULTATIONAUSCULTATION

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LABORATORY / DIAGNOSTIC TESTSNON-INVASIVE A. Blood Chemistry and electrolyte analysis 1. Cardiac enzymes: in MI

a. Troponin T: detected 3-12 hours after chest pain NV=<0.2 ng/mlb. Troponin I: detected 3-12 hrs NV= <0.03bg/dlc. Creatine phosphokinase (CPK – MB): 6-12Hrs NV=by ratiod. Aspartate aminotransferase (AST) (SGOT): 24 Hrs after chest pain NV=7-40 U/mle. Lactic dehydrogenase (LDH): 36 Hrs NV=14%- 26%

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2. Electrolytesa. Sodium (Na) 135-145meq/L

- hyponatremia: fluid excess- hypernatremia: fluid deficit

b. Potassium (K) 3.5-5 meq/L- inc. or dec. levels can cause

dysrhythmiasc. Magnesium (Mg) 1.3-2.1 meq/L

- dec. levels can cause dysrhythmias

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d. Calcium (Ca) 4.5-5.3 meq/L:- For blood clotting and neuromuscular

activity- dec. levels cause tetany, inc. levels

causes muscle atony- dec. and inc. levels cause dysrhythmias

3. Serum Lipidsa. Total Cholesterol 150-200mg/dl:

- high levels predispose to atherosclerotic HD

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b. High density lipids (HDL) 30-85 mg/dl- low levels predispose to CVD

c. Low density lipids (LDL) 50-140 mg/dl:- high levels predispose to

atherosclerotic plaque formationd. Triglycerides 10-150 mg/dl:

- high levels increase risk of atherosclerotic heart disease

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B. Hematologic Studies1. CBC2. Coagulation time: 5-15mins; inc. levels indicate bleeding tendency, used to monitor heparin tx.3. Prothrombin time (PT) 9.5-12sec.; used to monitor warfarin tx.4. Activated partial thromboplastin time (APTT) 20-45sec; used to monitor heparin therapy5. Erythrocyte sedimentation rate(ESR) <20mm/hr; inc. level indicate inflamm. process

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C. Urine Studies (routine U/A)D. Electrocardiogram (ECG)

1. Noninvasive ECG – a graphic record of the electrical activity of the heart2. Portable recorder (Holter monitor) – provides continuous recording of ECG for up to 24 hrs.

E. Exercise ECG (stress test): the ECG is recorded during prescribed exercise; may show heart disease when resting ECG does not

F. Echocardiogram: noninvasive recording of the cardiac structures using ultrasound

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STRESS TESTSTRESS TEST

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Nursing intervention:Nursing intervention:

Cardiac monitoringCardiac monitoring Invasive diagnostic testInvasive diagnostic test ECGECG Hemodynamic monitoringHemodynamic monitoring Swan gans cathetherSwan gans cathether Central venous pressureCentral venous pressure

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INVASIVE DIAGNOSTICS

G. Cardiac catheterization: invasive, but often definitive test for diagnosis of cardiac disease.1. A catheter is inserted into the right or left side of the heart to obtain information2. Purpose: to measure intracardiac pressures and oxygen levels in various parts of the heart; -with injection of a dye, it allows visualization of the heart chambers, blood vessels and blood flow (angiography)04/11/2304/11/23 sdelfin2010sdelfin2010

Cardiac Catheterization.mp4

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3. Nursing care: prior to the test- informed consent- any allergies esp. to iodine- keep client on NPO for 8-12 hrs- record height, weight, V/S- inform client that a feeling of warmth

and fluttering sensation as catheter is inserted

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4. Nursing care: post test- assess circulation to the extremity

used for catheter insertion- check peripheral pulses, color,

sensation of affected extremity- if protocol requires, keep affected

ext. straight for approx. 8 hrs.- observe catheter insertion site for

swelling, bleeding- assess V/S and report for sig.

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H. Coronary arteriography1. visualization of coronary arteries

by injection of radiopaque contrast dye and recording on a movie film.

2. Purpose: evaluation of heart disease and angina, location of areas of infarction and extent of lesions, ruling out coronary artery disease in clients with MI.

3. Nursing care: same as cardiac catheterization

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Coronary arteriography

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Hemodynamic Hemodynamic monitoringmonitoring Assessment of the patient’s Assessment of the patient’s

circulatory status and it includes:circulatory status and it includes:

1.1. Measurement of heart rateMeasurement of heart rate

2.2. Intra-arterial pressureIntra-arterial pressure

3.3. Pulmonary arteryPulmonary artery

4.4. Cardiac outputCardiac output

5.5. Blood volumeBlood volume04/11/2304/11/23 sdelfin2010sdelfin2010

HEMODYNAMIC MONITORING(Swan Ganz Catheter)A. A multilumen catheter with a balloon tip that is

advanced through the superior vena cava into the RA, RV, and PA. When it is wedged it is in the distal arterial branch of the pulmonary artery.

B. Purpose:1. Proximal port: measures RA pressure 2. Distal port:

a. measures PA pressure and PAWP b. normal values: PA systolic and

diastolic less than 20mmHg; PAWP 4-12mmHg

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PLANNING AND IMPLEMENTATION

C. Nursing care1. a sterile dry dressing should be applied to site and changed every 24 hours; inspect site daily and report signs of infection2. if catheter is inserted via an extremity, immobilize extremity to prevent catheter dislodgment or trauma.

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CENTRAL VENOUS PRESSURE (CVP)A. Obtained by inserting a catheter into the

external jugular, antecubital, or femoral vein and threading it into the vena cava. The catheter is attached to an IV infusion and H2O manometer by a three way stopcock

B. Purposes:1. Reveals RA pressure, reflecting alterations in the RV pressure

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2. Provides information concerning blood volume and adequacy of central venous return3. Provides an IV route for drawing blood samples, administering fluids or medication, and possibly inserting a pacing catheter

C. Normal range is 5-12 cmH20; elevation indicates hypervolemia, decreased level indicates hypovolemia

EVALUATION

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INTERVENTIONSCARDIAC MONITORINGA. ECG Indications for ordering an ECG:1. To determine cardiac rate2. To accurately define cardiac rhythm3. To diagnose old or new myocardial

infarction4. To identify intracardiac conduction

disturbances5. To aid in the diagnosis of ischemic HD,

pericarditis, myocarditis, electrolyte imbalances, and pacemaker malfunction.

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Impulse generationImpulse generation

Resting state- Resting state- cells is ready to cells is ready to receive an impulse.receive an impulse.

DepolarizationDepolarization- flow of electrical - flow of electrical along the cardiac membrane, along the cardiac membrane, initiating muscle contraction.initiating muscle contraction.

RepolarizationRepolarization- cells regain the - cells regain the electrical charge and are electrical charge and are returned to a resting state.returned to a resting state.

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1. strip: small square: 0.04secs. large square: 0.2secs.

