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CARDIOVASCULAR SYSTEM:
Heart: Location: MediastinumSize: Fist; wt= 300 g (10.6 oz) Characteristics: Four chambered muscular organFunctions: Pumps blood to the tissues, supplying
them with oxygen and other nutrientsComposed of:
a. Endocardium Consists of the endothelial tissue and lines inside the heart and valves.b. Myocardium Made up of muscle fibers and is responsible for the pumping action.c.Epicardium Exterior layer of the heart.
PericardiumCharacteristics: Thin, fibrous sacFunctions: Surrounds the heart, protects it from
traumas and infections.Composed of:
a. Visceral pericardium Adhering to the epicardiumb. Parietal pericardium A tough fibrous tissue that attaches to the great vessels, diaphragm,
sternum, and vertebral column and supports the heart in the mediastinum. c. pericardial space - space between two layers.
- normally filled with 20 mL of fluid, lubricates the surface of the heart and reduces friction during systole.
Four chambers of the heart
-Separated by the septum-pumping action of the heart accomplished by rhythmic relaxation and contraction of the heart.a. Diastole -Relaxation phase
-all four chambers relax simultaneously. -allows the ventricle to fill in preparation for contraction.-period of ventricular filling.
b. Systole -events in the heart during contraction of the two top chambers and 2 bottom chanbers.- Atrial systole occurs first just at the of diastole, followed by ventricular systole.- this sync, allows the ventricles to completely fill prior to ejection of blood from their chambers.
Composed of:a. Atria Upper collecting chambers
b.Ventricle Lower collecting chambers
Blood flow:
IVC
SVC
RA
TRICUSPID VALVE -prevents regurgitation.
RV
PULMONARY ARTERY
PULMONIC VALVE
BLOOD FROM THE LUNGS
LA
MITRAL VALVE- guarding atrium; prevents regurgitation.
LV
AORTIC VALVE
AORTA
SYSTEMIC CIRCULATION
FOUR VALVES OF THE HEART -keeps blood flowing in one directiona. Atrioventricular valves (tricuspid/ mitral valve)
Prevents backflow of blood into the atria at the start of each contraction.
b. Pulmonic and aortic valve -Prevents blood from regurgitating into the ventricles of each ventricular contraction. -“semilunar valves”
- Ventricular wall must expand in order to accommodate rapid ventricular
filling.
Name Description Characteristics Etiology Clinical manifestations
Nsg. Mangement
Sinus tachycardia rate is greater than 100
RATE: 100 to 180 bpmP WAVES: precede each QRS.PR INTERVAL: normalQRS COMPLEX: normalCONDUCTION: normalRHYTHM: normal
Causes:(asymptomatic)ExerciseAnxietyFeverDrugsAnemiaHeart failureHypovolemia
Occasional palpitationsHypotensionAngina with CVD
Prescribed treatmentCarotid massageNeta-adrenergic blockers
ShockSinus Bradycardia Heart rate is less
than 60 bpmRATE: less than 60P WAVES: precede each QRSPR INTERVAL: normalQRS COMPLEX: normalRHYTHM: normalCONDUCTION: normal
-DrugsVagal stimulationHypoendocrine statesanorexiahypothermiasinus node involvement in MI
-normal in athletes
FatigueLightheadednessSyncope
Maintain adequate COAnticholinergic drug (atropine
Premature Ventricular Tachycardia
-Increased automaticity of ventricular muscle cells.- harmful if more than 6.
