Cardiac Nursing

Applied Anatomy And Physiology:

hollow muscular behind the sternum and between the lungs has heart wall has 3 layers:

Endocardium – thin lining, covers valves Myocardium – muscular layer Epicardium – thin covering(mesothelium)

Pericardium – invaginated sac Visceral – attached to the exterior of myocardium Parietal – attached to the great vessels and diaphragm

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separated into 2 pumps: right heart – pumps blood through the lungs left heart – pumps blood through the peripheral organs

chambers of the heart atrium – weak pump and blood reservoir ventricle – main force that propels blood to pulmonary

and peripheral circulation Blood Supply

Arteries Coronary artery – 1st branch of aorta

• Right Coronaryo SA nodal Branch – supplies SA nodeo Right marginal Branch – supplies the

right border of the hearto AV nodal branch – supplies the AV nodeo Posterior interventricular artery –

supplies both ventricles• Left Coronary

o Circumflex branch – supplies SA node in 40 % of people

o Left marginal – supplies the left ventricleo Anterior interventricular branch aka Left

anterior descending(LAD)–supplies both ventricles and interventricular septum

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o Lateral branch – terminates in ant surface of the heart

Veins Coronary sinus – main vein of the heart Ant interventricular vein or Great Cardiac vein –

main tributary of the coronary sinus Post interventricular vein or Middle cardiac vein Small Cardiac vein Left Posterior ventricular vein Left Marginal Vein Oblique vein – remnant of SVC, small unsignificant Smallest cardiac veins- valveless

Action PotentialResting Membrane Potentials

-85 to -95 mV – cardiac muscle -90 to -100 mV – Purkinje fibers

Circulation

Blood from head and UE; Trunk and LE Superior Vena Cava: Inferior Vena Cava Right Atrium Tricuspid Valve Right Ventricle Pulmonary Valve Pulmonary Artery Lungs Pulmonary Vein Left Atrium

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Mitral Valve Left Ventricle Aortic valve Aorta

Myocardial cell Intercalated disks

Cell membranes that separates individual cells from each other

Two Groups of Myocardial Cells Cells specialized for impulse generation and

conduction• Automatic cells• Found in SA, AV nodes and Purkinje

system(transitional cells) Cells specialized for contraction

• Non Automatic Cells

Specialized Cardiac Cells

Nodal tissues SA Node( Sino-atrial, Keith and Flack)

• Primary Pacemaker• Between SVC and RA• Vagal and symphatetic innervation• Sinus Rhythms

AV Node( Atrioventricular , Kent and Tawara)• At the right atrium

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• 3 zoneso AN Zone(atrionodal)o N Zone (nodal)o NH zone (nodal –HIS)

Internodal and Interatrial Pathways Connects SA and AV Node Ant. Internodal(bachman) tract Middle Internodal(wenkebach) tract Posterior internodal(Thorel) tract

Bundle of His/ Purkinje Fibers Provides for ventricular conduction system Fastest conduction among cardiac tissues Right bundle Left Bundle

• Septal branches and 2 fascicles

Mechanism of Contraction of Contractile Cardiac Muscle Fibers

1. Na+ influx from extracellular space, causes positive feedback opening of voltage-gated Na+ channels; membrane potential quickly depolarizes (-90 to +30 mV); Na+ channels close within 3 ms of opening.

2. Depolarization causes release of Ca++ from sarcoplasmic reticulum (as in skeletal muscle), allowing sliding actin and myosin to proceed.

3. Depolarization ALSO causes opening of slow Ca++

channels on the membrane (special to cardiac muscle), further increasing Ca++ influx and activation of filaments. This causes more prolonged depolarization than in skeletal muscle, resulting in a plateau action potential, rather than a "spiked" action potential (as in skeletal muscle cells).

Differences Between Skeletal & Cardiac MUSCLE Contraction

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1. All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked electrochemically, so that activation of a small group of cells spreads like a wave throughout the entire heart. This is essential for "synchronistic" contraction of the heart as opposed to skeletal muscle.

2. Automicity (Autorhythmicity) - some cardiac muscle cells are "self-excitable" allowing for rhythmic waves of contraction to adjacent cells throughout the heart. Skeletal muscle cells must be stimulated by independent motor neurons as part of a motor unit.