2. P wave: produced by atrial depolarization; indicates SA node function

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3. P-R interval (N˚= 0.12 - 0.20 secs.)a. indicates AV conduction time or the time it takes an impulse to travel from the atria down and through the AV nodeb. measured from beginning of P wave to beginning of QRS complex

4. QRS complex (N˚= 0.06-0.10 secs.)a. indicates ventricular depolarizationb. measured from onset of Q wave to end of S wave

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5. ST segmenta. indicates time interval between complete depolarization of ventricles and repolarization of ventriclesb. measured after QRS complex to beginning of T wave

6. T wavea. represents ventricular repolarizationb. follows ST segment

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Normal ECGNormal ECG

P

Q S

R

T

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NORMAL SINUS.MP43d animation of a cardiac cycle + electrical activity.mp4

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Position of Chest Position of Chest LeadsLeadsLeads Position in the Leads Position in the

chestchest

V1 4V1 4thth ICS at the RSB ICS at the RSB

V2 4V2 4thth ICS at the LSB ICS at the LSB

V3 Halfway between V2 & V3 Halfway between V2 & V4V4

V4 5V4 5thth ICS at the MCL ICS at the MCL

V5 5V5 5thth ICS at the LAAL ICS at the LAAL

V6 5V6 5thth ICS at the LMAL04/11/2304/11/23 sdelfin2010sdelfin2010

DISORDERS OF THE CARDIOVASCULAR

SYSTEMHEARTCORONARY ARTERY DISEASE (CAD)A. General Information

1. refers to a variety of pathology that cause narrowing or obstruction of the coronary arteries, resulting in decreased blood supply to the myocardium2. major causative factor: Atherosclerosis3. bet 30-50 y.o., men>women4. may manifest as angina pectoris or MI

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CORONARY ARTERY DISEASE

5. Risk factors: - family history of CAD - DM- el. Serum lipoproteins - hypertension- cigarette smoking - obesity- el. serum uric acid - lifestyle

B. Medical management, assessment findings and nursing interventions – Angina pectoris and MI

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ANGINA PECTORIS

A. Gen. info:1. transient, paroxysmal chest pain produced by insufficient blood flow to the myocardium resulting in myocardial ischemia2. Risk factors:- CAD - DM- hypertension - aortic insufficiency- severe anemia - atherosclerosis- thromboangiitis obliterans

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ANGINA PECTORIS3. Precipitating factors: 5 E’s- Exertion- Exposure to cold- Emotion- Excessive eating- Excessive smoking

B. Medical mgt:1. Drug therapy: nitrates, beta adrenergic blocking agents, and/or calcium blocking agents, lipid reducing drugs if cholesterol is elevated

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ANGINA PECTORIS

2. Lifestyle modification 3. Surgery: coronary bypass surgery

C. Assessment Findings:1. Pain: substernal with possible radiation to the neck, jaw, back and arms, relieved by REST2. Palpitations, tachycardia, dyspnea, diaphoresis3. el. serum lipid levels

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ANGINA PECTORIS

4. Diagnostic tests:- ECG may reveal ST segment depression and T-wave inversion during chest pain- Stress test may reveal an abnormal ECG during exercise

D. Nursing interventions:1. administer oxygen2. give prompt pain relief with nitrates or narcotic analgesics as ordered.

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ANGINA PECTORIS

3. Monitor V/S, status of cardiopulmonary function, monitor ECG4. place patient in semi-high Fowler’s position5. provide emotional support, health teachings and discharge instructions.6. Instruct client to notify physician immediately if pain occurs and persists, despite rest and medication administration.

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MYOCARDiAL INFARCTiON

A. General information:1. The death of myocardial cells from inadequate oxygenation, often caused by a sudden complete blockage of a coronary artery; characterized by localized formation of necrosis (tissue destruction) with subsequent healing by scar formation and fibrosis.2. Risk factors: - atherosclerotic CAD - DM- thrombus formation - hypertension

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B. Assessment findings:1. Pain same as in angina, crushing, viselike with sudden onset; UNRELIEVED by rest or nitrates2. nausea/vomiting “indigestion”, dyspnea3. skin: cool & clammy4. elevated temperature5. initial increase in BP and pulse, with gradual drop in BP6. Restlessness

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7. Diagnostic tests:a. elevated WBC, cardiac enzymes (troponin, CPK-MB, LDH, SGOT)b. ECG changes (specific changes dependent on location of myocardial damage and phase of the MI; inverted T wave and ST segment changes seen with myocardial ischemiac. inc. ESR, el. serum cholesterol

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Acute myocardial injury: Acute myocardial injury: Inc. ST elevation, T wave Inc. ST elevation, T wave

invertioninvertion

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Old MI (healed/ scarred) : Old MI (healed/ scarred) : Normal ST & T Waves, Q Normal ST & T Waves, Q

wave persistswave persists

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Myocardial Infarction- Animation.mp4

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C. Nursing interventions:1. establish a patent IV line2. provide pain relief; morphine sulfate IV 3. Administer O2 as ordered to relieve dyspnea and prevent arrhythmias 4. Provide bed rest with semi fowler’s position 5. Monitor ECG and hemodynamic procedures6. Administer anti-arrhythmias as ordered.

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7. Monitor I & O, report if UO <30 ml/hr8. Maintain full liquid diet with gradual increase to soft, low salt9. Maintain quiet environment10. Administer stool softeners as ordered11. Relieve anxiety associated with CCU environment12. Administer anticoagulants, thrombolytics (tpa or streptokinase) as ordered and monitor for S/E

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13. Provide client teaching and discharge instruction concerning:- effects of MI, healing process and treatment regimen- Medication regimen: name, purpose, schedule, dosage, S/E- Risk factors with necessary lifestyle modification- Dietary restrictions: low salt, low cholesterol, avoidance of caffeine- Resumption of sexual activity as ordered (usually 4-6weeks)

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- Need to report the ff. symptoms:* increased persistent chest pain* pain, dyspnea, weakness, fatigue* persistence palpitations, light

headedness- Enrollment of client in a cardiac rehabilitation program

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PERCUTANEOUS TRANSLUMINAL

CORONARY ANGIOPLASTY (PTCA)

A. General information:1. PTCA can be performed instead of coronary artery bypass graft surgery in various clients with single vessel CAD.2. Aim: revascularize the myocardium

decrease angina – increase survival3. a balloon tipped catheter is inserted into the stenotic, diseased coronary artery. The balloon is inflated with a controlled pressure and thereby decreases the stenosis of the vessel

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Coronary Stent Animation.mp4

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CORONARY ARTERY BYPASS SURGERY

A. General information:1. A coronary artery bypass graft is the surgery of choice for clients with severe CAD2. new supply of blood brought to diseased/occluded coronary artery by bypassing the obstruction with a graft that is attached to the aorta proximally and to the coronary artery distally3. Procedure requires use of extracorporeal circulation (heart-lung machine, cardiopulmonary bypass) cORONARY aRTERY bYPASS gRAFT 2.mp4

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heart-lung machine

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B. Nursing interventions: preoperative1. Explain anatomy of the heart, function of coronary arteries, effects of CAD2. Explain events of the day of surgery3. Orient to the critical and coronary care units and introduce to staff4. Explain equipments to be used (monitors, hemodynamic procedures, ventilators, ET, etc)5. Demonstrate activity and exercise6. Reassure availability of pain medications

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C. Nursing interventions: post-operative1. Maintain patent airway2. Promote lung re-expansion3. monitor cardiac status4. maintain fluid and electrolyte balance5. maintain adequate cerebral circulation6. provide pain relief7. prevent abdominal distension

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8. Monitor for and prevent the ff. complications:a. Thrombophlebitis / pulmonary

embolismb. Cardiac tamponadec. arrhythmiasd. CHF

9. Provide client teaching and discharge planning concerning:

a. limitation with progressive increase in activities

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b. sexual intercourse can usually be resumed by 3rd or 4th week post-op

c. medical regimend. meal planning with prescribed

modificationse. Symptoms to be reported: - fever, dyspnea, chest pain with

minimal exertionCORONARY BYPASS SURGERY real .mp4

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DYSRHYTHMIAS

An arrhythmia is a disruption in the normal events of the cardiac cycle. It may take a variety of forms.

