cardiovascular & hematologic system

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CARDIOLOGY NURSING

THE CARDIOVASCULAR SYSTEM

HEART’S NORMAL ANATOMY

The heart is located in the LEFT side of the mediastinum

Consists of Three layers - epicardium, myocardium and endocardium

THE CARDIOVASCULAR SYSTEM

The epicardium covers the outer surface of the heart

The myocardium is the middle muscular layer of the heart

The endocardium lines the chambers and the valves

THE CARDIOVASCULAR SYSTEM

The layer that covers the heart is the PERICARDIUM

There are two parts - parietal and visceral pericardium

The space between the two pericardial layers is the pericardial space

THE CARDIOVASCULAR SYSTEM

The heart also has four chambers - two atria and two ventricles

The Left atrium and the right atrium

The left ventricle and the right ventricle

The Cardiovascular System

The heart chambers are guarded by valves

The atrio-ventricular valves - tricuspid and bicuspid

The semi-lunar valves - pulmonic and aortic valves

The Cardiovascular System

The Blood supply of the heart comes from the Coronary arteries

1. Right coronary artery supplies the RIGHT atrium and RIGHT ventricle, inferior portion of the LEFT ventricle, the POSTERIOR septal wall and the two nodes - AV (90%) and SA node (55%)

The Cardiovascular System

2. Left coronary artery- branches into the LAD and the circumflex branch

The LAD supplies blood to the anterior wall of the LEFT ventricle, the anterior septum and the Apex of the left ventricle

The CIRCUMFLEX branch supplies the left atrium and the posterior LEFT ventricle

The Cardiovascular System

The CONDUCTING SYSTEM OF THE HEART

Consists of the1. SA node- the pacemaker2. AV node- slowest conduction3. Bundle of His – branches into the Right and the Left bundle branch4. Purkinje fibers- fastest conduction

The Heart sounds

1. S1- due to closure of the AV valves

2. S2- due to the closure of the semi-lunar valves

3. S3- due to increased ventricular filling

4. S4- due to forceful atrial contraction

The Cardiovascular System

The Cardiovascular System

Heart rate

Normal range is 60-100 beats per minute

Tachycardia is greater than 100 bpm

Bradycardia is less than 60 bpm

Sympathetic system INCREASES HR

Parasympathetic system (Vagus) DECREASES HR

The Cardiovascular System

Blood pressure

Cardiac output X peripheral resistance

Control is neural (central and peripheral) and hormonal

Baroreceptors in the carotid and aorta

Hormones- ADH, aldosterone, epinephrine can increase BP; ANF can decrease BP

The Cardiovascular System

The vascular system consists of the arteries, veins and capillariesThe arteries are vessels that carry blood away from the heart to the peripheryThe veins are the vessels that carry blood to the heartThe capillaries are lined with squamos cells, they connect the veins and arteries

The Cardiovascular System

The lymphatic system also is part of the vascular system and the function of this system is to collect the extravasated fluid from the tissues and returns it to the blood

The Cardiovascular System

Cardiac Assessment

The Cardiovascular System

Laboratory Test Rationale

1. To assist in diagnosing MI

2. To identify abnormalities

3. To assess inflammation

The Cardiovascular System

Laboratory Test Rationale4. To determine baseline value 5. To monitor serum level of medications6. To assess the effects of medications

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC Proteins and enzymes

CK- MB ( creatine kinase)Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC Proteins and enzymes

CK- MB ( creatine kinase)Normal value is 0-7 U/L

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC Proteins and enzymesLactic Dehydrogenase (LDH)

Elevates in MI in 24 hours, peaks in 48-72 hours

Normally LDH1 is greater than LDH2

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC Proteins and enzymes

Lactic Dehydrogenase (LDH)MI- LDH2 greater than

LDH1 (flipped LDH pattern)Normal value is 70-200 IU/L

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC Proteins and enzymes

MyoglobinRises within 1-3 hoursPeaks in 4-12 hoursReturns to normal in a day

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC Proteins and enzymes

MyoglobinNot used aloneMuscular and RENAL disease

can have elevated myoglobin

The Cardiovascular SystemLABORATORY PROCEDURES

Troponin I and T

Troponin I is usually utilized for MI

Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks!

Normal value for Troponin I is less than 0.6 ng/mL

The Cardiovascular SystemLABORATORY PROCEDURES

Troponin I and T

REMEMBER to AVOID IM injections before obtaining blood sample!

Early and late diagnosis can be made!

The Cardiovascular SystemLABORATORY PROCEDURES

SERUM LIPIDSLipid profile measures the serum cholesterol, triglycerides and lipoprotein levelsCholesterol= 200 mg/dLTriglycerides- 40- 150 mg/dL

The Cardiovascular SystemLABORATORY PROCEDURES

SERUM LIPIDS

LDH- 130 mg/dL

HDL- 30-70- mg/dL

NPO post midnight (usually 12 hours)

The Cardiovascular SystemLABORATORY PROCEDURES

ELECTROCARDIOGRAM (ECG)A non-invasive procedure that evaluates the electrical activity of the heartElectrodes and wires are attached to the patient

The Cardiovascular SystemLABORATORY PROCEDURESHolter Monitoring

A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours

The Cardiovascular SystemLABORATORY PROCEDURES

Holter Monitoring

Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop

The Cardiovascular SystemLABORATORY PROCEDURES

ECHOCARDIOGRAMNon-invasive test that studies the structural and functional changes of the heart with the use of ultrasoundNo special preparation is needed

The Cardiovascular SystemLABORATORY PROCEDURES

Stress TestA non-invasive test that studies the heart during activity and detects and evaluates CADExercise test, pharmacologic test and emotional test

The Cardiovascular SystemLABORATORY PROCEDURES

Stress Test

Treadmill testing is the most commonly used stress testUsed to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise

The Cardiovascular SystemLABORATORY PROCEDURES

Stress TestPre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine

The Cardiovascular SystemLABORATORY PROCEDURES

Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath . Instruct client to avoid taking a hot shower for 10-12 hours after the test

The Cardiovascular SystemLABORATORY PROCEDURES

Pharmacological stress testUse of dipyridamoleMaximally dilates coronary arterySide-effect: flushing of face

The Cardiovascular SystemLABORATORY PROCEDURES

Pharmacological stress testPre-test: 4 hours fasting, avoid alcohol, caffeinePost test: report symptoms of chest pain

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC catheterizationInsertion of a catheter into the heart and surrounding vesselsDetermines the structure and performance of the heart valves and surrounding vessels

The Cardiovascular SystemLABORATORY PROCEDURES

CARDIAC catheterization

Used to diagnose CAD, assess coronary atery patency and determine extent of atherosclerosis

The Cardiovascular SystemLABORATORY PROCEDURES

Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses

The Cardiovascular SystemLABORATORY PROCEDURES

Pretest: Fast for 8-12 hours, teachings, medications to allay anxiety

The Cardiovascular SystemLABORATORY PROCEDURES

Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart; inform the patient that a feeling of warmth and metallic taste may occur when dye is administered

The Cardiovascular SystemLABORATORY PROCEDURES

Post-test: Monitor VS and cardiac rhythmMonitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion site Maintain sandbag to the insertion site if required to maintain pressureMonitor for bleeding and hematoma formation

The Cardiovascular SystemLABORATORY PROCEDURES

Maintain strict bed rest for 6-12 hours

Client may turn from side to side but bed should not be elevated more than 30 degrees and legs always straight

Encourage fluid intake to flush out the dye

Immobilize the arm if the antecubital vein is used

Monitor for dye allergy

The Cardiovascular SystemLABORATORY PROCEDURES

CVPThe CVP is the pressure within the SVCReflects the pressure under which blood is returned to the SVC and right atrium

The Cardiovascular SystemLABORATORY PROCEDURES

CVPNormal CVP is 0 to 8 mmHg/ 4-10 cm H2OElevated CVP indicates increase in blood volume, excessive IVF or heart/renal failureLow CVP may indicated hypovolemia, hemorrhage and severe vasodilatation

The Cardiovascular SystemLABORATORY PROCEDURES

Measuring CVP1. Position the client supine with bed elevated at 45 degrees2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL, 4th ICS 3. Instruct the client to be relaxed and avoid coughing and straining.

