Cardiovascular Study Guide for the CCRN

Heart Failure

Heart failure is the inability of the heart to pump out enough oxygen-rich blood to support the body’s needs. It is often called congestive heart failure (CHF) because the unpumped blood builds up and causes congestion in either the lungs or other parts of the body. It is diagnosed through a variety of methods, including an echocardiogram, an electrocardiogram, a chest x-ray, and blood tests such as B-type natriuretic peptide (BNP).

Heart failure is most commonly a chronic condition caused by a variety of factors such as lifestyle, hypertension, coronary artery disease, cardiomyopathies, diabetes, and kidney disease. It can also have an acute onset, such as after a myocardial infarction or arrhythmia. Those with chronic heart failure can have an acute episode of worsening symptoms. This is referred to as an exacerbation. Otherwise controlled heart failure can be exacerbated by things like injuries, infections, poor dietary consumption, and new medications.

Heart failure can be further classified into left-sided, right-sided, or biventricular (both left- and right-sided) heart failure depending on the affected side of the heart. Heart failure affecting the left side of the heart is more common. It can also be classified into the part of the cardiac cycle it affects: diastolic heart failure affects diastole, or the relaxation, and systolic heart failure affects systole, or the contraction.

Systolic Heart Failure

Systolic heart failure is the more common left-sided heart failure. In this condition, there is a reduction of blood ejected from the ventricle during contraction. This causes a decreased ejection fraction. You will often see this abbreviated HFrEF, which stands for “heart failure with reduced ejection fraction.” Ejection fraction is the percentage of blood pumped by the heart per beat. Normal is considered at 50 to 70%, and a value below 50% would be reduced. The body compensates by releasing catecholamines to support the myocardium; however, these catecholamines then destroy the beta and adrenergic receptors and cause myocardial damage.

When the muscle becomes damaged, the RAAS (renin-angiotensin-aldosterone system) cascade is initiated, causing the body to retain sodium and fluid, increasing the cardiac load. To support the increased fluid volume, the cardiac muscle thickens and remodels, ultimately leading to further decreased effectiveness in circulating the blood. Reduced blood flow to the capillaries increases tissue injury and ischemia.

Diastolic Heart Failure

Diastolic heart failure is another type of left-sided heart failure and is clinically similar to systolic heart failure. However, in diastolic heart failure, the ventricles are unable to fully relax to allow the ventricles to fill with blood. In other words, the heart pumping action is normal, but it is unable to fully fill with blood during the relaxation stage. You will often see this abbreviated as HFpEF, which stands for “heart failure with preserved ejection fraction.” The ejection fraction will be normal, >50%, but the same symptoms occur as with systolic heart failure. It most commonly occurs in females older than 75. Diastolic heart failure symptoms worsen with exertion, as the ventricles are unable to sustain the need for increased stroke volume and workload. Goals in the treatment of diastolic heart failure include reducing the cardiac workload, preventing further myocardial changes, and avoiding exacerbations.

Symptoms

Left-sided heart failure, either systolic or diastolic, will manifest with symptoms affecting the lungs. This is because when the left side of the heart does not work properly, fluid accumulates in the lungs. Common symptoms include shortness of breath, intolerance to physical activity, coughing, wheezing, and orthopnea (shortness of breath while lying flat). Weight gain and edema can be observed, but typically are not as pronounced as in right-sided heart failure.

Treatment

Common treatments for systolic and diastolic heart failure include medications, heart transplant, and lifestyle modifications. Nurses should educate patients and their families about lifestyle changes such as a low-sodium diet, supplemental oxygen, and monitoring daily weight changes. Patients should notify their primary care providers of weight gain greater than three pounds per day or greater than five pounds per week.

Right-sided Heart Failure

Right-sided heart failure is not as common as left-sided heart failure. It occurs when the right ventricle cannot pump effectively to send blood to the lungs to be oxygenated. The most common cause of right-sided heart failure is actually left-sided heart failure, as it puts extra strain on the right side. Other causes may include lung conditions such as severe COPD, pulmonary hypertension (when caused by this, it’s a type of heart failure called cor pulmonale), and pulmonary embolism. Congenital heart defects and heart valve issues can also contribute to its development.

Symptoms

Right-sided heart failure typically manifests with symptoms affecting the rest of the body and not typically the lungs. Symptoms include ascites, peripheral edema, enlarged liver and/or spleen, distended jugular veins, fatigue, weakness, and sudden weight gain.

