CARDIOVASCULAR DISORDERS

Introduction People are living longer than ever before.

However, they are living increasingly with chronic conditions or sequelae of acute ones. Of these conditions, disorders related to cardiovascular systems are currently one of the leading causes of death most countries worldwide, including the Philippines.

We, nurses will be caring for clients with cardiovascular disorders more often, in all health care settings. Therefore we will increasingly assume significant roles in providing individualized comprehensive, holistic, ethical, and quality care among the clients.

To provide effective care for these clients, we need a clear understanding of cardiovascular structures and functions, assessment techniques, diagnostic tests, pathophysiology, complications and collaborative management of the disorders. Moreover, we must include client education on the management of the disorders to empower the client’s and assist them assume self – responsibility in their health care.

  On the whole, such knowledge, skills and

attitudes allow us, nurses better promote recovery, improve client compliance, and ensure adequate home care. And finally, enable the clients achieve quality life.

Learning outcomes

1. Discuss the different assessment parameters for cardiac functioning.

2. Describe nursing care of clients undergoing diagnostics tests to assess cardiac functioning.

3. Describe treatment modalities for clients with cardiac disorders.

4. Explain the pathophysiology, clinical manifestations and collaborative management of cardiac disorders.

5. Design a nursing care plan for clients with cardiac disorders.

6. Teach clients with cardiac disorders about prevention, management and rehabilitation factors that optimize health.

Overview of anatomy and Physiology of the Heart

The heart is a small organ that weighs 300 g. and is approximately the size of a fist. It is located in the middle of the mediastinum.

Heart Wall The three layers of the heart are as follows: epicardium,

outermost layer; myocardium, the cardiac muscle; and endocardium, the endothelium.

The heart is enclosed by the pericardium which consist of two layers: visceral pericardium (inner layer) and parietal pericardium (outer layer). There is is 5 to 20 mls. Of fluid in the pericardial sac which prevents friction between the two pericardial layers.

Structure of the Heart

Chambers of the Heart

The four chambers of the heart are as follows: right atrium, right ventricle, left atrium and left ventricle. The right atrium receives venous blood returning to the heart via the superior and inferior vena cavae.The right ventricle receives venous blood from the right atrium, and ejects this blood into the lungs via the pulmonary artery.The left atrium receives oxygenated blood from the four pulmonary veins and serves as a reservoir during ventricular systole.The left ventricle receives blood from the left atrium and ejects blood into the systemic arterial circulation via the aorta.

Valves of the HeartThe two types of cardiac valves are the atrioventricular (AV) valves and the semilunar valves.

The Av valves are the tricuspid valve and bicuspid (mitral) valve. The tricuspid valve is located between the right atrium and right ventricle. The mitral valve is located between the left atrium and left ventricle.

The AV valves are held in place by the chorda tendinae cordis, which in turn are anchiored to the ventricular wall by the papillary muscles. The chorda tendinae cordis supports the AV valves during ventricular systole to prevent valvular prolapsed into the atrium.

The semilunar valves are the aortic valve and the pulmonic valve. The aortic valve lies between the left ventricle and the aorta. The pulmonic valve lies between the right ventricle and the pulmonary artery. These valves open during ventricular systole, and they close during ventricular diastole.

Coronary ArteriesThe coronary arteries originate from

the aorta, behind the cusps of the aortic valve, in an area known as Vasalva’s sinus.

The two main coronary arteries are the left coronary artery (LCA) and the right coronary artery (RCA).

The LCA divides into two branches namely, the circumflex coronary artery (CCA) and the left anterior descending artery (LADA).

The CCA supplies the following: left atrium, posterior lateral surface of the left ventricle.

The LADA supplies the anterior wall of the left ventricle, the anterior interventricular septum, the anterior papillary muscles and apex of the heart.

The RCA supplies the right atrium, right ventricle, a portion of the septum, SA node, AV node, and inferior portion of the left ventricle.

Coronary artery blood flow to the myocardium occurs during diastole, when coronary vascular resistance is reduced. During diastole, blood enters the coronary artery, which is called diastolic filling.

Conduction System:The normal pacemaker of the heart is he

sinoatrial (SA) node. The Sa node triggers electrical impulses at a rate of 60 to 100 beats per minute. The atria are then depolarized and the impulse is transmitted via the intermodal tracts into the atriventricular (AV) node. The impulse is delayed in the AV node, which enables atrial contraction to complete before the ventricles are stimulated and contract.

The electrical impulse is then transmitted into the Bundle of His, and into the Purkinje fibers

Electrophysiologic Properties of the heart

The electro physiologic properties of the heart are as follows: automaticity, excitability, conductivity, contractility, and refractioriness.

Automaticity is the ability of the heart to initiate impulses repetively and spontaneously (also called rhythmicity).

Excitability is the ability of cardiac cells to respond to a stimulus by initiating a cardiac impulse.

Conductivity is the ability of cardiac cells to respond to an impulse by transmitting the impulse along cell membranes.

Contractility is the ability of cardiac cells to respond to an impulse by contracting.

Refractoriness is the inability of the cardiac cells to respond to a new stimulus while it is in contraction in response to a previous stimulus.

Cardiac Conduction System

Cardiac CycleThe two phase of the cardiac cycle are diastole and systole. Relaxation and filling of the atria and ventricles occur during diastole. Contraction and emptying of the atria and ventricles occur during systole.

Cardiac OutputCardiac output (C.O) is the volume of

blood ejected from the left ventricle into the aorta per minute. C.O = Stroke Volume x Heart Rate (70 mls X 70 bpm = 4,900 mls or approximately 5 L)

The average cardiac output is approximately 5L/minute.

Stroke volume (SV) is the mount of blood rejected by the left ventricle into the aorta per beat. The stroke volume is determined by three factors, namely: preload, contractility and afterload. It is approximately 70 mls.

Preload is the degree of myocardial fiber stretch before contraction. It is related to the volume of blood distending the ventricles at the end of diastole. It is determined by the amount of venous return.

Frank – starling law of the heart conceptualizes that the greater the myocardial fiber stretch, within physiologic limits, the more forceful the ventricular contraction, thereby increasing stroke volume.

Contractility refers to a change in the inotropic state of the muscle without a change in myocardial fiber length or preload.

Afterload is the amount of tension the ventricle musty develop during contraction to eject blood from the left ventricle into the aorta.

Autonomic Influences on cardiac Activity

Autonomic nervous system provides an external influence on myocardial contractility and rate.

The sympathetic nervous system (SNS) releases norepinephrine which increases the heart rate and the force of contraction of the heart. The parasympathetic nervous system (PNS) releases acetycholine from vagal fibers which slows the heart rate and causes slight decrease in ventricular contractility.

Baroreceptors

The baroreceptors in the carotid and aortic bodies are pressure – sensitive structures. Decreased BP causes a reflex SNS response with increased pulse, increased contractility and vasoconstriction. Increased BP causes reflex vagal responces, which results in decreased heart rate and passive vasidilation in the systemic arterioles. This phenomenon is known as Marcy’s Law of the heart.

Chemoreceptors:

The major chemoreceptor of the heart is the medulla oblongata, and special receptors are found in the carotid and aortic bodies. A decreased pH or paO₂ level causes a reflex SNS response that results in tachycardia, vasoconstriction and increased ph level leads to passive vasodilation.

Cardiac Index

The cardiac index is a more accurate indicator of tissue perfusion. It represents the cardiac output in terms of liters per minute per square meter of body surface area. The normal range of cardiac index is 2.4 to 4.0 L/min.

Cardiac Index = C.O (L/min.)Body Surface Area (m²)

Physiologic Changes in the Heart with Aging

Decreased myocardial contractility. This reduces cardiac reserve.

General thickening of endocardium and valves. The valves tend to become rigid and incompetent. Heart murmurs develop.

Conducting fibers are replaced by fibrous tissue. This reduces the effectiveness of pacemaker cells, decreases conductivity and leads to dysrhythmias.

Assessment of the clients with Cardiovascular Disorders

Nursing historyThe risk factors cardiovascular disorders

may be classified as follows: Non-modifiable Risk factors (Unavoidable risk factors)

Modifiable Risk factors (Avoidable risk factors)

Physical examination Common Clinical Manifestations Diagnostic Tests

Non- Modifiable Risk factors Age – persons above 40 years of age are at

high risk to develop cardiovascular diseased. This is due to degenerative changes in the heart and blood vessels.

Gender – males are more prone to cardiovascular disorders before the age of 65 years. However, females have higher propensity to cardiovascular disorders after the age of 65 years. This is due to decreased estrogen levels in menopause. HDL (high density lipoprotein/ “good cholesterol”) decreases, LDL (low density lipoprotein/ “bad cholesterol”) increases. This causes development atherosclerosis.

Race – cardiovascular disorders are among the 10 leading causes of death worldwide in the U.S., cardiovascular disorders rank the number one causes of morbidity.

Heredity – person with family history for cardiovascular disorders are at risk to develop these diseases.

Modifiable Risk factors Stress – sympathetic response

stimulation causes increased secretion of norepinephrine. This results to vasoconstriction and tachycardia. Increased BP and increased cardiac workload occur.

Diet – increased dietary intake of foods high in sodium, fats and cholesterol predisposes a person to cardiovascular disorders. Sodium retains water and increases blood volume. This may cause hypertension. High fats and high cholesterol diet predisposes a person to atherosclerosis.

Exercise – regular pattern of exercise improves circulation to different body parts including the heart and blood vessels; maintains vascular tone; and enhances release of chemical activators (tissue – type plaminogen activators), which prevent platelet aggregation and prevent blood clotting. Sedentary lifestyle increases risk to cardiovascular disorders.

Cigarette smoking – nicotine causes vasoconstriction and spasm of the arteries; increases myocardial oxygen demands; and adhesion of platelets. In addition, cigarette smoking has been associated with decreased levels of HDL. In cigarette smoking, more carbon dioxide is inhaled than oxygen

Alcohol – it positively correlates with high blood pressure. Alcohol causes vasoconstriction. Thirty mls. Of alcohol is stimulant and causes vasodilatation. More than 30 mls. Of alcohol causes vasoconstriction and elevation of blood pressure.

Hypertension – increased systemic vascular resistance, endothelial damage, increased platelet adherence, and increased permeability of endothelial lining, result from elevated blood pressure.