Treatment varies on the type dysrhythmias

SINUS TACHYCARDIAA. General Information:

1. A heart rate of over 100 beats/min, originating in the SA node

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DYSRHYTHMIAS

2. May be caused by:- fever - anemia- apprehension - hyperthyroidism- physical activity - myocardial ischemia- caffeine - drugs (epi., theo)

B. Assessment findings:1. Rate: 100-160 beats /min2. Rhythm: regular

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DYSRHYTHMIAS

3. P wave: precedes each QRS complex with normal contour4. P-R interval: normal (0.08 sec)5. QRS complex: normal (0.06 sec)

C. Treatment;- correction of underlying cause, elimination of stimulants, sedatives, propranolol (Inderal)

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Sinus tachycardiaSinus tachycardia

SINUS TACH.mp4

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DYSRHYTHMIAS

SINUS BRADYCARDIAA. General Information:

1. A slowed heart rate initiated by SA node2. Caused by:- excessive vagal or decreased sympathetic tone - MI - IC tumors- meningitis- cardiac fibrosis

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DYSRHYTHMIAS

B. Assessment findings:1. Rate: <60 beats/min2. Rhythm: regular3. P wave: precedes each QRS with a normal contour4. P-R interval: normal5. QRS complex: normal

C. Treatment: usually not needed- if cardiac output is inadequate: atropine and isoproterenol; pacemaker

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Sinus BradycadiaSinus Bradycadia

SINUS BRADY.mp4

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DYSRHYTHMIAS

ATRIAL FIBRILLATIONA. General information

1. An arrhythmia in which ectopic foci cause rapid, irregular contractions of the heart2. seen in clients with - rheumatic mitral stenosis - thyrotoxicosis- cardiomyopathy - pericarditis- hypertensive heart disease - CHD

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DYSRHYTHMIAS

B. Assessment findings:1. Rate: 350-600 beats/min2. Rhythm: atrial and ventricular regularly

irregular3. P wave: no definite P wave; 4. P-R interval: not measurable5. QRS complex: generally normal

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Atrial FibrillationAtrial Fibrillation ATRIAL FIB.mp4

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DYSRHYTHMIAS

C. Treatment: digitalis preparations, propanolol, verapamil in conjunction with digitalis; direct current cardioversion

PREMATURE VENTRICULAR CONTRACTIONSA. General Information:

1. Irritable impulses originate in the ventricles2. Caused by:- electrolyte imbalance (hypokalemia)- digitalis drug therapy

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DYSRHYTHMIAS

Cont’d: (causes)- stimulants( caffeine, epinephrine, isoproterenol)- hypoxia- CHF

B. Assessment findings:1. Rate: varies according to no. of PVC’s2. Rhythm: irregular because of PVC’s3. P wave: normal; however, often lost in QRS complex

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DYSRHYTHMIAS

4. P-R interval: often not measurable5. QRS complex: greater then 0.12secs, wide

C. Treatment: 1. IV push of Lidocaine (50-100mg) followed by IV drip of lidocaine at rate of 1-4 mg/min2. Procainamide, quinidine3. Treatment of underlying cause

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PVCPVC PVC'S & ARREST.mp4

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DYSRHYTHMIAS

VENTRICULAR TACHYCARDIAA. General information:

1. 3 or more consecutive PVC’s; occurs from repetitive firing of an ectopic focus in the ventricles2. caused by:- MI - CAD- digitalis intoxication - hypokalemia

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DYSRHYTHMIAS

B. Assessment findings:1. Rate: ventricular: 110-250 beats/min2. Rhythm: atrial(regular), ventricular (occly. irregular) 3. P wave: often lost in QRS complex4. P-R interval usually not measurable5. QRS complex: greater than 0.12 secs, wide

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Ventricular Ventricular TachycardiaTachycardia

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DYSRHYTHMIAS

C. Treatment:1. IV push of lidocaine (50-100mg), then IV drip of lidocaine 1-4 mg/min2. Procainamide via IV infusion of 2-6 mg/min3. direct current cardioversion4. bretylium, propanolol

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CONGESTIVE HEART FAILURE

A. Gen. Info:- Inability of the heart to pump an adequate supply of blood to meet the metabolic needs of the body

B. Types:1. Left sided heart failure2. Right sided heart failure

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1. LEFT SIDED HEART FAILUREa. Left ventricular damage causes blood to back up through the left atrium and into the pulmonary veins. Increased pressure causes transudation into the interstitial tissues of the lungs with resultant pulmonary congestionb. Caused by:- left ventricular damage (MI, CAD)- hypertension, aortic valve disease (AS)- mitral stenosis, cardiomyopathy

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c. Assessment findings:Signs:- easy fatigability, dyspnea on exertion, PND, orthopnea, cough, nocturia, confusion

Symptoms:- S3 gallop, tachycardia, tachypnea, rales, wheezing, pleural effusion

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d. Diagnostic tests:- ECG, chest x-ray (cardiomegaly, pleural effusion), echocardiography, cardiac catheterization

2. RIGHT SIDED HEART FAILUREa. weakened RV is unable to pump blood into the pulmonary system; systemic venous congestion occurs as pressure builds up.

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b. caused by:- left sided heart failure- RV infarction- atherosclerotic heart disease- COPD, pulmonic stenosis, pulmonary embolism

c. Assessment findings:Symptoms:- easy fatigability, lower extremity swelling, RUQ discomfort

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Signs:- elevated jugular venous pressure, hepatomegaly, ascites, lower extremity edema

d. Diagnostic tests:- chest x-ray: reveals cardiac hypertrophy- echocardiography: indicates inc. size of cardiac chambers- elevated CVP, dec. PO2, inc. ALT(SGPT)

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C. Medical Management:1. determination and elimination/control of underlying cause2. Drug therapy:- Diuretics: Furosemide, Spironolactone- Dilators: ACE inhibitors, nitrates- Digitalis: digoxin3. Diet: low salt, low cholesterol

* If medical therapies unsuccessful, mechanical assist devices (intra-aortic balloon pump), cardiac transplantation or mechanical hearts may be employed.

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D. Nursing Interventions:1. Monitor respiratory status and provide adequate ventilation (when CHF progresses to pulmonary edema)2. Provide physical and emotional rest3. Increase cardiac output4. Reduce/eliminate edema5. Provide client teaching and discharge planning

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CARDIAC ARREST

A. General Info:- sudden, unexpected cessation of breathing and adequate circulation of blood by the heart

B. Medical management:1. Cardiopulmonary resuscitation (CPR)2. Drug therapy:

a. lidocaine, procainamide, verapamilb. Dopamine, isoproterenol,

Norepinephrine

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CARDIAC ARREST

c. Epinephrine to enhance myocardial automaticity, excitability, conductivity, and contractilityd. Atropine sulfate to reduce vagus nerve’s control over the heart, thus increasing the heart ratee. Sodium bicarbonate: administered during first few moments of a cardiac arrest to correct respiratory and metabolic acidosisf. Calcium chloride: calcium ions help the heart beat more effectively by enhancing the myocardium's contractile force

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3. Defibrillation

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CARDIAC ARRESTC. Assessment findings:

- unresponsiveness, cessation of respiration, pallor, cyanosis, absence of heart rate/ BP/pulses, dilation of pupils, ventricular fibrillation

D. Nursing interventions:1. Begin precordial thump and if successful, administer lidocaine2. If unsuccessful, defibrillation - CPR3. Assist with administration of and monitor effects of emergency drugs

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CARDIOPULMONARY RESUSCITATION

A. General info: process of externally supporting the circulation and respiration of a person who has had a cardiac arrest

B. Nursing interventions: unwitnessed cardiac arrest1. Assess LOC

a. Shake victim’s shoulder and shoutb. if no response, summon for help

2. Position victim supine on a firm surface

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C P R

3. Open airwaya. Use head tilt, chin lift maneuverb. Place ear into nose and mouth- look to see if chest is moving- listen for escape of air- feel for movement of air against

facec. If no respiration, proceed to #4

4. Ventilate twice, allowing for deflation between breaths

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C P R

5. Assess circulation: if not present, proceed to #66. Initiate external cardiac compressionsa. Proper placement of hands: lower half of the sternumb. Depth of compressions: 1½ - 2 in. for adultsc. One rescuer: 15 compressions (80-100/min) with 2 ventilationsd. Two rescuers: 5 compressions (80-100/min)with 1 ventilation04/11/2304/11/23 sdelfin2010sdelfin2010

WHEN TO S.T.O.P. CPRWHEN TO S.T.O.P. CPR

1.1. SPONTANEOUSSPONTANEOUS signs of circulation are signs of circulation are restored.restored.

2. TURNED 2. TURNED over to medical services or properly over to medical services or properly trained and authorized personnel.trained and authorized personnel.