3. Length of Absolute Refractory Period - The absolute refractory period of cardiac muscle cells is much longer than skeletal muscle cells (250 ms vs. 2-3 ms), preventing wave summation and tetanic contractions which would cause the heart to stop pumping rhythmically.

Internal Conduction (Stimulation) System of the Heart

A. General Properties of Conduction

1. heart can beat rhythmically without nervous input2. nodal system (cardiac conduction system) - special

autorhythmic cells of heart that initiate impulses for wave-like contraction of entire heart (no nervous stimulation needed for these)

3. gap junctions - electrically couple all cardiac muscle cells so that depolarization sweeps across heart in sequential fashion from atria to ventricles

B. "Pacemaker" Features of Autorhythmic Cells

1. pacemaker potentials - "autorhythmic cells" of heart muscle create action potentials in rhythmic fashion; this is due to unstable resting potentials which slowly drift back toward threshold voltage after repolarization from a previous cycle.

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Theoretical Mechanism of Pacemaker Potential:

a. K+ leak channels allow K+ OUT of the cell more slowly than in skeletal muscle

b. Na+ slowly leaks into cell, causing membrane potential to slowly drift up to the threshold to trigger Ca++ influx from outside (-40 mV)

c. when threshold for voltage-gated Ca++ channels is reached (-40 mV), fast calcium channels open, permitting explosive entry of Ca++ from of the cell, causing sharp rise in level of depolarization

d. when peak depolarization is achieved, voltage-gated K+

channels open, causing repolarization to the "unstable resting potential"

e. cycle begins again at step a.

C. Anatomical Sequence of Excitation of the Heart

1. Autorhythmic Cell Location & Order of Impulses

(right atrium) sinoatrial node (SA) (right AV valve) atrioventricular node (AV) atrioventricular bundle (bundle of His) right & left bundle of His branches Purkinje fibers of ventricular walls

(from SA through complete heart contraction = 220 ms = 0.22 s)

a. sinoatrial node (SA node) "the pacemaker" - has the fastest autorhythmic rate (70-80 per minute), and sets the pace for the entire heart; this rhythm is called the sinus rhythm; located in right atrial wall, just inferior to the superior vena cava

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b. atrioventricular node (AV node) - impulses pass from SA via gap junctions in about 40 ms.; impulses are delayed about 100 ms to allow completion of the contraction of both atria; located just above tricuspid valve (between right atrium & ventricle)

c. atrioventricular bundle (bundle of His) - in the interATRIAL septum (connects L and R atria)

d. L and R bundle of His branches - within the interVENTRICULAR septum (between L and R ventricles)

e. Purkinje fibers - within the lateral walls of both the L and R ventricles; since left ventricle much larger, Purkinjes more elaborate here; Purkinje fibers innervate “papillary muscles” before ventricle walls so AV can valves prevent backflow

External Innervation Regulating Heart Function

1. heart can beat without external innervation2. external innervation is from AUTONOMIC SYSTEM

Parasympathetic (acetylcholine) DECREASES rate of contractions cardioinhibitory center (medulla) vagus nerve (cranial X) heart

Sympathetic (norepinephrine) INCREASES rate of contractions cardioacceleratory center (medulla) lateral horn of spinal cord to preganglionics Tl-T5 postganlionics cervical/thoracic ganglia heart

The Normal Cardiac Cycle

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A. General Concepts

1. systole - period of chamber contraction2. diastole - period of chamber relaxation3. cardiac cycle - all events of systole and diastole

during one heart flow cycleB. Events of Cardiac Cycle

1. mid-to-late ventricular diastole: ventricles filled

the AV valves are open pressure: LOW in chambers; HIGH in aorta/pulmonary trunk aortic/pulmonary semilunar valves CLOSED blood flows from vena cavas/pulmonary vein INTO atria blood flows through AV valves INTO ventricles (70%) atrial systole propels more blood > ventricles (30%) atrial diastole returns through end of cycle

2. ventricular systole: blood ejected from heart

filled ventricles begin to contract, AV valves CLOSE isovolumetric contraction phase - ventricles CLOSED contraction of closed ventricles increases pressure ventricular ejection phase - blood forced out semilunar valves open, blood -> aorta & pulmonary trunk

3. isovolumetric relaxation: early ventricular diastole

ventricles relax, ventricular pressure becomes LOW semilunar valves close, aorta & pulmonary trunk backflow dicrotic notch - brief increase in aortic pressure