Treatment

Treatment is similar to left-sided heart failure. This type has an especially big emphasis on diuretics and monitoring daily weights. Utilizing things like compression stockings and teaching patients to keep their legs elevated can promote venous return and help reduce edema.

Acute Heart Failure or Exacerbation

Acute heart failure or an exacerbation of chronic heart failure occurs when the body can no longer compensate for the decreased efficacy of the heart. This can be left-sided, right-sided, or both, but as mentioned before, left-sided is the most common. When the cardiac output cannot meet the body’s metabolic demand, acute decompensation of the patient occurs. This condition may be triggered by dysrhythmias, illness, changes or non-compliance in medication administration, acute trauma, fluid overload, and hypertension.

Symptoms

Cough, edema, dyspnea, ascites, increased jugular venous pressure, fatigue, cool extremities, hypotension, and altered mental status are all symptoms of acute heart failure. Nurses must quickly recognize these symptoms and notify the provider of any acute changes to prevent organ failure and death. Diagnosis of acute heart failure is supported by testing, such as chest x-ray, ECG, exam, and blood work, including BMP, BUN, creatinine, and BNP.

Treatment

Expected interventions of treatment include stabilization of the patient, diuretics (Lasix®, Bumex®, etc.), vasodilators to decrease pulmonary congestion, monitoring urine output, sodium restriction, and prophylaxis for thromboembolism.

Medications

Medications for heart failure help reduce the workload on the heart and improve its function. To understand how they work, it’s important to understand four concepts:

Preload: The amount of blood returning to the heart. High preload means the heart is overloaded with fluid and needs to stretch more to pump.

Afterload: This is the resistance the heart must pump against. High afterload makes it harder for the heart to pump blood.

Contractility: This is the heart’s ability to squeeze. Low contractility means the heart cannot squeeze effectively.

Cardiac (ventricular) remodeling: This consists of changes in the size, shape, and function of the heart, specifically after damage. You may hear medications that reverse these changes referred to as cardioprotective, as they protect the heart from damage.

• ACE inhibitors (ACEIs) decrease afterload and preload, as well as reverse ventricular remodeling. Avoid use in renal insufficiency, renal artery stenosis, and pregnancy. Persistent dry cough, hyperkalemia, hypotension, hypoglycemia in diabetic patients, angioedema (ACEI are one of the most common causes of drug-induced angioedema), dizziness, and weakness are the most common side effects of ACE inhibitors. The most common drugs in this category include captopril (Capoten®), enalapril (Vasotec®), and lisinopril (Prinivil®).

• Angiotensin receptor blockers (ARBs) are similar to ACE inhibitors in that they decrease afterload and preload and reverse ventricular remodeling. ARB medications are used for those who cannot tolerate ACE inhibitors. Side effects are also similar to ACE inhibitors; however, ARBs may present additional side effects of headache, metallic taste, and rash. Common drugs in this category include losartan (Cozaar®) and valsartan (Diovan®).

• Beta-blockers are used to slow the heart rate, reduce hypertension, prevent dysrhythmias, and reverse ventricular remodeling. Tachycardia can occur in heart failure when the heart tries to compensate for the lack of proper pumping. While short term, it boosts cardiac output and it can be damaging to the heart if it goes on for too long. Patients with bradycardia, decompensated heart failure, uncontrolled hypo- or hyperglycemia, and airway disease should not be prescribed beta-blockers. Patients taking this medication generally tolerate it very well. Side effects include bradycardia, hypotension, and bronchospasm. They may also overshadow signs of hypoglycemia. Common medications in this class include metoprolol (Lopressor®), carvedilol (Coreg®), and esmolol (Brevibloc®).

• Aldosterone agonists mimic the action of the natural hormone aldosterone, a hormone secreted by the adrenal glands that regulates blood pressure through potassium and sodium levels. In heart failure, they are used to decrease preload and myocardial hypertrophy. However, patients should be monitored for hyperkalemia. The most common of these agents is spironolactone (Aldactone®), which is also a diuretic.

• Diuretics are primarily used to help control congestive heart failure and renal insufficiency. They help to reduce preload and reduce the inflammatory response post-cardiac surgery. The most commonly prescribed diuretic is furosemide (Lasix®). This medication commonly causes hypokalemia and may need to be given with a potassium supplement to prevent this.