3. OPERATOR 3. OPERATOR is already exhausted and cannot is already exhausted and cannot continue CPR.continue CPR.

4. PHYSICIAN 4. PHYSICIAN assumes responsibility (declares assumes responsibility (declares death, take over, etc.).death, take over, etc.).

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INFLAMMATORY DISEASES OF THE

HEARTENDOCARDITISA. General Info:

1. Inflammation of the endocardium; platelets and fibrin deposit on the mitral and/or aortic valves causing deformity, insufficiency or stenosis 2. caused by bacterial infection:- commonly S. aureus. S. viridans, B hemolytic streptococcus, gonococcus

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ENDOCARDITIS

B. Medical management:1. Drug therapy:

a. antibiotics specific to sensitivity or organism cultured

b. PenG and streptomycin if org. not known

c. antipyretics2. Cardiac surgery to replace valve

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ENDOCARDITIS

C. Assessment findings:1. Fever, malaise, fatigue, dyspnea and cough acute upper quadrant pain, joint pain2. petechiae, murmurs, edema, splenomegaly, hemiplegia and confusion, hematuria3. elevated WBC & ESR, decreased Hgb & Hct.4. Diagnostic tests: positive blood culture for causative organism

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ENDOCARDITIS

D. Nursing interventions:1. antibiotics as ordered2. control temperature3. assess for vascular complications and pulm. embolism4. Provide client teaching and discharge planning

- types of procedures, antibiotic therapy- S/S to report: persistent fever, fatigue, chills, anorexia, joint pains- avoidance of individuals with known infections

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MYOCARDITIS

A. General Info: an acute or chronic inflammation of the myocardium as a result of pericarditis, systemic infection or allergic response.

B. Assessment:- fever, pericardial friction rub, - murmur, signs of heart failure, fatigue, dyspnea- tachycardia, chest pain

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MYOCARDITIS

C. Implementation:1. Assist client to assume a position of comfort2. Administer analgesics, salicylates, NSAIDS3. Administer O2, provide adequate rest periods4. Limit activities, to dec. workload of heart5. Treat underlying cause6. Administer meds. as ordered:- antibiotics, diuretics, ACE inhibitors, digitalis 7. Monitor complications: thrombus, heart failure, cardiomyopathy

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PERICARDITIS

A. General Info: 1. An inflammation of the visceral and parietal pericardium2. caused by bacterial, viral, or fungal infection; collagen diseases; trauma; acute MI, drugs (procainamide, hydralazine, Doxorubicin HCL)

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PERICARDITIS

B. Medical management:1. Determination and elimination/control of underlying cause2. Drug therapya. Medication for pain reliefb. Corticosteroids, *salicylates (aspirin), indomethacin, to reduce inflammation3. Specific antibiotic therapy against the causative organism may be indicated

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PERICARDITIS

C. Assessment findings:1. chest pain with deep inspiration (relieved by sitting up), cough, hemoptysis, malaise2. tachycardia, fever, pericardial friction rub, cyanosis or pallor, jugular vein distension3. Elevated WBC and ESR, normal or inc. SGOT4. Diagnostic test:

a. chest x-ray may show increased heart size

b. ECG: ST elevation, T wave inversion

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PERICARDITIS

D. Nursing Interventions:1. Ensure comfort, bed rest with semi- or high Fowler’s position2. Monitor hemodynamic parameters 3. Administer medications as ordered and monitor effects4. Provide client teaching and discharge planning:- S/S of pericarditis indicative of recurrence (chest pain intensified by lying down and relieved when sitting up; medication regimen

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HAVE A HAVE A BREAK… BREAK…

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CONGENITAL HEART DISEASE (CHD)

A. General Info:1. CHDs are structural defects of the heart, great vessels, or both that are present from birth2. 2nd only to prematurity as a cause of death in the first year of life

B. Clinical Classification of Congenital heart disease1. Acyanotic: PDA, ASD, VSD2. Cyanotic: TOF, TGV, Truncus arteriosus3. Obstructive: Coarctation of Aorta, AS, PS

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ACYANOTIC CHD (PDA)

ACYANOTIC CHDA. PATENT DUCTUS ARTERIOSUS (PDA)

- results when the fetal ductus arteriosus fails to close completely after birth

1. Pathophysiology- blood flows from the aorta through the PDA and back to the pulmonary artery and lungs, causing inc. LV workload and increase pulmonary vascular congestion

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ACYANOTIC CHD (PDA)

2. Assessment findings:a. Clinical manifestations:

1. if defect is small, child may be aysmptomatic

2. a loud machine like murmur is characteristic

3. child may have frequent resp. infections4. child may have CHF with poor feeding,

fatigue, poor weight gain, tachypnea and irritability

5. widened pulse pressure and bounding pulse rate maybe detected

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ACYANOTIC CHD (PDA)b. Laboratory and diagnostic findings:

1. ECG – normal but may show ventricle enlargement if the shunt is large

3. Nursing management:a. Provide family teaching abt. treatment options- some close spont; others can be closed surgically or nonsurgicallyb. In premature infants, PDA sometimes can be closed using prostaglandin synthetase inhibitors (Indomethacin) w/c stimulate closure of the ductus arteriosus

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ACYANOTIC CHD (ASD)

B. ATRIAL SEPTAL DEFECT- an abnormal communication between the atria; results when the atrial septal tissue does not fuse properly during embryonic devt.

1. Pathophysiologya. pressure is higher in the left atrium than the right, causing blood to shunt from left to rightb. the RV and PA enlarge because they are handling more blood

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ACYANOTIC CHD (ASD)

2. Assessment findings:a. Clinical manifestations:- most infants tend to be aysmptomatic until early childhood and many defects close spont. By 5y.o.- symptoms vary with the size of the defect, fatigue and dyspnea on exertion are the most common- slow weight gain and frequent respiratory infections may occur- systolic ejection murmur may be auscultated, usually most prominent at the 2nd ICS

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ACYANOTIC CHD (ASD)

b. Laboratory and diagnostic study findings:- echocardiography with doppler gen. reveals the enlarged R side of the heart and the inc. pulmonary circulation

- cardiac catheterization demonstrates the separation of the R atrial septum and the inc. oxygen saturation in the R atrium

3. Nursing management:a. Provide family teaching abt. treatment options:- defects are usually repaired in girls due to possibility of clot formation during child bearing years- small ASDs are left open in boys, larger ones are repaired- surgical closure is performed during the school age years

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ACYANOTIC CHD (VSD)

C. VENTRICULAR SEPTAL DEFECT- the most common CHD, is an abnormal opening between the right and left ventricles- the degree of this defect vary from a pinhole between the R & L ventricles to an absent septum

1. Pathophysiologya. pressure from the LV causes blood to flow through the defect to RV, resulting in increased pulmonary vascular resistance and right heart enlargement

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ACYANOTIC CHD (VSD)

b. RV and PA pressures increase, leading eventually to obstructive pulmonary vascular disease

2. Assessment findings:- symptoms vary with the size of the defect, age and amt of resistance, usually the child is asymp.- failure to thrive, excessive sweating, fatigue- more susceptible to pulmonary infections- may exhibit s/s of CHF

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ACYANOTIC CHD (VSD)

b. Laboratory and diagnostic study findings:- Echocardiography with Doppler U/S or MRI reveals RVH and possible PA dilatation from the inc. blood flow

- ECG shows RVH

3. Nursing managementa. provide family teaching abt treatment options- some VSDs close spontaneously

- others are closed with a Dacron patch, recommended for large defects, PA hypertension, CHF, recurrent resp. infxns. FTT

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CYANOTIC CHD (TOF)

CYANOTIC CHDCYANOTIC CHDA. TETRALOGY OF FALLOT (TOF)

- consists of 4 major anomalies:a. VSD c. PSb. RVH d. overriding aorta

1. Pathophysiology a. PS impedes the flow of blood to the lungs, causing increased pressure in the RV, forcing deoxygenated blood through the septal defect to the LV

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CYANOTIC CHD (TOF)

b. the increased workload on the RV causes hypertrophy. The overriding aorta receives blood from both right and left ventricles.

