*DIVERSE GROUP OF DISORDERS THAT AFFECT BOTH SYSTOLIC & DIASTOLIC FUNCTIONS, MAY BE PRIMARY OR SECONDARY

*PRIMARY-IDIOPATHIC-OF UNKNOWN CAUSE

*SECONDARY-OCCUR AS A RESULT OF OTHER PROCESSES SUCH AS ISCHEMIA, DISEASES, TOXINS, CONNECTIVE TISSUE DISORDERS, NUTRITIONAL DEFICIENCIES

*AFFECTS THE HEART MUSCLE ITSELF

*MOST COMMON TYPE; ALSO COMMON CAUSE OF HEART FAILURE

*HEART CHAMBERS DILATE & VENTRICULAR CONTRACTION IS IMPAIRED

*CARDIAC OUTPUT DECREASES R/T LOWER LEFT VENTRICULAR

EJECTION FRACTION

*LEFT VENTRICULAR DILATION PROMINENT, HYPERTROPHY MINIMAL

*RIGHT VENTRICLE MAY BE ENLARGED

*CHARACTERIZED BY DECREASED COMPLIANCE OF LEFT VENTRICLE & HYPERTROPHY OF VENTRICULAR MASS/SEPTAL WALL

*IMPAIRS VENTRICULAR FILLING LEADING TO SMALL END-DIASTOLIC VOLUMES & LOW CARDIAC OUTPUT

*MUSCLE MAY NOT HYPERTROPHY EQUALLY

*ALSO KNOWN AS IDIOPATHIC HYPERTROPHIC SUBAORTIC STENOSIS OR HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY

*LEAST COMMON FORM-CHARACTERIZED BY RIGID VENTRICULAR WALLS THAT IMPAIR DIASTOLIC FILLING

*DECREASED VENTRICULAR COMPLIANCE IMPAIRS FILLING, DECREASED VENTRICULAR SIZE, ELEVATED END-DIASTOLIC PRESSURES, & DECREASED CARDIAC OUTPUT

*CONTRACTILITY IS UNAFFECTED, EJECTION FRACTION IS NORMAL

*RELATIVELY RARE BUT SERIOUS

*DYSFUNCTION OF LEFT VENTRICLE THAT MAY OCCUR IN LAST MONTH OF PREGNANCY OR FIRST 5 MONTHS POSTPARTUM IN WOMAN WITH NO PREVIOUS HX OF HEART DISEASE

*SUBSEQUENT PREGNANCY IS STRONGLY DISCOURAGED BECAUSE THE DISEASE TENDS TO RECUR

*DEVELOPS GRADUALLY  *HF PRESENTS YRS AFTER ONSET OF DILATION & PUMP FAILURE

*BOTH R & L SIDED HF OCCUR   *DYSPNEA ON EXERTION

*ORTHOPNEA   *PAROXYSMAL NOCTURNAL DYSPNEA

*WEAKNESS  *FATIGUE  *PERIPHERAL EDEMA  *ASCITES

*DYSRHYTHMIAS COMMON (SUPRAVENTRICULAR TACHY, A-FIB, COMPLEX VENTRICULAR TACHY)-CAN LEAD TO SUDDEN DEATH IF UNTREATED

*MURAL THROMBI(CLOTS IN HEART WALL) MAY FORM IN LEFT VENTRICULAR APEX & EMBOLIZE TO OTHER PARTS OF THE BODY

*MAY BE ASYMPTOMATIC FOR MANY YRS  *SYMPTOMS USUALLY OCCUR WHEN INCREASED O2 DEMAND CAUSES INCREASED VENTRICULAR CONTRACTILITY OR MAY DEVELOP SUDDENLY DURING/AFTER PHYSICAL ACTIVITY

*SUDDEN CARDIAC DEATH(SCD) MAY BE FIRST SIGN IN CHILDREN/YOUNG ADULTS   *DYSPNEA, ANGINA, SYNCOPE COMMON   *VENTRICULAR DYSRHYTHMIAS COMMON, A-FIB MAY DEVELOP   *FATIGUE  *DIZZINESS  *PALPITATIONS  *HARSH CRESCENDO-DECRESCENDO SYSTOLIC MURMUR OF VARIABLE INTENSITY IS CHARACTERISTIC (AUSCULTATED @ LOWER LEFT STERNAL BORDER & APEX)  *S4 MAY BE NOTED