CARDIAC ASSESSMENT

ASSESSMENT1. Health History

Obtain description of present illness and the chief complaintChest pain, SOB, Edema, etc.Assess risk factors

CARDIAC ASSESSMENT2. Physical examination

Vital signs- BP, PP, MAPInspection of the skinInspection of the thoraxPalpation of the PMI, pulsesAuscultation of the heart sounds

CARDIAC ASSESSMENT3. Laboratory and diagnostic studiesCBC cardiac catheterizationLipid profile arteriographyCardiac enzymes and proteinsCXR CVPEEGHolter monitoringExercise ECG

CARDIAC IMPLEMENTATION

1. Assess the cardio-pulmonary status

VS, BP, Cardiac assessment

2. Enhance cardiac output

Establish IV line to administer fluids

CARDIAC IMPLEMENTATION

3. Promote gas exchange

Administer O2

Position client in SEMI-Fowler’s

Encourage coughing and deep breathing exercises

CARDIAC IMPLEMENTATION4. Increase client activity tolerance

Balance rest and activity periodsAssist in daily activities

5. Promote client comfortAssess the client’s description of pain and chest discomfortAdminister medication as prescribed

CARDIAC IMPLEMENTATION

6. Promote adequate sleep7. Prevent infection

Monitor skin integrity of lower extremitiesAssess skin site for edema, redness and warmthMonitor for feverChange position frequently

CARDIAC IMPLEMENTATION

8. Minimize patient anxietyEncourage verbalization of feelings, fears and concernsAnswer client questions. Provide information about procedures and medications

CARDIAC DISEASESCoronary Artery DiseaseMyocardial InfarctionCongestive Heart FailureInfective EndocarditisCardiac TamponadeCardiogenic Shock

VASCULAR DISEASES

HypertensionBuerger’s diseaseVaricose veinsDeep vein thrombosisAneurysm

CAD

CAD results from the focal narrowing of the large and medium-sized coronary arteries due to deposition of atheromatous plaque in the vessel wall

CADRISK FACTORS

1. Age above 45/55 and Sex- Males and post-menopausal females2. Family History3. Hypertension4. DM5. Smoking6. Obesity7. Sedentary lifestyle8. Hyperlipedimia

CADRISK FACTORS

Most important MODIFIABLE factors:

Smoking

Hypertension

Diabetes

Cholesterol abnormalities

CADPathophysiology

Fatty streak formation in the vascular intima T-cells and monocytes ingest lipids in the area of deposition atheroma narrowing of the arterial lumen reduced coronary blood flow myocardial ischemia

CADPathophysiology

There is decreased perfusion of myocardial tissue and inadequate myocardial oxygen supplyIf 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, this becomes significantPotential for Thrombosis and embolism

Angina Pectoris

Chest pain resulting from coronary atherosclerosis or myocardial ischemia

Angina Pectoris: Clinical SyndromesThree Common Types of

ANGINA1. STABLE ANGINA

The typical angina that occurs during exertion, relieved by rest and drugs and the severity does not change

Angina Pectoris: Clinical SyndromesThree Common Types of ANGINA

2. Unstable anginaOccurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and drug

Angina Pectoris: Clinical SyndromesThree Common Types of ANGINA

3. Variant anginaPrinzmetal angina, results from coronary artery VASOSPASMS, may occur at rest

Angina Pectoris

ASSESSMENT FINDINGS1. Chest pain- ANGINA

The most characteristic symptomPAIN is described as mild to severe retrosternal pain, squeezing, tightness or burning sensationRadiates to the jaw and left arm

Angina Pectoris

ASSESSMENT FINDINGS

1. Chest pain- ANGINA

Precipitated by Exercise, Eating heavy meals, Emotions like excitement and anxiety and Extremes of temperature

Relieved by REST and Nitroglycerin

Angina Pectoris

ASSESSMENT FINDINGS2. Diaphoresis3. Nausea and vomiting4. Cold clammy skin5. Sense of apprehension and doom6. Dizziness and syncope

Angina Pectoris

LABORATORY FINDINGS1. ECG may show normal tracing if patient

is pain-free. Ischemic changes may show ST depression and T wave inversion

2. Cardiac catheterizationProvides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions

Angina Pectoris

NURSING MANAGEMENT1. Administer prescribed medications

Nitrates- to dilate the coronary arteriesAspirin- to prevent thrombus formationBeta-blockers- to reduce BP and HRCalcium-channel blockers- to dilate coronary artery and reduce vasospasm

2. Teach the patient management of anginal attacksAdvise patient to stop all activities Put one nitroglycerin tablet under the tongueWait for 5 minutesIf not relieved, take another tablet and wait for 5 minutesAnother tablet can be taken (third tablet)If unrelieved after THREE tablets seek medical attention

Angina Pectoris3. Obtain a 12-lead ECG4. Promote myocardial perfusion

Instruct patient to maintain bed restAdminister O2 @ 3 lpmAdvise to avoid valsalva maneuversProvide laxatives or high fiber diet to lessen constipationEncourage to avoid increased physical activities

Angina Pectoris

5. Assist in possible treatment modalitiesPTCA- percutaneous transluminal coronary angioplasty

To compress the plaque against the vessel wall, increasing the arterial lumen

CABG- coronary artery bypass graftTo improve the blood flow to the myocardial tissue

Angina Pectoris

6. Provide information to family members to minimize anxiety and promote family cooperation

7. Assist client to identify risk factors that can be modified

8. Refer patient to proper agencies

Myocardial infarction

Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood supply

Myocardial infarction

ETIOLOGY and Risk factors1. CAD2. Coronary vasospasm3. Coronary artery occlusion by embolus and thrombus4. Conditions that decrease perfusion- hemorrhage, shock

Myocardial infarction

Risk factors1. Hypercholesterolemia2. Smoking3. Hypertension4. Obesity5. Stress6. Sedentary lifestyle

Myocardial infarction

PATHOPHYSIOLOGYInterrupted coronary blood flow myocardial ischemia anaerobic myocardial metabolism for several hours myocardial death depressed cardiac function triggers autonomic nervous system response further imbalance of myocardial O2 demand and supply

Myocardial infarction

ASSESSMENT findings1. CHEST PAIN

Chest pain is described as severe, persistent, crushing substernal discomfortRadiates to the neck, arm, jaw and back