TOTAL CARDIAC CYCLE TIME = 0.8 second(normal 70 beats/minute)

atrial systole (contraction) = 0.1 secondventricular systole (contraction) = 0.3 secondquiescent period (relaxation) = 0.4 second

Heart Sounds: Stethoscope Listening

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A. Overview of Heart Sounds

1. lub-dub, - , lub, dub, -2. lub - closure of AV valves, onset of ventricular systole3. dub - closure of semilunar valves, onset of diastole4. Pause - quiescent period of cardiac cycle5. Tricuspid valve (lub) - RT 5th intercostal, medial6. Mitral valve (lub) - LT 5th intercostal, lateral7. Aortic semilunar valve (dub) - RT 2nd intercostal8. Pulmonary semilunar valve (dub) - LT 2nd intercostals

1. S1- due to closure of the AV valves2. S2- due to the closure of the semi-lunar valves3. S3- due to increased ventricular filling4. S4- due to forceful atrial contraction

B. Heart Murmurs

1. murmur - sounds other than the typical "lub-dub"; typically caused by disruptions in flow

2. incompetent valve - swishing sound just AFTER the normal "lub" or "dub"; valve does not completely close, some regurgitation of blood

3. stenotic valve - high pitched swishing sound when blood should be flowing through valve; narrowing of outlet in the open state

Cardiac Output - Blood Pumping of the Heart

A. General Variables of Cardiac Output

1. Cardiac Output (CO) - blood amount pumped per minute CO (ml/min) = HR (beats/min) X SV (ml/beat) normal CO = 75 beats/minX 70 ml/beat = 5.25 L/min

2. Stroke Volume (SV) - ventricle blood pumped per beat3. Heart Rate (HR) - cardiac cycles per minute

Normal range is 60-100 beats per minute

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Tachycardia is greater than 100 bpm Bradycardia is less than 60 bpm Sympathetic system INCREASES HR Parasympathetic system (Vagus) DECREASES HR

4. 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 BPB. Regulation of Stroke Volume (SV)

1. end diastolic volume (EDV) - total blood collected in ventricle at end of diastole; determined by length of diastole and venous pressure (~ 120 ml)

2. end systolic volume (ESV) - blood left over in ventricle at end of contraction (not pumped out); determined by force of ventricle contraction and arterial blood pressure (~50 ml)

SV (ml/beat) =EDV (ml/beat) - ESV (ml/beat)normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat

3. Frank-Starling Law of the Heart - critical factor for stroke volume is "degree of stretch of cardiac muscle cells"; more stretch = more contraction force

a. increased EDV = more contraction force

i. slow heart rate = more time to fillii. exercise = more venous blood return

C. Regulation of Heart Rate (Autonomic, Chemical, Other)

1. Autonomic Regulation of Heart Rate (HR)

a. sympathetic - NOREPINEPHRINE (NE) increases heart rate (maintains stroke volume which leads to increased Cardiac Output)

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b. parasympathetic - ACETYLCHOLINE (ACh) decreases heart rate

c. vagal tone - parasympathetic inhibition of inherent rate of SA node, allowing normal HR

d. baroreceptors, pressoreceptors - monitor changes in blood pressure and allow reflex activity with the autonomic nervous system

2. Hormonal and Chemical Regulation of Heart Rate (HR)

a. epinephrine - hormone released by adrenal medulla during stress; increases heart rate

b. thyroxine - hormone released by thyroid; increases heart rate in large quantities; amplifies effect of epinephrine

c. Ca++, K+, and Na+ levels very important;

* hyperkalemia - increased K+ level; KCl used to stop heart on lethal injection

* hypokalemia - lower K+ levels; leads to abnormal heart rate rhythms

* hypocalcemia - depresses heart function* hypercalcemia - increases contraction phase* hypernatremia - HIGH Na+ concentration; can

block Na+ transport & muscle contraction

3. Other Factors Effecting Heart Rate (HR)

a. normal heart rate - fetus 140 - 160 beats/minutefemale 72 - 80 beats/minutemale 64 - 72 beats/minute

b. exercise - lowers resting heart rate (40-60)c. heat - increases heart rate significantlyd. cold - decreases heart rate significantlye. tachycardia - HIGHER than normal resting heart

rate (over 100); may lead to fibrillation f. bradycardia - LOWER than normal resting heart rate (below 60); parasympathetic drug side effects;

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physical conditioning; sign of pathology in non-healthy patient