*SAME AS HEART FAILURE & DECREASED TISSUE PERFUSION

*DYSPNEA ON EXERTION/EXERCISE INTOLERANCE

*JUGULAR VENOUS PRESSURE INCREASED/ELEVATED

*S3 & S4 COMMON

*USUALLY PRESENTS WITH ANEMIA & INFECTION

*CXR

*ECHOCARDIOGRAPHY

*ELECTROCARDIOGRAPHY & AMBULATING ECG

*HEMODYNAMIC STUDIES

*RADIONUCLEAR SCANS

*CARDIAC CATH/CORONARY ANGIOGRAPHY

*MYOCARDIAL BIOPSY

*DIAGNOSIS BEGINS WITH HISTORY/PHYSICAL ASSESSMENT TO RULE OUT KNOWN CAUSES OF HEART FAILURE

*DILATED/RESTRICTIVE: SAME DRUG REGIMEN USED TO TX HF-ACE INHIBITORS, VASODILATORS, DIGITALIS. BETA BLOCKERS MAY BE USED WITH CAUTION IN DILATED.  ANTICOAGULANTS USED TO DECREASE RISK OF THROMBUS/EMBOLI, ANTIDYSRHTYMICS AVOIDED BECAUSE TENDENCY TO PRECIPITATE FURTHER DYSRHYTHMIAS

*HYPERTROPHIC: BETA-BLOCKERS DRUG OF CHOICE, ALSO CALCIUM CHANNEL BLOCKERS-DECREASE MYOCARDIAL CONTRACTILITY THUS DECREASING OBSTRUCTION OF OUTFLOW TRACT.  BETA BLOCKERS ALSO DECREASE HR AND INCREASE VENTRICULAR COMPLIANCE THUS INCREASING DIASTOLIC FILLING TIME & CARDIAC OUTPUT.  AMIODARONE MAY BE USED TO TREAT VENTRICULAR DYSRHYTHMIAS.  VASODILATORS, DIGITALIS, NITRATES, & DIURETICS ARE CONTRAINDICATED

DILATED

*REVERSIBLE FORMS-ALCOHOL/COCAINE ABUSE, CHEMOTHERAPEUTIC DRUGS, PREGNANCY & SYSTEMIC HTN. MAY BE GENETIC.  USUALLY IDIOPATHIC, MAY BE SECONDARY TO CHRONIC ALCOHOLISM OR MYOCARDITIS.  PRIMARILY A DISEASE OF MIDDLE AGED MALES, BLACKS @ HIGHER RISK THAN WHITES

RESTRICTIVE

*MYOCARDIAL FIBROSIS & INFILTRATIVE PROCESSES(AMYLOIDOSIS)-FIBROSIS OR MYO/ENDOCARDIUM CAUSES EXCESSIVE STIFFNESS & RIGIDITY OF VENTRICLES

PERIPARTUM

*UNKNOWN CAUSE OR SPECIFIC RISK FACTORS

HYPERTROPHIC

*AUTOSOMAL DOMINANT TRANSMISSION CAUSED BY MUTATIONS-HEREDITARY

*MAY BE SECONDARY TO CHRONIC HTN

***HTN, EXCESSIVE ALCOHOL CONSUMPTION, & VALVULAR HEART DISEASE IS RISK FACTOR FOR ALL CARDIOMYOPATHIES***

DILATED/RESTRICTIVE

*TREAT UNDERLYING CAUSE IF KNOWN. TX FOCUSES ON MANAGING HF & DYSRHYTHMIAS

HYPERTROPHIC

*TX FOCUSES ON REDUCING CONTRACTILITY & PREVENTING SCD

*STRENUOUS PHYSICAL EXERTION RESTRICTED

*DIETARY/SODIUM RESTRICTION

PERIPARTUM

*MAY RESOLVE WITH BEDREST AS HEART GRADUALLY RETURNS TO NORMAL SIZE

DILATED: CARDIAC TRANSPLANT DEFINITIVE TX. VENTRICULAR ASSIST DEVICES MAY BE USED TO SUPPORT CARDIAC OUTPUT UNTIL DONOR AVAILABLE

RESTRICTIVE: TRANSPLANT NOT VIABLE B/C UNDERLYING CAUSE CAN AFFECT NEW ORGAN

HYPERTROPHIC: EXCESS MUSCLE MAY BE SURGICALLY RESECTED; SEPTUM INCISED, TISSUE REMOVED.  IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR TO TREAT POTENTIALLY LETHAL DYSRHYTHMIAS, DUAL CHAMBER PACEMAKER MAY ALSO BE USED

*C/O SOB, DYSPNEA ON EXERTION, DECREASED ACTIVITY INTOLERANCE, OR PAROXYSMAL NOCTURNAL DYSPNEA

*# OF PILLOWS USED FOR SLEEPING

*RECENT WT GAIN  *ANOREXIA OR NAUSEA

*PRESENCE OF COUGH

*CHEST PAIN OR ABDOMINAL PAIN

*HX OR CARDIAC DISEASE/PREVIOUS EPISODES OF HF

*OTHER IMPORTANT FACTORS: HTN, DM, CURRENT MEDS, USUAL DIET/ACTIVITY, ANY RECENT CHANGES

*GENERAL APPEARANCE  *EASE OF BREATHING (CONVERSING, CHANGING POSITIONS)