Myocardial infarction

ASSESSMENT findings1. CHEST PAIN

Occurs without cause, primarily early morningNOT relieved by rest or nitroglycerinLasts 30 minutes or longer

Myocardial infarctionAssessment findings

2. Dyspnea3. Diaphoresis4. cold clammy skin5. N/V6. restlessness, sense of doom7. tachycardia or bradycardia8. hypotension9. S3 and dysrhythmias

Myocardial infarction

Laboratory findings1. ECG- the ST segment is ELEVATED. T wave inversion, presence of Q wave2. Myocardial enzymes- elevated CK-MB, LDH and Troponin levels3. CBC- may show elevated WBC count 4. Test after the acute stage- Exercise tolerance test, thallium scans, cardiac catheterization

Myocardial infarctionNursing Interventions

1. Provide Oxygen at 2 lpm, Semi-fowler’s2. Administer medications

Morphine to relieve pain nitrates, thrombolytics, aspirin and anticoagulantsStool softener and hypolipidemics

3. Minimize patient anxietyProvide information as to procedures and drug therapy

Myocardial infarction

4. Provide adequate rest periods

5. Minimize metabolic demands

Provide soft diet

Provide a low-sodium, low cholesterol and low fat diet

6. Minimize anxiety

Reassure client and provide information as needed

Myocardial infarction

7. Assist in treatment modalities such as PTCA and CABG

8. Monitor for complications of MI- especially dysrhythmias, since ventricular tachycardia can happen in the first few hours after MI

9. Provide client teaching

MI

Medical Management

1. ANALGESICThe choice is MORPHINE

It reduces pain and anxiety

Relaxes bronchioles to enhance oxygenation

MI

Medical Management

2. ACEPrevents formation of angiotensin II

Limits the area of infarction

MI

Medical Management

3. ThrombolyticsStreptokinase, Alteplase

Dissolve clots in the coronary artery allowing blood to flow

Myocardial infarction

NURSING INTERVENTIONS AFTER ACUTE EPISODE1. Maintain bed rest for the first 3 days2. Provide passive ROM exercises3. Progress with dangling of the feet at side of bed

Myocardial infarction

NURSING INTERVENTIONS AFTER ACUTE EPISODE4. Proceed with sitting out of bed, on the chair for 30 minutes TID5. Proceed with ambulation in the room toilet hallway TID

Myocardial infarction

NURSING INTERVENTIONS AFTER ACUTE EPISODE

Cardiac rehabilitationTo extend and improve quality of lifePhysical conditioningPatients who are able to walk 3-4 mph are usually ready to resume sexual activities

CARDIOMYOPATHIES

Heart muscle disease associated with cardiac dysfunction

CARDIOMYOPATHIES

1. Dilated Cardiomyopathy

2. Hypertrophic Cardiomyopathy

3. Restrictive cardiomyopathy

DILATED CARDIOMYOPATHY

ASSOCIATED FACTORS

1. Heavy alcohol intake

2. Pregnancy

3. Viral infection

4. Idiopathic

DILATED CARDIOMYOPATHY

PATHOPHYSIOLOGYDiminished contractile proteins poor contraction decreased blood ejection increased blood remaining in the ventricle ventricular stretching and dilatation. SYSTOLIC DYSFUNCTION

HYPERTROPHIC CARDIOMYOPATHY

Associated factors:

1. Genetic

2. Idiopathic

HYPERTROPHIC CARDIOMYOPATHY

Pathophysiology

Increased size of myocardium reduced ventricular volume increased resistance to ventricular filling diastolic dysfunction

RESTRICTIVE CARDIOMYOPATHY

Associated factors

1. Infiltrative diseases like AMYLOIDOSIS

2. Idiopathic

RESTRICTIVE CARDIOMYOPATHY

Pathophysiology

Rigid ventricular wall impaired stretch and diastolic filling decreased output

Diastolic dysfunction

CARDIOMYOPATHIESAssessment findings

1. PND

2. Orthopnea

3. Edema

4. Chest pain

5. Palpitations

6. dizziness

7. Syncope with exertion

CARDIOMYOPATHIES

Laboratory Findings1. CXR- may reveal cardiomegaly2. ECHOCARDIOGRAM3. ECG4. Myocardial Biopsy

CARDIOMYOPATHIES

Medical Management

1. Surgery

2. pacemaker insertion

3. Pharmacological drugs for symptom relief

CARDIOMYOPATHIES

Nursing Management

1.Improve cardiac output

Adequate rest

Oxygen therapy

Low sodium diet

CARDIOMYOPATHIES

Nursing Management

2. Increase patient tolerance

Schedule activities with rest periods in between

CARDIOMYOPATHIES

Nursing Management3. Reduce patient anxiety

SupportOffer information about transplantationsSupport family in anticipatory grieving

Infective endocarditis

Infection of the heart valves and the endothelial surface of the heart

Can be acute or chronic

Infective endocarditis

Etiologic factors

1. Bacteria- Organism depends on several factors

2. Fungi

Infective endocarditis

Risk factors1. Prosthetic valves2. Congenital malformation3. Cardiomyopathy4. IV drug users5. Valvular dysfunctions

Infective endocarditisPathophysiology

Direct invasion of microbes microbes adhere to damaged valve surface and proliferate damage attracts platelets causing clot formation erosion of valvular leaflets and vegetation can embolize

Infective endocarditisAssessment findings

1. Intermittent HIGH fever2. anorexia, weight loss3. cough, back pain and joint pain4. splinter hemorrhages under nails

Infective endocarditis

Assessment findings

5. Osler’s nodes- painful nodules on fingerpads

6. Roth’s spots- pale hemorrhages in the retina

Infective endocarditis

Assessment findings

7. Heart murmurs

8. Heart failure

Infective endocarditis

Prevention

Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc.

Infective endocarditis

LABORATORY EXAM

Blood Cultures to determine the exact organism

Infective endocarditis

Nursing management

1. regular monitoring of temperature, heart sounds

2. manage infection

3. long-term antibiotic therapy

Infective endocarditis

Medical management

1. Pharmacotherapy

IV antibiotic for 2-6 weeks

Antifungal agents are given – amphotericin B

Infective endocarditis

Medical management

2. Surgery

Valvular replacement

CHF

A syndrome of congestion of both pulmonary and systemic circulation caused by inadequate cardiac function and inadequate cardiac output to meet the metabolic demands of tissues

CHF

Inability of the heart to pump sufficientlyThe heart is unable to maintain adequate circulation to meet the metabolic needs of the bodyClassified according to the major ventricular dysfunction- Left or Right

CHFEtiology of CHF

1. CAD2. Valvular heart diseases3. Hypertension4. MI5. Cardiomyopathy6. Lung diseases7. Post-partum8. Pericarditis and cardiac tamponade

New York Heart Association

Class 1Ordinary physical activity does NOT cause chest pain and fatigueNo pulmonary congestionAsymptomaticNO limitation of ADLs

New York Heart Association

Class 2SLIGHT limitation of ADLsNO symptom at restSymptom with INCREASED activityBasilar crackles and S3

New York Heart Association

Class 3

Markedly limitation on ADLs

Comfortable at rest BUT symptoms present in LESS than ordinary activity

New York Heart Association

Class 4

SYMPTOMS are present at rest

CHF

PATHOPHYSIOLOGYLEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion

CHF

PATHOPHYSIOLOGYLEFT ventricular failure decreased cardiac output decreased perfusion to the brain, kidney and other tissues oliguria, dizziness

