Page 3 Cardiovascular Study Guide for the CCRN®
Cardiac catheterization is both a diagnostic and interventional procedure when vascular occlusion is suspected. Nurses must understand the indications for each type of catheterization as well as any interventions to perform post-operatively.
In diagnostic cardiac catheterization, a catheter is inserted in an artery or vein in the groin, neck, or arm (large vessel) and threaded through blood vessels to the heart. The catheters can be used to assess for blockages and perform pressure measurements of the associated cardiac chambers and vessels. It can also be used to perform right or left ventriculogram and cardiac biopsy. A coronary angiogram is the catheterization of the coronary vessels to determine their perfusion and function. A right heart catheterization may be used to determine right sided chamber pressures and blood flow. Congenital heart defects, such as septal defects, patent processes, and other cardiac anomalies may also be diagnosed with cardiac catheterization.
Interventional cardiac catheterization occurs in response to a cardiac event in which vessels are blocked or narrowed. It is frequently used as an alternative to open heart surgery. Common types of interventional cardiac catheterization include coronary angioplasty, coronary stenting, angioplasty with or without stent placement, fixing congenital defects, replacing or repairing valves, cardiac ablation, balloon valvuloplasty (open narrowed heart valves), and balloon angioplasty (open narrowed arteries in or near the heart).
In the event of a patient undergoing cardiac catheterization, the nurse should anticipate interventions regarding preparation for and recovery of this procedure. Risk factors of cardiac catheterization include bleeding, heart attack, stroke, damage to the artery, arrhythmia, allergic reaction to contrast or medication, renal damage, infection, and clots. Post-surgical observation and assessment of the puncture site and dressing should be performed regularly. The dressing should not be prematurely removed and the nurse should monitor for clot dislodgement or internal bleeding (hematoma, ecchymosis), especially if the patient is coughing or vomiting. Generally, the dressing can be removed after 24 hours.
To help prevent internal or external bleeding from the puncture site, patients undergoing diagnostic cardiac catheterization are required to have strict bedrest and lie flat (no greater than 30-degree head of bed elevation) for 4 hours. If an interventional cardiac catheterization was performed, the patient’s bed rest and flat time increases to 6 hours.
Just as with any surgical procedure, postoperative nursing assessment should include monitoring for infection and thrombus formation. Frequent neurovascular checks to assess distal extremity circulation are also required. Retroperitoneal bleeding is a significant concern and may be indicated by fluctuating blood pressure response, bradycardia, hypotension, abdominal pain, groin and/or back pain, and diaphoresis. Other signs of bleeding include tachycardia, hypotension, decreased peripheral perfusion, increasing pulse pressure, agitation, and decreased haemoglobin.
Cardiogenic shock occurs when the heart cannot pump enough blood for the needs of the body. It is most often caused by a severe myocardial infarction. It can also be caused by myo- and endocarditis, cardiomyopathy, and drug overdose/poisoning. Those at highest risk include older age, history of prior heart failure or myocardial infarction, coronary artery disease, diabetes, hypertension, and females. While rare, it is an extremely fatal condition if not treated promptly.
Symptoms of cardiogenic shock include severe shortness of breath, tachycardia, loss of consciousness, thready pulse, hypotension, diaphoresis, pallor, clammy hands and feet, and decreased urination. This condition is diagnosed by ECG changes, chest x-ray, echocardiogram, and cardiac catheterization (angiogram).
Treatment medications include inotropic agents such as norepinephrine (Levophed®) or dopamine; aspirin; thrombolytics such as alteplase (Activase®) or reteplase (Retavase ®); antiplatelet medication such as clopidogrel (Plavix®), abciximab (Reopro®), tirofiban (Aggrastat®), and eptifibatide (Integrilin®). Understand the indication for these medications, side effects, and contraindications to administration.
In addition to pharmacologic support, the patient must be placed on oxygen and undergo therapy to restore blood flow to and through the heart. The patient may have to undergo angioplasty with stenting to remove and/or stent a blocked vessel; balloon pump to decrease the workload of the heart; and/or mechanical circulatory support such as extracorporeal membrane oxygenation (ECMO). If these measures fail to treat the shock, surgical measures such as coronary artery bypass surgery, ventricular assistive device (LVAD), and heart transplant may be considered.