Hyperlipidemia – hypercholesterolemia. Increased LDL cholesterol damages endothelium and causes accumulation of fatty plaques on endothelial lining and proliferation of smooth muscle cells.

Diabetes Mellitus

Glucose from carbohydrates cannot be transported into the cells due to insulin deficiency or increased resistance to insulin.

The body then, mobilizes fats (lipolysis), to become a source of glucose. However, not all of the fats mobilized are converted into glucose. Most of it remain as lipids. Hyperlipidemia results, which enhances the risk of atherosclerosis.

Obesity – this results to increased cardiac workload. The heart has to pump blood supply to a larger body surface area. May also be characterized by rise in serum lipid levels.

Personality type or Behavioral Factors – the type A behavior pattern characterized by competitiveness, impatience, aggressiveness and time urgency has been correlated to coronary artery diseases (Cad). Although the mechanism is unknown.

Contraceptive pills – may precipitate thromboembolism and hypertension. The estrogen component of oral contraceptive pills increase blood viscosity, thereby increasing the risk to thromboembolism. It also stimulates the liver to synthesize angiotensinogen. The angiotensinogen triggers production of pulmonary converting enzymes. This in turn causes conversion of angiotensinogen to angiotensin I, a vasoconstrictor. Angiotensin I is further acted upon by pulmonary converting enzyme and converted to Angiotensin II, a very potent vasoconstrictor.

Physical Examination Inspection

Skin color – note for pallor, cyanosis or jaundice. Pallor and cyanosis are due to inadequate oxygenation. Jaundice is due to hemolysis of rbc. The bilirubin component of the rbc is released into the systematic circulation causing yellowish discoloration of the skin and scelerae.

Neck vein distension (jugular vein distension). This is due to venous congestion.

Respiration note for signs of dyspnea. This indicates inadequate oxygenation.

Point of Maximalo Impulse (PMI). It is located in the left , mid- clavicular, fifth intercostals space (ICS).

Peripheral edema. This is due to venous insufficiency.

PalpationPeripheral pulses. Weak or bounding and

irregular pulses may indicate presence of cardiovascular disorders.

Apical pulse. It is assessed at the point of maximum impulse.

PercussionPulmonary edema produces dullness on

percussion of the chest. Auscultation

Heart sounds S1 is produced by asynchronous closure of the mitral and tricuspid valves. It signals the onset of ventricular systole (“lubb”).

S2 is produced by asynchronous closure of the aortic and pulmonic valves. It signals the onset of ventricular diastole (“dubb”).

S3 or ventricular diastolic gallop is a faint, low pitched sound produced by rapid ventricular filling in early diastole. It is normal in children and in young adults. It indicates congestive heart failure (CHF) in older adults.

S4 or atrial diastolic gallop is a low frequency sound which is present in congestive heart failure. It is abnormal in all ages.

Murmurs. These are audible vibrations of the heart and great vessels that are produced by turbulent blood flow.

Pericardial friction rub. It is an extra heart sound originating from the pericardial sac. This may be a sign of inflammation, infection or infiltration. It is described as a short, high pitched, scratchy sound.

Common Clinical manifestations of Cardiovascular Disorders

 Dyspnea – the client experiences shortness of breath.

Dyspnea on exertion (DOE). This may indicate decreased cardiac reserve (heart’s ability to adjust and adapt to increased demands).

Orthopnea – is usually a symptom of more advanced heart failure. The client experiences difficulty of breathing when in lying position and relieved by upright position. The client may need several pillows to be able to sleep during the night.

Paroxysmal nocturnal dyspnea – is manifested by severe shortness of breath that usually occurs 2 to 5 hours after the onset of sleep. During waking hours, the client usually assumes upright position most of the time. This causes venous pooling. When the client lies recumbent during the night, the blood from the lower extremities are distributed to the upper parts of the body and lung congestion may occur and the client experiences difficulty of breathing. It takes 2 to 5 hours for the blood from the lower extremities to be distributed to the upper parts of the body.

Chest pain – this may be due to decreased coronary tissue perfusion and oxygenation. Anaerobic metabolism causes production of lactic acid. Lactic acid causes irritation of nerve endings in the myocardium. This results to chest pain.

Edema – increased hydrostatic pressure in the venous system causes shifting of plasma. Therefore, accumulation of fluids in the interstitial compartment occurs.

Syncope – the client experiences generalized muscle weakness with an inability to stand upright, followed by loss of consciousness. This is due to decreased cerebral tissue perfusion.

Palpitations – the client experiences unpleasant awareness of the heartbeat. This is described by the client as “pounding,” “racing” or “skipping”. Palpitations that occur during mild exertion may indicate the presence of heart failure, anemia or thyrotoxicosis.

Fatigue – this may be a consequence of inadequate cardiac output.

Laboratory and Diagnostic Test Related to Cardiovascular

Function Laboratory Tests

Complete blood count For evaluation of general health status.

Elevated RBC”s suggests inadequate tissue oxygenation. Hypoxia stimulates renal secretion of erythropoietin. This stimulates the bone marrow to increase rbc production (polycythemia).

Elevated WBC’s may indicate infectious heart diseases and myocardial infarction.

Erythrocyte Sedimentation Rate (ESR) It is a measurement of the rate at which RBC’s “settle out” of anticoagulated blood in an hour.

It is elevated in infectious heart disorders or myocardial infarction.

Normal range is as follows:Males: 15 – 20 mm/hr.Females: 20 – 30 mm/hr.

Blood Coagulation Tests Prothrombin time (PT, pro time)

It measures the time required for clotting to occur after thromboplastin and calcium are added to decalcified plasma.

It is valuable in evaluating the effectiveness of Coumadin. Therapeutic range is 1.5 to 2 times the normal value or control.

Normal range is 11 to 16 seconds

Partial thromboplastin Time (PTT) It measures the time required for clotting to

occur after a “partial thromboplastin reagent” is added to blood plasma.

It is the best single screening test for disorders of coagulation.

It is determined to evaluate the effectiveness of Heparin. Therapeutic range is 2 to 2.5 times the normal value or control.

Normal range is 60 to 70 secs. Activated Partial Thromboplastin Time (APTT).

It has the same purpose as PTT. It is the most specific test to evaluate effectiveness of Heparin.

Normal range is 30 to 45 secs.

Blood urea Nitrogen (BUNIt is an indicator of renal function.Decreased cardiac output leads to low

renal tissue perfusion and reduction in glomerular filtration rate. The Bun level becomes elevated

Normal range is 10 to 20 mg/dl (5 to 25 mg/dl is also acceptable level).

Blood LipidsSerum cholesterolThe client should be on NPO for 10 to

12 hrs.Normal range is 150 to 200 mg/dl.Serum triglyceridesThe client should observe fasting for

10-12 hours.Normal range is 140 to 200 mg/dl.

Blood CulturesTo assist in the diagnosis of infectious

diseases of the heart, e.g., pericaditis.Caution is taken to prevent

contamination of the specimen. To ensure accuracy of results.

Serum Enzyme StudiesAspartyate Aminotranferase (AST)

Formerly, SGOT. Elevated level indicates tissue necrosis. Normal range I 7 to 40 mu/ml. Range with Myocardial Infarction

Initial elevation: 4 to 6 hrs.Peaks: 24 to 36 hrs.Returns to normal: 4 to 7 days Creatine

Phosphokinase (CK-MB)

It is the most cardiac specific enzyme. It is an accurate indicator of Myocardial

damage. Normal range is:

Males: 50-325 mu,/mlFemales: 50-250 mu./ml.

Range with Myocardial infarctionOnset: 3 to 6 hrs.Peaks: 12 to 18hrs.Returns to normal: 3 to 4 datys

Lactic Dehydrogenase (LDH) Among the five LDH isoenzymes, LDh1 is

the most sensitive indicator of myocardial damage.

In Ml, LDH1 is elevated and its level exceeds LDH2. This makes LDH1/LDH2 ratio “flipped”.

Normal range is 100 to 225 mU/ml. Range with myocardial infarction

Onset: 12 hrs.Peaks: 48 hrs.Returns to normal: 10 to 14 days

Hydroxybutyrate Dehydrogenase (HBD

Elevation of HBD is always accompanied by elevation of LDH levels.

It is valuable in detecting “silent M.I.” because it remains elevated for a long period of time, even after the other enzymes have returned to normal.

The HBD/LDH ratio may be increased in M.I. Normal range is 140 to 350 u Range with myocardial infraction

Onset: 10 to 12 hrs.Peaks: 48 to 72 hrs.Returns to normal: 12 to 13 days

Troponin

Most specific laboratory test to detect MI.

Troponin has three components: I, C and T.

Troponin I modulates the contractile state. Troponin C binds calcium and troponin T binds I and C.

Elevated troponin T is as sensitive as CK-MB for the detection of myocardial injury.

Troponin I persists for 4 to 7 days.

Urinalysis

This test is performed to assess the effects of cardiovascular diseases on renal function and the existence of concurrent renal or systemic diseases, e.g., glomerulonephritis, hypertension or diabetes mellitus.

Albuminuria is detected in clients with malignant hypertension and CHF (congestive heart failure).

Myoglobinuria supports diagnosis of M.I.

Blood Uric Acid (BUA)

This test reflects adequacy of renal tissue perfusion thereby glomerular filtration of metabolities.

Cardiovascular disorders result to decreased renal tissue perfusion. This will cause impairment of the ability of the kidneys to clear the plasma of end products of metabolism like uric acid.

Normal range is 2.5 to 8 mg./dl

Serologic Tests

VDRL helps indicate presence of syphilis. This disease involves development of aortic disorders.

Serum electrolytesElectrolytes affect cardiac contractility,

specifically Na+,k+,ca+Normal ranges are as follows:

Na+: 135 to 145 mEq./L K+: 3.5 to 5 mEq/L Ca+: 4.5 to 5.5 mEq/L (or 8.6 to 10 mg/dl)

Diagnostics Tests

Electrocardiography (ECG, EKG) It is graphical recording of the electrical

activities of the heart. It is the first diagnostic test done when

cardiovascular disorder is suspected. Inform the client that the procedure is

painless. He will not experience electrocution or a shock.

Waves, complexes and intervals

P wave. Depolarization of atria. Duration is 0.04 to 0.11 secs.