*APPARENT ANXIETY   *VITAL SIGNS (APICAL PULSE)

*COLOR OF SKIN/MUCOUS MEMBRANCES

*NECK VEIN DISTENTION

*PERIPHERAL PULSES, CAP REFILL, EDEMA

*HEART/BREATH SOUNDS

*ABDOMINAL CONTOUR

*BOWEL SOUNDS/TENDERNESS

*RIGHT UPPER ABDOMINAL TENDERNESS/LIVER ENLARGEMENT

*ACTIVITY RESTRICTIONS/DIETARY CHANGES TO REDUCE MANIFESTATIONS/PREVENT COMPLICATIONS

*DRUG THERAPY-REASON, INTENDED/ADVERSE EFFECTS

*DISEASE PROCESS, EXPECTED OUTCOME, TX OPTIONS

*HEART TRANSPLANT-PRE/POST PROCEDURE CARE & TX

*SYMPTOMS TO REPORT TO HCP THAT REQUIRE IMMEDIATE CARE

*CPR & AVAILABLE TRAINING SITES

*REFERENCES TO HOME/SOCIAL SERVICES, COUNSELING, SUPPORT GROUPS, & AHA

*AN OPENING IN THE VENTRICULAR SEPTUM THAT CAUSES INCREASED PULMONARY BLOOD FLOW

*BLOOD IS SHUNTED FROM THE LEFT VENTRICLE DIRECTLY ACROSS THE OPEN SEPTUM INTO THE PULMONARY ARTERY

*MOST COMMON CONGENITAL HEART DEFECT

*CAN CAUSE CHF, INCREASED # OF PULMONARY INFECTIONS, & PULMONARY HTN (<15% OF CASES)

*SYSTOLIC MURMUR AUSCULTATED @ 3RD OR 4TH LEFT INTERCOSTAL SPACE @ STERNAL BORDER

*CHEST XRAY

*ECG

*ECHOCARDIOGRAM (ESTABLISHES DIAGNOSIS)

*CARDIAC CATH-ONLY USED IN PREPERATION OF SURGERY

*MOST WILL CLOSE SPONTANEOUSLY WITHIN FIRST 6MO OF LIFE

*TX CONSERVATIVE WHEN NO S/S OF CHF OR PULMONARY ARTERY HTN

*SURGICAL PATCHING DURING INFANCY WHEN POOR GROWTH PRESENT

*CLOSURE BY TRANSCATHETER DEVICE (RASHKIND DEVICE)

*PROPHYLAXIS FOR INFECTIVE ENDOCARDITIS

*HIGH RISK WITH SURGICAL REPAIR IN FIRST FEW MO OF LIFE

*CHILDREN RESPOND WELL TO SX & EXPERIENCE SUBSTANTIAL CATCH UP GROWTH

*TACHYARRHYTHMIAS & RIGHT BUNDLE BRANCH BLOCK ARE POSSIBLE COMPLICATIONS

*FAILURE OF DUCTUS ATERIOSIS TO CLOSE WITHIN THE FIRST WEEK OF LIFE

*COMMON PROBLEM OF PRETERN INFANTS AND IS PRESENT IN NEARLY ALL PRETERN INFANTS DELIVERED AT <27WKS

*DYSPNEA, TACHYPNEA  *TACHYCARDIA  *FULL BOUNDING PULSE, WIDENED PULSE PRESSURE, POSSIBLY HYPOTENTION  *CHF  *INTERCOSTAL RETRACTIONS  *HEPATOMEGALY  *GROWTH FAILURE IN LARGE DEFECTS

*CONTINUOUS "MACHINERY" MURMUR DURING SYSTOLE & DIASTOLE  *THRILL IN PULMONIC AREA  *HIGH RISK FOR RESPIRATORY INFECTIONS, PNEUMONIA, & INFECTIVE CARDITIS