Dilated cardiomyopathy (DCM) is characterized by an enlarged left ventricle limiting effective blood flow to the body. It is often caused by coronary artery disease, excessive alcohol intake, metabolic disease (thyroid, diabetes, etc.), viral infections, anatomic abnormalities (valve concerns), drugs (cocaine), and heavy metal poisoning (cobalt). The damaged cardiac muscle is replaced with scar tissue that then stimulates overgrowth of healthy cardiac cells. The overgrowth of the cardiac cells causes hypertrophy and muscle stretching. The muscle weakens, stresses the cardiac valves, and becomes ineffective in pumping blood.
Symptoms of DCM include dyspnea, shortness of breath, tachycardia, S3/S4 heart sounds, holosystolic murmur, wheezes/crackles, pleural effusions, edema, jugular vein distension (JVD), and ascites. ECG testing often shows tachycardia with T-wave changes, cardiomegaly will be present on chest x-ray, and echocardiogram testing may show valve regurgitation and decreased ejection fraction.
Treatment for dilated cardiomyopathy includes medications such as beta-blockers, ACE inhibitors, and diuretics. A low-sodium diet should also be implemented. Surgical interventions may include placement of a pacemaker, especially in light of cardiac dysrhythmia, and repair of the left ventricle. In severe cases, a heart transplant may be indicated.
Hypertrophic cardiomyopathy is a genetic disorder causing idiopathic thickening of the heart muscle, particularly the ventricular septum and left ventricle. Other characteristics of this disease include asymmetrical septum, forceful systole, cardiac dysrhythmias, and myocardial disarray. It may not be diagnosed until middle or late adulthood when symptoms become apparent.
Common symptoms of hypertrophic cardiomyopathy include exertional or atypical chest pain, dyspnea at rest, syncope, and palpitations. Diagnostic studies such as echocardiogram, ECG, x-ray, and a thorough family history can help to identify this condition.
The primary treatment measure is a septal myectomy. While this has a higher mortality rate (3-10%), the outcome, when successful, increases cardiac output and quality of life. An alternate therapy is the alcohol-based septal ablation, where ethanol 100% is injected into the heart, creating a controlled infarction and consequential thinning of the septum. Nurses must frequently assess these patients prior to and after treatment to monitor for significant changes in heart rate, blood pressure, and respiratory status.
Families should be educated on the genetic factor of this condition and educate them regarding the early signs, symptoms, and treatments to help identify and prevent extensive cardiac damage.
Idiopathic cardiomyopathy tends to occur in younger patients, 20 to 60 years old. Theories for this disease progression include overactive immune response (immune-mediated), toxic or metabolic injury, tachycardia induced, viral, or inherited cause. A thorough family history, cardiac history, and any unusual recent changes in health should be documented. Treatment medications include ACE inhibitors, angiotensin II receptor antagonists, beta-blockers, diuretics, aldosterone antagonists, and digitalis.
In restrictive cardiomyopathy, the ventricles stiffen due to the infiltration of fibroelastic tissues into the cardiac muscle. This decreases the compliance of the ventricles, thus decreasing the end-diastolic cardiac refill volume. Atrial enlargement occurs due to this resistance, which can lead to atrial fibrillation.
Symptoms of restrictive cardiomyopathy include exercise intolerance/fatigue, edema, crackles, elevated central venous pressure (CVP), S3/S4 heart sounds, cardiac murmur, and dyspnea at rest. It can be diagnosed with echocardiogram testing (showing an enlarged atria), hemodynamic monitoring (increased right atrial pressure, pulmonary wedge pressure, and systemic vascular resistance), x-ray, ECG, and cardiac biopsy. There may not be an identifying cause to the restrictive cardiomyopathy.
Treatment plans include diuretics, calcium-channel blockers, beta-blockers, ACE inhibitors, anticoagulants, lifestyle changes (low sodium), and even heart transplant in advanced cases.
Dysrhythmias occur when the heart beats abnormally as a result of internal or external factors. Electrocardiograms (ECG) are used to trace the activity of the heart and help define normal rates from abnormal ones. ECGs have a variety of settings.
The most common and conventional test is a 12-lead ECG, in which 10 electrodes are placed in various spots among the extremities and chest to trace these electrical impulses. Below is a list of dysrhythmias the nurse may encounter in practice. Please use your nursing texts to visualize lead placement in the 12-lead ECG and arrhythmia tracings, as you will need to know this for future testing purposes.