• B-type natriuretic peptide (BNP) medications are synthetic versions of the natural B-type natriuretic peptide, which is a protein made by the heart that tells the body to release more water and to dilate the blood vessels. It does this so the heart does not have to work as hard. This explains why the BNP lab level is high in heart failure. These medications are used to promote vasodilation, decrease filling pressure, decrease vascular resistance, and increase urine output. It is primarily used in worsening congestive heart failure. It should be avoided in patients with a systolic blood pressure less than 90 mmHg, cardiogenic shock, constrictive pericarditis, and valve stenosis. Patients should be monitored for hypotension, headache, bradycardia, and nausea. The most common BNP medication is nesiritide (Natrecor®).

• Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a newer class of medications, initially approved for use in diabetic patients, but recently gained approval for heart failure as well. The mechanism of action is not fully understood, as more research is needed. What is known is that the medications block a protein in the kidneys that reabsorbs sodium and glucose. Therefore, the unabsorbed glucose and sodium are excreted out of the body, via the osmotic effect of pulling water with it, through urine. Look out for dehydration, hypotension, and hypoglycemia, and the associated symptoms with those. Examples of these are dapagliflozin (Farxiga®) and empagliflozin (Jardiance®).

• Positive intropes are medications that increase the contractility of the heart. Dobutamine (Dobutrex®) is a medication used in acute heart failure or decompensation. It increases contractility and serves as a temporary measure to improve hemodynamic stability mostly in critically ill patients. It has an increased risk of arrhythmias. Milrinone (Primacor®) is similar to dobutamine; it increases contractility and is used short term in critically ill patients. Milrinone has a greater vasodilating effect, meaning hypotension is seen more commonly with this medication.

• Digoxin (Lanoxin®) is also a positive inotrope, but also a cardiac glycoside and has more special considerations. It is used to increase myocardial contractility, left ventricular output, and decrease conduction of impulses through the AV node. It is commonly prescribed in cases of heart failure to improve heart function. This medication comes with strict regulations to promote effectiveness and prevent toxicity. Digoxin blood levels should be maintained between 0.5 and 2.0 ng/mL. Nurses should also monitor for early signs of digoxin toxicity, including fatigue, lethargy, depression, nausea, and vomiting. Late signs of digoxin toxicity include severe diarrhea, blurred vision, yellow or green halos around lights, and extreme fatigue or weakness. ECG changes may note SA or AV block, ventricular tachycardia or fibrillation, multiple PVC episodes, and bradycardia. If necessary, digoxin immune FAB (Digibind®) may be used to bind to digoxin and inactivate its reaction, thus lowering serum levels and returning to a therapeutic response.

Supportive Cardiac Devices

Cardiac devices are devices that are inserted or implanted into the body to help the heart function better. They can support the electrical or pumping action of the heart. Furthermore, they can be permanent or temporary. Temporary cardiac devices are used in critically ill patients and require careful monitoring.

Intra-Aortic Balloon Pump

An intra-aortic balloon pump is a catheter used to assist in cardiac function for patients with decreased function. This device works by threading a catheter with a balloon at the tip through the femoral artery into the descending thoracic aorta. The balloon inflates with diastole and deflates with systole. This helps to increase circulation to the coronary arteries while also decreasing the afterload of the heart. Patients with acute heart failure, unstable angina, papillary or septal rupture, and cardiogenic/septic shock may be candidates for this therapy. Aortic valve stenosis and large aortic aneurysms would be contraindications for this therapy.

Placement Concerns

Patients with an intra-aortic balloon pump will get daily chest x rays to ensure placement of the balloon. Nurses should be aware of the placement of the intra-aortic balloon pump and the associated symptoms with incorrect placement. If the placement of the balloon is too high, it will occlude the left subclavian artery and cause dizziness and decreased radial pulse. If the placement is too low, occlusion of the renal artery will occur and cause acute flank pain with reduced urine output.

Patient Care

Nurses should prevent extra movement of the balloon by instructing the patient to not bend their knee or flex their hips greater than 45 degrees. The nurse should also monitor for ECG changes, noting that the balloon inflates with the T wave and deflates with the R wave. Frequently assess the controller to ensure it is at the right settings. Neurovascular checks, neurologic status checks, site checks, and fluid balance should be monitored hourly. It is critical that if the balloon pump errors, a leak alarm sounds, or blood is visualized in the catheter, the nurse must stop the machine, place the patient in Trendelenburg, and notify the provider. This emergent situation should be addressed immediately to prevent blood flow occlusion, leakage, embolus formation, and cardiac overload.

When the provider thinks the patient is ready to have the balloon catheter removed, a weaning strategy is commonly used to ensure they tolerate it first. This is done by reducing the volume and/or frequency of the balloon. The pump should not remain in place long if turned off and no longer inflating, as it carries a high risk of thrombosis.