2. Assessment findings:a. Clinical manifestations: vary, depending on the size of the VSD and the degree of PS.

1. Acute episodes of cyanosis (“tet spells”) and transient cerebral ischemia. “Tet spells” are char. By irritability, pallor, and blackouts or convulsions.

2. Cyanosis occurring at rest (as PS worsens)

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CYANOTIC CHD (TOF)

3. Squatting (a char. posture of older children that serves to decrease the return of poorly oxygenated venous blood from the lower extremities and to inc. SVR, w/c increases pulmonary blood flow and eases respiratory effort)

4. slow weight gain5. clubbing, exertional dyspnea, fainting, or

fatigue slowness due to hypoxia6. a murmur may be heard at the mid-

lower left sternal border

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CYANOTIC CHD (TOF)

b. Laboratory and diagnostic study findings1. echocardiography and ECG show the

enlarged chambers of the right side of the heart2. echocardiography also demonstrates

the decrease in the size of the PA and the reduced blood flow through the lungs

3. cardiac catheterization and angiography allow definitive evaluation of the extent of the defect, particularly the PS and the VSD

4. CBC reveals polycythemia, ABG demonstrate reduced oxygen saturation

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CYANOTIC CHD (TOF)

3. Nursing managementa. Provide family teaching about treatment options

1. elective repair is usually performed during the infant’s 1st year of life, but palliative repairs may be warranted for infants who cannot undergo primary repair

2. total repair involves VSD closure, infundibular stenosis resection, and pericardial patch to enlarge RV outflow tractb. Provide preoperative and postoperative care

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CYANOTIC CHD (TGV)

B. TRANSPOSITION OF GREAT VESSELS (TGV)- in TGV, the PA leaves the LV and the aorta exits the RV, there is no communication between the systemic and pulmonary circulations

1. Pathophysiologya. this defect results in two separate circulatory patterns; the right heart manages systemic circulation and the left manages pulmonary circulationb. to sustain life, the child must have an associated defect.

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CYANOTIC CHD (TGV)

Associated defects such as septal defects or a PDA, permit oxygenated blood into the systemic circulation but cause increased cardiac workload.c. Potential complications include CHF, infective endocarditis, brain abscess, and cerebral vascular accidents resulting from hypoxia or thrombosis.

2. Assessment findings:a. Clinical manifestations vary, depending on associated defects

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CYANOTIC CHD (TGV)

1. In infants with minimal communication (no associated defects), severe respiratory depression and cyanosis, will be evident at birth

2. In infants with associated defects, there is less cyanosis but the infant may have symptoms of CHF

3. easily fatigued, FTT

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CYANOTIC CHD (TGV)

3. Nursing managementa. Provide family teaching about the treatment options

1. Prostaglandin E is administered to maintain a PDA and further blood mixing.

2. An arterial switch procedure within the 1st week of life is the surgical procedure of choice

C. TRUNCUS ARTERIOSUS - failure of normal septation and division of the embryonic bulbar trunk into the PA and aorta, resulting in a single vessel that overrides both ventricles

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CYANOTIC CHD

1. Pathophysiologya. blood ejected from the ventricles enters the common artery and flows either the lungs or aortic arch.b. pressure in both ventricles is high and blood flow to the lungs is markedly increased.

2. Assessment findings:a. neonates with this defect appear normal; however, as pulmonary vascular resistance decreases after birth, severe pulmonary edema and CHF commonly develop

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CYANOTIC CHD

2. marked cyanosis, especially on exertion; S/S of CHF; LVH, dyspnea, marked activity intolerance, and retarded growth3. loud systolic murmur best heard at the lower left sternal border and radiating throughout the chest

b. Laboratory and diagnostic study findings:- echocardiography reveals the defect

4. Nursing managementa. surgical repair is necessary in the 1st few months of life, the mortality rate associated with surgery is greater than 10%; w/o surgery, children die w/in 1 yr.

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OBSTRUCTIVE CHD (COA)

OBSTRUCTIVE CHDA. COARCTATION OF AORTA (COA)

- a defect that involves a localized narrowing of the aorta

1. Pathophysiology

a. COA is char. by inc. pressure proximal to the defect and decreased pressure distal to itb. restricted blood flow through the narrowed aorta increases the pressure on the LV and causes dilation of the proximal aorta and LVH, w/c may lead to LVF

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c. eventually, collateral vessels develop to bypass the coarctated segment and supply circulation to the LE

2. Assessment findings:a. Clinical manifestations

1. the child may be asymptomatic or may experience the classic difference in BP and pulse quality between the upper and lower ext. – the BP is elevated in the UE and dec. in the LE while the pulse is bounding in the UE and dec. or absent in the LE. Thus femoral pulse are weak or absent

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2. epistaxis, headaches, fainting and lower leg cramps

3. a systolic murmur may be heard over the left anterior chest and between the scapula posteriorly

4. rib notching may be observed in an older childb. Laboratory and diagnostic findings

1. ECG, echocardiography, and chest x-ray may reveal left sided heart enlargement resulting from back pressure

2. the radiograph may also demonstrate rib notching from enlarged collateral vessels

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3. Nursing managementa. repair involves surgical removal of the stenotic area

b. nonsurgical repair via balloon angioplasty

B. AORTIC STENOSIS (AS)- a defect that primarily involves an obstruction to the LV outflow of the valve

1. Pathophysiologya. LV pressure inc. to overcome resistance of the obstructed valve and allow blood to flow into the aorta, eventually producing LVH

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OBSTRUCTIVE CHD (AS)

b. MI may develop as the inc. O2 demands of the hypertrophied LV go unmet

2. Assessment findings:a. clinical manifestations:

1. faint pulse, hypotension, tachycardia, and poor feeding pattern

2. exercise intolerance, chest pain, and dizziness when standing for long periods

3. a systolic ejection murmur may be heard best at the 2nd ICS

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OBSTRUCTIVE CHD (AS)

b. Laboratory and diagnostic study findings:

1. ECG or echocardiography reveals LVH2. cardiac catheterization demonstrates

degree of the stenosis

3. Nursing management:a. if the child’s symptoms warrant, surgical aortic valvulotomy or prosthetic valve replacement is necessary

b. balloon angioplasty can be used to dilate the narrow valve

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OBSTRUCTIVE CHD (PS)

C. PULMONIC STENOSIS (PS)- a defect that involves obstruction of blood flow from the right ventricle

1. Pathophysiologya. RV pressure increases leading to RVH and eventually RV failure may occur

2. Assessment findings:a. Clinical manifestations

1. may be asymptomatic or may have mild cyanosis or CHF

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2. a systolic murmur may be heard over the pulmonic area; a thrill may be heard if stenosis is severe

3. in severe cases, decreased exercise tolerance, dyspnea, precordial pain and generalized cyanosis may occur

b. Laboratory and diagnostic findings:1. ECG or echocardiography reveals RVH2. cardiac catheterization demonstrates

the degree of stenosis

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3. Nursing managementa. provide family teaching about treatment options

1. Balloon angioplasty techniques are being widely used to treat PS

2. Surgical valvulotomy may be performed (although the need for surgery is uncommon due to the widespread use of balloon angioplasty techniques)b. provide preoperative and postoperative care

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POST POST TEST?TEST?

