Cardiovascular Study Guide for the CCRN

Myocardial Conduction System Defects

Review the following conduction system defects and cardiac block rhythms. Please use your nursing text to visualize these events.

first-degree AV block—The impulses from the atrium to the ventricle are slower than normal. First-degree AV block is classified by typically normal P and QRS but with lengthened PR interval >0.20 seconds and a P:QRS ratio of 1:1. The width of the QRS helps to determine if the changes are just present in the AV node or also in the bundle branches. A narrowed QRS will signify abnormality in the AV node and a widened complex will show that greater anatomy has been damaged.

Chronic first-degree AV block is often left untreated. Acute first-degree block is more concerning. Risk factors for first-degree AV block include digoxin toxicity, beta-blocker medications, amiodarone, myocardial infarction, hyperkalemia, or edema. Treatment of acute first-degree AV block includes removing the agents causing the dysrhythmia. 0.5 to 1.0 mg of atropine may also be given if the heart rate drops too low.

second-degree AV block—There are two types of second-degree AV block, Type I, or the Mobitz Type I Block (Wenckebach), and Mobitz Type II. Both block some of the atrial beats of the heart.

• In Type I second-degree AV block, the atrial beats occur further and further apart until one is completely dropped. More P waves than QRS complexes will present themselves on an ECG reading. Also, the length between the R waves will gradually shorten with each heartbeat. Morbidity of this dysrhythmia is low unless complicated by an inferior wall infarct.

• Type II, or Mobitz, second-degree AV block is different in that the dropped atrial impulses are irregular. The block of impulse from the AV node to the SA node occurs after the AV node, bundle of His, bundle branches, or Purkinje fibers. Evidence on a rhythm strip would show a normal P wave when atrial conduction occurs, followed by a widened QRS. Understand that this heart block is more serious than Type I as it may progress to a complete heart block and may require a cardiac pacemaker and/or close access to a defibrillator. Chest pain may be a sign of this disorder.

Third-degree AV block—This is also referred to as a complete heart block. Third-degree AV block is classified by more P waves than QRS complexes. There is a dysfunction of either the AV node or the SA node, which creates a rhythm of contractility that ineffectively pumps blood from the heart. Due to this AV dissociation, bradycardia occurs with widened QRS complexes, and the heart struggles to maintain compensatory mechanisms. Dyspnea, chest pain, hypotension, dizziness, and death may occur. IV atropine may be used but it is typically ineffective as it works on the AV node, which, as we mentioned, is dissociated from the ventricles. Atropine is still given as it won’t hurt the patient, but the ultimate intervention is transcutaneous pacing. Pacing should not be delayed to administer atropine.

Transcutaneous pacing is when electrical impulses are sent through pads placed on the patient’s chest. This method of pacing is temporary in emergencies and quite uncomfortable for the patient. Sedative medications and oxygen are usually given. The rate is typically set around 80 bpm or according to the provider’s order. The current or electrical flow is increased until capture occurs. Capture will appear as a pacemaker spike just before the QRS complex. The goal is to use just enough current to maintain capture.

bundle branch block—Bundle branch blocks are classified as either right (RBBB) or left (LBBB). The type of block depends on which ventricle is affected by the blocked impulse past the bundle of His. In RBBB, a normal P wave with a widened and “rabbit-eared” notched QRS will be present. LBBB will show normal P waves but widened and “M-shaped” notched QRS complexes. Both block types exhibit a regular rhythm and a 1:1 P:QRS ratio. This pattern can be visualized best in lead I. Both of these can be caused by various cardiac conditions, such as hypertension, myocardial infarction, heart disease, cardiomyopathy, and heart failure. Sometimes the bundle branch block has no known cause (idiopathic), and the risk of having a BBB increases with age. Most people are asymptomatic but occasionally can present with fatigue, dizziness, or chest pain.