CHF

PATHOPHYSIOLOGYRIGHT ventricular failure blood pooling in the venous circulation increased hydrostatic pressure peripheral edema

CHF

PATHOPHYSIOLOGY

RIGHT ventricular failure blood pooling venous congestion in the kidney, liver and GIT

LEFT SIDED CHFASSESSMENT FINDINGS

1. Dyspnea on exertion2. PND3. Orthopnea4. Pulmonary crackles/rales5. cough with Pinkish, frothy sputum6. Tachycardia

LEFT SIDED CHFASSESSMENT FINDINGS

7. Cool extremities8. Cyanosis9. decreased peripheral pulses10. Fatigue11. Oliguria12. signs of cerebral anoxia

RIGHT SIDED CHFASSESSMENT FINDINGS

1. Peripheral dependent, pitting edema2. Weight gain3. Distended neck vein4. hepatomegaly5. Ascites

RIGHT SIDED CHFASSESSMENT FINDINGS

6. Body weakness

7. Anorexia, nausea

8. Pulsus alternans

CHF

LABORATORY FINDINGS1. CXR may reveal cardiomegaly2. ECG may identify Cardiac hypertrophy3. Echocardiogram may show hypokinetic heart

CHF

LABORATORY FINDINGS

4. ABG and Pulse oximetry may show decreased O2 saturation

5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF

CHF

NURSING INTERVENTIONS

1. Assess patient's cardio-pulmonary status

2. Assess VS, CVP and PCWP. Weigh patient daily to monitor fluid retention

CHF

NURSING INTERVENTIONS

3. Administer medications- usually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators and hypolipidemics are prescribed

CHF

NURSING INTERVENTIONS4. Provide a LOW sodium diet. Limit fluid intake as necessary5. Provide adequate rest periods to prevent fatigue

CHF

NURSING INTERVENTIONS6. Position on semi-fowler’s to fowler’s for adequate chest expansion7. Prevent complications of immobility

CHF

NURSING INTERVENTION AFTER THE ACUTE STAGE1. Provide opportunities for verbalization of feelings2. Instruct the patient about the medication regimen- digitalis, vasodilators and diuretics3. Instruct to avoid OTC drugs, Stimulants, smoking and alcohol

CHF

NURSING INTERVENTION AFTER THE ACUTE STAGE4. Provide a LOW fat and LOW sodium diet5. Provide potassium supplements6. Instruct about fluid restriction

CHF

NURSING INTERVENTION AFTER THE ACUTE STAGE7. Provide adequate rest periods and schedule activities8. Monitor daily weight and report signs of fluid retention

CARDIOGENIC SHOCKHeart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion

ETIOLOGY1. Massive MI2. Severe CHF3. Cardiomyopathy4. Cardiac trauma5. Cardiac tamponade

CARDIOGENIC SHOCKASSESSMENT FINDINGS

1. HYPOTENSION2. oliguria (less than 30 ml/hour)3. tachycardia4. narrow pulse pressure5. weak peripheral pulses6. cold clammy skin7. changes in sensorium/LOC8. pulmonary congestion

CARDIOGENIC SHOCK

LABORATORY FINDINGS

Increased CVPNormal is 4-10 cmH2O

CARDIOGENIC SHOCK

NURSING INTERVENTIONS

1. Place patient in a modified Trendelenburg (shock ) position

2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE

3. Administer O2

4. Morphine is administered to decreased pulmonary congestion and to relieve pain

CARDIOGENIC SHOCK

5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz cath and IABP

6. Monitor urinary output, BP and pulses

7. cautiously administer diuretics and nitrates

CARDIAC TAMPONADE

A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion)

CARDIAC TAMPONADE

This condition restricts ventricular filling resulting to decreased cardiac outputAcute tamponade may happen when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac

CARDIAC TAMPONADE

Causative factors

1. Cardiac trauma

2. Complication of Myocardial infarction

3. Pericarditis

4. Cancer metastasis

CARDIAC TAMPONADE

ASSESSMENT FINDINGS

1. BECK’s Triad- Jugular vein distention, hypotension and distant/muffled heart sound

2. Pulsus paradoxus

3. Increased CVP

4. decreased cardiac output

CARDIAC TAMPONADE

ASSESSMENT FINDINGS

5. Syncope

6. anxiety

7. dyspnea

8. Percussion- Flatness across the anterior chest

CARDIAC TAMPONADE

Laboratory FINDINGS

1. Echocardiogram

2. Chest X-ray

CARDIAC TAMPONADE

NURSING INTERVENTIONS

1. Assist in PERICARDIOCENTESIS

2. Administer IVF

3. Monitor ECG, urine output and BP

4. Monitor for recurrence of tamponade

Pericardiocentesis

Patient is monitored by ECG

Maintain emergency equipments

Elevate head of bed 45-60 degrees

Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration and myocardial trauma

HYPERTENSION

A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over a sustained period, based on two or more BP measurements.

HYPERTENSION

Types of Hypertension

1. Primary or ESSENTIAL

Most common type

2. Secondary

Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushing’s, Conn’s , SIADH

HYPERTENSION

CLASSIFICATION OF HYPERTENSION by JNC-VII

HYPERTENSION

PATHOPHYSIOLOGY

Multi-factorial etiology

BP= CO (SV X HR) x TPR

Any increase in the above parameters will increase BP

1. Increased sympathetic activity

2. Increased absorption of Sodium, and water in the kidney

HYPERTENSION

PATHOPHYSIOLOGY

Multifactorial etiology

BP= CO (SV X HR) x TPR

Any increase in the above parameters will increase BP

3. Increased activity of the RAAS

4. Increased vasoconstriction of the peripheral vessels

5. insulin resistance

HYPERTENSION

ASSESSMENT FINDINGS

1. Headache

2. Visual changes

3. chest pain

4. dizziness

5. N/V

HYPERTENSIONRisk factors for Cardiovascular Problems in Hypertensive patients

Major Risk factors1. Smoking2. Hyperlipidemia3. DM4. Age older than 60 5. Gender- Male and post menopausal W6. Family History

HYPERTENSION

DIAGNOSTIC STUDIES

1. Health history and PE

2. Routine laboratory- urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS

3. Other lab- CXR, creatinine clearance, 24-huour urine protein

HYPERTENSION

MEDICAL MANAGEMENT

1. Lifestyle modification

2. Drug therapy

3. Diet therapy

HYPERTENSIONMEDICAL MANAGEMENT

Drug therapyDiureticsBeta blockersCalcium channel blockersACE inhibitorsA2 Receptor blockersVasodilators

HYPERTENSION

NURSING INTERVENTIONS1. Provide health teaching to patientTeach about the disease processElaborate on lifestyle changesAssist in meal planning to lose weight

HYPERTENSION

NURSING INTERVENTIONS1. Provide health teaching to the patientProvide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/dayLimit alcohol intake to 30 ml/dayRegular aerobic exerciseAdvise to completely Stop smoking

HYPERTENSIONNursing Interventions2. Provide information about anti-hypertensive drugsInstruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved conditionInstruct to avoid over-the-counter drugs that may interfere with the current medication