Assessment

Diagnostic Tests:

Laboratory Test Rationale

1. To assist in diagnosing MI2. To identify abnormalities3. To assess inflammation4. To determine baseline value5. To monitor serum level of medications6. To assess the effects of medications

LABORATORY PROCEDURES

CARDIAC Proteins and enzymes1. CK- MB ( creatine kinase)

Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days

Normal value is 0-7 U/L2. Lactic Dehydrogenase (LDH)

Elevates in MI in 24 hours, peaks in 48-72 hours Normally LDH1 is greater than LDH2 Lactic Dehydrogenase (LDH) MI- LDH2 greater than LDH1 (flipped LDH pattern) Normal value is 70-200 IU/L

3. Myoglobin Rises within 1-3 hours Peaks in 4-12 hours

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Returns to normal in a day Not used alone Muscular and RENAL disease can have elevated

myoglobin4. 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 REMEMBER to AVOID IM injections before obtaining

blood sample! Early and late diagnosis can be made!

5. SERUM LIPIDS Lipid profile measures the serum cholesterol,

triglycerides and lipoprotein levels Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL LDH- 130 mg/dL HDL- 30-70- mg/dL NPO post midnight (usually 12 hours)

ELECTROCARDIOGRAM (ECG)

A non-invasive procedure that evaluates the electrical activity of the heart

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A. Deflection Waves of ECG1. P wave - initial wave, demonstrates the depolarization from

SA Node through both ATRIA; the ATRIA contract about 0.1 s after start of P Wave

2. QRS complex - next series of deflections, demonstrates the depolarization of AV node through both ventricles; the ventricles contract throughout the period of the QRS complex, with a short delay after the end of atrial contraction; repolarization of atria also obscured

3. T Wave - repolarization of the ventricles (0.16 s)

4. PR (PQ) Interval - time period from beginning of atrial contraction to beginning of ventricular contraction (0.16 s)

5. QT Interval the time of ventricular contraction (about 0.36 s); from beginning of ventricular depolarization to end of repolarization

Electrodes and wires are attached to the patient

Holter Monitoring

A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded

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continuously over a period of 24 hours

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

ECHOCARDIOGRAM

Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound

No special preparation is needed

Stress Test A non-invasive test that studies the heart during activity and

detects and evaluates CAD Exercise test, pharmacologic test and emotional test Treadmill testing is the most commonly used stress test Used to determine CAD, Chest pain causes, drug effects

and dysrhythmias in exercise Pre-test: consent may be required, adequate rest , eat a light

meal or fast for 4 hours and avoid smoking, alcohol and caffeine

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

Pharmacological stress test Use of dipyridamole

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Maximally dilates coronary artery Side-effect: flushing of face Pre-test: 4 hours fasting, avoid alcohol, caffeine Post test: report symptoms of chest pain

Cardiac Catheterization Insertion of a catheter into the heart and surrounding vessels Determines the structure and performance of the heart

valves and surrounding vessels Used to diagnose CAD, assess coronary atery patency and

determine extent of atherosclerosis Pretest: Ensure Consent, assess for allergy to seafood and

iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses

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

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

Post-test: Monitor VS and cardiac rhythm Monitor peripheral pulses, color and warmth and sensation

of the extremity distal to insertion site Maintain sandbag to the insertion site if required to maintain

pressure Monitor for bleeding and hematoma formation

Central Venous Pressure(CVP)

Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O Elevated CVP indicates increase in blood volume, excessive

IVF or heart/renal failure Low CVP may indicated hypovolemia, hemorrhage and

severe vasodilatation

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

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3. Instruct the client to be relaxed and avoid coughing and straining.

CARDIAC IMPLEMENTATION

1. Assess the cardio-pulmonary status VS, BP, Cardiac assessment

2. Enhance cardiac output Establish IV line to administer fluids

3. Promote gas exchange Administer O2 Position client in semi-Fowler’s Encourage coughing and deep breathing exercises

4. Increase client activity tolerance Balance rest and activity periods Assist in daily activities

5. Promote client comfort Assess the client’s description of pain and chest discomfort Administer medication as prescribed

6. Promote adequate sleep 7. Prevent infection

Monitor skin integrity of lower extremities Assess skin site for edema, redness and warmth Monitor for fever Change position frequently

8. Minimize patient anxiety Encourage verbalization of feelings, fears and concerns

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Answer client questions. Provide information about procedures and medications