*CXR, ECG-LEFT VENTRICULAR HYPERTROPHY

*CAN BE VISUALIZED

*ECHOCARDIOGRAM-LEFT TO RIGHT SHUNT CAN BE MEASURED

*SURGICAL LIGATION IS TX OF CHOICE

*IV INDOMETHACIN OFTEN STIMULATES CLOSURE IN PREMATURE INFANTS

*TRANSCATHETER CLOSURE BY OBSTRUCTIVE DEVICE  SOMETIMES ATTEMPTED IN CHILDREN >18MO

*PROPHYLAXIS FOR INFECTIVE ENDOCARTITIS REQUIRED UNTIL CLOSURE

*NO LONG TERM SEQUELAE OCCUR IF TREATED BEFORE PULMONARY VASCULAR DISEASE DEVELOPS

*IF NOT TREATED, CHILDS LIFE SPAN SHORTENED BECAUSE PULMONARY HTN & PERIPHERAL VASCULAR DISEASE DEVELOP

*A DEFECT IN THE HEART OR GREAT VESSELS THAT RESULTS FROM AN ALTERATION IN NORMAL FETAL DEVELOPMENT  OR PERSISTENCE OF A FETAL STRUCTURE THAT DOES NOT CONVERT TO EXTRAUTERINE ANATOMY AFTER BIRTH

CATEGORIZATIONS OF CONGENITAL HEART DEFECTS

*DEFECTS INCREASING PULMONARY BLOOD FLOW

    -SEPTAL DEFECTS, PATENT DUCTUS ARTERIOSIS,

     AV CANAL

*DEFECTS DECREASING PULMONARY BLOOD FLOW

    -PULMONIC STENOSIS, TETRALOGY OF FALLOT,     

     PULMONARY/TRICUSPID ATRESIA

*MIXED DEFECTS

    -TRANSPOSITION OF THE GREAT ARTERIES, 

     TRUNCUS ARTERIOSUS, TOTAL ANOMALOUS

     PULMONARY VENOUS RETURN

*DEFECTS OBSTRUCTING SYSTEM BLOOD FLOW

    -AORTIC STENOSIS, COARCTION OF THE AORTA,

     HYPOPLASTIC LEFT HEART SYNDROME

*AKA THROMBOPHLEBITIS

*A CONDITION IN WHICH A BLOOD CLOT(THROMBUS) FORMS ON THE WALL OF A VEIN, ACCOMPANIED BY INFLAMMATION OF THE VEIN & SOME DEGREE OF OBSTRUCTED VENOUS BLOOD FLOW

*******************************

*OCCURS WHEN THE THROMBOSIS IS LOCATED IN A DEEP VEIN OF THE BODY

*THE DEEP VEINS OF THE LEGS, CLAF & PELVIS PRIMARILY, PROVIDE MOST HOSPITABLE ENVIRONMENT FOR VENOUS THROMBOSIS

*USUALLY ASYMPTOMATIC

*WHEN PRESENT, THEY ARE: -DULL ACHING PAIN IN AFFECTED EXTREMITY, ESPECIALLY WHEN WALKING

-POSSIBLE TENDERNESS, WARMTH, & ERYTHEMA ALONG AFFECTED VEIN

-CYANOSIS OF AFFECTED EXTREMITY

-EDEMA OF AFFECTED EXTREMITY

*DUPLEX VENOUS ULTRASONOGRAPHY: NONINVASIVE, VISUALIZES VEIN/MEASURES VELOCITY OF BLOOD FLOW

*PLETHYSMOGRAPHY: NONINVASIVE, MEASURES CHANGES IN BLOODFLOW THROUGH VEINS

*MRI: NONINVASIVE, USED FOR SUSPECTED CLOTS IN VENAE CAVAE OR PELVIS

*ASCENDING CONTRAST VENOGRAPHY: INJECTED DYE TO ASSESS/LOCATE EXTENT OF CLOT.  MOST ACCURATE DIAGNOSTIC TOOL FOR VENOUS THROMBOSIS

**********************************************

LAB STUDIES: D-DIMER, PROTHROMBIN TIME, PARTIAL PROTHROMBIN TIME, BLEEDING TIME, & PLATELET COUNT

*ANTICOAGULANTS: PREVENT CLOT PROPAGATION & ENABLE BODYS LYTIC SYSTEM TO DISSOLVE CLOTS

*FIBRINOLYTIC DRUGS: MAY ACCELERATE PROCESS OF CLOT LYSIS & PREVENT DAMAGE TO VENOUS VALVES

*NSAIDS: REDUCE INFLAMMATION IN VEINS & PROVIDE SYMPTOMATIC RELIEF (PARTICULARLY FOR SUPERFICIAL VENOUS THROMBOSIS)

*VENOUS THROMBECTOMY: PERFORMED WHEN THROMBI LODGE IN FEMORAL VEIN & REMOVAL IS NECESSARY

*FILTER: MAY BE INSERTED INTO VENA CAVA TO CAPTURE EMBOLI FROM PELVIS/LOWER EXTREMITIES WHEN ANTICOAGULANT THERAPY CONTRAINDICATED