HYPERTENSION

Nursing Intervention

3. Promote Home care management

Instruct regular monitoring of BP

Involve family members in care

Instruct regular follow-up

4. Manage hypertensive emergency and urgency properly

Vascular Diseases

ANEURYSM

Dilation involving an artery formed at a weak point in the vessel wall

ANEURYSM

Saccular= when one side of the vessel is affected

Fusiform= when the entire segment becomes dilated

ANEURYSM

RISK FACTORS

1. Atherosclerosis

2. Infection= syphilis

3. Connective tissue disorder

4. Genetic disorder= Marfan’s Syndrome

ANEURYSM

PATHOPHYSIOLOGY

Damage to the intima and media weakness outpouching

Dissecting aneurysm tear in the intima and media with dissection of blood through the layers

ANEURYSM

ASSESSMENT

1. Asymptomatic

2. Pulsatile sensation on the abdomen

3. Palpable bruit

ANEURYSM

LABORATORY:

• CT scan

• Ultrasound

• X-ray

• Aortography

ANEURYSM

Medical Management:

• Anti-hypertensives

• Synthetic graft

ANEURYSM

Nursing Management:

• Administer medications

• Emphasize the need to avoid increased abdominal pressure

• No deep abdominal palpation

• Remind patient the need for serial ultrasound to detect diameter changes

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis.

Usually found in males age 50 and above

The legs are most often affected

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Risk factors for Peripheral Arterial occlusive disease

Non-Modifiable

1. Age

2. gender

3. family predisposition

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Risk factors for Peripheral Arterial occlusive disease

Modifiable1. Smoking 2. HPN3. Obesity4. Sedentary lifestyle5. DM6. Stress

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

ASSESSMENT FINDINGS1. INTERMITTENT CLAUDICATION- the hallmark of PAODThis is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of exercise or activity

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

ASSESSMENT FINDINGS1. INTERMITTENT CLAUDICATION- the hallmark of PAODThis pain is RELIEVED by RESTThis commonly affects the muscle group below the arterial occlusion

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Assessment Findings2. Progressive pain on the extremity as the disease advances3. Sensation of cold and numbness of the extremities

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Assessment Findings4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position5. Muscle atrophy, leg ulceration and gangrene

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Diagnostic Findings

1. Unequal pulses between the extremities

2. Duplex ultrasonography

3. Doppler flow studies

PAOD

Medical Management

1. Drug therapy

Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles

Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation

2. Surgery- Bypass graft and anastomoses

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Nursing Interventions

1. Maintain Circulation to the extremity

Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time

Administer post-operative care to patient who underwent surgery

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Nursing Interventions2. Monitor and manage complications

Note for bleeding, hematoma, decreased urine outputElevate the legs to diminish edemaEncourage exercise of the extremity while on bedTeach patient to avoid leg-crossing

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Nursing Interventions

3. Promote Home management

Encourage lifestyle changes

Instruct to AVOID smoking

Instruct to avoid leg crossing

BUERGER’S DISEASE

Thromboangiitis obliterans

A disease characterized by recurring inflammation of the medium and small arteries and veins of the lower extremities

Occurs in MEN ages 20-35

RISK FACTOR: SMOKING!

BUERGER’S DISEASE

PATHOPHYSIOLOGY

Cause is UNKNOWN

Probably an Autoimmune disease

Inflammation of the arteries thrombus formation occlusion of the vessels

BUERGER’S DISEASE

ASSESSMENT FINDINGS

1. Leg PAIN

Foot cramps in the arch (instep claudication) after exercise

Relieved by rest

Aggravated by smoking, emotional disturbance and cold chilling

2. Digital rest pain not changed by activity or rest

BUERGER’S DISEASE

ASSESSMENT FINDINGS

3. Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances

4. Paresthesia

BUERGER’S DISEASE

Diagnostic Studies

1. Duplex ultrasonography

2. Contrast angiography

BUERGER’S DISEASE

Nursing Interventions

1. Assist in the medical and surgical management

Bypass graft

amputation

2. Strongly advise to AVOID smoking

3. Manage complications appropriately

Medical Management

1. Drug therapy

Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles

Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation

2. Surgery- Bypass graft and anastomoses

BUERGER’S DISEASENursing Interventions

Post-operative care: after amputationElevate stump for the FIRST 24 HOURS to minimize edema and promote venous returnPlace patient on PRONE position after 24 hoursAssess skin for bleeding and hematomaWrap the extremity with elastic bandage

RAYNAUD’S DISEASE

A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain and pallor of the fingertips or toes

Cause : UNKNOWNMost commonly affects WOMEN, 16- 40 years old

RAYNAUD’S DISEASE

ASSESSMENT FINDINGS1. Raynaud’s phenomenon

A localized episode of vasoconstriction of the small arteries of the hands and feet that causes color and temperature changes

RAYNAUD’S DISEASE

W-B-RPallor- due to vasoconstriction, thenBlue- due to pooling of Deoxygenated bloodRed- due to exaggerated reflow/hyperemia

RAYNAUD’S DISEASE

ASSESSMENT FINDINGS2. tingling sensation

3. Burning pain on the hands and feet

RAYNAUD’S DISEASE

Medical management

Drug therapy with the use of CALCIUM channel blockers

To prevent vasospasms

RAYNAUD’S DISEASE

Nursing Interventions1. instruct patient to avoid situations that may be stressful2. instruct to avoid exposure to cold and remain indoors when the climate is cold3. instruct to avoid all kinds of nicotine4. instruct about safety. Careful handling of sharp objects

Venous diseases

VARICOSE VEINS

THESE are dilated veins usually in the lower extremities

VARICOSE VEINS

Predisposing FactorsPregnancyProlonged standing or sittingConstipation (for hemorrhoids)Incompetent venous valves

VARICOSE VEINS

PathophysiologyFactors venous stasis increased hydrostatic pressure edema

VARICOSE VEINS

Assessment findingsTortuous superficial veins on the legs

Leg pain and Heaviness

Dependent edema

VARICOSE VEINS

Laboratory findingsVenography

Duplex scan pletysmography

VARICOSE VEINS

Medical managementPharmacological therapy

Leg vein stripping

Anti-embolic stockings

VARICOSE VEINS

Nursing management

1. Advise patient to elevate the legs

2. Caution patient to avoid prolonged standing or sitting

VARICOSE VEINS

Nursing management

3. Provide high-fiber foods to prevent constipation

4. Teach simple exercise to promote venous return

VARICOSE VEINS

Nursing management

5. Caution patient to avoid knee-length stockings and constrictive clothings

VARICOSE VEINS

Nursing management6. Apply anti-embolic stockings as directed7. Avoid massage on the affected area

DVT- Deep Vein Thrombosis

Inflammation of the deep veins of the lower extremities and the pelvic veins

The inflammation results to formation of blood clots in the area

DVT- Deep Vein Thrombosis

Predisposing factorsProlonged immobility

Varicosities

Traumatic procedures

DVT- Deep Vein Thrombosis

Complication

PULMONARY thromboembolism

DVT- Deep Vein Thrombosis

Assessment findings

Leg tenderness

Leg pain and edema

Positive HOMAN’s SIGN

DVT- Deep Vein Thrombosis

Laboratory findings

Venography

Duplex scan

DVT- Deep Vein Thrombosis

Medical managementAntiplatelets

Anticoagulants

Vein stripping and grafting

Anti-embolic stockings

DVT- Deep Vein Thrombosis

Nursing management

1. Provide measures to avoid prolonged immobility

Repositioning Q2

Provide passive ROM

Early ambulation

DVT- Deep Vein Thrombosis

Nursing management

2. Provide skin care to prevent the complication of leg ulcers

3. Provide anti-embolic stockings

DVT- Deep Vein Thrombosis

Nursing management

4. Administer anticoagulants as prescribed

5. Monitor for signs of pulmonary embolism

Blood disordersBlood disorders

AnemiaAnemiaNutritional anemiaNutritional anemiaHemolytic anemiaHemolytic anemiaAplastic anemiaAplastic anemiaSickle cell anemiaSickle cell anemia