PR interval. Time of impulse transmission from the SA node to the AV node. Duration is 0.12 to 0.20 secs.

QRS complex. Depolarization of the ventricles. Duration is 0.05 to 0.10 secs.

St segment. Represents the plateau phase of the action potential.

T wave. Ventricular repolarization. Should not exceed 5 mm amplitude.

Common ECG changesHypokalemia

U-wave Depresses ST segment Peaked T wave

Hyperkalemia Prolonged QRS complex Elevated ST segment Peaked T wave

Myocardial Infraction Elevated ST segment (this is the first ECG change that

occurs in MI) Inverted T wave Pathologic Q wave (this becomes permanent in the

ECG complexes of the post M.I. client. It is generated from the area of infarction that becomes scarred).

Holter Monitoring It is continuous (24-hour) ECG

monitoring. The portable monitoring system is

called telemetry unit. This attempts to assess the activities

which precipitate dysrthythmias, and the time of the day when the client experiences dysrhythmias.

The nurse (or the client or significant others) should log / record the activities of the client, and any unusual sensations experienced.

Invasive hemodynamic monitoring

Central Venous Pressure Monitors the pressures within the right

atrium. Monitors blood volume, adequacy of venous

return to the heart, pump function of the right side of the heart.

The level of the water manometer should be placed at the right, mid-axillary, 4th ICS. This is the approximate level of the right atrium when the client is in supine position.

Place the client in supine position or in the same position as during the initial reading. To get accurate readings. Position can affect CVP readings.

Practice strict asepsis. To prevent infection.

CENTRAL VENOUS PRESSURE MONITORING

Normal reading.

Superior vena cava : 0-12 cm. H₂O

Right atrium : 5-12 cm. H₂OUse other parameters to validate CVP reading –BP, urine output, pulse. Hypervolemia is manifested by elevated CVP reading, hypertension, polyuria, and bounding pulse. Hypovolemia and dehydration are characterized by low CVP reading, hypertension,oliguria and rapid, weak, thread pulse.

Pulmonary Artery Pressure (PAP) and Pulmonary Capillary Wedge Pressure (PCWP)

Swan – Ganz catheter is inserted via antecubital vein into the right side of the heart and is floated into the pulmonary artery.it reflects pressure in the left heart. Left-sided congestive heart failure may lead to pulmonary edema. This in turn, causes congestion of blood in the pulmonary artery (pulmonary hypertension). Elevated PAP and PCWP readings indicate left side congestive heart failure.

SWAN GANZ CATHETERIZATION

Swan – ganz catheter is a flow – directed, balloon – tipped, 4 – lumen catheter.

The catheter allows continuous monitoring of

Right and left ventricular functionPulmonary artery pressures (Pap,PCWP)Cardiac outputArterial-venous oxygen difference

Normal range:PAP : 4-12 mmHgPCWP : 4-12 mmHg

PCWP reading above 25 mmHg suggests impending pulmonary edema.

Nursing Interventions:

Inflate balloon only for PCWP readings: deflate between readings.

Observe catheter insertion site; culture site every 48 hours as prescribed.

Assess extremity for color, temperature, capillary filing and sensation. To observe for signs and symptoms of circulatory impairment in the extremity involved.

Sonic studies

Echocardiography Uses ultrasound to assess cardiac

structure and mobility. No special preparation is required It is painless and takes approximately 30

to 60 minutes to complete. The client has to remain still, in supine

position slightly turned to the left side with HOB elevated 15 to 20 degrees

Transesophageal Echocardiography (TEE)

Allows ultrasonic imaging of the cardiac structures and great vessels via esophagus.

Nursing Interventions Before TEEAscertain history of esophageal

surgery, malignancy, or allergy to anesthetics or sedatives.

NPO for 4 to 6 hrs. before the procedure. To prevent aspiration.

Encourage to void before the procedure. To promote comfort.

Remove dentures and other oral prosthetics. To prevent airway obstruction.

Administer sedatives as ordered. To relieve anxiety.

Keep suction and resuscitation equipment readily available.

Cardiac monitoring is done during the entire procedure. To assess for dysrhythmias.

Topical spray anesthetic is administered to depress gag reflex. This facilities insertion of the transducer into the esophagus.

Place the patient in chin – to – chest position to facilitate passage of endoscope.

Nursing Interventions after TEE

NPO until gag reflex returns. To prevent aspiration.

Place in lateral or semi – fowler’s position. To promote drainage of secretions from the mouth.

Encourage to coughThroat lozenges or rinses may be

used to relieve throat soreness.Observe for signs and symptoms of

complications, e.g. pharyngeal bleeding, cardiac dysrhythmias, vasovagal reaction, and transient hypoxemia.

Phonocardiography

Involves the use of electrically recorded amplified cardiac sounds.

It is helpful in assessing the exact timing characteristics of murmurs and extra heart sounds.

Preparation of client is similar to echocardiogram

Stress Testing or Exercise Testing Involves the use of electrically

recorded amplified cardiac sounds.

It is helpful in assessing the exact timing characteristics of murmurs and extra heart sounds.

Preparation of client is similar to echocardiogram

Stress Testing or Exercise Testing

ECG is monitored during exercise on a treadmill or a bicycle – like device.

The purposes of stress test are as follows: Identify ischemic heart disease Evaluate patients with chest pain Evaluate effectiveness of therapy Develop individual fitness program during cardiac rehabilitation.

Nursing Interventions: treadmill Test Patient teaching includes the following:

Get adequate sleep the night before the test Avoid tea, coffee and alcohol on the day of

the test. These may affect the test results. Avoid smoking and taking nitroglycerine, 2

hours before the test. To prevent postural hypotension.

Wear comfortable, loose-fitting clothes Eat a light breakfast/lunch at least 2 hours

before the test Wear low-heeled, rubber-soled pair of shoe.

For comfort during the test. Inform the physician if any unusual

sensations develop during the test, e.g., shortness of breath, dizziness, faintness.

Rest after the test.

Radiolic TestsChest Roentgenograms (X-Rays)

To determine overall size and configuration of the heart and size of the cardiac chambers.

Cardiac Flouroscopy Facilities observation of the heart from varying views while the heart is in motion.

Cardiac Catheterization The purposes of the test are as follows:

Assess: oxygen levels, pulmonary blood flow, cardiac output, heart structures.

Coronary artery visualization. Right – sided heart catheterization is

done by insertion of a catheter via a cut down into a large vein, e.g., medial cubital or brachial vein.

Left – sided heart catheterization is done by passing a catheter into the aorta via the brachial or femoral artery.

Nursing Interventions: Cardiac CatheterizationBefore The Procedure

Provide psychosocial support. To allay anxiety. Assess for allergy to iodine/ seafood's. The contrast

medium used is iodinated. Obtain baseline VS. Withhold meals before the procedure. To prevent

nausea and vomiting. Have client void. To promote comfort. Administer sedative as ordered. Mark distal pulses. Do cardiac monitoring. To assess for dysrhythmias. Done under local anesthesia. May experience warm or flushing sensation as the

contrast medium is injected. “Fluttering” sensation is felt, as the catheter enters

the chambers of the heart.

After the procedure:

Bed rest: if the catheter insertion site is an upper extremity, until VS are stable; while if it is in a lower extremity, bed rest fro 6 to 8 hrs. to prevent bleeding.

Monitor VS, especially peripheral pulses. Diminished or absent pulse indicates circulatory impairment. This may be due to vasopasm or obstruction caused by thromboembolism.

Monitor ECG, note for dysrhythmias.

Apply pressure dressing and a small sand bag or ice over the puncture site. To prevent bleeding.

Immobilize affected extremity in extension. To promote circulation.

Do not elevate HOB more than 30° if femoral site was used. Acute hip flexion causes circulatory impairment.

Monitor extremity for color, temperature, pulse and sensation. Impaired circulation in the affected extremity is manifested by pallor or cyanosis, cold skin, diminished pulse or pulselessness, and numbness or tingling sensation.

Angiography / Arteriography

Involves introduction of contrast medium into the vascular system to outline the heart and blood vessels.

It may be done during cardiac catheterization.

Nursing interventions are similar to that of cardiac catheterization.

Observe for hypertension after the procedure because the contrast medium uses in

Magnetic Resonance Imaging (MRI) Strong magnetic field and

radiowaves are used to detect and defined differences between healthy and diseased tissues.

MRI can actually show the heart beating and the blood flowing in any direction. It can image over three spatial dimensions and overtime.

It is used for examination of the aorta, detection f tumors, cardiomyopathies and pericardiac disease

Nursing Interventions: MRI Secure written consent. Consent is required for

diagnostic tests that involve use of contrast medium. In MRI, gandolinium is commonly used.

Inform the client that the procedure may last 45 to 60 minutes. The client is less anxious when he knows what to expect.

Assess for claustrophobia. The client will be placed in a tunnel – like device.

Remove all metals items, e.g., watch, eyeglasses and jewelry. these affect accuracy of results.

Instruct the client to remain still during the procedure.

Inform the client that MRI unit makes a loud, knocking noise.

CAUTION: clients with pacemakers, prosthetic valves or recently implanted clips or wires are not eligible for MRI scans.

Myocardial Scintigraphy The procedure involves intravenous

injection of a radioactive isotope via a catheter.

Myocardial function, motion and perfusion are studied through the use of an external gamma camera.

Techniques used are as follows: Thalium 201 scintigraphy Dipyridamole – thalium – 201 test Technetium 99m Ventriculography First – pass cardiac study

Nursing interventions: Myocardial Scintigraphy

Informs client that ECG or treadmill test may be done during the procedure.

Assess for pregnancy because the test involves radiation exposure.

Instruct the client to take a light meal, to prevent nausea and stomach cramping during exercise and for better uptake of the radioisotope.

Omit the usual dose of prescribed beta – blockers, calcium – channel blockers and xanthenes before the procedure.

Instruct the client to report any chest pain experienced during the procedure.

Invasive Hemodynamic Monitoring: Intra – arterial Pressure Monitoring This provides continuous detection of arterial BP via

an indwelling intra – arterial catheter. It is valuable in monitoring the BP of the clients

with low cardiac output, fluctuating hemodynamic status and excessive peripheral vasoconstriction and in whom cuff BP measurements are undetectable.

Intra – arterial readings are at least 10mmHg higher than cuff BP readings.