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THE BLOOD VESSELS

A. HYPERTENSION- persistent elevation of the SBP above 140mmHg and of DBP above 90mmHg (WHO)

manifestations:asymptomatic, occipital

headache is a common complaint.

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HYPERTENSION

Risk Factors:- (+) family history, obesity, stress, cigarette smoking, hypercholesterolemia, inc. sodium intake

B. Medical management:1. Diet and weight reduction (restricted sodium, kcal, cholesterol)2. Lifestyle changes: alcohol moderation, exercise regimen, cessation of smoking3. Antihypertensive drug therapy

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ARTERIOSCLEROSIS OBLITERANS

- a chronic occlusive arterial disease that may affect the abdominal aorta or the LE. The obstruction to blood flow with resultant ischemia usually affects the femoral, popliteal, aortic and iliac arteries

- occurs most often in men ages 50-60- caused by atherosclerosis- Risk Factors: cigarette smoking,

hyperlipidemia, hypertension, DM

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B. Medical management:1. Drug therapy

a. Vasodilators: papaverine, Isoxsuprine Hcl (Vasodilan), Nylidrin Hcl (Arlidin), nicotinyl alcohol (Roniacol) cyclandelate (Cyclospasmol), tolazoline Hcl (priscoline) to improve arterial circulation;

b. Analgesics to relieve ischemic painc. Anticoagulants to prevent thrombus

formationd. Lipid reducing drug: simvastatin, (Lopid),

niacin, lovastatin (Mevacor), atorvastatin

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2. Surgery: bypass grafting, endarterectomy, balloon catheter dilation, lumbar sympathectomy (to increase blood flow), amputation may be necessary

C. Assessment findings:1. Pain both intermittent claudication and rest pain,

numbness or tingling of the toes2. Pallor after 1-2 mins. Of elevating feet, and

dependent hyperemia/rubor; diminished or absent dorsalis pedis, posterior tibial and femoral pulses; shiny, taut skin with hair loss on lower legs

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3. Diagnostic tests:a. Oscillometry may reveal decrease pulse volume b. Doppler U/S reveals decreased blood flow through affected vesselsc. Angiography reveals location and extent of obstructive process

4. Elevated serum triglycerides; sodium

D. Nursing Interventions:1. Encourage slow, progressive physical activity 04/11/2304/11/23 sdelfin2010sdelfin2010


2. Administer medications as ordered3. Assist with Buerger-Allen exercises qid

a. client lies with legs elevated above heart for 2-3 minsb. client sits on edge of bed with legs and feet dependent and exercises feet and toes – upward and downward, inward and outward – for 3 minsc. client lies flat with legs at heart level for 5 mins

4. Assess for sensory function; protect client from injury

5. Provide client teaching and discharge planning: stop cigarette smoking, diet, drug compliance, exercise

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THROMBOANGIITIS OBLITERANS (BUERGER’S DISEASE)

- Acute inflammatory disorder affecting medium/smaller arteries and veins of the LE. Occurs as focal, obstructive process; results in occlusion of a vessel with subsequent development of collateral circulation

- Most often affects men ages 25-40; disease is idiopathic; high incidence among smokers

A. Medical management: same as arteriosclerosis obliterans but only cessation of smoking is effective treatment

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B. Assessment findings:1. Intermittent claudication, sensitivity to cold (skin

of extremity may at first be white, changing to blue then red)

2. Decreased or absent peripheral pulses (post. tibial and dorsalis pedis), ulceration and gangrene (advanced)

3. Diagnostic tests: same as arteriosclerosis obliterans

C. Nursing Interventions:

1. Prepare client for surgery04/11/2304/11/23 sdelfin2010sdelfin2010


2. Provide client teaching and discharge planning- drug regimen, avoidance of trauma to the affected extremity, need to maintain warmth esp. during cold weathers, importance of stopping smoking

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RAYNAUD’S PHENOMENON

- intermittent episode of arterial spasms, most frequently involving the fingers; most often affects women between the teenage years and age 40; cause unknown

- Predisposing factors: collagen diseases (SLE, RA), trauma (from typing, playing piano)

A. Medical management: vasodilators

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RAYNAUD’S PHENOMENON

B. Assessment findings:1. coldness, numbness, tingling in one or more digits;

pain (usually pptd. By exposure to cold, emotional upsets, tobacco use)

2. intermittent color changes (pallor, cyanosis, rumor); small ulcerations and gangrene tips of digits

C. Nursing interventions1. provide client teaching concerning:

- importance of stopping smoking; need to maintain warmth; need to use gloves in handling cold objects; drug regimen

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ANEURYSM

- a sac formed by dilation of an artery secondary to weakness and stretching of an arterial wall. The dilation may involve one or all layers of the arterial wall.

Classification1. Fusiform: uniform spindle shape involving the

entire circumference of the artery

2. Saccular: outpouching on one side only, affecting part of the arterial circumference

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ANEURYSM

3. Dissecting: separation of the arterial wall layers to form a cavity that fills with blood

4. False: the vessel wall is disrupted, blood escapes into surrounding area but is held in place by surrounding tissue

A. General info:

1. usually occurs in men ages 50-70; caused by arteriosclerosis, infection, syphilis, hypertension

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ANEURYSM

B. Medical management:1. control of underlying hypertension2. Surgery: resection of the aneurysm and

replacement with a Teflon/Dacron graft; coiling and clipping.

aneurysym.mp4

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ANEURYSM

3. Diagnostic tests:a. Aortography shows exact location of the aneurysm

b. X-rays: chest film reveals abnormal widening of aorta; abdominal film may show calcification within walls of aneurysm

4. Nursing interventions: Do not vigorously palpate the area Maintain BP normal to dec. risk of rupture Monitor for hemorrhage Prepare client for surgery

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THROMBOPHLEBITIS

A. General info:1. Inflammation of the vessel wall with formation of a

clot (thrombus); may affect superficial or deep veins

2. Most frequent veins affected are the saphenous, femoral, and popliteal.

3. Can result in damage to the surrounding tissues, ischemia and necrosis

4. Risk Factors: obesity, CHF, prolonged immobility, MI, pregnancy, oral contraceptives, trauma, sepsis, cigarette smoking, dehydration, severe anemias, venous cannulation, complication of surgery

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THROMBOPHLEBITIS

B. Medical management:1. Anticoagulation therapy:

a. Heparin: blocks conversion of prothrombin to thrombin and reduces formation of thrombus

- S/E: spontaneous bleeding, injection site reactions, ecchymoses, tissue irritation and sloughing, reversible transient alopecia, cyanosis, pain in arms or legs, thrombocytopeniab. Warfarin (coumadin): blocks prothrombin synthesis by interfering with vit. K synthesis

- S/E: GI: anorexia, nausea/vomiting, diarrhea, stomatitis

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THROMBOPHLEBITIS

2. Surgerya. Vein ligation and strippingb. venous thrombectomy: removal of a clot in the iliofemoral regionc. insertion of an umbrella-like prosthesis into the lumen of the vena cava to filter incoming clots

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THROMBOPHLEBITIS

C. Assessment findings:1. Pain in the affected extremity2. Superficial vein: tenderness, redness, induration

along course of the vein3. Deep vein: swelling, venous distension of limb,

tenderness over involoved vein, (+) Homan’s sign4. Elevated WBC and ESR5. Diagnostic tests:

a. venography (phlebography): inc. uptake of radioactive material

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THROMBOPHLEBITIS

b. Doppler ultrasonography: impairment of blood flow ahead of thrombus

D. Nursing interventions1. Provide bed rest, elevating involved extremity2. Apply continuous warm, moist soaks to dec.

lymphatic congestion3. Administer anticoagulants as ordered

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THROMBOPHLEBITIS

a. Heparin1. monitor PTT, use infusion pump to administer IV

heparin2. assess for bleeding tendencies (hematuria;

hematemesis; bleeding gums; epistaxis, melena) 3. have antidote ( protamine sulfate) availableb. Warfarin (Coumadin)1. assess PT daily, advise client to withhold dose and

notify physician immediately if bleeding or signs of bleeding occurs

2. instruct client to use a soft toothbrush and to floss gently, prepare antidote: Vit. K