Imbalance of Cardiac Output & Heart Pathologies

1. congestive heart failure - heart cannot pump sufficiently to meet needs of the body

a. coronary atherosclerosis - leads to gradual occlusion of heart vessels, reducing oxygen nutrient supply to cardiac muscle cells; (fat & salt diet, smoking, stress)

b. high blood pressure - when aortic pressure gets too large, left ventricle cannot pump properly, increasing ESV, and lowering SV

c. myocardial infarct (MI) - "heart cell death" due to numerous factors, including coronary artery occlusion

d. pulmonary congestion - failure of LEFT heart; leads to buildup of blood in the lungs

e. peripheral congestion - failure of RIGHT heart; pools in body, leading to edema (fluid buildup in areas such as feet, ankles, fingers)

Angina Pectoris

Chest pain resulting from coronary atherosclerosis or myocardial ischemia

Clinical Syndromes:

Three Common Types of ANGINA

1. STABLE ANGINA The typical angina that occurs during exertion, relieved by rest

and drugs and the severity does not change2. Unstable angina

Occurs unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and drug

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

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ASSESSMENT FINDINGS: Chest pain- ANGINA The most characteristic symptom PAIN is described as mild to severe retrosternal pain,

squeezing, tightness or burning sensation Radiates to the jaw and left arm Precipitated by Exercise, Eating heavy meals, Emotions like

excitement and anxiety and Extremes of temperature Relieved by REST and Nitroglycerin Diaphoresis Nausea and vomiting Cold clammy skin Sense of apprehension and doom Dizziness and syncope

LABORATORY FINDINGS ECG may show normal tracing if patient is pain-free. Ischemic

changes may show ST depression and T wave inversion Cardiac catheterization Provides the MOST DEFINITIVE source of diagnosis by

showing the presence of the atherosclerotic lesionsNURSING MANAGEMENT

Administer prescribed medications Nitrates- to dilate the coronary arteries Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP and HR Calcium-channel blockers- to dilate coronary artery and reduce

vasospasm Teach the patient management of anginal attacks Advise patient to stop all activities Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention Obtain a 12-lead ECG

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Promote myocardial perfusion Instruct patient to maintain bed rest Administer O2 @ 3 lpm Advise to avoid valsalva maneuvers Provide laxatives or high fiber diet to lessen constipation Encourage to avoid increased physical activities Assist in possible treatment modalities

o PTCA- percutaneous transluminal coronary angioplasty To compress the plaque against the vessel wall,

increasing the arterial lumeno CABG- coronary artery bypass graft

To improve the blood flow to the myocardial tissue Provide information to family members to minimize anxiety and

promote family cooperation Assist client to identify risk factors that can be modified Refer patient to proper agencies

Myocardial Infarction terminal stage of coronary art dse resulting from permanent

mal-occlussion, necrosis and scarringtypes of MI:1. Transmural

most dangerous form of MI characterized by occlussion of right and left coronary art.

2. Subendocardial critical period of MI: 24-48 hours - arrythmias, PVC (lidocaine

as ordered)S/S:a. Pain: sharp, excruciating visceral pain

substernal: radiates to back, arms, shoulder, axilla, jaw and abdominal ms

not usually received by restb. Dyspneac. Hyperthermiad. Mild restlessness or apprehensione. Initial inc in bld pressuref. Occasional findings:

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Rales or crackles upon auscultation Pericardial friction rub Split S1 and S2 Atrial gallop (S4)

Dx procedures1. Cardiac enzymes

CPK-MB Lactic dehydrogenase SGPT (ALT) SGOT (AST)

2. Troponin test: inc3. ECG tracing reveals:

ST segment elevation Widening of QRS complex Arrythmia in MI: PVCs

4. Serum uric acid and cholesterol: inc5. CBC: inc in WBC count

Nursing Management:1. Administer meds as ordereda. Narcotic analgesic: morphine sulfate - induce vasodilation, reduce levels of anxiety

side effect: resp depression: antidote - NaloxoneNaloxone toxicity: - tremor2. Administer O2 inhalation as ordered3. Enforce complete bedresta. Bedside commode

dec myocardial O2 demand4. Instruct client to avoid vasalva manuever5. semi-fowler's pos'n6. General liquid -> soft diet7. Avoid foods rich in caffeine, sodium and saturated fats8. Monitor VS, I and O9. Administer meds as ordered:a. Vasodilators