ANEMIAANEMIA

A condition in A condition in which the which the hemoglobin hemoglobin concentration is concentration is lower than normallower than normal

ANEMIAANEMIA

Three broad categoriesThree broad categories1. Loss of RBC- occurs with 1. Loss of RBC- occurs with

bleedingbleeding2. Decreased RBC 2. Decreased RBC

productionproduction3. Increased RBC 3. Increased RBC

destructiondestruction

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency Anemia–Results when the Results when the dietary intake of iron dietary intake of iron is inadequate to is inadequate to produce hemoglobinproduce hemoglobin

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency Anemia–Etiologic FactorsEtiologic Factors–1. Bleeding- the most 1. Bleeding- the most common causecommon cause

–2. Mal-absorption2. Mal-absorption–3. Malnutrition3. Malnutrition–4. Alcoholism4. Alcoholism

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency Iron Deficiency AnemiaAnemia

PathophysiologyPathophysiology–The body stores of iron The body stores of iron decrease, leading to decrease, leading to depletion of depletion of hemoglobin synthesishemoglobin synthesis

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency AnemiaPathophysiologyPathophysiology

–The oxygen carrying The oxygen carrying capacity of hemoglobin is capacity of hemoglobin is reducedreduced tissue hypoxia tissue hypoxia

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency AnemiaAssessment FindingsAssessment Findings1. Pallor of the skin and 1. Pallor of the skin and mucous membranemucous membrane

2. Weakness and fatigue2. Weakness and fatigue3. General malaise3. General malaise4. Pica4. Pica

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency AnemiaAssessment FindingsAssessment Findings5. Brittle nails5. Brittle nails6. Smooth and sore 6. Smooth and sore tonguetongue

7. Angular cheilosis7. Angular cheilosis

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency AnemiaLaboratory findingsLaboratory findings1. CBC- Low levels of Hct, 1. CBC- Low levels of Hct, Hgb and RBC countHgb and RBC count

2. low serum iron, low 2. low serum iron, low ferritinferritin

3. Bone marrow aspiration- 3. Bone marrow aspiration- MOST definitiveMOST definitive

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency AnemiaMedical managementMedical management1. Hematinics1. Hematinics2. Blood transfusion2. Blood transfusion

Hypoproliferative AnemiaHypoproliferative Anemia

Iron Deficiency AnemiaIron Deficiency AnemiaNursing ManagementNursing Management1. Provide iron rich-foods1. Provide iron rich-foods

–Organ meats (liver)Organ meats (liver)–BeansBeans–Leafy green vegetablesLeafy green vegetables–Raisins and molassesRaisins and molasses

Hypoproliferative AnemiaHypoproliferative Anemia

Nursing ManagementNursing Management2. Administer iron 2. Administer iron Oral preparations tablets- Fe Oral preparations tablets- Fe

fumarate, sulfate and gluconatefumarate, sulfate and gluconate Advise to take iron ONE hour Advise to take iron ONE hour

before mealsbefore meals Take it with vitamin CTake it with vitamin C Continue taking it for several Continue taking it for several

monthsmonths

Hypoproliferative AnemiaHypoproliferative AnemiaNursing ManagementNursing Management2. Administer iron 2. Administer iron Oral preparations- liquidOral preparations- liquid It stains teethIt stains teeth Drink it with a strawDrink it with a straw Stool may turn blackish- dark Stool may turn blackish- dark

in colorin color Advise to eat high-fiber diet to Advise to eat high-fiber diet to

counteract constipationcounteract constipation

Hypoproliferative AnemiaHypoproliferative AnemiaNursing ManagementNursing Management2. Administer iron 2. Administer iron IM preparationIM preparation Administer DEEP IM using the Administer DEEP IM using the

Z-track methodZ-track method Avoid vigorous rubbingAvoid vigorous rubbing Can cause local pain and Can cause local pain and

stainingstaining

APLASTIC ANEMIAAPLASTIC ANEMIA

A condition A condition characterized by characterized by decreased number decreased number of RBC as well as of RBC as well as WBC and plateletsWBC and platelets

APLASTIC ANEMIAAPLASTIC ANEMIA

CAUSATIVE FACTORSCAUSATIVE FACTORS1. Environmental toxins- 1. Environmental toxins-

pesticides, benzenepesticides, benzene2. Certain drugs- 2. Certain drugs-

Chemotherapeutic agents, Chemotherapeutic agents, chloramphenicol, chloramphenicol, phenothiazines, Sulfonamidesphenothiazines, Sulfonamides

3. Heavy metals3. Heavy metals4. Radiation4. Radiation

APLASTIC ANEMIAAPLASTIC ANEMIA

PathophysiologyPathophysiologyToxins cause a direct bone Toxins cause a direct bone marrow depressionmarrow depression acellualr bone marrowacellualr bone marrow decreased production of decreased production of blood elementsblood elements

APLASTIC ANEMIAAPLASTIC ANEMIA

ASSESSMENT FINDINGSASSESSMENT FINDINGS1. fatigue1. fatigue2. pallor2. pallor3. dyspnea3. dyspnea4. bruising4. bruising5. splenomegaly5. splenomegaly6. retinal hemorrhages6. retinal hemorrhages

APLASTIC ANEMIAAPLASTIC ANEMIA

LABORATORY FINDINGSLABORATORY FINDINGS1. CBC- decreased blood 1. CBC- decreased blood cell numberscell numbers

2. Bone marrow 2. Bone marrow aspiration confirms the aspiration confirms the anemia- hypoplastic or anemia- hypoplastic or acellular marrow acellular marrow replaced by fatsreplaced by fats

APLASTIC ANEMIAAPLASTIC ANEMIA

Medical ManagementMedical Management1. Bone marrow 1. Bone marrow transplantationtransplantation

2. Immunosupressant 2. Immunosupressant drugsdrugs

3. Rarely, steroids3. Rarely, steroids4. Blood transfusion4. Blood transfusion

APLASTIC ANEMIAAPLASTIC ANEMIA

Nursing managementNursing management1. Assess for signs of 1. Assess for signs of bleeding and bleeding and infectioninfection

2. Instruct to avoid 2. Instruct to avoid exposure to offending exposure to offending agentsagents

Megaloblastic AnemiasMegaloblastic Anemias

Anemias characterized Anemias characterized by abnormally large RBC by abnormally large RBC secondary to impaired secondary to impaired DNA synthesis due to DNA synthesis due to deficiency of Folic acid deficiency of Folic acid and/or vitamin B12 and/or vitamin B12

Megaloblastic AnemiasMegaloblastic Anemias

Folic Acid deficiencyFolic Acid deficiencyCausative factorsCausative factors1. Alcoholism1. Alcoholism2. Mal-absorption2. Mal-absorption3. Diet deficient in 3. Diet deficient in uncooked vegetablesuncooked vegetables

