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 clients 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.

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.

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.

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.

The 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.

The coronary arteries originate from the aorta, behind the cusps of the aortic valve, in an area known as Vasalvas 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.

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

The

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.

 The

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 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 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.

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 Marcys Law of the heart.

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 paO level causes a reflex SNS response that results in tachycardia, vasoconstriction and increased ph level leads to passive vasodilation.

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 (m)

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.

Nursing history The 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

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.

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.

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.

Palpation Peripheral pulses. Weak or bounding and irregular pulses may indicate presence of cardiovascular disorders. Apical pulse. It is assessed at the point of maximum impulse. Percussion Pulmonary edema produces dullness on percussion of the chest. Auscultation

 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.

Dyspnea the client experiences shortness of breath.

Dyspnea on exertion (DOE). This may indicate decreased cardiac reserve (hearts 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 Tests Complete blood count For evaluation of general health status. Elevated RBCs suggests inadequate tissue oxygenation. Hypoxia stimulates renal secretion of erythropoietin. This stimulates the bone marrow to increase rbc production (polycythemia). Elevated WBCs may indicate infectious heart diseases and myocardial infarction.

Erythrocyte Sedimentation Rate (ESR) It is a measurement of the rate at which RBCs 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 (BUN It 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 Lipids Serum cholesterol The client should be on NPO for 10 to 12 hrs. Normal range is 150 to 200 mg/dl. Serum triglycerides The client should observe fasting for 10-12 hours. Normal range is 140 to 200 mg/dl.

Blood Cultures To 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.

Aspartyate 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,/ml Females: 50-250 mu./ml. Range with Myocardial infarction Onset: 3 to 6 hrs. Peaks: 12 to 18hrs. Returns to normal: 3 to 4 datys

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

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

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.

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.

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

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

Serum electrolytes
Electrolytes 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)

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.

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.

Hypokalemia 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).

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.

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.

 Superior vena cava : 0-12 cm. HO Right atrium : 5-12 cm. HO Use 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.

 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 catheter is a flow directed, balloon tipped, 4 lumen catheter.

The catheter allows continuous monitoring of Right and left ventricular function Pulmonary artery pressures (Pap,PCWP) Cardiac output Arterial-venous oxygen difference Normal range: PAP : 4-12 mmHg PCWP : 4-12 mmHg PCWP reading above 25 mmHg suggests

impending pulmonary edema.

 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.

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

Allows ultrasonic imaging of the cardiac structures and great vessels via esophagus. Nursing Interventions Before TEE Ascertain 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.

NPO until gag reflex returns. To prevent aspiration. Place in lateral or semi fowlers position. To promote drainage of secretions from the mouth. Encourage to cough Throat 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.

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

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

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.

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 Tests Chest 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.

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.

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.

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

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

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

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

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.

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.

Referred to MS Word Figure 1. page.14

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.

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.

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

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 (prinzmetals 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 angina Occurs only during the night and is possibly associated with rapid eye movement (REM) sleep. Angina decubitus Paroxysmal chest pain that occurs when the clients sits or stands up. Intractable angina Chronic, incapacitating angina unresponsive to intervention. Postinfarction angina Occurs after MI, when residual ischemia may cause episodes of angina.

Precipitating events of angina pectoris

1.

2. 3. 4.

Exertion vigorous exercise done very sporadically. Emotions excitement, sexual activity. Eating a heavy meal Environment. Exposure to cold.

These events increase myocardial oxygen demands. Further disequilibrum between oxygen supply and oxygen demand occurs. Collaborative management for angina pectoris Medications Vasodilators: 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

 Effects

Decrease 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.

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.

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 blockers Assess heart rate and BP (blood pressure) Monitor hepatic and renal function Administer 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.

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

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.

Promoting comfort Relieve pain Nitroglycerine is the drug of choice for relief of pain from acute ischemic attacks. Promoting tissue perfusion Instruct 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 rest Encourage slower activity or shorter periods of activity with more rest periods. Avoid over exertions. Plan for regular activity program Take 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

Activity Activities are encouraged within the patients 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.

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

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.

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 handclutching). 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 basis
Pathologic 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 Basis These 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.

(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 therapy To 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 fowlers 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 pulse Administer 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 activity Gradual 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 being Provide an opportunity for the client and family to explore their concerns and to identify alternative methods of coping as necessary. Facilitating learning Teaching 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.

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 hearts ability to respond to activity and stress.

Progressive activity Activity 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.

Self management education guide: discharge after MI Discontinue smoking Control 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.

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.

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

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 (PVCs.) PVCs of 6 or more per minute is life threatening.

Referred to MS word figure 4. pg. 29

Sinus Sinus tachycardia Sinus bradycardia Sinus dysrhythmia Sick sinus syndrome Atrial Premature Atrial contraction Paroxysmal Atrial tachycardia Atrial flutter Atrial fibrillation

Ventricular Premature ventricular contractions Ventricular bigeminy Ventricular fibrillation Conduction defects First degree AV block Second degree AV block Third degree block

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. Treatment Digitalis 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.

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

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. PVCs 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 dW 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 is altered at the level of the AV node 1. 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 pacemaker Summary of therapeutic modalities for dysrhythmias Antidysrhythmis drugs Artificial cardiac pacemaker Cardioversion / defibrillation Cardiopulmonary resuscitation

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)

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.

Clinical indications Symptomatic bradyarrhythmias Sinoatrial bradyarrhythmias Sinoatrial arrest Sick sinus syndrome Heart block Second degree heart block Complete heart block

Prophylaxis Following acute MI; arrhythmias and conduction defects Before or following cardiac surgery During coronary arteriography Before permanent pacing Tachyarrythmias Supraventricular Ventricular

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 patients 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 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 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.

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 radar TV and radio transmitter Electrocautery machines Airport screening devices Antitheft 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 device Wear loose fitting clothing around the area of the pacemaker Observe for signs and symptoms of infection around generator and leads fever, heat, pain, skin impairment at the implant site. Avoid contact sports Electrode may be displaced

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.

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.

Indication

Cardiopulmonary arrest or clinical death (breathlessness, pulselessness). CPR is initiated within 4 to 6 minutes after the arrest, to prevent brain death. 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.

Crucial time

Two types of CPR

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

Step I. assess level of consciousness

Shake the victims 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 ventilation Mouth to mouth ventilation Mouth to nose ventilation Mouth to stoma ventilation Mouth to barrier ventilation
*note give 2 initial breaths lasting for 1 to 2 seconds. If no rise and fall of the chest is observed, consider airway obstruction.

Step IV. Assess circulation Check 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 message Depress the sternum with heels of both hands, one on top of the other 1 to 2 inches (adult); heel of one hand 1 to 1 inches (child); 2 fingers 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.

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 Fowlers 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

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.

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.

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

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

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.

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

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

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

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.

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 manifestations Anorexia Nausea and vomiting Diarrhea Dysrhythmias (most dangerous) Altered visual perceptions (yellow or green vision; blurred vision; halos or rainbows around the lights among elderly) In males: anitiandrogenic effects Gynecomastia Decreased libido Impotence

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)

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 Dopamine Dobutamine Treatment Diet sodium restricted diet to prevent fluid excess. Activity balances program of activity and rest Oxygen therapy to increase oxygen supply

(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 fowlers or high fowlers 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 fowlers 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 valsalvas 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 fowlers 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.

(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.

a. Fever. Temperature of 38C (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. Roths 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. Oslers nodes painful, erythematous around a small, infected embolus. i. Clubbing of fingers. j. Janeways 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.

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.

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

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 diseases Aortic 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 contractions corrigans 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.