The intra-arterial BP line can be used for obtaining blood samples for ABG and blood studies.

Heparinize the catheter to maintain patency. Check the catheter insertion site for hemorrhage,

hematoma, redness or signs of infection. Do neurovascular check distal to catheter insertion

site – color, temperature, capillary filling and sensation.

Coronary Heart Disease (CHD)Pathophysiology: ATHEROGENESIS

Referred to MS Word Figure 1. page.14

Pathophysiology of Atherosclerosis

Self management education guide: decreasing risk for

coronary heart disease Daily management of hypertension.

Take medications at regular basis. Do not stop.

Stop smoking as soon as possible. Smoking reduces available oxygen to the heart and can precipitate angina. Smoking increases heart rate and blood pressure.

Avoid passive smoke. Two hours of passive smoke decreases oxygen to the heart and increases heart rate and blood pressure. Plan a regular exercise under medical supervision.

Self management education guide: decreasing risk for

coronary heart disease If overweight. Lose weight. Seek help

from professionals Follow a healthy heart diet. Reduce

cholesterol and increase fiber. Reduce stress. Allow adequate time for rest and

relaxation. These are life – long life – style changes.

Angina pectoris(Myocardial ischemia)

Transient chest pain caused by insufficient blood flow to the myocardium resulting in myocardial ischemia. It results when myocardial oxygen demand exceeds myocardial oxygen supply.

Pathophysiology of angina pectoris

Refered to MS word Figure 2. pg. 16

Types of angina pectoris

Stable angina Chest pain lasts for less than 15 minutes. Recurrence is less frequent.

Unstable angina (preinfarction angina, crescendo angina, intermittent coronary syndrome) Chest pain lasts for more than 15 minutes but less

than 30 minutes. Recurrence is more frequent, may occur at night. Intensity of pain increases.

Variant angina (prinzmetal’s angina) Chest pain is of longer duration and may occur at

rest. The attacks tend to occur in the early hours of the

day. May result from coronary artery spasm.

Pallor Diaphoresis Dyspnea Faintness Palpitations Dizziness Digestive disturbances Angina: PQRST pain assessment

Method of assessment of chest pain P – rovocative

“what activities bring on the apin?” Q – uality

“what does the pain feel like/” R – egion / radiation

“where is the pain?” “does it radiate elsewhere?”

S – everity “how does the pain rate on a scale of 1 to 10?”

T – iming/treatment “when did the pain begin?” “how long does it last?” What do you do to relieve the pain?” Are these measures effective?”

Nocturnal anginaOccurs only during the night and is

possibly associated with rapid eye movement (REM) sleep.

Angina decubitusParoxysmal chest pain that occurs

when the clients sits or stands up. Intractable angina

Chronic, incapacitating angina unresponsive to intervention.

Postinfarction anginaOccurs after MI, when residual

ischemia may cause episodes of angina.

Precipitating events of angina pectoris

1. Exertion – vigorous exercise done very sporadically.

2. Emotions – excitement, sexual activity.3. Eating a heavy meal4. Environment. Exposure to cold.

These events increase myocardial oxygen demands. Further disequilibrum between oxygen supply and oxygen demand occurs.

Collaborative management for angina pectoris

MedicationsVasodilators: nitroglycerine, amyl nitrate,

isosorbide Effects:Direct relaxing effect on vascular smooth muscle, resulting in generalized vasodilation

Decrease peripheral resistance, decrease systolic pressure, produce venous pooling, and decrease preload.

Coronary vasodilation redistributes myocardial blood flow more efficiently. Beta – adrenergic blocking agents Propranolol (inderal) Metorolol (lopressor) Nadolol (corgard) Atenolol (tenormin) Pindolol (visken) Esmolol (brevibloc

EffectsDecrease myocardial oxygen demand by decreasing heart rate, BP, myocardial contractility and calcium output. Calcium – channel blockers.

Verapamil (isoptin, calan) Nifedipine (procardia, adalat calcibloc)

Diltiazem (cardizem) Amlodipine (norvasc) Nicardipine(cardene)

Effects Inhibit ion transportation into myocardial cells to depress inotropic and choronotropic activity, decreasing cardiac workload.

It has vasodilation effect It reduces coronary vasopasm. Other medications.

Platelet aggregation inhibitors ASA (aspirin) Dipyridamole (persantin) Clopidogrel (plavix) Ticlopidine (ticlid) Effects; inhibit platelet aggregation

Anticoagulants Heparin sodium (clexane, fragmin, lovenox, innohep)

Effects: inactivates thrombin and other clotting factors inhibiting conversion off fibrinogen to fibrin, finrin clot formation is prevented.

Warfarin sodium (Coumadin) Dicumarol Effect: inhibit hepatic systhesis of vit. K.

Nursing interventions in drug therapy

Nitroglycerine therapy Assume sitting or supine position when

taking the drug. To prevent hypostatic hypotension.

Take maximum of three doses at five – minute interval.

Practice gradual change of position to prevent orthostatic hypotension.

If taken sublingual, the medication causes burning or stinging sensation under the tongue. This indicates that the medication is potent.

Sublingual route produces onset of action within 1 to 2 minutes, duration of action is 30 minutes.

offer sips of water before giving sublingual nitrates; dryness of mouth may inhibit drug absorption.

Instruct client to avoid drinking alcohol, to avoid hypotension, weakness and faintness.

Advise client to always carry three tablets in his pocket.

Store nitroglycerine in cool, dry place; use dark / amber – colored, air-tight container. Do not store nitroglycerine in the refrigerator. It may be destroyed by het, light or moisture.

Change stock of nitroglycerine every 3 months. Observe for side effects: headache, flushed face,

dizziness, faintness, tachycardia; these are common during first few doses of the medication. Do not discontinue the drug.

Transderm – nitropatch is applied once a day, usually in the morning. Rotation of skin sites is necessary, usually on the chest wall. Remove the patch during the night to prevent tolerance.

Evaluate effectiveness: relief of chest pain.

Beta – adrenergic blockers Assess pulse rate before administration

of the drug; withhold if bradycardia is present.

Administer with food to prevent GI upset.

Do not administer inderal (propanolol) to clients with asthma. It causes bronchoconstriction.

Do not administer propranolol to clients with DM. it causes hypoglycemia.

Give with extreme caution in clients with heart failure.

Observe for side – effects which are as follows: nausea, vomiting, mental depression, mild diarrhea, fatigue and impotence.

The antidote for beta blocker poisoning is Glucagon.

Calcium – channel blockersAssess heart rate and BP (blood

pressure)Monitor hepatic and renal functionAdminister 1 hour before or 2 hours

after meals. Food delays absorption and decreases plasma levels of the drug.

The antidote for calcium – channel blocker poisoning is glucagon.

1.Heparin Sodium Assess for signs and symptoms of

bleeding. Keep protamine sulfate available. It is

administered as antidote if bleeding occurs in heparin therapy.

If administered subcutaneously, do not aspirate, do not massage site of heparin injection. To prevent hematoma formation.

Monitor PTT or APTT levels. (therapeutic effect: PTT/APTT x 2 to 2.5).

Used for a maximum of 2 weeks.

2.Coumadin (warfarin sodium) Assess for signs and symptoms of bleeding. Keep vitamin K (e.g., aquamephyton)

readily available. It is administered as antidote if bleeding occurs in Coumadin therapy

Monitor prothrombin time (therapeutic effect; PT x 1.5 to2; INR = 2 toCoumadin therapy

Monitor prothrombin time (therapeutic effect; PT x 1.5 to2; INR = 2 to 3)

Minimize green leafy vegetables in the diet, these contain vitamin k and antagonize the effect of Coumadin.

Do not give ASA and Coumadin together. To prevent bleeding.

Treatment and surgical interventions. Percutaneous transluminal coronary angioplasty

(PTCA) Mechanical dilatation of the coronary vessel wall by

compressing the atheromatous plaque. A specially design balloon – tipped catheter is inserted

under the fluoroscopic guidance and advanced to the site of the coronary obstruction.

It is recommended for clients with single – vessel coronary artery disease.

Intravascular stenting Biologic stent is produced through coagulation of

collagen, elastin and other tissues in the vessel wall by laser , photocoagulation, or radio frequency – induced heat.

Prosthetic intravascular cylindric stents maintain good luminal geometry after balloon deflation and withdrawal.

Intravascular stenting is done to prevent restenosis after PTCA.

Percutaneous Coronary Intervention

Laser therapy Laser light produces necrosis, hemostasis,

coagulation, evaporation of tissue. Coronary artery bypass graft (CABG)

Reduces angina and improves activity tolerance

It is recommended if severe narrowing of one or more branches of the coronary artery exists.

The main purpose of CABG is myocardial revascularization.

The commonly used grafts are the saphenous vein and internal mammary artery.

Greater and lesser saphenous veins are commonly used for bypass graft procedures.

Nursing Interventions In Clients With Angina Pectoris Promoting comfort

Relieve painNitroglycerine is the drug of choice

for relief of pain from acute ischemic attacks.

Promoting tissue perfusionInstruct the client to avoid over –

fatigue.Stop activity immediately in the

presence of chest pain, dyspnea, lightheadedness or faintness which indicates low tissue perfusion

Promoting activity and restEncourage slower activity or shorter

periods of activity with more rest periods.Avoid over exertions.Plan for regular activity programTake nitroglycerine before exercise Increase extent of exercise gradually.

Facilitating learning Promote a positive attitude and active

participation of the client and the family to encourage compliance.

Promoting relief of anxiety and feeling of well – being Facilitate reduction in clients present level of

anxiety Advise the client to minimize emotional

outbursts, worry and tension Encourage to maintain an optimistic outlook

to help relieve the work of the heart. Diet

Low sodium, low fat and low cholesterol, high fiber diet.

Avoid saturated fats (animal fats). White meat, e.g., chicken without skin, turkey,

fish are low in cholesterol. Read labels

ActivityActivities are encouraged within the

patient’s limitations.Myocardial Infraction (MI)The formation of localized necrotic

areas within the myocardium. MI usually follows sudden coronary occlusion and the abrupt cessation of blood and oxygen flow to the heart muscle.

Prolonged ischemia lasting more than 3 to 45 minutes produces irreversible cellular damage and necrosis of the myocardium.

Pathophysiology of myocardial infarction

Referred to MS word figure 3. pg. 21

Ischemic injury evolves over several hours toward complete necrosis and infarction.