RATE: 60 TO 100 BPM P WAVES: no P wavesPR INTERVAL: no PR intervalQRS COMPLEX: -wide and bizarre (0.1 second)-multifocal-results in many different configurations RHYTHM: BigeminyCONDUCTION: retrograde through the conduction system
Irritability of ventricular musclesExerciseIncreasd catecholaminesElectrolyte ImbalanceDigoxin ToxicityHypoxiaMyocardial Damage
(asymptomatic)PalpitationsWeaknessLightheadedness
AssessmentSevere, may lead to Fibrillation or V tach.Admin lidocaine- short termProcainamide- long term
Name Description Characteristics Etiology Clinical manifestations
Nsg. Mangement
Ventricular Tachycardia
Three or more consecutive PVC’s
Decreased in diastolic filling
RATE: 100-250P wave: blurred ; QRS has no association with the P wavePR interval: not presentQRS complex: wide and bizarre, T wave is in the opposite directionConduction: abnormal in ventricular tissueRhythm: usually regular
Irritability of ventricular muscle
Light-headednessWeaknessDyspneaUnconscious
Antiarrhythmic drud Lidocaine Procainamide/ AmiodaroneCardioversion –if meds unsuccessful.Severe- defibrillation
Ventricular fibrillation Rapid, ineffective RATE: rapid and Untreated VT LOC Assist with
quivering of ventricles that may be rapidly fatal.
uncoordinatedP wave: not seenPR interval: not seenQRS complex: undulation with no specific patternConduction: unorganized; foci firing at onceRhythm: Irregular with rhythm
Digoxin and quinidine toxicityHypothermia
PulselessnessLoss of BPCessation of respirationsPossible seizuresSudden death
defibrillationAntiarrythmic medAvoid automated external devices
Disease Definition Diagnostic exams Etiology Clinical manifestations Nsg. ManagementCoronary artery disease
Narrowing of large and medium sized coronary arteries due to intimal plaque formation
ECG 1. ST depression2. T wave
inversion
1. Advanced age2. Chronic stress3. DM4. Family history5. Contraceptives6. Hyperlipidemia7. Hypertension8. Male/ post
menopausal female
9. Obesity10. Sedentary lifestyle11. Smoking
Angina N and V Dizziness Syncope Diaphoresis,
cool clammy skin
Apprehension or a sense of impending doom
Nitrates Antiplatelets Antilipidemics Beta-adrenergic
blockers Ca channel
blockers
*Anginal attack1. Stop all activity,
Place one NTG tablet under the tongue adnw ait for 5 min,
2. Stay with him at all times
3. STAT 12- lead ECG
4. Family teaching
*Treatment:1. PTCA- percutaneous
transluminal Coronary angioplasty
2. CABG- coronary Artery bypass graft
*family Teaching1. Participate in
cardiac rehab.2. Advise family to
take CPR courseDisease Definition Diagnostic exams Etiology Clinical manifestations Nsg. ManagementMyocardial Infarction
1. Destruction of myocardial tissue in regions of the heart .
2. Deprivation of adequate blood supply.
ECG T wave to be larger and inverted(epicardial MI)St segment elevated(endocardial MI)
Serum enzyme tests:Creatinine phosphokinaseLactate dehydrogenaseTroponin
WBC elevated
1. Atherosclerosis2. Coronary Artery
Spasm3. Complete arterial
occlusion by embolism or thrombus
4. Decreased coronary blood flow due to hemorrhage or shock
Chest painDiaphoresisN and VDyspneaPalpitations or syncopeAnxietyTachycardia/ bradycardiaDec. BPAltered S3 (L ventricular failure)
Drug therapy Morphine Nitrates Antilipidemics Thrombolytics AnticoagulantsAssess Px Monitor cardiac enzymes Hemodynamic parametersAnxietyDiet: liquid dietLow sodium dietLow fat
Treatment PTCA CABGFamily teaching
CARDIAC REHABILITATION
Goal: help px live a life that is full, vital, and productive but within the hearts ability
Objective:
Limit the effects and progression of atherosclerosis
Return px to work and pre-illness lifestyle
Enhance the pfychosocial and vocational status of the Px
Prevent another cardiac event
Causes:CVD:ASHDMIHYPERTENSIONRHDIschemic Heart DiseaseArrythmiasValvular disease
Non- CVDPregnancy and childbirthSevere Physical and mental stressThrotoxicosisAcute Blood LossSevere infectionCOPD
NSG. Management CBR
Semifowlers position- promote oxygenation
Nitroglycerin1. Inorder to preserve
med: do not place on light.