Types of Dysrhythmia
Sinus Bradycardia— Sinus bradycardia is classified by a decreased rate of heart beat impulses. It has normal P waves and QRS complexes but occur at a rate <50-60 beats per minute. It may be considered a normal condition especially for athletes, older adults, and during sleep. Medications such as calcium channel blockers and beta-blockers, increased cranial pressure, and recent myocardial infarction may result in bradycardia. If acute and symptomatic, atropine 0.5-1mg IV may be given.
Sinus Tachycardia— Sinus tachycardia is classified by an increase in impulse frequency. The P waves, QRS, and T waves are usually normal shape, though the QRS and T waves may overlap. The whole complex may be irregular as well. The patient will have a rapid pulse and may experience hypotension, dizziness, and pulmonary edema. Causes of this condition include acute volume loss (blood, shock, etc.), hypovolemic heart failure, fever, infection, anxiety, exercise, and some medications. Calcium channel blockers and beta-blockers help to reduce heart rate.
Supraventricular Tachycardia— Supraventricular tachycardia (SVT) is defined as >100 beats per minute. At times, SVT ranges from 200-300 beats per minute. This may decrease heart function and cause congestive heart failure. In this rhythm, there is some oburity between the P and preceding T waves, though the QRS complex appears normal. Treatment for SVT includes adenosine, digoxin, verapamil, vagal maneuvers, and cardioversion. In some cases, cardiac ablation may be required.
Sinus Arrhythmia— Sinus arrhythmia is often a paradoxical heart rhythm in which heart impulse increases with inspiration and decreases with expiration due to the altering stimulation of the vagus nerve. This arrhythmia is most often noticed when the nurse palpates the pulse fluctuations. This arrhythmia is most prevalent in children and young adults and tends to decrease with age. The P waves and QRS complexes are generally normal with this condition, just the rate and rhythm are mildly irregular. Treatment may be indicated if this rhythm occurs with bradycardia.
Premature Atrial Contractions— Premature Atrial Contractions (PAC) are extra atrial impulses that act as extra beats or palpitations. On ECG tracing, the nurse will see extra P waves, a normal to slightly abnormal QRS complex, and irregular rhythm. It can be caused by caffeine, nicotine, alcohol, increased fluid volume, decrease potassium levels, metabolic conditions, atrial ischemia, or myocardial infarction. Patients may experience palpitations with this condition. If the PACs occur greater than 6 episodes per hour or with severe palpitations, further testing is indicated.
Atrial Flutter— Atrial flutter is characterized by a fast atrial rate, usually 250-400 beats per minute with or without excessive ventricular activity (general rates 75-150 beats per minute). It may be caused by coronary artery disease, valvular disease, pulmonary disease, alcohol ingestion, and cardiac surgery. Symptoms of this condition include chest pain, difficulty breathing, and decreased blood pressure. If unstable, cardioversion may be implemented. Medications to help slow ventricular rate include non-dihydropyridine calcium channel blockers and beta-blockers. For converting back to sinus rhythm, Tikosyn® and amiodarone may be used.
Atrial Fibrillation— Atrial fibrillation is the constant, disorganized beating of the atrium which can cause decreased blood movement and blood clots. The patient may experience palpitations and fatigue as the ventricles try to compensate for the decreased stroke volume and overactivity of the atrum. The atrial rate may be 300-600 beats per minute, while the ventricular rate ranges from 120-200 beats per minute. Risk factors for acquiring and treatment of atrial fibrillation are the same as atrial flutter.
Premature Junctional Contractions— Junctional dysrhythmias arise from the dysfunction of the area around the AV node. Premature junctional contractions (PJC) is a premature impulse to the AV node prior to the normal sinus impulse. It is similar to premature atrial contractions (PAC); however, PJCs may be a sign of digoxin toxicity. In this rhythm, the QRS complex may come early and a P wave may or may not be present. The interval of the rhythm is usually regular and symptoms of this condition are rare.
Junctional Rhythms— Junctional rhythms are the result of the AV node taking over the role of initiating cardiac rhythm. Instead of sinus node impulse initiation, which occurs at 60-100 beats per minute, the atrial node dictates the pace at 40-60 beats per minute. The P wave may be absent or inverted but the QRS complex will appear normal. This rhythm may also be defined as the junctional escape rhythm and is a protective measure to prevent asystole with sinus node failure. Junctional tachycardia occurs when the junctional rate is greater than 100 beats per minute.