Ischemia almost immediately alters the integrity and permeability of the cell membrane to vital electrolytes, thereby decreasing myocardial contractility.

The autonomic nervous system attempts to compensate for the depressed cardiac performance. This results to further imbalance between myocardial oxygen supply and demand.

MI almost always occurs in the left ventricle and often significantly depress left ventricular function. This is due to occlusion of the LADA (left anterior descending artery). This is referred to as anterior wall infarction.

Alterations in function in the necrotic area ceases permanently.

The three areas which develop in MI are as follows: Zone of infarction which records pathologic

Q wave in the ECG Zone of injury which gives rise to elevated

ST segment Zone of ischemia which produces inversion

of T wave

Effects of Ischemia, Injury, and Infarction on ECG

MI may be classified as follows:Transmural infarct, which extends from

endocardium to epircardium.Subendocardial infarct, which affects

the endocardial muscles.Intramural infarction, which is seen in

patchy areas of the myocardium and is usually, associated with longstanding angina pectoris.

Healing requires formation of scar tissues that replace the necrotic myocardial muscle; scar tissue inhibits contractility.

Clinical Manifestations Of Myocardial Infraction Pain

Crushing, severe, prolonged, unrelieved by rest or nitroglycerine; often radiating to one or both arms, the neck and the back.

Characterized by “Levine's sign” (chest hand- clutching). This is the universal sign of distress in angina pectoris and MI.

Pathophysiologic basis Cessation of blood supply to myocardium

due to thrombotic occlusion causes accumulation of metabolities (e.g., lactic acid) within ischemic part of myocardium. lactic acid irritates nerve endings, resulting to pain.

Anxiety and apprehension Feeling of “doom”, restlessness. Pathophysiologic basis:Severe pain of a heart attack is terrifying; most clients are aware of the significance of a heart attack; restlessness results from shock and pain.

Shock This is manifested by systolic pressure

below 80mmHg, gray, facial color, lethargy, cold diaphoresis, peripheral cyanosis, tachycardia /bradycardia, weak pulse.

Pathophysiologic basis:This may due to severe pain, severe reduction in cardiac output and inadequate tissue perfusion, thereby causing tissue hypoxia. Oliguria

Urine flow of less than 30ml/ hour. Pathophysiologic basis:

This indicates renal hypoxia due to inadequate tissue perfusion

Fever Slight elevation of temperature occurs within

24 hours and extend 3 to 7 days accompanied by leukocytosis and elevated ESR.

Pathophysiologic basis Fever and leukocytosis result from destruction of myocardial tissue and ensuring inflammatory process. “indigestion”

“gas pains around the heart,” nausea and vomiting.

Pathophysiologic basis: Client may prefer to believe that pain is caused by “gas” or “indigestion” rather than by heart disease; nausea and vomiting may result from sever pain or from vasovagal reflexes conducted from an area of damaged myocardium to gastrointestinal tract.

Acute pulmonary edema Sense of suffocation, dyspnea, orthoea, gurgling / bubbling respiration.

Pathophysiologic basis:Left ventricle becomes severely weakened in pumping action owing to infarction; severe pulmonary congestion results. ECG Changes.

Mi causes elevation of ST segment, inversion of T wave and enlargement of Q wave.

Pathophysiologic basisPathologic Q wave develops from the area of infarction; elevated St segment results from the area of injury; and inverted T wave originates from the zone of ischemia.

Elevation of ST segment heralds a pattern of injury and usually occurs as an initial ECG change in acute MI.

Elvated CK – MB, elevated LDH, elevated AST. Pathophysiologic BasisThese cardiac enzymes are produced in abnormally large amounts because of cellular damage and death.

CK – MB is the most cardiac- specific enzyme. Elevated CK- MB in the presence of increased levels of LDH strongly support presence of MI.

Elevated troponin levels. These are the most definitive laboratory findings in MI.

Collaborative Management for Myocardial Infarction(1) Medications Analgesic.

For relief of pain. This is priority.Morphine sulfate, lidocaine or

nitroglycerine are administered intravenously. The drug of choice is Morphine.

Thrombolytic therapyTo disintegrate blood clot by activating

the fibronolytic processes. Streptokinase, urokinase and tissue

plasminogen activator (TPA) are currently used

Administration of thrombolytic is most crucial between 3 to 6 hours after the initial infarction has occurred.

Detect for occult bleeding during and after thrombolytic therapy.

Assess neurologic status changes which may indicate G.I. bleeding or cardiac tamponade.

The effectiveness of the medication is evidenced by absence of chest pain. Absence of blood clots improves blood flow and oxygen support to the myocardium.

Anticoagulant and antiplatelet medications are administered after thrombolytic therapy to maintain arterial patency.

Other medication: Beta – adrenergic blocking agents; diazepam (valium).

(3) Nursing interventions Promoting oxygenation and tissue perfusion

Instruct the patient to avoid over fatigue; stop activity immediately in the presence of chest pain, dyspnea, lightheadedness or faintness.

Oxygen therapy by cannula for the first 24 to 48 hours or longer if pain, hypotension, dyspnea or dysrhythmias persist. Monitor VS changes, indicative of complications.

Position the client in semi – fowler’s to allow greater diaphragm expansion, thereby lung expansion and better carbon dioxide – oxygen exchange. Promoting adequate cardiac output.

Monitor the following parameters: Dysrhythmias on ECG tracings VS (vital signs) Effects of daily activities on cardiac status

Rate and rhythm of pulseAdminister pharmacotherapy as

prescribed. Promote rest and minimize unnecessary

disturbances

Promoting comfort Relieve pain. Administer morphine sulfate as

ordered. This is to decrease sympathetic stimulation, which increases myocardial oxygen demand. In addition, this will prevent shock which may result from severe pain. Providing rest.

The client is usually placed on bed rest with commode privileges for 24 to 48 hours.

Administer diazepam (valium) as ordered. Explain that the purpose of CCU (coronary

care unit) is for continuous monitoring and safety during the early recovery period.

Provide psychosocial support to the client and his family. Calmness and competency are extremely reassuring.

Promoting activityGradual increase in activity is

encouraged. After the first 24 to 48 hours, the client may be allowed to sit on a chair for increasing periods of time and begins ambulation on the 4th or 5th day.

Monitor for signs of dysrhythmias, chest pain and changes in VS during activity.

Promoting nutrition and elimination Provide small, frequent feedings. Provide low – calorie. Low cholesterol, low –

sodium diet. Avoid stimulants. Avoid taking very hot or very cold foods.

Vasovagal stimulation may occur this may lead to bradycardia and cardiac arrest.

Use of bedpan and straining at stool should be avoided. Valsalva maneuver causes changes in blood pressure and heart rate, which may trigger ischemia, dysrhythmias, pulmonary embolism or cardiac arrest.

Use bedside commode Administer stool softener as ordered, e.g., Sodium decussate (colace).

Promoting relief of anxiety and feeling of well – beingProvide an opportunity for the client and

family to explore their concerns and to identify alternative methods of coping as necessary.

Facilitating learningTeaching is started once the client is free

of pain and excessive anxiety.Promote a positive attitude and active

participation of the client and the family.

Cardiac Rehabilitation Is a process by which a person is restored to

health and maintains optimal physiologic, psychosocial, vocational and recreational functions.

It begins the moment a client is admitted to the hospital for emergency care, it continues four months and even years after the client is discharged from the health care facility.

Goals of rehabilitation To live as full, vital and productive a life as

possible. Remain within the limits of the heart’s ability

to respond to activity and stress.

Progressive activityActivity progression is based on the

metabolic equivalent of the task (MET), the energy expenditure for various activities.

In the hospital, exercise may be gradually implemented as follows: Lying or sitting exercises ( arms, legs, and trunk), then exercises progress to standing and slow walking in the hall. (VS and heart rhythms are constantly monitored).

An exercise session is terminated if any one of the following occurs: cyanosis, cold sweats, faintness, extreme fatigue, severe dyspnea, pallor, chest pain, PR more than 100 beats/min., dysrhythmias, BP greater than 160 / 95 mmHg.

Exercise must be done twice a day for about 20 minutes.

Exercise provides the clients a positive sign of progress and recovery, a sense of control over their bodies, and tends to decrease anxiety and depression during the recovery period.

Home exercise program includes 2 to 12 week structured walking program.

Teaching and Counseling Self – management education guide:

discharge after MIDiscontinue smokingControl hypertension with continued

medical supervision.Eat a diet low in calories, saturated fats

and cholesterol; decrease in salt intake.Participate in weight reduction program.Progressive exercise based on the

discharge MET level under medical supervision.

Take prescribed medications at regular basis.

Resumption of sexual activity after 4 to 6 weeks from discharge, if appropriate. Or when the client with uncomplicated MI (no dysrhythmias, shock or CHF) is capable of walking one to two flights of stair without difficulty.

Stress management techniques.Return to usual home activities,

relationships and to work at earliest opportunity would be beneficial.

Teaching guide on resumption sexual activity

Assume less fatiguing position. Let the couple decide on their less fatiguing position.

The non – MI partner takes the active role. Perform sexual activity in a cool, familiar

environment. Take nitroglycerine before sexual activity. Refrain from sexual activity during a fatiguing

day, after eating a large meal, or after drinking alcohol.

If dyspnea, chest pain, dizziness or palpitations occur, moderation should be observed; if symptoms persist, stop sexual activity.

Develop other means of sexual expression.

COMPLICATION OF MI

Dysrhythmias Cardiogenic shock Thromboembolism Pericarditis Rupture of myocardium Ventricular aneurysm Congestive heart failure

Dysrhythmias Abnormal cardiac rhythms which are due to the following

factors: Tissue ischemia Hypoxemia SNS and PNS influences Lactic acidosis Hemodynamic abnormalities Drug toxicity Electrolyte imbalances

These are due to abnormal automaticity, abnormal conduction or both.

The most common complication and most major cause of death among clients with MI.

The most common dysrhythmias in MI is premature ventricular contractions (PVC’s.)

PVC’s of 6 or more per minute is life threatening.