2. Lifetime: 6 mths3. Vasodilatory function
(check BP)4. If not relieved give
every 5 min. O2- tissue hypoxia ECG- Hemodynamic
procedure Stool softeners-dec.
constipation-risk of bradycardia
Thrombolytic Therapy- effective during 3 to 5 hrs.
After therapy—take heparin: to prevent recurence
Admin antiarryhythmias
CATEGORIES:1. Right-L sided HF-Cor pulmonale-R ventricular infarction
2.Left-Disease of coronary arteriesHypertensionCardiomyopathyRHD
Maintain a quite envi.
MIO
HEART FAILURE Syndrome of pulmonary or systemic circulatory congestion caused by decreased myocardial contractility.
CHEST RADIOGRAPH
CardiomegalyVascular congestion
ELECTROCARDIOGRAM:HypertrophyMyocardial damage
ABGDecreased partial pressure of arterial oxygen Increased partial pressure of arterial carbon dioxide
PULSE OXIMETERLess than 95 %
MULTILUMEN PULMONARY ARTERY L SIDE:Elevated pulmonary artery and capillary wedge pressures
R side:Elevated CVP
LEFT SIDED:DyspneaCracklesFrothy blood tinged sputumTachycardia with s3soundPale cool extremitiesPeripheral and central cyanosisDec. peripheral pulsesDec. urinary outputEasy fatigabilityInsomnia
RIGHT SIDEDEdemaWt. gainNauseaAnorexiaJVDLiver congestion
Medications: Cardiac glycosides Diuretics Angiotensin
converting enzyme inhibitors
Vasodilator therapy
Antilipemics
Provide ongoing assessment: Multilumen pulmonary
artery catheter: -Hemodynamic parameters Heart rate and rhythm
Weigh client
Monitor serum electrolyte
Prevent complication of immobility: Apply antiembolism stockings
Provide a low low sodium diet- dec. fluid retention and subsequently the workload of the heart.
Provide a client and family teaching
Internal ballon- mech. Device that diverts blood to an ext pump.
ANGINA
Types: Stable angina-
paroxysmal chest pain. Predictable.
Unstable angina- pre infarction. Unpredictable degree
Variant angina- similar to classic angina. Appears at early HRS of the day.
Nocturnal Angina- during night
Angina Decubitus- recline and lessens when the clients stands up
Intractable- not responsive to intervention
Post infarction- occurs after heart attack
LABS and Dx’s test: ECG Exercise stress
test Echocardiogram C-reactive protein Coronary
Angiography Cardiac
catheterization
Chest pain upon :Physical exertionExposure to coldEating a heavy mealstress
DRUG THERAPY: Nitrates Beta blockers Ca channel
blockers Antiplatelet anti coagulant
medications1. aspirin2. eplidogrel3. heparin4. LMWH
Acute Pulmonary edema-L side HF
Heart failure
CO reduced increased left atrial pressure
Increased pulmonary vein and capillary pressure exceeding intravascular osmotic pressure
Serous fluid is forced rapidly into the alveoli
Reaches the bronchioles and bronchi
Assessment
Restlessness and vague uneasiness
Profound dyspnea
Pallor
Cough
Productive frothy blood tinged –classic symptom
sputum
Audible wheezing
Cyanosis
Tachycardia
Treatment
CBRSemifowlers positionOxygen (40 to 70)Drug therapy Digitalis Diuretics Vasodilators Morphine IV AminophyllineRotating Tourniquet or phlebotomyHemodynamic Monitoring –CVPEndotracheal/ nasotracheal intubation
Px’s with cardiac failure- careful in positioning
- Semi-fowlers-
- Inc. in fluid in change of positions
- Lungs is affected
Dx’s test: Chest radiographvascular congestion of lung fields (butterfly appearance)
Multilumen Pulmonary artery catheter-
Elevated central venousPulmonary arteryCapillary wedge pressures
ABG Decreased partial pressure of arterial oxygen Co2
STRUCTURAL HEART FAILURE
Congenital Heart Failurea. Volume overload-occurs when greater than normal amount of blood enters either the ventricular chambers.
b.Ventricular Septal Defect-abnormal opening between R and L ventricles.