AV Nodal Reentry Tachycardia— AV nodal reentry tachycardia is also known as paroxysmal atrial tachycardia or supraventricular tachycardia. It occurs as impulses are sent quickly to both the AV node and ventricles. Atrial heart rate may be 150-250 whereas the ventricular rate is 75-250. P waves may be difficult to see and are small if present. The QRS complex is generally normal. Symptoms include chest pain, dyspnea, and hypotension. It may be corrected with vagal maneuvers, adenosine, verapamil, or diltiazem, and/or cardioversion.
Premature Ventricular Contractions— Premature ventricular contractions (PVC) occur when impulses begin in the ventricles during a beat cycle. The abnormal impulses cause an irregular QRS complex. Patient will also have an irregular heartbeat. PVCs can be caused by electrolyte imbalances, caffeine, nicotine, and alcohol. It may be a precursor to ventricular tachycardia, especially if there is a presence of more than 6 PVCs in one hour. Treatment measures include lidocaine, procainamide, and treating any underlying cause.
Ventricular Tachycardia— Ventricular tachycardia is the presence of greater than 3 PVCs in a row. This must coincide with a ventricular rhythm rate of 100-200 beats per minute. This rate of contraction disables the heart from pumping blood effectively. Patients with this condition may be unconscious without a palpable pulse. If a pulse is palpated, synchronized cardioversion and adenosine may be given to convert the rhythm back to normal. If a pulse is not palpated, emergency defibrillation, epinephrine, and amiodarone will be used to try to regain a normal rhythm.
Narrow Complex and Wide Complex Tachycardias— Narrow and wide complex tachycardias are classified by the width of the QRS complex. Wide complex tachycardia occurs when the QRS is >0.12 seconds and extra impulses are introduced below the AV node. The most common wide complex tachycardia is ventricular tachycardia. It may cause palpitations, difficulty breathing, diaphoresis, anxiety, and cardiac arrest. Narrow complex tachycardia, then, is defined by a QRS <0.12 seconds and is usually supraventricular in origin. It may additionally present with symptoms peripheral edema.
Ventricular Fibrillation— Ventricular fibrillation is a rapid, irregular beating (often greater than >300 beats per minute) of the ventricles without atrial input. There are no recognizable P waves or QRS complexes. This is a pulseless rhythm and will result in death if not immediately treated. Emergency defibrillation followed by IV push epinephrine 1mg every 3-5 minutes and amiodarone 300mg (1st dose) and 150mg (2nd dose).
Idioventricular Rhythm— Idioventricular rhythms occur when the Purkinje fibers create impulses due to sinus node failure or AV node blockage. The rate will be regular between 20-40 beats per minute. The tracing of this rate shows an absent P wave and an abnormally shaped QRS complex. A patient in this rhythm may lose consciousness.
Ventricular Asystole— Ventricular asystole or asystole is the absence of heart activity. It is also known as cardiac arrest. There may be an occasional beat, known as an “escape beat” or “agonal rhythm”. CPR with mechanical airway and intravenous access is required in this situation as it will result in death without treatment. This rhythm, or absence of rhythm, cannot be defibrillated. Epinephrine can be given every 3-5 minutes to attempt to restart the heart.
Sinus Pause— Sinus pauses occur when the impulses fail to stimulate heart contraction. Pauses may last from seconds to minutes and appear similar to ventricular asystole. Frequent pauses may lead to symptoms such as dizziness. The underlying cause for the pauses should be addressed; however, if no cause is identified or the pauses continue to be frequent and symptomatic, a pacemaker would be indicated.
Some medications can be used to prevent or treat dysrhythmias. There are four classes of medications that can be used. These medications act on the conduction system of the heart and help to control ventricular and/or atrial impulses. Review these medications and classes as you prepare for your exam.
- Class I: sodium channel blockers (quinidine, lidocaine, procainamide)
- Class II: beta-receptor blockers (esmolol, propranolol)
- Class III: amiodarone and ibutilide (slow repolarization)
- Class IV: calcium channel blockers (diltiazem, verapamil)
- Unclassified: adenosine