nitroglycerin isosorbide dinitrate

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b. Anti-arrhythmic agents xylocaine

c. Beta blockers propanolol

d. ACE-inhibitors captopril, enalopril

e. Thrombolytic/fibrinolytic agents streptokinase urokinase TPAF (tissue plasminogen activating factor): monitor bleeding

timef. Anticoagulants

heparin and coumadin simultaneously: late effect of coumadin - 3 days

heparin: monitor PTT (partial thromboplastin time) heparin antidote: protamine sulfate coumadine antidote: vit K

g. Antiplatelet anti thrombotic property

10. Assist in surgical procedure coronary art by pass PTCA

11. Provide client health teaching concerning:a. Avoidance of precipitating factorsb. Dietary restrictionsc. Prevention of Complications

arrhythmia: PVCs shock: cardiogenic - oliguria as late sign congestive heart failure thrombophlebitis CVA Dressler's Syndrome: post MI syndrome - resistance to

pharmacologocal agents: administer 450,000 units of streptokinase as ordered

d. Instruct client re resumption of ADL sexual intercourse: 3-6 weeks post carrdiac rehab sex before meals assume a non wt-bearing position

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importance of follow-up care

Congestive Heart Failure inability to pump blood toward systemic circulation

I. Left-sided heart failurePred. Factors1. 90% mitral valve stenosis (RHD, aging): ASO titer (anti streptolysin O) = > 300 Todd units

complication of RHD -> CHF

steroids

penicillin aspirin

2. IHD3. Hypertension4. MI5. Aortic stenosisSigns and symptoms:1. Pulmonary edema and congestion2. Paroxysmal nocturnal dyspnea (PND)3. Orthopnea: place client in high Fowler's pos'n4. Productive cough with bld tinge sputum5. Frothy salivation6. Cyanosis7. Rales or crackles8. Bronchial wheezing9. Pulsus alternans10. Anorexia, gen body malaise11. Point of max impulse displaced laterally

PMI 4th-5th ICS mid clavicular line12. S3 (ventricular gallop)

Dx procedures1. Chestx-ray:cardiomegaly2. Angiography, echocardiography: site and extent of mal occlusion3. ABG: pCO2 inc, pO2 dec -> resp acidosis, hypoxemia4. PAP (pulmonary art pressure), pulmonary capillary wedge pressure (PCWP): inc

Swan Ganz catheterization: done at bedside tracheostomy: bedside, done in O.R if pt has laryngeal or

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thyroid cancer

Right sided HF

Predisposing factors1. Tricuspid v stenosis2. Pulm edema3. COPD

4. Pulm valve stenosis5. left sided heart failure

B. S/S1. Jugular vein distention2. Pitting edema3. Ascites4. Wt gain5. Hepatosplenomegaly

6. Jaundice7. Pruritus8. Anorexia, gen body malaise9. Esophageal varices

Dx procedure1. Chest x-ray: cardiomegaly2. Echocardiogram: enlarged heart chamber3. Central venous pressure: measures right atrium pressure

- N = 4-10 cm of H2O- if CVP is dec -> hypovolemia -> fluid challenge- if CVP is inc -> hypervolemia- trendelenberg pos'n: CVP catheter insertion

4. Liver enzymes: incA. SGPT (ALT)B. SGOT (AST)

Nursing Mgt1. Administer meds as orderedA. Cardiac glycoside (Digoxin - lanoxin): monitor heart rate before admin > 60

digitalis toxicity: digibind (antidote)B. Bronchodilator

aminophylline (theophylline) toxicity: tachycardia, tremors

C. Narcotic analgesic morphine sulfate

D. Loop diuretics

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Lasix (furosemide): 6 hrs max effect, onset 15 minsE. Vasodilators

ISDNF. Anti arrhythmic agents

lidocaine bretylium

2. Restrict fluids3. VS, I and O, breath sounds4. Weigh pt daily, assess for pitting edema5. Measure abdominal girth -> notify physician6. O2 inhalation: 3-4 liters/min via nasal cannula - high inflow7. High Fowler's position8. Bloodless phlebotomy: rotating tournique - 3 tournique rotated clockwise every 15 mins to dec venous return9. Health teaching

A. Dietary modification: low Na, saturated fats, caffeineB. Prevent complications

Arrhythmia MI Thrombophlebitis Cor pulmonale

C. Follow-up care

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