cardiovascular & hematologic system
TRANSCRIPT
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