Clinical manifestations
CHF Murmur Risk for bacterial
endocarditis and pulmonary vascular obstructive
Tachypneic Diaphoretic Fatigue Emboli formation
Dx
Chest XrayEchocardiogram
Surgical management
Pallative surgeryCABG -closure or patch graft performed
Atrial septal defect:Surgical Dacron patchCP bypass
OBSTRUCTION OF THE FORWARD FLOW
Coarctation of the aorta
-caused by narrowing of aorta that impedes blood flow, can occur anywhere between the origin of the aortic arch and bifurcation of the aorta in the lower abd.
Aortic Stenosis-fusion of the three cusps of the aortic valve-causing resistance to the blood flow in the L ventricles-L ventricular Hypertrophy-Pulmonary Vascular congestion-Hypertrophy of the L ventricular wall lead to decrease end diastolic pressure; results to pulmonary venous and pulmonary arterial HPN
MANIFESTATIONS:
s/sx of CHF in infanthigh BP and bounding
pulse in the armsWeak or absent femoral
pulseColl lower extremitiesChildren exp:HeadacheDizzinessFaintingEpistaxis resulting from
hypertension
MurmurDec cardiac output withfaint pulsesHypotensionTachycardiaPoor feeding
Children show signs of:Exercise intoleranceChest paindizziness
High risk for:HPNRuptured aortaAortic aneurysmStroke
Surgical management
Resection of the coarcted portion with an end to end anastomosis of the aorta
Enlargement of the constricted section
Percutaneous balloon angioplasty
Aortic ValvulotomyBalloon angioplasty
Disease Pathophysiology Assessment Treatment Dx’s exams Etiology
CONGENITAL PULMONIC STENOSIS
-narrowing of pulmonary valve-resistance to blood flow causes R ventricular hypertrophy and decreased pulmonary BF
PULMONARY ATRESIA- extreme form of pulmonary stenosis in that there is total fusion of the commisures and no blood flow to the lungs
Manifestations:
MurmurMild cyanosis of CHFCyanosisSevere: CHF
Treatment;Surgery
Transventricular valvutomy
Pulmonary valvutomy
CONDITIONS OF DESATURATION
Assessment:Infant:-acutely cyanotic progresses as pulmonic
MANAGEMENT:
Knee chest and squatting position
Tetralogy of fallota. structural defect – complex of shunting of the blood due to multiple structural alterationsb. Ventricular Septal defectc. Pulmonic Stenosisd. Overriding of the aortae.R ventricular hypertrophy
stenosis worsens-murmur-episode of cyanosis, hypoxia, blue spells or tet spellsCharacterized by:Sudden, marked inc. of cyanosis followed by syncope, hypoxic brain and injury
Children:Inc. cyanosis, squatting, clubbing of fingers, poor growth may occur
Dec. exercise toleranceInc. DOBEating difficultiesSquatting SOBClubbing of fingers and toes
- Cuts offcirculationVolume resuscitationOxygen- ineffective in treating hypoxic spells
Pharmacologic
BetablockerMorphinePhenylephrine HCL
SurgeryPallative shunt
Closure of Vsd- complete repair
PATENT DUCTUS ARTERIOSUS
-failure of the fetal ductus ateriosus to close w/in the 1st wk of life
Manifestations:AsymptomaticSx CHFMURMUR- machinery likeWidened PPBounding PulseRisk for bacterial endocarditis
Med mgmt:Indomethacin- helps close the PDA in premature infants. Stimulate PDA to constrict tighten closing the connection.