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THROMBOPHLEBITIS

4. monitor for chest pain or SOB (possible pulmonary embolism)

5. Provide client teaching and discharge planning:a. need to avoid standing, sitting for long periods; constrictive clothing; crossing legs at the knees; smoking; oral contraceptivesb. importance of adequate hydration c. use of elastic stockings when ambulatoryd. importance of planned rest with elevation of feete. importance of weight reduction and exercise

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VARICOSE VEINS

A. General info:1. Dilated veins that occur most often in the lower

extremities and trunk. As the vessel dilates, the valves become stretched and incompetent with resultant venous pooling/edema

2. most common between ages 30-503. predisposing factor: congenital weakness of the

veins, thrombophlebitis, pregnancy, obesity, heart disease

B. Medical management: sclerotherapy vein ligation (involves ligating the saphenous vein

where it joins the femoral vein and stripping the saphenous vein system from groin to ankle)

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VARICOSE VEINS

C. Assessment findings:1. Pain after prolonged standing (relieved by elevation)2. Swollen, dilated, tortuous skin veins3. Diagnostic tests:

a. Trendelenburg test: varicose veins distend very quickly (less than 35 secs)b. Doppler U/S: decreased or no blood flow heard after calf or thigh compression

D. Nursing interventions:1. Elevate legs above heart level

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VARICOSE VEINS

2. Apply knee length elastic stockings3. Provide adequate rest4. Prepare client for vein ligation, if necessary

a. Provide routine pre-op careb. keep affected extremity elevated above

the level of the heart to prevent edemac. apply elastic bandages and stockings,

which should be removed every 8hrs for short periods.

d. assist out of bed within 24hrs, ensuring that elastic stockings are applied.

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RHEUMATIC FEVERRHEUMATIC FEVER

Main problem:Main problem:

An inflammatory autoimmune disease An inflammatory autoimmune disease that affects connective tissue of the that affects connective tissue of the heart, joints, subcutaneous tissues heart, joints, subcutaneous tissues and blood vessels of the CNS; most and blood vessels of the CNS; most serious complication- RHD affecting serious complication- RHD affecting the cardiac valves; presents 2-6 wks the cardiac valves; presents 2-6 wks following an untreated group A following an untreated group A hemolytic strephemolytic strep

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INITIAL MANIFESTATIONS:INITIAL MANIFESTATIONS:

Signs of carditis, SOB, edema of the Signs of carditis, SOB, edema of the face, abdomen or ankles, precordial face, abdomen or ankles, precordial pain; signs of polyarthritis: edema, pain; signs of polyarthritis: edema, inflammation of the large joints, joint inflammation of the large joints, joint pain; erythema marginatum: pain; erythema marginatum: macular rash on trunk and macular rash on trunk and extremities; subcutaneous nodules; extremities; subcutaneous nodules; feverfever

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LABORATORY DATA:LABORATORY DATA:

elevated ESR; elevated WBCelevated ESR; elevated WBC

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NURSING INTERVENTION:NURSING INTERVENTION: Dec. activity; bed rest if pulse Dec. activity; bed rest if pulse

rate is inc. or if child is febrilerate is inc. or if child is febrile Friends may visit for short Friends may visit for short

periods; child is not contagiousperiods; child is not contagious Maintain adequate hydrationMaintain adequate hydration Maintain adequate nutritionMaintain adequate nutrition

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Administer analgesics for arthralgiaAdminister analgesics for arthralgia Teach parents importance or Teach parents importance or

preventing recurring infxnpreventing recurring infxn Importance of prophylactic therapy Importance of prophylactic therapy

before invasive medical proc.before invasive medical proc. Continue medical follow-up for the Continue medical follow-up for the

development of valvular prob. as development of valvular prob. as child grows.child grows.

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RHEUMATIC RHEUMATIC HEART DISEASEHEART DISEASE

Rheumatic heart disease is an inflammatory Rheumatic heart disease is an inflammatory disease, primarily affecting connective disease, primarily affecting connective tissue, especially cardiac valves.tissue, especially cardiac valves.

A. Usually preceded by a group A beta-A. Usually preceded by a group A beta-hemolytic streptococcal infection.hemolytic streptococcal infection.

1. Tissue damage is believed to be 1. Tissue damage is believed to be related to an autoimmune related to an autoimmune process. process.

2. Antibiotics produced in response to 2. Antibiotics produced in response to streptoccocal infection react with connective streptoccocal infection react with connective tissue ( cardiac tissue, joints)tissue ( cardiac tissue, joints)

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RHEUMATIC HEART RHEUMATIC HEART DISEASEDISEASE

B. Myocardial involvement is B. Myocardial involvement is characterized by inflammation of the characterized by inflammation of the endocardium, pericardium, and endocardium, pericardium, and myocardium.myocardium.

1. Endocarditis produces scarring of 1. Endocarditis produces scarring of the cardiac valves.the cardiac valves.

2. Mitral and aortic valves are most 2. Mitral and aortic valves are most commonly affected, either by valvular commonly affected, either by valvular stenosis or valvular insufficiency.stenosis or valvular insufficiency.

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ASSESSMENT:ASSESSMENT:

A.A. Risk factors/etiology: previous infection by beta Risk factors/etiology: previous infection by beta hemolytic streptococcus.hemolytic streptococcus.

B.B. Clinical manifestations: symptoms vary; no Clinical manifestations: symptoms vary; no specific symptoms or sign is diagnostic of specific symptoms or sign is diagnostic of rheumatic fever. Criteria for the diagnosis rheumatic fever. Criteria for the diagnosis require a combination of sympyoms to be require a combination of sympyoms to be present:present:

1. carditis1. carditis

2. migratory polyarthritis2. migratory polyarthritis

3. erythema marginatum3. erythema marginatum

4. subcutaneous nodules4. subcutaneous nodules04/11/2304/11/23 sdelfin2010sdelfin2010


TREATMENTTREATMENT

1.1. Adequate tx of streptococcal infxnAdequate tx of streptococcal infxn

2.2. Bed rest until tachycardia subsidesBed rest until tachycardia subsides

3.3. Salicylates to control inflammatory Salicylates to control inflammatory processprocess

4.4. Prophylactic tx:Prophylactic tx: Initiated after immediate therapyInitiated after immediate therapy Monthly administration of penicillinMonthly administration of penicillin Administration of prophylactic pen. Administration of prophylactic pen.

Before and after medical proc.Before and after medical proc.04/11/2304/11/23 sdelfin2010sdelfin2010


COMPLICATION:COMPLICATION:

Severe valvular damage Severe valvular damage precipitates the development of precipitates the development of CHF and may require open heart CHF and may require open heart surgery for replacement of surgery for replacement of diseased valve.diseased valve.

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CARDIAC TAMPONADECARDIAC TAMPONADE

Main problem:Main problem: Fluid accumulation in the Fluid accumulation in the

pericardial sacpericardial sac

Initial manifestation:Initial manifestation: Hypotension muffled heart Hypotension muffled heart

sounds is a common signsounds is a common sign

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CARDIAC TAMPONADECARDIAC TAMPONADELaboratory data:Laboratory data: ECG reveals ST and T wave ECG reveals ST and T wave

abnormalitiesabnormalities

Intervention:Intervention: Prepare the px for pericardiocentesis. Prepare the px for pericardiocentesis.

This involves aspirating the fluid or air This involves aspirating the fluid or air from the pericardial sac.from the pericardial sac.