Papillary Muscle Rupture

Papillary muscle rupture is a rare but deadly complication of myocardial infarction. Responsible for the movement of the tricuspid and mitral valves, these muscles prevent blood regurgitation and valve prolapse. When ruptured, the muscles can no longer prevent the backflow of blood through the heart, which can result in cardiogenic shock.

Symptoms of this condition include acute heart failure, pulmonary edema, tachycardia, diaphoresis, loss of consciousness, pallor, tachypnea, mental status change, weak/thready pulse, and decreased urinary output.

Diagnosis can be achieved with transesophageal echocardiography (TEE), which is used to visualize the papillary muscles. Color flow Doppler and echocardiogram can help identify the flow and severity of the valve prolapse/regurgitation within the heart. Nurses must be aware of any new holosystolic murmurs noted from the apex radiating to the axilla. Emergent surgical repair of the affected valve is indicated when diagnosed to prevent further cardiac damage and death.

Structural Heart Defects

Structural heart defects are issues with physical parts of the heart, including chambers, walls, or valves. Some of these defects include faulty valves, holes, or muscle thickening. These can be defects that someone is born with (congenital) or defects that develop later in life (acquired) due to a variety of reasons. If left untreated, heart defects can cause several issues including the development of heart failure.

Acquired Defects

Acquired cardiac defects occur due to wear and tear on the tissues and valves of the cardiac system. They often develop over time and may be complicated by other diseases (diabetes, cardiac disease, connective tissue disorders, alcoholism, drug use, etc.). Valvular disease includes stenosis or prolapse of the pulmonic, aortic, mitral, and tricuspid valves. The most common is aortic valve stenosis. Stenosed valves increase intrathoracic cardiac pressure and stress the chambers of the heart, thus decreasing pumping efficacy and increasing cardiac remodeling and hypertrophy. Cardiomyopathy, myocarditis, and left ventricular hypertrophy are also acquired defects that result from bacterial, viral, or inflammatory events.

Symptoms

Symptoms of acquired cardiac defects include murmurs, shortness of breath, cough, excessive fatigue, weight gain, swollen extremities, and poor cognition. ECG, echocardiogram, chest x-rays, cardiac MRI, cardiac catheterization, urinalysis, and lab tests (BMP, CBC, thyroid levels) are useful in diagnosing these defects.

Treatment

Treatment of acquired defects includes cardiac medications to reduce the cardiac workload, antihypertensive medications, surgical replacement or repair of valves and vessels, and heart transplant, when indicated. Replacement for aortic valves can be done surgically, surgical aortic valve replacement (SAVR), or minimally invasive, transcatheter aortic valve replacement (TAVR). TAVR is a newer development, but it offers a great option for less complex cases or for those unable to withstand open-heart surgery. Nurses should educate patients on lifestyle changes to prevent these defects, including taking prescribed medications, managing hypertension, encouraging a low-sodium diet, limiting alcohol use, and avoiding illicit drug use.

Congenital Defects

Congenital heart defects are most often diagnosed in infancy or early childhood. Adult-diagnosed congenital defects are usually the result of increased symptoms or cardiac complications. Atrial septal and ventricular septal defects are the most commonly diagnosed adult congenital defects. These defects cause a shunt of blood. The higher-pressure left side of the heart shunts oxygen-rich blood back to the right side of the heart to be sent to the lungs again. Depending on the size of the defect, it can overload the lungs, decrease cardiac output, and damage the right side of the heart.

Symptoms

Symptoms of these defects include cardiac murmur, cyanosis, clubbing of the fingernails, dyspnea, fatigue, syncope, palpitations, and unexplained edema. Physical assessment, ECG, echocardiogram, CT, and MRI may aid in the diagnosis of these defects. Sometimes, a bubble study can be performed during an echocardiogram, which involves pushing air through a patient’s vein to see where it travels in the heart.

Treatment

Correction of congenital defects often consists of surgical repair of the cardiac muscle. Nurses should monitor for complications of decreased or ineffective circulation prior to surgery, as well as post-surgical recovery.