-continued patency of this vessel allows blood to flow from the higher pressure aorta to the lower pressure aorta to the lower pulmonary artery causing a L to R shunt
Pulmonary vascular Obstructive
ADULTS:DyspneaFatigability
TRANSPOSITION OF GREAT ARTERIES
Pulmonary artery leaves L ventricle, and the aorta exits from the R ventricle with no communication between the systemic and pulmonary circulation
Assessment:Infants- cyanosis
Children- Cyanosis- Respi infections- diminished exercise
tolerance- fatigabilityclubbing of
fingers
MAngement:
Mechanical ventilationPharmacologic support for poor cardiac outputProstaglandinCorrection of metabolic acidosis
Interventions:V/sRespi stat.Auscultate breath sounds for crackles, rhonchi, or ralesAdmin. O2Provide endotracheal tube and ventilator careMonitor for hypercyanotic spellsAsses for S/sx of CHFPeripheral pulsesIOWt. dailyFluid restrictionAdmin. MedsStress freePrepare family for possibility of surgery
CARDIOMYOPATHY-heart muscle disorder of unknown etiology-heart muscle disorder associated with cardiac dysfunction-dominant feature: involvement of heart muscle itself-Four conditions that increases threshold:
Categories:DILATED cardiomyopathy
-known as congestive cardiomyopathy-the heart chambers are dilated and ventricular contraction is impaired-common type- heart ejects less than 40 % of the blood in the L
CAUSES:Idiopathic
Result of damage to the myocardium, produced by a variety of toxic, metabolic or infectious agents. It may be due to fibrous change of the myocardium from a prev. MI
Assessment:S/ sx of L ventricular failureWeakness, fatigueActivity intoleranceChest painDysrhythmiasEventually signs of R ventricular failure
TreatmentDiureticsCardiac GlycosidesVasodilatorsAnti dysrhythmias Instruct the client to avoid ingestion of alcoholHeart Transplant
Chronic alcohol ingestion PregnancySystemic HPNVarious infections
ventricle- red. CO may lead to HF
Hypertrophic Cardiomyopathy
-characterized by decreased compliance of the L ventricle and hypertrophy of the ventricle muscle massa. impaired ventricular fillingb. Small end diastolic pressurec.Low cardiac output
Characterized by Massive Ventricular Hypertrophy
Heart Muscle asymmetrically increase in size and mass esp. along the septum
1. Obstructive – septum thickens and bulges into the L ventricle. This will block the blood out out of the ventricle
2.Non obstructive – thickened heart muscle does not block the flow of blood out of the ventricle amy become thicker or may happen only at the bottom
s/sx chest paindizzinessSOBFainting
Exertional DyspneaSyncopeChest pain @rest, not relieved by nitratesDysrhythmias
Instruct the px to report s/sx of dizziness or faintingIntruct the Px to avoid ingestion of alcohol
Restrictive cardiomyopathy
-least common
DIGITALIS TOXICITYGI:AnorexiaN and VDiarrheaAbd. Cramps
CNS:FatigueLethargy
Guidelines for digitalis prep:1. Take pulse for 1 minute2. Heartbeat is below 60, dc drug3.S/sx for digitalis toxicity4.hypokalemic – withhold drug and notify doctor
Depression restlessness irritabilityDrowsinessConvulsionsNeuralgiaDelusionsHallucinationAphasiaMemory loss
CVSBradycardia Ventricular bigeminyTrigeminyVTAV blockAtrial tachycardia
Eyes:Flickering flashes of lightHalo around lightsPhotophobiaBlurringDiplopiaScomata (blind spots on visual field
Dopamine and Dobutamine-facilitate myocardial contractilityAnd enhanced stroke volume
Dopaminerenal dose- less than 4 ug/ kg/ min-stimulates dopaminergic receptors in the renal, mesenteric, cerebral and coronary vascular bed which causes vasodilation:Inc. renal flowIncrease GFR and Na excretion
Dobutamine-inc. HR and produces more myocardial contractility than dopamine
Moderate dose- 4-8 ug / kg/ min- inc. HR. SV and Co
Large dose8-vasoconstriction
PHARMACOLOGIC THERAPIES FOR HEART PROBLEMS:
Sinus Tachycardia:
Beta blockers Ca channel blocker
Sinus Bradycardia
Atropine- 0.5 as an IV bolus every 3-5 m until 3 mg
PVC
Short term- lidocaineLong- procainamide
V TACHAmiodarone –IV for stable PxProcainamideSotalolLidocaine –shortIsoproterenol- correct electrolyte imbalance
ASHDLow dose aspirinNiacin or nicotinic acidBile acid binding resins- Cholestyramine
Lowers cholesterol levelLovastin
ANGINANITRATESBeta blockersCa channel blockersAntipaltelet and anticoagulant meds (aspirin, clopidogrel, heparin, LMWH)
Pravastatinsimvastatin
MI
ThrombolyticsAnticoagu;lants and antiplateletrsAnalgesicsACE inhibitorsStool softeners
Heart failures
ACE inhibitorsDigitalisDopamineDobutamineDiureticsVasodilating agentsBetablockersCa channel blockers
Acute pulmonary edema
DigitalisDiureticsVasodilatorsMorphine IVAminophyline
Conditions of desaturation
Beta blockerMorphinePhenylephrine Hcl
Patent Ductus Arteriosus
Indomethacin
Dilated Cardiomyopathy
DiureticsCardiac glycosidesVasodilatorsAntidysrhythimias
Medical therapies:
Defibrillation-SA node to resume it’s role as the pace maker of the heart-pulseless and unconscious
Before:
Check ECG results for the presence of VF and VT
Pulse Remove any Topical
Nitroglycerin Patches
During:
Lubricate the paddles to enhance conduction and prevent skin burn
Turn defibrillator on and confirms that synchronizer switch off.
25-30 lbs of poressure (anterolateral; paddles are placed @ 2nd ICS Right and anterior axillary line 5th ICS left
Stay away from bed
After:
Assess the pulse and ECGFirst countershock , if unsuccessful, defilbrate againTerminate of resuscitation after 15-20 min of CPR andACLs1st: 2002nd:3003rd:360 (max energy; last)
Cardioversion-elective procedure-use of electricity to convert cardiac dysrythmia to NSR.-electrical discharged is synchronized with or triggered by
Before:
Check ECG results for the presence of VF and VT
Pulse Remove any Topical
During:
Set machine within range 50-200 joulesTurn on synchronizer, deliver during QRS complex and not on
After:
Asses V/sMaintain patent airwayAdminister O2Assess v/s and LOC
the client’s QRS complex for avoidance of accidental discharge during the repolarization phase when the ventricle is vulnerable to the development of VF.-indications include tachycardia developing in atrial, junctional, ventricular-QRS complex- present for successful conversion of the dysrythmia
Nitroglycerin Patches the downslope of T wave(may inc. in ventricular irritability, causing VF)Lubricate padsWhen ensuring O2, move pads awayMove away from bed
Asmin antiarrythmic drugsMonitor for dysrythmiasAssess for chest burnsProvide emotional supportDocument
Automatic Implantable Cardioverter- Defibrillator (AICD)
Device itended to convert life threatening rhythms of the heart which may cause sudden cardiac death/ arrest
PACEMAKERa. TemporaryTranscutaneous- for life threatening situationsTransvenous-
Epicardial
b.Permanent fixed rate Demand or stand by mode
After careAfter insertion
Provide cont. ECG monitoring
Chart the type of insertion, lead system, pacemaker mode and pacing guidelines
VS every 30 min ‘til stable
Be on guard for perforated ventricles
Asses for insertion sites for infection
First 24 hrs, ROM in affected arm—active ROM in 2 wks
Homecare
Take pulse before getting out of bed
Check implantation everydaySpecial precautions to prevent disruptionAvoid strong magnetic forcesAvoid placing excessive pressureFollow normal routinesTake note of follow up orders
Vagal Maneuvers-used to terminate tachydysrthmia
Carotid massage-last pulse to be checked.
Valsalva maneuver-bring out parasympathetic impulses
Cough CPR-cough and deep breathing
S1 S2 Abnormal heart
sounds:Onset of systoleApex of the heartClosure of AV valves
DiastoleBase of the heartClosure of semilunar valves