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