Megaloblastic AnemiasMegaloblastic AnemiasPathophysiology of Folic acid Pathophysiology of Folic acid

deficiencydeficiencyDecreased folic acidDecreased folic acid impaired impaired

DNA synthesis in the bone DNA synthesis in the bone marrowmarrow impaired RBC impaired RBC development, impaired nuclear development, impaired nuclear maturation but CYTOplasmic maturation but CYTOplasmic maturation continuesmaturation continues large large sizesize

Megaloblastic AnemiasMegaloblastic Anemias

Vitamin B12 deficiencyVitamin B12 deficiencyCausative factorsCausative factors1. Strict vegetarian diet1. Strict vegetarian diet2. Gastrointestinal 2. Gastrointestinal

malabsorptionmalabsorption3. Crohn's disease3. Crohn's disease4. gastrectomy4. gastrectomy

Megaloblastic AnemiasMegaloblastic Anemias

Vitamin B12 deficiencyVitamin B12 deficiency

Pernicious AnemiaPernicious Anemia Due to the absence of intrinsic Due to the absence of intrinsic

factor secreted by the parietal factor secreted by the parietal cells cells

Intrinsic factor binds with Vit. Intrinsic factor binds with Vit. B12 to promote absorptionB12 to promote absorption

Megaloblastic AnemiasMegaloblastic Anemias

Assessment findingsAssessment findings 1. weakness1. weakness 2. fatigue2. fatigue 3. listless3. listless 4. neurologic manifestations 4. neurologic manifestations

are present only in Vit. B12 are present only in Vit. B12 deficiencydeficiency

Megaloblastic AnemiasMegaloblastic Anemias

Assessment findingsAssessment findings Pernicious AnemiaPernicious Anemia

– Beefy, red, swollen tongueBeefy, red, swollen tongue– Mild diarrheaMild diarrhea– Extreme pallorExtreme pallor– Paresthesias in the extremitiesParesthesias in the extremities

Megaloblastic AnemiasMegaloblastic Anemias

Laboratory findingsLaboratory findings 1. Peripheral blood smear- 1. Peripheral blood smear-

shows giant RBCs, WBCs with shows giant RBCs, WBCs with giant hypersegmented nucleigiant hypersegmented nuclei

2. Very high MCV2. Very high MCV 3. Schilling’s test3. Schilling’s test 4. Intrinsic factor antibody test4. Intrinsic factor antibody test

Megaloblastic AnemiasMegaloblastic Anemias

Medical ManagementMedical Management 1. Vitamin supplementation1. Vitamin supplementation

– Folic acid 1 mg dailyFolic acid 1 mg daily 2. Diet supplementation2. Diet supplementation

– Vegetarians should have vitamin Vegetarians should have vitamin intakeintake

3. Lifetime monthly injection 3. Lifetime monthly injection of IM Vit B12of IM Vit B12

Megaloblastic AnemiasMegaloblastic Anemias

Nursing ManagementNursing Management 1. Monitor patient1. Monitor patient 2. Provide assistance in 2. Provide assistance in

ambulationambulation 3. Oral care for tongue sore3. Oral care for tongue sore 4. Explain the need for 4. Explain the need for

lifetime IM injection of vit B12lifetime IM injection of vit B12

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

A severe chronic A severe chronic incurable hemolytic incurable hemolytic anemia that results anemia that results from heritance of the from heritance of the sickle hemoglobin sickle hemoglobin gene.gene.

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Causative factorCausative factor–Genetic inheritance Genetic inheritance of the sickle gene- of the sickle gene- HbS geneHbS gene

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

PathophysiologyPathophysiologyDecreased O2, Cold, Decreased O2, Cold, Vasoconstriction can Vasoconstriction can precipitate sickling precipitate sickling processprocess

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCellPathophysiologyPathophysiology

FactorsFactors cause defective cause defective hemoglobin to acquire a hemoglobin to acquire a rigid, crystal-like C-shaped rigid, crystal-like C-shaped configurationconfiguration Sickled Sickled RBCs will adhere to RBCs will adhere to endotheliumendothelium pile up and pile up and plug the vesselsplug the vessels ischemia resultsischemia results pain, pain, swelling and feverswelling and fever

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Assessment FindingsAssessment Findings1. jaundice1. jaundice2. enlarged skull and 2. enlarged skull and facial bonesfacial bones

3. tachycardia, 3. tachycardia, murmurs and murmurs and cardiomegalycardiomegaly

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Assessment FindingsAssessment FindingsPrimary sites of Primary sites of thrombotic occlusion: thrombotic occlusion: spleen, lungs and CNSspleen, lungs and CNS

Chest pain, dyspneaChest pain, dyspnea

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Assessment FindingsAssessment Findings1. Sickle cell crises1. Sickle cell crises

–Results from tissue hypoxia Results from tissue hypoxia and necrosisand necrosis

2. Acute chest syndrome2. Acute chest syndrome–Manifested by a rapidly Manifested by a rapidly falling hemoglobin level, falling hemoglobin level, tachycardia, fever and tachycardia, fever and chest infiltrates in the CXRchest infiltrates in the CXR

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Medical ManagementMedical Management1. Bone marrow 1. Bone marrow transplanttransplant

2. Hydroxyurea2. Hydroxyurea–Increases the HbFIncreases the HbF

3. Long term RBC 3. Long term RBC trnasfusiontrnasfusion

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Nursing ManagementNursing Management1. manage the pain1. manage the pain

–Support and elevate Support and elevate acutely inflamed jointacutely inflamed joint

–Relaxation techniquesRelaxation techniques–analgesicsanalgesics

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Nursing ManagementNursing Management2. Prevent and manage 2. Prevent and manage infectioninfection–Monitor status of Monitor status of patientpatient

–Initiate prompt Initiate prompt antibiotic therapyantibiotic therapy

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Nursing ManagementNursing Management3. Promote coping skills3. Promote coping skills

–Provide accurate Provide accurate informationinformation

–Allow patient to verbalize Allow patient to verbalize her concerns about her concerns about medication, prognosis medication, prognosis and future pregnancyand future pregnancy

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Nursing ManagementNursing Management4. Monitor and prevent 4. Monitor and prevent potential complicationspotential complications–Provide always adequate Provide always adequate hydrationhydration

–Avoid cold, temperature Avoid cold, temperature that may cause that may cause vasoconstrictionvasoconstriction

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Nursing ManagementNursing Management4. Monitor and 4. Monitor and prevent potential prevent potential complicationscomplications–Leg ulcerLeg ulcer

Aseptic techniqueAseptic technique

Hemolytic Anemia: Sickle Hemolytic Anemia: Sickle CellCell

Nursing ManagementNursing Management4. Monitor and prevent 4. Monitor and prevent potential complicationspotential complications–PriapismPriapism

Sudden painful erectionSudden painful erectionInstruct patient to empty Instruct patient to empty bladder, then take a warm bladder, then take a warm bathbath

PolycythemiaPolycythemia

Refers to an INCREASE Refers to an INCREASE volume of RBCsvolume of RBCs

The hematocrit is The hematocrit is ELEVATED to more than ELEVATED to more than 55%55%