Pathophysiology of premature ventricular contractions

Referred to MS word figure 4. pg. 29

Common dysrhythmias after MI

SinusSinus tachycardiaSinus bradycardiaSinus dysrhythmiaSick sinus syndrome

AtrialPremature Atrial contractionParoxysmal Atrial tachycardiaAtrial flutterAtrial fibrillation

Common dysrhythmias after MI

VentricularPremature ventricular contractionsVentricular bigeminyVentricular fibrillation

Conduction defectsFirst degree AV blockSecond degree AV block

Third degree block

Sinus Dysrhythmias Sinus tachycardia is a dysrhythmia that

where the heart rate exceeds 100 beats per minute.Etiology:

The sympathetic fibers are stimulated thereby, speeding up excitation of the SA node.

TreatmentDigitalis administration.Treat underlying cause (fever, shock, electrolyte disturbances etc.)

Sinus bradycardia is a dysrhythmia where the heart rate fails below 60 beats per minute.Etiology

The parasympathetic fibers (vagal tone) are stimulated and cause the sinus node to slow.

Treatment atropine 0.5 to 1.0 mg / IV push to block vagal stimulation

isopproterenol 1mg. / 500 ml D5w to stimulate sympathetic response.

Pacemaker insertion

Sinus arrhythmia is a regular irregularity in rhythm which is related to respiratory exchange. No treatment is necessary.

Sick sinus syndrome is dysrhythmia that is caused by a diseased sinus node. The sinus node conducts at a slow rate or may fail to conduct at all, producing sinus block or pauses. There is related tachycardia. Thus it is also called “brady – tachycardia syndrome”.Treatment

Treatment of ischemia due to arteriosclerotic heart disease, MI.

Pacemaker insertion.

Atrial Dysrhythmias Premature atrial contraction (PAC) is an

ectopic beat that originates in the atria and is discharged at a rate faster than that of the sinus node.Treatment

Generally does not require treatment. Quinidine or calcium – channel blocker may be prescribed if PAC increases if frequency.

Paroxysmal atrial tachycardia (PAT) is a sudden onset of an atrial tachycardia with rates that vary between 140 and 250 beats per minute. Treatment

Valsalva maneuver to reduce the heart rate through vagal stimulation

Digitalis Beta adrenergic blockers (propranolol) Calcium – channel blockers (Verapamil) Cardioversion Morphine sulfate, diazepam

*Avoid excess use of alcohol, cigarettes, caffeine.

Atrial flutter is a dysrhythmia in which an ectopic atrial focus captures the heart rhythm and discharges impulses at a rate of between 200 and 400 times per minute. Treatment

Digitalis preparation Quinidine Calcium – channel blockers Beta – adrenergic blockers Cardioversion

Atrial fibrillation is a dysrhythmia that is caused by the rapid and chaotic firing of atrial impulses by a multitude of foci.Treatment

Digitalis, if uncontrolled fibrillation (rate is above 100 beats per minute)

Quinidine Beta adrenergic blockers

Ventricular Dysrhythmias Premature ventricular contraction (PVC) is a

dysrhythmia that is produced by an ectopic beat originating in a ventricle and being discharged at a rate faster than that of the next normally occurring beat. PVC’s of 6 /minute or more is life threatening. Treatment

Lidocaine / IV push, drip Initial bolus close: 75 – 100 mg then 50 – 100 mg. within

10-15 min. as needed Continuous IV drip in d₅W 4:1 concentration

Procainamide IV push, drip bolus dose: 300mg. Bretylium continuous infusion if lidocaine and

procainamide are ineffective.

Ventricular bigeminy is a PVC where every other beat is a ventricular complex Treatment

Refer to PVC Ventricular tachycardia is a life threatening

dysrhythmia that originates from an irritable focus within the ventricle. It is an inaffective rhythm for maintaining cardiac output. It is emergency. Treatment

Epinephrine 1mg /IV every 3 to 5 minutes or vasopressin 40 units/ IV; amniodarone 300mg/ IV push, then 150 mg/ IV push in 3 to 5 minutes or licodaine 1 to 1.5 mg/kg, then 0.5 to 0.75 mg/kg., total of 3mg/kg.

Defibrillation, if loss of consciousness occurs. Cardioversion if conscious. Sodium bicarbonate is administered to relieve

lactic acidosis.

Ventricular Fibrillation is a dysrhythmia that is characterized by the random and chaotic discharging of impulses within the ventricle at rates that exceed 300 beats per minute. It produces clinical death and must be reversed immediately. It is an emergency.Treatment

Immediate defibrillation; use 200 – 360 watt/sec. (joules)

Na Bicarbonate to relieve lactic acidosis, which causes unsuccessful defibrillation.

Epinephrine

Conduction Defects/Heart Blocks/ AV Blocks Conduction is altered at the level of the AV

node1. First degree AV block – the impulse is

transmitted normally, but it is delayed longer at the level of the AV node.

2. Second degree AV block – some, but not all of the impulses are transmitted. The AV node becomes selective about which impulses are conducted to the ventricles.

3. Third degree AV block – no impulses from the SA node is transmitted by the AV node.

Treatment of AV blocks First degree AV block requires no treatment Second degree AV block requires treatment if

the ventricular rate falls too low to maintain effective cardiac output.

Third degree AV block requires treatment if C.O. is compromised.

*Treatment of choice: ventricular pacemakerSummary of therapeutic modalities for

dysrhythmias Antidysrhythmis drugs Artificial cardiac pacemaker Cardioversion / defibrillation Cardiopulmonary resuscitation

Antidysrhythmic drugs Class I

Fast (sodium) channel blockers I Disopyramide (norpace) Procainamide (pronestyl) Quinidine sulfate (cardioquin)

Fast(sodium) channel blockers II Licodaine (xylocaine) Mexitiline hcL (Mexitil)

Fast (sodium) channel blockers III Flecainide (tambocor) Propafenone (rythmol) Tocaidine (tonocard)

Class II Beta – adrenergic blockers

Acebutolol HCI (spectral) Propranolol (inderal)

Class III Prolong repolirization

Adenosine (adenocard) Amiodarone (cardarone) Bretylium tosylate (bretylol)

Class IV Calcium channel blockers

Verapamil HCI (calan) Ditiazem (cardizem)

Others Phenytoin (dilantin) Digoxin (lanoxin)

Pacemakers A cardiac pacemaker is an electronic

device that delivers direct stimulation to the heart, causing electrical depolarization and cardiac contraction

The pacemaker initiates and maintains the heart rate when the natural pacemakers of the heart are unable to do so.

Implanted Transvenous Pacemaker

Clinical indications Symptomatic bradyarrhythmias

Sinoatrial bradyarrhythmiasSinoatrial arrestSick sinus syndrome

Heart blockSecond degree heart blockComplete heart block

ProphylaxisFollowing acute MI; arrhythmias and

conduction defectsBefore or following cardiac surgeryDuring coronary arteriographyBefore permanent pacing

TachyarrythmiasSupraventricularVentricular

Pacing modes Demand (synchronous, non – competitive)

atrial/ ventricular It triggers electrical firings only when the

heart rate goes slow It does not compete with the hearts basic

rhythm If the clients hearts rate falls below a

predetermined escape interval (programmed into pulse generator), an electrical stimulus is delivered to the heart.

Fixed rate (asynchronous, competitive) atrial / ventricular It delivers an electrical stimulus at a preset

constant rate that is independent of the patients own rhythm.

Does not allow atrial contribution to the cardiac output. May be valuable in complete heart block. Synchronous atrial / ventricular.

A demand form of pacing which is able to increase heart rate to accompany the physiological demands of the body

An actual electrode senses the patient’s atrial depolarization, waits for a preset interval (simulated PR interval) and triggers firing of ventricular pacer.

If rapid atrial rhythm occurs, the ventricular pacemaker stimulates the ventricle at a fixed rate independent of atrial activity.

Temporary pacemakers Temporary pacing of the heart is usually

done as an emergency procedure that allows observation of the effects of pacing on heart function before a permanent pacemaker is implanted.Transvenous approach to position the

electrode in the apex of right ventricle is done.

The external pulse generator is attached to the patient.

Permanent pacemakers Permanent pacing of the heart may be implanted

through the following techniques: Transvenous (endocardial)

The electrode is threaded through cephalic or external jugular vein into the right ventricle. This is done under local anesthesia.

The peripheral end of the electrode is connected to the pulse generator which is implanted underneath the skin below the right or left pectoral region.

Transthoracic (epicardial) Anterior chest is opened and electrodes are sutured

to the surface of the right or left ventricle or atrium, then threaded subcutaneously to the abdominal wall either above or below the waist.

*note pace beats are characterized by sharp spikes that preceded each ECG complex.

Nursing interventions for Clients with artificial cardiac pacemakers Monitor ECG following implantation of pacemaker,

including VS. Observe for indications of pacemaker malfunction like

dizziness, faintness, lightheadedness, chest pain, shortness of breath.

Make sure all equipment in the clients unit is grounded, to prevent wound infection

Provide psychosocial support: Explore concerns of the client Encourage to utilize coping mechanism Ensure client comfort Maintain a positive body image

Provide client education which includes the following:Take daily pulse for one full minute.

Report any sudden slowing of pulse greater than 4 to 5 beats per minute or any increase in pulse rate.

The best time to take the daily pulse is in the morning upon awakening

Report signs and symptoms of dizziness, fainting, palpitation, prolonged hiccups and chest pain to the physician (indicative of pacemaker failure)

May use electrical devices with caution.

If dizziness occurs, stop using the device

Sources of electromagnetic inference (EMI) that may affect some pulse generators are as follows:High – energy radarTV and radio transmitterElectrocautery machinesAirport screening devicesAntitheft devices (inform the security guard on presence of pacemaker)

Move to 5 to 10 feet away from the source of EMI if dizziness occurs.

Avoid going near or using microwave oven

Move 3 feet away from the deviceWear loose – fitting clothing around the

area of the pacemakerObserve for signs and symptoms of

infection around generator and leads fever, heat, pain, skin impairment at the implant site.

Avoid contact sportsElectrode may be displaced

Cardioversion and Defibrillation Cardioversion is the synchronous

application of an electrical shock of short duration to the heart through the use of the chest paddles. It is done to convert cardiac

dysrhythmia (other than ventricular fibrillation) into a more hemodynamically stable, sinus rhythm.

Electric shock is applied during the R wave; never on the T wave

Defibrillation is unsynchronized passing of an electric shock of short duration through the heart to terminate ventricular fibrillation or ventricular tachycardia without pulse.