*LIGATION/DIVISION OF SAPHENOUS VEIN: PERFORMED WHEN EXTENSIVE THROMBOSIS OF SAPHENOUS VEIN WHERE IT JOINS FEMORAL VEIN TO PREVENT CLOT EXTENTION INTO DEEP VEIN SYSTEM

-A VEIN AFFECTED BY SEPTIC VENOUS THROMBOSIS IS EXCISED TO CONTROL INFECTION

*SUPERFICIAL: APPLY WARM, MOIST COMPRESSES OVER AFFECTED VEIN, EXTREMITY REST, & ANTI-INFLAMMATORY AGENTS TO RELIEVE SYMPTOMS

*DEEP: BEDREST MAY BE ORDERED.  EXTENT DEPENDS ON EXTENT OF LEG EDEMA.  LEGS ELEVATED 15-20 WITH

KNEES SLIGHTLY FLEXED ABOVE LEVEL OF HEART.  TED HOSE OR SCD BOOTS, AVOID PROLONGED SITTING/STANDING, OR CROSSING LEGS, ALSO NO TIGHT FITTING GARMENTS OR STOCKINGS THAT BIND

*C/O LEG OR CALF PAIN: DURATIONS & CHARACTERISTICS, EFFECT OF WALKING ON PAIN

*HX OF VENOUS THROMBOSIS OR OTHER CLOTTING DISORDERS

*CURRENT MEDICATIONS

*REDNESS & EDEMA OF AFFECTED EXTREMITY

*TENDERNESS, WARMTH, & CORDLIKE STRUCTURES ON PALPATION

*BODY TEMPERATURE

*EXPLANATION OF DISEASE PROCESS

*TX MEASURES, INCLUDING LAB TESTS & PURPOSE

*MEDICATIONS, REASON, EXPECTED & ADVERSE EFFECTS

*APPROPRIATE METHODS OF HEAT APPLICATION

*PRESCRIBED ACTIVITY RESTRICTIONS

*MEASURES TO PREVENT FUTURE EPISODES

*IMPORTANCE OF FOLLOW UP VISITS & LABS AS SCHEDULED

*REFER TO OUTSIDE NURSING & THERAPY ASSISTANCE

*COMPLEX SYNDROME RESULTING F/CARDIAC DISORDERS THAT IMPAIR THE ABILITY OF THE VENTRICLES TO FILL WITH & EFFECTIVELY PUMP BLOOD-UNABLE TO MEET METABOLIC DEMANDS

*END RESULT OF MANY CONDITIONS

*MAY BE ACUTE OR CHRONIC

*CLASSIFIED AS: SYSTOLIC VS DIASTOLIC,

 L SIDED VS R SIDED, LOW OUTPUT VS HIGH OUTPUT, ACUTE VS CHRONIC

*FRANK STARLING MECHANISM: GREATER STRETCH-GREATER CONTRACTION

*NEUROENDOCRINE RESPONSE: RELEASE OF CATECHOLAMINES, RENIN ANGIOTENSIN, ALDOSTERONE, ADH, ANP, BNP

*VENTRICULAR HYPERTROPHY: HYPERTROPHY OF MYOCARDIAL MUSCLE & DILATION OF VENTRICLES

*HF FAILURE PROCESSES AS COMPLICATIONS ARISE FROM MECHANISMS-HERALDED BY DECOMPENSATION

*CLIENTS WITH HF HAVE LITTLE TO NO CARDIAC RESERVE

*ACTIVITY INTOLERANCE @ REST INDICATES CRITICAL LEVEL OF CARDIAC DECOMPENSATION

*CLIENTS WITH HF HAVE INCREASED CHANCE OF SUDDEN CARDIAC DEATH

*OCCURS WHEN THE VENTRICLE FAILS TO CONTRACT ADEQUATELY TO EJECT A SUFFICIENT VOLUME OF BLOOD INTO THE ARTERIAL SYSTEM

*FUNCTION IS AFFECTED BY LOSS OF MYOCARDIAL CELLS AS A RESULT OF ISCHEMIA & INFARCTION, CARDIOMYOPATHY, OR INFLAMMATION

*RESULTS WHEN THE HEART CANNOT COMPLETELY RELAX, DISRUPTING NORMAL FILLING

*DYSFUNCTION RESULTS FROM DECREASED VENTRICULAR COMPLIANCE CAUSED BY HYPERTROPHIC & CELLULAR CHANGES & IMPAIRED RELAXATION OF HEART MUSCLE

*CORONARY HEART DISEASE & HTN ARE CDOMMON CAUSES

*PRESSURES IN VENTRICLE & ATRIUM INCREASE AS THE AMT OF BLOOD REMAINING IN VENTRICLE AFTER SYSTOLE INCREASES

*INCREASED PRESSURES IMPAIR FILLING, CAUSING CONGESTION & INCREASED PRESSURES IN PULMONARY VASCULAR SYSTEM(NORMALLY LOW PRESSURE SYSTEM)