Clasified as Primary or Clasified as Primary or SecondarySecondary

PolycythemiaPolycythemia

POLYCYTHEMIA VERAPOLYCYTHEMIA VERA–Primary PolycythemiaPrimary Polycythemia–A proliferative disorder A proliferative disorder in which the myeloid in which the myeloid stem cells become stem cells become uncontrolled uncontrolled

PolycythemiaPolycythemia

POLYCYTHEMIA VERAPOLYCYTHEMIA VERACausative factorCausative factor

–unknownunknown

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERAPathophysiologyPathophysiology

–The stem cells grow The stem cells grow uncontrollablyuncontrollably

–The bone marrow becomes The bone marrow becomes HYPERcellular and all the blood HYPERcellular and all the blood cells are increased in numbercells are increased in number

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERAPathophysiologyPathophysiology

–The spleen resumes its function The spleen resumes its function of hematopoiesis and enlargesof hematopoiesis and enlarges

–Blood becomes thick and Blood becomes thick and viscous causing sluggish viscous causing sluggish circulationcirculation

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERAPathophysiologyPathophysiology

–Overtime, the bone Overtime, the bone marrow becomes fibroticmarrow becomes fibrotic

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERAAssessment findingsAssessment findings

–1. Skin is ruddy1. Skin is ruddy–2. Splenomegaly2. Splenomegaly–3. headache3. headache–4. dizziness, blurred vision4. dizziness, blurred vision–5. Angina, dyspnea and 5. Angina, dyspnea and thrombophlebitisthrombophlebitis

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERALaboratory findingsLaboratory findings

–1. CBC- shows elevated RBC 1. CBC- shows elevated RBC massmass

–2. Normal oxygen saturation2. Normal oxygen saturation–3 Elevated WBC and 3 Elevated WBC and PlateletsPlatelets

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERAComplicationsComplications

–1. Increased risk for 1. Increased risk for thrombophlebitis, CVA and thrombophlebitis, CVA and MIMI

–2. Bleeding due to 2. Bleeding due to dysfunctional blood cellsdysfunctional blood cells

PolycythemiaPolycythemiaPOLYCYTHEMIA VERAPOLYCYTHEMIA VERAMedical ManagementMedical Management

–1. To reduce the high blood cell 1. To reduce the high blood cell mass- PHLEBOTOMYmass- PHLEBOTOMY

–2. Allopurinol2. Allopurinol–3. Dipyridamole3. Dipyridamole–4. Chemotherapy to suppress 4. Chemotherapy to suppress bone marrowbone marrow

PolycythemiaPolycythemia Nursing ManagementNursing Management

– 1. Primary role of the nurse is 1. Primary role of the nurse is EDUCATOREDUCATOR

– 2. Regularly asses for the 2. Regularly asses for the development of complicationsdevelopment of complications

– 3. Assist in weekly phlebotomy3. Assist in weekly phlebotomy– 4. Advise to avoid alcohol and aspirin4. Advise to avoid alcohol and aspirin– 5. Advise tepid sponge bath or cool 5. Advise tepid sponge bath or cool

water to manage prurituswater to manage pruritus

LeukemiaLeukemiaMalignant disorders of blood Malignant disorders of blood

forming cells characterized by forming cells characterized by UNCONTROLLED proliferation UNCONTROLLED proliferation of WHITE BLOOD CELLS in the of WHITE BLOOD CELLS in the bone marrow- replacing bone marrow- replacing marrow elements . The WBC marrow elements . The WBC can also proliferate in the can also proliferate in the liver, spleen and lymph nodes.liver, spleen and lymph nodes.

LeukemiaLeukemia

The leukemias are named The leukemias are named after the specific lines of after the specific lines of blood cells afffected blood cells afffected primarilyprimarily– MyeloidMyeloid– LymphoidLymphoid– MonocyticMonocytic

LeukemiaLeukemia

The leukemias are named also The leukemias are named also according to the maturation of according to the maturation of cellscells

ACUTEACUTE– The cells are primarily immatureThe cells are primarily immature

CHRONICCHRONIC– The cells are primarily mature The cells are primarily mature or diferentiatedor diferentiated

LeukemiaLeukemia

ACUTE myelocytic leukemiaACUTE myelocytic leukemiaACUTE lymphocytic leukemiaACUTE lymphocytic leukemia

CHRONIC myelocytic leukemiaCHRONIC myelocytic leukemiaCHRONIC lymphocytic leukemiaCHRONIC lymphocytic leukemia

LeukemiaLeukemia

ETIOLOGIC FACTORSETIOLOGIC FACTORS– UNKNOWMUNKNOWM– Probably exposure to Probably exposure to radiationradiation

– Chemical agentsChemical agents– Infectious agentsInfectious agents– GeneticGenetic

LeukemiaLeukemia

– PATHOPHYSIOLOGY of PATHOPHYSIOLOGY of ACUTE LeukemiaACUTE Leukemia

Uncontrolled proliferation of Uncontrolled proliferation of immature cellsimmature cells suppresses bone marrow suppresses bone marrow functionfunction severe anemia, severe anemia, thrombocytopenia and thrombocytopenia and granulocytopeniagranulocytopenia

LeukemiaLeukemia

– PATHOPHYSIOLOGY of PATHOPHYSIOLOGY of CHRONIC LeukemiaCHRONIC Leukemia

Uncontrolled proliferation of Uncontrolled proliferation of DIFFERENTIATED cellsDIFFERENTIATED cells slow suppression of bone slow suppression of bone marrow functionmarrow function milder milder symptomssymptoms

LeukemiaLeukemia

ASSESSMENT FINDINGSASSESSMENT FINDINGS ACUTE LEUKEMIAACUTE LEUKEMIA

– PallorPallor– FatigueFatigue– DyspneaDyspnea– HemorrhagesHemorrhages– OrganomegalyOrganomegaly– HeadacheHeadache– vomitingvomiting

LeukemiaLeukemia

ASSESSMENT FINDINGSASSESSMENT FINDINGS CHRONIC LEUKEMIACHRONIC LEUKEMIA

– Less severe symptomsLess severe symptoms– organomegalyorganomegaly

LeukemiaLeukemia

LABORATORY FINDINGSLABORATORY FINDINGS Peripheral WBC count varies Peripheral WBC count varies

widely widely Bone marrow aspiration biopsy Bone marrow aspiration biopsy

reveals a large percentage of reveals a large percentage of immature cells- BLASTSimmature cells- BLASTS

Erythrocytes and platelets are Erythrocytes and platelets are decreaseddecreased

LeukemiaLeukemia

Medical ManagementMedical Management

1.1. ChemotherapyChemotherapy

2.2. Bone marrow transplantationBone marrow transplantation

LeukemiaLeukemia

Nursing ManagementNursing Management 1. Manage AND prevent 1. Manage AND prevent

infectioninfection– Monitor temperatureMonitor temperature– Assess for signs of infectionAssess for signs of infection– Be alert if the neutrophil count Be alert if the neutrophil count

drops below 1,000 cells/mm3drops below 1,000 cells/mm3

LeukemiaLeukemia

Nursing ManagementNursing Management 2. Maintain skin integrity2. Maintain skin integrity

3. Provide pain relief3. Provide pain relief

4. Provide information as to 4. Provide information as to therapy- chemo and bone therapy- chemo and bone marrow transplantationmarrow transplantation

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