Nursing Interventions During Cardioversion And Defibrillation

Place the client in a flat, firm surface. Apply interface material (gel, paste, saline

pads) to the paddles.This is for better contact with the skin and

to prevent burns Grasp the paddles only by the insulated

handles. To prevent electrocution. Give command for personnel to STAND

CLEAR of the client and the bed.

Apply the chest paddles as follows: one of the right of the sternum, third ICS; and the other one on the left midaxillary, fifth ICS.

Push the discharge buttons in both paddles simultaneously.

For defibrillation, release 200 to 360 watts/sec. (joules); for cardioversion, lower energy is required

Defibrillation is done before initiating CPR if the client is monitored.

CPR id done before defibrillation if the client is unmonitored.

Cardiopulmonary Resuscitation (CPR)

Indication Cardiopulmonary arrest or clinical death

(breathlessness, pulselessness). Crucial time

CPR is initiated within 4 to 6 minutes after the arrest, to prevent brain death.

Two types of CPR Basic life support (BLS)

Involves the use of the hands, mouth and the sincere desire to give the person a second chance for life.

Advanced cardiac life support (ACLS) Involves BLS and the use of equipment,

emergency drugs and fluids to monitor the client and stabilize his condition.

CPR Involves The ABCD Of Life Support

A – open airway B – restore breathing C – restore circulation D – provide definitive treatment (ACLS)

Techniques Of Basic Life Support

Step I. assess level of consciousness Shake the victim’s shoulders and ask “are you

okay?” If no response, place the client in supine position on

a firm surface Step II. Open the airway

The tongue is the most common cause of airway obstruction in the unconscious person.

Use the head tilt – chin lift and the jaw thrust methods for opening and maintaining airway.

Jaw thrust is recommended fro clients with suspected neck injury.

Take 3 to 5 seconds to look, listen and feel for spontaneous breathing.

Step III. Initiate artificial ventilationMouth to mouth ventilationMouth to nose ventilationMouth to stoma ventilationMouth to barrier ventilation

  *note give 2 initial breaths lasting for 1

½ to 2 seconds. If no rise and fall of the chest is observed, consider airway obstruction.

Step IV. Assess circulationCheck carotid pulse (adult) for 5 to 10

seconds; brachial pulse for infant and child.

No pulse, cardiac compressions are initiated.

Step V. initiates external cardiac compressions / external cardiac messageDepress the sternum with heels of both

hands, one on top of the other 1 ½ to 2 inches (adult); heel of one hand 1 to 1 ½ inches (child); 2 fingers ½ to 1 inch (infant).

Ratio for compressions and ventilation for adult, child, and infant is 30:2. An equivalent of 100 compressions per minute and 8 to 10 rescue breaths per minute.

Hand position for adults and children is center of chest (between nipples in children0. For infants, use the area just below the nipple line.

Reassess the client after 2 cycles; if pulse is absent, continue CPR.

Recheck pulse every 3 to 4 minutes thereafter.

Most common complication of CPR is fracture of ribs. Most commonly punctured internal organ during CPR is the liver.

When to stop CPR? When the client is revived. When the EMS has been activated. When the rescuer is exhausted. When the client is dead.

Nursing Interventions

Perform hemodynamic monitoring; PAP, PCWP measurements, intra – arterial BP.

Administer oxygen therapy. Correct hypovelemia. Administer IV fluids as

ordered. Pharmacotherapy:

Vasodilators: nitroprusside, p hentolamine, nitroglycerine.

Inotropic agents: digitalis, dopamine, doputamine Diuretics: forusemide Na bicarbonate to relieve lactic acidosis

Monitor hourly urine output, LOC, arrhythmias. Provide psychosocial support.

Decrease pulmonary edema. Ausculate lung fields for crackles and

wheezes Note for dyspnea, cough, hemoptysis,

orthopnea Monitor ABG for hypoxia and metabolic

acidosis. Place the client in Fowler’s position to reduce

venous return Administer during therapy as ordered:

Morphine sulfate to reduce venous return Aminophylline to reduce bronchospasm

caused by severe congestion Vasodilators to reduce venous return

(nitroprusside, nitroglycerine) Diuretics to decrease circulating volume.

Utilize counter pulsation to decrease ventricular work of the client with severe shock Counter pulsation device (mechanical cardiac

assistance / diastolic augmentation) involve introduction of the intra – aortic balloon catheter via the femoral artery into the aorta.

The intra – aortic balloon pump (IABP) augments diastole, resulting in increased perfusion of the coronary arteries and the myocardium and a decrease in left ventricular workload.

The balloon is inflated during diastole; it is deflated during systole.

Indications: Cardiogenic shock AMI (acute myocardial infarction) Unstable angina pectoris Open heart surgery

Thromboembolism

It results when platelets aggregate at the area of necrosis, an attempt of the body to repair the tissue injury.

Emboli occur because clots formed in the healing area of the myocardium break loose and escape into the circulation.

Pulmonary embolism may develop and proves to be fatal.

Nursing Interventions For Thromboembolism

Administer pharmacotherapy as ordered Anticoagulants Thrombolytics

Observe for signs and symptoms indicative of pulmonary embolism Dyspnea Chest pain Coughing Hemoptysis Rapid, weak pulse Pallor

Early ambulation is encouraged to prevent venous stasis. Venous stasis enhances thromboembolism.

Pericarditis (Dressler’s Syndrome)

Is an inflammation of the pericardium which occurs approximately 1 to 6 weeks after acute MI.

In MI, pericarditis results as an antigen – antibody response. The necrotic tissues play the role of an antigen, which trigger antibody formation. Inflammatory process follow.

Pericardial effusion / cardiac tamponade is outpouring of fluid into the pericardial sac. Compression of the heart occurs, followed by decrease in ventricular emptying. This further, may lead to cardiac failure, shock and death. This may follow pericarditis.

Constrictive pericarditis is a condition in which a chronic inflammatory thickening of the pericardium compresses the heart so that it is unable to fill normally during diastole.

Clinical manifestations of pericarditis include the following:

Pain in the anterior chest, aggravated by coughing, yawning, swallowing, twisting and turning the torso; relieved by upright, leaning forward position.

Pericardial friction rub – scratchy, grating or creaking sound.

Dyspnea Fever, sweating, chills Joint pains Arrhythmias

Nursing Interventions For Pericarditis Elevate head of bed, place pillow on the overbed table

so that the patient can lean on it. Promote bed rest Administer prescribed pharmacotherapy

ASA to suppress inflammatory process. Corticosteroids for more severe symptoms.

Cardiac tamponade is accumulation of blood in the pericardial sac. It reduces myocardial compliance and contractility. It occurs following pericarditis. The manifestations of cardiac tamponade are as

follows: jugular vein distention, muffled heart sounds, diminished or absent pulse (Beck’s triad).

The management of cardiac tamponade is pericardiocentesis (aspiration of blood from the pericardial sac).

Rupture of the myocardium It is common in transmural MI (there is necrosis

of the entire heart wall – from epicardium to endocardium).

It causes immediate cardiac tamponade and death.

Ventricular aneurysm It involves thinning, ballooning and hypokinesis

of the left ventricular wall after a transmural MI. The dysfunctional area often becomes filled

with necrotic debris and clot and sometimes is rimmed by the calcium ring.

The debris or clot may fragment and travel into the systemic arterial circulation, thereby embolization.

The aneurysm may rupture causing cardiac tamponade and death.

Congestive Heart Failure It is state of circulatory congestion

produced by myocardial dysfunction. MI compromises myocardial function

by reducing contractility and producing abnormal wall motion.

The ability of the ventricle to empty lessens, the stroke volume falls, residual volume increases.

Heart failure is the inability of the heart to pump the amount of the oxygenated blood necessary to effect venous return and to meet the metabolic requirements of the body

Causes of congestive heart failure Direct damage to the heart, e.g. mitral

myocarditis, ventricular aneurysm. Ventricular overload

Increased preload, e.g. mitral aortic regurgitation, atrial or ventricular septal defects, or rapid infusion of large volume of IV fluids.

Increased afterload, e.g. aortic or pulmonary valve stenosis, systemic hypertension, pulmonary hypertension.

Constriction of the ventricles, e.g. cardiac tamponade, pericarditis, restrictive cardiomyopathies

Classification Of Heart Failure Backward heart failure results from damming

up of blood in the vessels proximal to the heart.

Forward heart failure results from inability of the heart to maintain cardiac output.

Referred to MS word figure 6. pg. 40

Pathophysiology: RIGHT –SIDED CONGESTIVE HEART FAILURE (RSCHF)

Referred to MS word figure 7. pg. 41

The RSCHF which results from pulmonary disorders is called COR PULMONALE

The signs and symptoms of LSCHF are due to pulmonary edema, cellular hypoxia, and activation of Rennin- angiotensin- aldosterone system (RAAS).

The signs and symptoms of RSCHF are due to venous back-up. Collaborative management. Congestive heart failure.

Medications

Digitalis therapy It is the major therapy for CHF. It has positive inotropic effect (strengthens force of cardiac contractility), negative chronotropic effect (decreases heart rate), and negative dromotropic effect(decreases conduction of the heart cells).

Assess heart rate before administration of digitalis. If the heart rate is 60 bpm and below or 120 bpm and above, withhold the drug. Bradycardia or rebound tachycardia may occur.

Monitor serum potassium (k) level. Hypokelemia enhances digitalis toxicity because it potentiates the effect of the drug. Commonly used digitalis (cardiac glycosides)Lanoxin (digitoxin)Crystodigin (digitoxin)Lanatoside C (cedilanid C)Deslanoside (cedilanid D)

Evaluate effectiveness of digitalis. There should be increased cardiac output, increased urine output, stronger pulse, lowering of BP, absence of rales or crackles

Assess for signs and symptoms of digitalis toxicity: Bradycardia G.G manifestationsAnorexiaNausea and vomitingDiarrhea

Dysrhythmias (most dangerous) Altered visual perceptions (yellow or green vision; blurred vision; halos or rainbows around the lights among elderly)

In males: anitiandrogenic effectsGynecomastiaDecreased libidoImpotence

The Antidote Of Digitalis Toxicity Is Digoxin Immune Fab (Digibind).

Diuretic therapy The purpose of diuretic therapy is to decreases

cardiac workload by reducing circulating volume and thereby reducing preload.