*INCREASED PRESSURE INCREASES FLUID MOVEMENT FROM BLOOD VESSELS INTO INTERSTITIAL TISSUES & ALVEOLI

*MANIFESTATIONS RESULT FROM PULMONARY CONGESTION (BACKWARD EFFECTS) AND DECREASED CO (FORWARD EFFECTS)

*CAUSED BY CONDITIONS THAT RESTRICT BLOOD FLOW TO LUNGS

*VENTRICLE & ATRIUM BECOME DISTENDED & BLOOD ACCUMULATES IN THE SYSTEMIC VENOUS SYSTEM

*INCREASED PRESSURES IN PULMONARY VASCULATURE OR VENTRICULAR MUSCLE DAMAGE IMPAIRS VENTRICLES ABILITY TO PUMP BLOOD INTO PULMONARY CIRCULATION

*INCREASED VENOUS PRESSURES CAUSE ABD ORGANS TO BECOME CONGESTED & PERIPHERAL TISSUE EDEMA TO DEVELOP

*DEPENDENT TISSUES TEND TO BE AFFECTED BC OF THE EFFECTS OF GRAVITY

*RESULTS IN CLIENTS WITH CORONARY HEART DISEASE, HTN, CARDIOMYOPATHY & OTHER PRIMARY CARDIAC DISORDERS

*DECREASED CARDIAC OUTPUT AS A RESULT OF CARDIAC DISORDERS

*RESULTS IN CLIENTS WITH HYPERMETABOLIC STATES SUCH AS HYPERTHYROIDISM, INFECTION, ANEMIA, OR PREGNANCY

*REQUIRES INCREASED CO TO MAINTAIN BLOOD FLOW & OXYGEN TO TISSUES. IF INCREASED BLOOD FLOW CANNOT MEET OXYGEN DEMANDS, COMPENSATORY MECHANISMS ARE ACTIVATED TO FURTHER INCREASE CO WHICH FURTHER INCREASES OXYGEN DEMAND

*EVEN THOUGH CO IS HIGH, HEART IS UNABLE TO MEET INCREASED OXYGEN DEMANDS

*ABRUPT ONSET OF MYOCARDIAL INJURY SUCH AS MASSIVE MI

*RESULTS IN SUDDEN DECREASE IN CARDIAC FUNCTION AND SIGNS OF DECREASED CARDIAC OUTPUT

*PROGRESSIVE DETERIORATION OF THE HEART MUSCLE AS A RESULT OF CARDIOMYOPATHIES, VALVULAR DISEASE, OR CORONARY HEART DISEASE

*THE CONTRACTILITY OF THE L VENTRICLE IS SEVERLY IMPAIRED

*EJECTION FRACTION FALLS B/C VENTRICLE IS UNABLE TO EJECT BLOOD THAT ENTERS IT, CAUSING SHARP RISE IN END-DIASTOLIC VOLUME & PRESSURES

*HYDROSTATIC PRESSURES RISE EXCEEDING OSMOTIC PRESSURE OF BLOOD RESULTING IN FLUID LEAKING F/THE PULMONARY CAPILLARIES

*CONGESTED INTERSTITIAL TISSUES, DECREASING LUNG COMPLIANCE, AND IMPAIRED GAS EXCHANGE OCCUR

*ISCHEMIC HEART DISEASE (CORONARY) IS LEADING CAUSE; CARDIOMYOPATHIES ARE SECOND.

*LESS COMMON CAUSES ARE HTN, CONGENITAL HEART DEFECTS & VALVULAR DISEASE

*INCIDENCE/PREVALENCE INCREASES WITH AGE, HIGHER AMONG BLACKS THAN WHITES

*FAMILY HISTORY, CARDIOTOXIC DRUGS, SOME CHEMO/CANCER DRUGS, SMOKING, OBESITY, ALCOHOL ABUSE, & DM

*MANY SHOW S/S OF BOTH TYPES

*SAME AS MANIFESTATIONS OF DECREASED CO: WEAKNESS, FATIGUE, & DECREASED EXERCISE TOLERANCE

*****************************************

*SOB, TACHYPNEA, RESPIRATORY CRACKLES IF

 LEFT VENTRICLE AFFECTED

*DISTENDED NECK VEINS, LIVER ENLARGEMENT, ANOREXIA/NAUSEA IF RIGHT VENTRICLE AFFECTED

*FATIGUE & ACTIVITY INTOLERANCE COMMON EARLY SIGNS

*DIZZINESS, SYNCOPE, PULMONARY CONGESTION, DYSPNEA, SOB, COUGH, POSSIBLE ORTHOPNEA, CYANOSIS FROM IMPAIRED GAS EXCHANCE, INSPIRATORY CRACKES/WHEEZES IN LUNG BASES, S3 GALLOP MAY BE PRESENT