Important Cardiac Calculations

In critical care, understanding cardiac calculations is pivotal to assessing hemodynamic status and heart function. These values provide insight into how effectively the heart is pumping and whether the circulatory system is delivering enough blood to meet the body’s needs. Frequent monitoring of these can allow for the detection of deterioration and early intervention.

The most common method of obtaining most of these values is through a Swan-Ganz or pulmonary artery catheter. The catheter is inserted into the neck, goes through the right side of the heart, and sits in the pulmonary artery. Other methods include diagnostic tests like echocardiograms and blood pressure readings.

You should be familiar with how to calculate or measure all of these values:

• Cardiac output (CO) is a measure of the volume of blood that can be ejected from the heart in one minute. It is calculated by multiplying heart rate (HR) and stroke volume (SV):

\[CO = HR \times SV\]

A normal cardiac output ranges between \(4\) and \(8\) liters per minute.

• Cardiac index (CI) helps measure the heart performance of an individual. It can be calculated by dividing cardiac output by body surface area (BSA):

\[CI = CO \div BSA\]

A normal cardiac index range would be \(2.5\) to \(4.2\) liters per minute per square meter (L/min/m\(^2\)). Cardiac output and index measurements can help manage medications such as inotropes and vasodilators.

• Stroke volume (SV) is the amount of blood released with each heartbeat. It can be calculated by dividing cardiac output by the heart rate and then multiplying by \(1\text{,}000\):

\[SV = (CO \div HR) \times 1\text{,}000\]

Alternatively, it can also be calculated by subtracting end systolic volume (ESV) from end diastolic volume (EDV):

\[SV = EDV - ESV\]

Normal volume is \(60\) to \(100\) milliliters per beat. The stroke volume can then be divided by the body surface area to find the stroke volume index:

\[SVI = SV \div BSA\]

A normal stroke volume index ranges from \(35\) to \(60\) milliliters per square meter. Stroke volume is factored by preload, afterload, and contractility of the heart.

• Ejection fraction (EF) is the percentage of blood ejected from the heart with every beat. A normal value is between \(50\) to \(70\%\). The most common test to measure ejection fraction is an echocardiogram.

• Preload is the end diastolic volume. The right ventricle’s preload can be assessed by central venous pressure (CVP), right atrial (RA) pressure, or right ventricular end-diastolic volume (RVEDV). Left ventricular preload can be calculated by the pulmonary arterial occlusion pressure (​​PAOP; also known as pulmonary arterial wedge pressure [PAWP]). An average CVP measurement is \(8\) millimeters of mercury (mmHg) with a range of \(2\) to \(12\) centimeters of mercury (cmHg). A normal PAOP pressure ranges from \(6\) to \(12\) mmHg and is optimal up to \(14\) to \(18\) mmHg for the critically ill patient.

  • The Frank-Starling curve shows how changes in a patient’s preload (e.g., IV fluids, passive leg raise) should affect their stroke volume. Medications that can decrease preload include diuretics such as furosemide (Lasix), torsemide (Demadex), and hydrochlorothiazide. Additionally, nitrates such as nitroglycerin and isosorbide reduce venous return. Most angiotensin-converting-enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) have a decreasing effect on preload as well.

  • Medications that are used directly to increase preload are primarily IV fluids, as they add to the circulating volume.

• Afterload is the force at which the heart must contract to eject blood during systole. This is otherwise known as ventricular contraction. The afterload is assessed by measuring the systemic vascular resistance (SVR) in the left ventricle and the pulmonary vascular resistance (PVR) in the right. Increased afterload results in increased oxygen demands and may, over time, decrease the contractility of the heart.

  • Medications that can decrease afterload include nitroglycerin, nicardipine, hydralazine (Apresoline), isosorbide dinitrate (Isordil), calcium channel blockers, sodium nitroprusside, and ACE inhibitors/ARBs.