Assess for signs and symptoms for hypokalemia when administering thiazides and loop diuretics.

Give potassium supplement and potassium-rich foods.

Diuretics are best administered early morning and / or early afternoon to prevent sleep pattern disturbance related to nocturia.

If thiazides are ineffective, an oral aldosterone antagonist (potassium- sparing diuretic) may be given with thiazides.

The diuretics used in the treatment of CHF are as follow: Thiazides (potassium- wasting)

Chlorothiazide (diuril) Hydrochlorothiazide (esidrix, hydrodiuril)

Loop diuretics (potassium- wasting) Furosemide (lasix) Bumetamide (bumex)

Potassium – sparing Spironolactone (aldatone) Triamterene (dyrenium)

Vasodilators

To decrease afterload by decreasing resistance to ventricular emptying

The most commonly used drugs are as follows:Nitroprusside (nipride)Hydralazine (apresoline)Nifedipine ( a calcium – channel

blocker with vasodilator effect)Captoril (capoten) – also has a

vasodilator effect

Other drugs Sympathomimetics

DopamineDobutamine

Treatment Diet – sodium – restricted diet to prevent

fluid excess. Activity – balances program of activity and

rest Oxygen therapy – to increase oxygen

supply

Nursing Interventions : Congestive Heart Failure

(a) Providing oxygenation.

Administer oxygen therapy per nasal cannula at 2 to 6 L / min. as ordered

Evaluate arterial blood gas analysis results

Maintain semi – fowler’s or high fowler’s position to maximize oxygenation by promoting greater lung expansion.

(b) Promoting rest and activity

Bed rest or limited activity may be necessary during the acute phase.

Provide and overbed table close to the patient to allow resting the head and arms.

The arms may be supported on pillows to reduce the pull on the shoulder muscles when in high – fowler’s position, which is most comfortable for the patient

Administer diazepam (valium) 2 to 10 mg. 3 to 4 times a day as ordered to alley apprehension.

Gradual ambulation is encouraged to prevent risk of venous thrombosis and embolism due to prolonged immobility.

Activities should progress through dangling, sitting up in a chair and then walking in increased distances under close supervision.

Assess for signs of activity intolerance such as dyspnea, fatigue and increased pulse rate that do not stabilize readily.

(C) Decreasing anxiety

Identifying feeling and concerns related to these feelings.

Indentify strengths that can be used for coping

Learn what can be done to decrease anxiety.

Note: anxiety causes increased breathlessness which may be perceived by the client as an increase in the severity of the heart failure and this turn increases the anxiety.

(d) Facilitating fluid balance

Control of sodium intake Administer diuretics and digitalis as prescribed Monitor I and O, weight and VS

(e) Providing skin care

Edematous skin is poorly nourished and susceptible to pressure sores.

Change position at frequent intervals Assess the sacral area regularly Use protective devices to prevent pressure sores.

(f) Promoting nutrition

Provide bland, low – calorie, low – residue with vitamin supplement during the acute phase.

Frequent small feedings minimize exertion and reduce gastrointestinal blood requirements.

There may be no need to severely restrict sodium intake of the client who receives diuretic. However, “no added salt” diet is prescribed. Salty foods must be omitted.

(g) Promoting elimination

Advise the client to avoid straining at defecation which involves valsalva’s maneuver. Valsalva maneuver increases cardiac workload. Administer laxative as ordered. E.g. colace (decussate sodium)

Encourage use of bedside commode.

(h) Facilitating learning

Teach the client and his family about the disorder and self – care. Monitor sign and symptoms of recurring CHF, e.g.

weight gain, loss of appetite, dyspnea, orthopnea, edema of the legs, persistent cough report these to the physician

Avoid fatigue, balance rest with activity. Observe prescribed sodium restrictions Eat small, frequent meals rather than 3 large

meals a day. Take prescribed medications at regular basis, e.g.

digitalis,diuretics, vasodilators Observe regular flow – up care as directed

If acute pulmonary edema occurs in the client with CHF, the following are the appropriate collaborative management: Place in high – fowler’s position, with legs

slightly lowered to facilitate breathing and to reduce preload

Morphine sulfate 10 to 15 mg./ IV as ordered. To primarily reduce preload and afterload, and to allay anxiety.

Oxygen therapy at 40% to 70% by nasal cannula or face mask

Aminophyline / IV as ordered. To relieve bronchospasm, increase urinary output and increase cardiac output.

Rapid digitalization. Diuretic therapy Vasodilators Dopamine or dobutamine Monitor serum potassium. Dieresis may result

to hypokalemia.

Infectious Disorders Of The Heart

(1.) Rheumatic fever. Is diffuse inflammatory disease, that results as a delayed response to an infection by group A beta – hemolytic streptococci.Poor hygiene, crowding, and poverty are

risk factors for acute rheumatic fever.The heart, joints, subcutaneous tissue,

central nervous system and the skin are effected in rheumatic fever.

Complications of rheumatic fever include valvular disorders, cardiomegaly, and heart failure.

The Clinical Manifestations Of Rheumatic Fever Include The Following:

a. Fever. Temperature of 38°C (104.4°) or higher that alternates with normal temperature.

b. Arthritis. It is painful and migratory. It affects larger joints, such as ankles, knees, elbows, shoulders, and wrists.

c. Carditis. It is characterized by murmur, cardiomegaly, pericarditis with friction rub, and heart failure. Chest pain may be present.

d. Subcutaneous nodules. These are small, painless, firm nodules in the knees, knuckles, and elbows.

e. Erythema marginatum. Rash seen on the trunk. The lesions are crescent shaped and have clear centers.

f. Chorea. This is characterized by sudden, irregular, aimless, involuntary movements.

g. Abdominal pain. This is due to the engorgement of the liver.

The laboratory findings in rheumatic fever are as follows: elevated ESR, wbc, and C-reactive protein; positive throat culture for GABHS; elevated ASO titer.

The collaborative management for rheumatic fever are as follows: Corticosteroids to treat carditis. ASA to relieve manifestations of arthritis. But this drug may mask the symptoms of the disease.

Bed rest High – protein, high – carbohydrate diet.

To provide adequate nutrition

2.Infective endocarditis. Is an inflammatory process of the endocardium, especially the valves.

Subacute bacterial endocarditis (SBE). Develops gradually over several weeks or months; caused by streptococcus viridians.

Acute bacterial endocarditis. Develops over days or weeks; caused by staphylococcus, aureus.

The clinical manifestations of endocarditis are as follows: fever, chills, malaise, weakness, anorexia, weight loss, pallor, backache, splenomegaly (flu – like manifestations).

Embolization may occur, producing the following signs and symptoms:a. Stroke, transient ischemic attacks, asphasia and ataxia.

b. Loss of vision (brain, retinal artery are affected)

c. Petechiae on the neck, conjunctiva, chest, abdomen and mouth.

d. Roth’s spots - a white or yellow center surrounded by a bright red irregular halo seen by opthalmoscope

e. Myocardial infarction (coronary artery is affected).

f. Pulmonary embolism.g. Splinter hemorrhages (tiny splinters under the nails).

h. Osler’s nodes – painful, erythematous around a small, infected embolus.

i. Clubbing of fingers.j. Janeway’s lesions – flat small, nontender red spots on the palms of the hands and the soles of the feet.

k. Arthralgia, proteinuria,hematuria, casts and acidosis.

The collaborative management for encarditis are as follows: Antibiotic (penicillin, streptomycin)

Treat fever (fluids, rest, cooling measures, salicylates).

Monitor for signs of heart failure and embolic manifestations.

Valvular heart disease

1. Mitral valve disease

a. Mitral stenosis. Is narrowing of the mitral valve.

b. Mitral regurgitation. Is ejection of blood from the left ventricle to the left atrium.

c.. Mitral valve prolapsed. The valve leaflets bulge into the left atrium during ventricular systole.

The Clinical Manifestations Are As Follows:

a. Mitral stenosis Diastolic murmur Atrial fibrillation Systemic embolization

b. Mitral regurgitation Fatigue, dyspnea Orthhopnea, paroxysmal nocturnal dyspnea (PND),

peripheral edema Systolic murmur Atrial fibrillation

c. Mitral valve prolapsed Tachycardia, lightheadedness, syncope, fatigue,

weakness, dyspnea, chest discomfort, anxiety, palpitations.

Regurgitant murmur

The Collaborative Management For Valvular Disorders Are As Follows:a. Mitral stenosis

Oral diuretics Sodium – restricted diet Digitalis for atrial fibrillation Beta – blockers to decrease the heart rate Anticoagulants to prevent embolization.

b. Mitral regurgitation Diuretics and reduction of sodium – intake. To

reduce cardiac workload. Nitrates, digitalis, ACE inhibitors

c. Mitral valve prolapsed. Beta – blockers to relieve syncope, palpitations

and chest pain. Antibiotic prophylaxis for invasive procedures.

Aortic valve diseasesAortic stenosis. Is narrowing of the orifice

of aortic valve. The signs and symptoms of aortic stenosis are as follows: chest pain, syncope, dyspnea, PND, pulmonary edema, left ventricular hypertrophy, systolic murmur.

The collaborative management for aortic stenosis are as follows:Avoid vigorous exercise.Prophylactic antibiotic for invasive procedures.

b. Aortic regurgitation. Blood propelled into the aorta regurgitates back into the left ventricle. The signs and symptoms of aortic regurgitation are as follows: palpitations, permanent pulsation in the neck, sinus tachycardia, premature ventricular contraction’s corrigan’s or water – hammer pulse (sudden sharp pulse followed by a swift collapse of the diastolic pulse).

The collaborative management is the same as for aortic stenosis.

3. Tricuspid valve diseases Tricuspic stenosis and regurgitation usually develop from rheumatic fever.

The clinical manifestations are dyspnea, fatigue, pulsations in the neck, hepatomegaly, peripheral edema, diastolic murmur.

The collaborative management includes diuretics and digitalis therapy surgery may required.

4. Pulmonic valve diseases These are pulmonic valve stenosis and regurgitation. These are usually congenital defects.

The clinical manifestations are usually due to right – sided congestive heart failure. Dyspnea and fatigue are common.

Pulmonic stenosis is characterized by crescendo – decrescendo murmur.

The collaborative management is the same as right – sided CHF.