*EDEMA DEVELOPS IN FEET & LEGS, SACRUM ALSO IF PT IS ON COMPLETE BEDREST

*ANOREXIA & NAUSEA FROM CONGESTION OF GI VESSELS

*RIGHT UPPER QUADRANT PAIN FROM LIVER ENGORGEMENT

*NECK VEIN DISTENTION VISIBLE R/T INCREASED VENOUS PRESSURE

*HEPATOMEGALY & SPLENOMEGALY: INCREASED ABDOMINAL PRESSURE, ASCITES, & GI PROBLEMS

*IMPAIRED LIVER FUNCTION WITH PROLONGED RIGHT SIDED HF

*DYSRHYTHMIAS R/T MYOCARDIAL DISTENTION

*PLEURAL EFFUSIONS

*RESPIRATORY: TACHYPNEA, PND, LABORED RESPIRATIONS, FROTHY COUGH WITH PINK TINGED SPUTUM, DYSPNEA, CRACKES & WHEEZES, ORTHOPNEA

*CARDIOVASCULAR: TACHYCARDIA, COOL CLAMMY SKIN, HYPOTENSION, HYPOXEMIA, CYANOSIS, VENTRICULAR GALLOP

*NEUROLOGIC: RESTLESSNESS, FEELING OF IMPENDING DOOM, ANXIETY

*SLOW PROGRESSION

*REDUCE CARDIAC WORKLOAD

*IMPROVE CARDIAC FUNCTION

*CONTROL FLUID RETENTION

*MAIN DRUG CLASSES ARE: ACE INHIBITORS, ARBS, BETA BLOCKERS (USED IN LOW DOSES), DIURETICS, POSITIVE INOTROPIC MEDICATIONS, DIRECT VASODILATORS, & ANTIDYSRHYTHMICS

ARBS=ANGIOTENSIN II RECEPTOR BLOCKERS

*HAWTHORN (A SHRUBBY TREE) CONTAINS NATURAL CARDIOTONIC INGREDIENTS- INCREASE FORCE OF CONTRACTION, DILATES BLOOD VESSELS, & HAS NATURAL ACE INHIBITOR

*COENZYME Q10(INCEASES MITOCHONDRIA FUNCTION & ENERGY), MAGNESIUM, & THIAMINE MAY BE USED IN CONJUNCTION WITH OTHER TREATMENTS

*MODERATE NA+ RESTRICTED DIET (1.5-2G/DAY)

*ACTIVITY MAY BE RESTRICTED TO BEDREST DURING ACUTE EPISODES-PROLONGED BEDREST NOT RECOMMENDED

*EXERCISE SHOULD BE PERFORMED 3-5X/WK WITH 10-15 MIN WARM UP, 20-30 MIN EXERCISE, COOL DOWN PERIOD... WALKING ENCOURAGED ON NON TRAINING DAYS

*ANP/BNP-HORMONES RELEASED BY HEART IN RESPONSE TO CHANGES IN BLOOD VOLUME; BNP MAY BE ELEVATED IN WOMEN & PPL >60YO

*SERUM ELECTROLYTES: NA, K, CL, CA, MAGNESIUM

*UA, BUN, SERUM CREATININE: EVALUATE RENAL FUNCTION

*LIVER FUNCTION TESTS: BILIRUBIN, TOTAL PROTEIN & ALBUMIN

*THYROID FUNCTION TESTS: TSH, LEVELS OF THYROID HORMONE

*ABG'S: GAS EXCHANGE IN ACUTE HF

*ECG: IDENTIFY CHANGES & DYSRHYTHMIAS, ISCHEMIA, & INFARCTION

*ECHOCARDIOGRAM C DOPPLER FLOW STUDIES: EVALUATE LEF VENTRICULAR FUNCTION

*ASSESSES CARDIOVASCULAR FUNCTION IN CRITICALLY ILL OR UNSTABLE CLIENTS

*MAIN GOALS ARE TO EVALUATE CARDIAC/CIRCULATORY FUNCTION & RESPONSE TO INTERVENTIONS

*MEASURES THE PRESSURE WITHIN A VESSEL & CONVERTS SIGNAL INTO AN ELECTRICAL WAVEFORM THAT IS AMPLIFIED AND DISPLAYED

*MAY BE USED TO MEASURE PERIPHERAL AFTERY PRESSURES OR CENTRAL PRESSURES SUCH AS CENTRAL VENOUS PRESSURE, RIGHT ARIAL PRESSURE, & PULMONARY ARTERY PRESSURE