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PERICARDIOCENTESISPERICARDIOCENTESIS

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COMPLETE HEART COMPLETE HEART BLOCKBLOCKMain problem:Main problem: Altered transmission of wave Altered transmission of wave

impulses from the SA node to impulses from the SA node to the AV nodethe AV node

Initial manifestation:Initial manifestation: BRADYCARDIABRADYCARDIA

Laboratory data:Laboratory data: ECG reveals prolonged PR ECG reveals prolonged PR

intevalinteval04/11/2304/11/23 sdelfin2010sdelfin2010

COMPLETE HEART COMPLETE HEART BLOCKBLOCK

Nursing interventions:Nursing interventions: Monitor patients’ ECGMonitor patients’ ECG Prepare patient for pacemaker Prepare patient for pacemaker

insertioninsertion A common sign of pacemaker A common sign of pacemaker

failure is hiccupsfailure is hiccups Atropine sulfate is given as a Atropine sulfate is given as a

vagolyticvagolytic04/11/2304/11/23 sdelfin2010sdelfin2010

Artificial pacemakerArtificial pacemaker

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SICKLE CELL ANEMIASICKLE CELL ANEMIA

Gen. info:Gen. info: Sickle cell anemia is a problem Sickle cell anemia is a problem

characterized by the sickling effect characterized by the sickling effect of the erythrocytes.of the erythrocytes.

Sickle cell dse is a genetic disorder.Sickle cell dse is a genetic disorder. Sickling problem is not apparent Sickling problem is not apparent

until around 6 months of ageuntil around 6 months of age Predominantly a problem of children Predominantly a problem of children

and adolescents. A child maybe and adolescents. A child maybe asymptomatic between crises.asymptomatic between crises.04/11/2304/11/23 sdelfin2010sdelfin2010

Inheritance pattern for Inheritance pattern for sickle cell diseasesickle cell disease

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SICKLE CELL ANEMIASICKLE CELL ANEMIA

Pathological changes of sickle cell dse Pathological changes of sickle cell dse results from:results from:

1.1. Inc. viscosity of bloodInc. viscosity of blood

2.2. Inc. RBC destructionInc. RBC destruction

3.3. Inc. viscosity eventually precipitates Inc. viscosity eventually precipitates ischemia & tissue necrosis caused ischemia & tissue necrosis caused by capillary stasis and thrombosisby capillary stasis and thrombosis

4.4. Cycle of occlusion, ischemia, & Cycle of occlusion, ischemia, & infarction to vascular organs.infarction to vascular organs.

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SICKLE CELL ANEMIASICKLE CELL ANEMIASickle cell disease is a multiple body Sickle cell disease is a multiple body

systems involvement.systems involvement.

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ImplementationImplementation:: Administer oxygen and blood transfusionsAdminister oxygen and blood transfusions Administer analgesicsAdminister analgesics Maintain adequate hydration and blood Maintain adequate hydration and blood

flow with IV normal saline as prescribed flow with IV normal saline as prescribed and with oral fluidsand with oral fluids

Avoid putting strain on painful jointsAvoid putting strain on painful joints Encourage consumption of a high calorie, Encourage consumption of a high calorie,

high protein diet with folic acid high protein diet with folic acid supplementationsupplementation

Monitor for signs of increasing anemia Monitor for signs of increasing anemia and shock (pallor, vital sign changes)and shock (pallor, vital sign changes)

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HemophiliaHemophilia

Deficiency of clotting factors. Sex-Deficiency of clotting factors. Sex-linked trait more common in linked trait more common in males. Von willebrands disease is males. Von willebrands disease is transmitted to both male and transmitted to both male and female offspring of a carrier.female offspring of a carrier.

Males to manifest, female carrierMales to manifest, female carrier

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X linked recessive traitX linked recessive trait Males inherit hemophilia from Males inherit hemophilia from

their mothers and females their mothers and females inherit the carrier status from inherit the carrier status from their fathers.their fathers.

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2 forms:2 forms: Classic hemophiliaClassic hemophilia

hemophilia A Factor VIII def.hemophilia A Factor VIII def. Christmas factorChristmas factor

hemophilia B Factor IXhemophilia B Factor IX

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Assessment:Assessment: Prolonged bleeding after minor Prolonged bleeding after minor

injuryinjury

1. after cutting a cord at birth1. after cutting a cord at birth

2. following circumcision2. following circumcision

3. following IM immunization3. following IM immunization

4. increase bruising as child 4. increase bruising as child learns learns to crawl and walkto crawl and walk

Abnormal bleeding in response to Abnormal bleeding in response to traumatrauma

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Joint bleeding- pain, tenderness, Joint bleeding- pain, tenderness, swelling limited range of motion swelling limited range of motion tendency to bruise easilytendency to bruise easily

Prolonged PTTProlonged PTT

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Implementation:Implementation: Prepare to administer Factor VIII Prepare to administer Factor VIII

concentrate/ cryoprecipitateconcentrate/ cryoprecipitate Monitor for bleedingMonitor for bleeding Monitor for joint pain; immobilize the Monitor for joint pain; immobilize the

affected extremity if joint pain occursaffected extremity if joint pain occurs Monitor urine for hematuriaMonitor urine for hematuria Control bleeding by immobilization, Control bleeding by immobilization,

elevation, application of ice; apply elevation, application of ice; apply pressure (15 mins) for superficial pressure (15 mins) for superficial bleedingbleeding

Avoidance of contact sportsAvoidance of contact sports04/11/2304/11/23 sdelfin2010sdelfin2010

Disseminated Disseminated Intravascular Intravascular

Coagulation (DIC)Coagulation (DIC) Main problem:Main problem: wide spread wide spread

coagulation all over the body coagulation all over the body resulting to subsequent depletion resulting to subsequent depletion of clotting factorsof clotting factors

Initial manifestation:Initial manifestation: petechiae petechiae and ecchymosis on the skin, and ecchymosis on the skin, mucous membrane, heart, lungs mucous membrane, heart, lungs and other organsand other organs

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Laboratory data:Laboratory data: prolonged PT prolonged PT and PTTand PTT

Interventions:Interventions:

1.1. Monitor for signs of bleeding ( tarry Monitor for signs of bleeding ( tarry stool, hemoptysis, nosebleeding)stool, hemoptysis, nosebleeding)

2.2. Administer heparin as ordered. Administer heparin as ordered. Heparin inhibits thrombin thus Heparin inhibits thrombin thus preventing further clot formation preventing further clot formation and allowing coagulation factors to and allowing coagulation factors to accumulate. Administer blood accumulate. Administer blood transfusion as ordered.transfusion as ordered.

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Kawasaki disease Kawasaki disease (mucocutaneous lymph (mucocutaneous lymph

node syndrome)node syndrome) Main problem:Main problem: acute systemic acute systemic

inflammatory illness of unknown inflammatory illness of unknown cause; cardiac involvement- most cause; cardiac involvement- most serious complication.serious complication.

Initial manifestations:Initial manifestations: fever, fever, conjunctival infection, red throat, conjunctival infection, red throat, “strawberry tongue”, swollen hands, “strawberry tongue”, swollen hands, rash, enlargement of the cervical rash, enlargement of the cervical lymph nodes.lymph nodes.

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InterventionsInterventions::

1.1. Monitor temperature frequentlyMonitor temperature frequently

2.2. Assess heart sounds and rhythmAssess heart sounds and rhythm

3.3. Assess extremities for edema, Assess extremities for edema, redness, desquamationredness, desquamation

4.4. Monitor mucus membrane for Monitor mucus membrane for inflammationinflammation

5.5. Weigh dailyWeigh daily

6.6. Administer IV immune globulinAdminister IV immune globulin

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NO PERMIT, NO EXAMNO PERMIT, NO EXAM

THE ENDTHE END

GODBLESS ON YOUR EXAMGODBLESS ON YOUR EXAM

PLEASE READ YOUR BOOKSPLEASE READ YOUR BOOKS

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WAIT FOR ME AMERICA!! IM WAIT FOR ME AMERICA!! IM COMING!!COMING!!

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4. cardiovascular delfin

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