  • Medications that can increase afterload include vasopressors, such as high-dose epinephrine, phenylephrine (Neo-Synephrine), norepinephrine (Levophed), high-dose dopamine, and vasopressin.

• Systemic vascular resistance (SVR) measures the amount of resistance vessels transmit to the heart during blood ejection. It can be calculated by multiplying the mean arterial pressure (MAP) multiplied by the central venous pressure, dividing that result by cardiac output, and multiplying everything by \(80\):

\[SVR = [(MAP \times CVP) \div CO] \times 80\]

A normal range is \(800\) to \(1\text{,}200\) dynes per second per centimeter to the fifth power (dyn/sec/cm\(^5\)). The systemic vascular resistance index (SVRI) measures systemic vascular resistance relative to the body surface area:

\[SVRI = SVR \times BSA\]

Increased SVR can be caused by anything that is or causes vasoconstriction. Therefore, it may result from hypertension, atherosclerosis, diabetes, peripheral artery disease, pulmonary hypertension, low cardiac output states, hypothermia, increased blood viscosity, hypovolemia, vasopressors, left ventricular failure, and alpha-adrenergic agents.

Decreased SVR can be caused by anything that is or causes vasodilation. These things may include shock, cirrhosis, hemorrhage, diuretics, vasodilators, hyperdynamic phase of sepsis, peripheral vasodilation, and loss of vasomotor tone.

• Pulmonary vascular resistance (PVR) measures the resistance to right ventricular blood ejection. It is measured by multiplying pulmonary artery wedge pressure by mean pulmonary artery pressure (PAP), dividing that result by cardiac output, and multiplying everything by \(80\):

\[PVR = [(PAP \times PAWP) \div CO] \times 80\]

A normal range for PVR is \(1.2\) to \(3.0\) units or \(100\) to \(250\) dyn/sec/cm\(^5\).

• The pulmonary vascular resistance index (PVRI) measures PVR relative to the body surface area:

\[PVRI = PVR \times BSA\]

Increased PVR causes stroke volume to decrease. It may result or occur in the event of hypoxia, pulmonary edema, acute respiratory distress syndrome (ARDS), pulmonary emboli, congenital heart defects, positive end-expiratory pressure (PEEP), pulmonary hypertension, sepsis, and vascular heart disease. It is managed by vasodilator therapy, correction of hypoxia, prostaglandins, and prostacyclin.

• Mean arterial pressure (MAP) is the average pressure in the arteries throughout one complete heartbeat. It is one of the most common ways to evaluate cardiac perfusion of vital organs. A normal MAP range is from \(70\) to \(100\) mmHg. MAP is calculated by multiplying diastolic blood pressure by \(2\) and adding systolic blood pressure, then dividing by \(3\):

\[MAP = [SBP + (2 \times DBP)] \div 3\]

A MAP less than \(60\) mmHg indicates the start of perfusion deficit, while a MAP less than \(40\) mmHg is considered cardiovascular collapse. Increased MAP may be due to volume infusions, peripheral vasoconstriction, increased contractility, hypervolemia, and vasopressors. Decreased MAP may occur due to diuretic therapy, vasodilation, inotropic therapy, hypovolemia, and vasodilators.

• Central venous pressure (CVP) is the measurement of blood pressure in the vena cava outside of the right atrium. This may also be referred to as right atrial pressure. It helps to identify the amount of blood returning to the heart and can be used to monitor fluid status. CVP levels range from \(0\) to \(12\) mmHg. A lowered CVP may indicate hypovolemia or venodilation, whereas an elevated CVP may indicate decreased contractility, valve abnormalities, dysrhythmias, and cardiac tamponade. Decreased intrathoracic pressure and forced inspiration can cause the vena cava to collapse, decreasing the venous return and the CVP. Any increases in pulmonary arterial resistance (e.g., PEEP, valve stenosis, pulmonary hypertension) will, in turn, increase the CVP.