*BLEEDING, HEMATOMA

*HEMOTHORAX, PNEUMOTHORAX

*ARTERIAL PUNCTURE

*DYSRHYTHMIAS

*VENOSPASM

*INFECTION

*AIR EMBOLISM, THROMBOEMBOLISM

*BRACHIAL & THORACIC NERVE INJURY

*MEASURE OF BLOOD VOLUME & VENOUS RETURN

*ALSO REFLECTS RIGHT HEART FILLING PRESSURES-ELEVATED IN RIGHT SIDED HF

*PRIMARILY USED TO MONITOR FLUID VOLUME STATUS

*HYPOVOLEMIA/SHOCK=DECREASED LEVEL

*FLUID OVERLOAD, VASOCONSTRICTION, CARDIAC TAMPONADE=INCREASED LEVEL

*NORMAL RANGE: 2-8CM H2O OR 2-6MMHG-VARIES INDIVIDUALLY

*BLEEDING MAJOR CONCERN EARLY POSTOP PERIOD

*CHEST TUBE DRAINAGE, CO, PULMONARY ARTERY PRESSURES & CVP MONITORED FREQUENTLY. CHEST TUBES GENTLY MILKED TO MAINTAIN PATENCY

*HYPOTHERMIA INDUCED DURING SX, CLIENT GRADUALLY REWARMED OVER 1-2HRS POST OP. RAPID REWARMING PREVENTE TO MAINTAIN HEMODYNAMIC STABILITY & REDUCE O2 CONSUMPTION

*INFECTION/REJECTION MAJOR POST OP CONCERNS

*REJECTION: MAY DEVELOP IMMEDIATELY AFTER TRANSPLANT, WITHIN WEEKS TO MONTHS OR EVEN YEARS

*INFECTIONS: EARLY POST OP-COMMONLY BACTERIAL OR FUNGAL

*PREVENTION IS VITAL: LIMIT VISITORS WITH COMMUNICABLE DISEASES, PULMONARY HYGIENE MEASURES, EARLY AMBULATION, & STRICT ASEPTIC TECHNIQUE

*CLOSE MONITORING OF PT DURING POSITION CHANGES, STRESS EXERCISE, ALSO MONITOR HR & DRUG EFFECTS

*C/O INCREASED SOB, DYSPNEA WITH EXERTION, DECREASED ACTIVITY INTOLERANCE, PND, # OF PILLOWS USED FOR SLEEPING, RECENT WT GAIN, ANOREXIA/NAUSEA, PRESENCE OF COUGH, CHEST/ABD PAIN, HX OF CARDIAC DISEASE OR PREVIOUS EPISODES OF HF, HTN, DM, CURRENT MEDICATIONS, USUAL DIET & ACTIVITY, ANY RECENT CHANGES

*GENERAL APPEARANCE, EASE OF BREATHING DURING CONVERSATIONS, CHANGING OF POSITIONS, APPARENT ANXIETY, VS(APICAL PULSE), COLOR OF SKIN/MUCOUS MEMBRANES, NECK VEIN DISTENTION, PERIPHRAL PULSES, CAP REFILL, DEGREE OF EDEMA, HEART & BREATH SOUNDS, ABD CONTOUR, BOWEL SOUNDS, TENDERNESS, RIGHT UPPER QUADRANT ABD TENDERNESS & LIVER ENLARGEMENT

*DISEASE PROCESS/EFFECTS ON QUALITY OF LIFE

*WARNING SIGNS OR CARDIAC DECOMPENSATION THAT REQUIRE TX

*IMPORTANCE OF COMPLIANCE WITH DRUG THERAPY, FOLLOW UP APPTS.  EXPLAIN DRUG ACTION, REASON, & DESIRED/ADVERSE EFFECTS

*PRESCRIBED NA+ RESTRICTED DIET, SUGGESTIONS FOR REDUCING INTAKE, & AHA FOR MATERIALS/RECIPES

*EXERCISE RECOMMENDATIONS TO STRENGTHEN HEART MUSCLE & IMPROVE AEROBIC CAPACITY

*REFERALS TO NSG/THERAPY, SUPPORT GROUPS, AHA

*DISCUSS ADVANCE DIRECTIONS DIFFERENTIATING IN EVENTS WHICH RECOVERY WOULD/WOULD NOT BE ANTICIPATED

*SEVERE DYSPNEA COMMON-MAY BE MANAGED WITH NARCOTIC ANALGESICS OR WITH FREQUENT IV DIURETICS AND CONTINUOS INFUSION OF A POSITIVE INOTRPIC AGENT