Left-Ventricular Assist Devices (LVAD)

LVAD is a surgically implanted device that takes over the pumping action of the left ventricle. They are indicated for patients with severe heart failure. The LVAD pump is connected to a controller outside of the body, worn on a belt or strap. These devices can be temporary to allow healing of a damaged heart, a bridge to a heart transplant, or permanent for those not eligible for transplant.

Complications

As with any surgery, there’s a risk of bleeding, infection, and death. Specifically to the LVAD, blood clots can form causing issues with the device or even a stroke, right-sided heart failure, arrhythmias, and device malfunction. The device will display or sound an alarm in the event of a malfunction. It is important that patients and nurses understand these alarms and troubleshoot.

Patient Care

LVAD placement is considered open-heart surgery and the patient is admitted to the ICU initially. These devices require lots of education. The patient must understand how the device works, as it is literally taking over the pumping action of the heart, and if used incorrectly, can stop the patient’s heart. Patients need a stable home environment with a good support system. The device needs to be on a battery or plugged in to work. The device can never be unpowered or it will stop working. Most patients with LVADs require blood-thinning medications. They will also need to understand proper dressing change technique to prevent infections at the insertion site.

There are also lifestyle modifications, such as no vigorous exercise, avoiding extremely hot or cold temperatures for long periods of time, drinking plenty of water, and maintaining a healthy weight. Patients with an LVAD typically do not have a palpable pulse and automatic blood pressure readings are not accurate. A Doppler and a manual blood pressure cuff are used for a blood pressure reading. You can also auscultate a “whir” sound made by the pump when running.

Extracorporeal Membrane Oxygenation (ECMO)

ECMO is a short-term life-support machine that acts as an artificial heart and/or lungs. There are two types of ECMO. Veno-venous VV ECMO supports the function of the lungs but not the heart, meaning a patient’s heart of this type is 100% responsible for the pumping function. The VV ECMO is simply doing the gas exchange portion. Veno-arterial VA ECMO supports the function of both the heart and lungs by pumping oxygenated blood through the body. It works through two cannulas that are inserted into the body. An access cannula is placed into a large vein and drains deoxygenated blood out of the body. The return cannula will either be in a large vein (VV ECMO) or artery (VA ECMO). These cannulas are connected to a circuit machine outside of the body that oxygenates and can help pump the blood. It is a last-resort measure for critically ill patients with diagnoses such as cardiogenic shock, cardiac arrest, or a bridge to transplant.

Patient Care and Complications

ECMO is a complex treatment that requires diligence and a multidisciplinary approach. Nurses must assess and monitor patients on ECMO closely.These patients are typically mechanically ventilated and sedated. Cannula sites should be checked for bleeding, clotting, and signs of infection. These patients are almost always on anticoagulation, such as heparin, due to the risk of blood clots. Patients on ECMO are more prone to hyperthermia due to blood circulating through a circuit. Nurses should monitor other organ systems for signs of dysfunction and watch for limb ischemia. Additionally, nurses need to be familiar with the machine itself and be able to recognize different alarms and basic troubleshooting to respond quickly to device issues.

Pacemaker

Pacemakers are artificial implanted devices that may be placed temporarily or permanently to provide regulation of the electrical impulses of the heart. They are commonly used in events such as symptomatic bradycardia, symptomatic tachycardia, heart failure, and heart block. Demand pacing and rate-response pacing are the two common types of programming for these devices. The typical pacemakers used in emergent events include the transcutaneous pacemaker and transvenous pacemaker. These pacemakers are not permanent and may be removed after the patient recovers from their acute cardiac event.

Complications

After pacemaker placement, nurses should monitor for complications related to the device. In temporary pacemaker sites, monitor for bleeding, infection, and hematoma. Ectopic beats or tachycardia may occur if the ventricular wall is irritated by the implanted electrodes. If the pacemaker becomes dislodged or the electrode perforates the cardiac muscle, the device is likely to malfunction, causing irregular or absent electric impulses. Persistent hiccupping in a patient with a pacemaker may indicate dislocation of the leads, causing phrenic nerve stimulation. Upon removal of the electrode and pacemaker, the patient should be monitored for cardiac tamponade.

Pacemaker syndrome is also a concern with the placement of any pacemaker device. This is caused by dyssynchrony between the electrical impulses from the pacemaker and the natural impulses from the myocardium. This is characterized by decreased cardiac output with inadequate ventricular filling. Symptoms of this syndrome may be mild to severe.

• Mild symptoms include visible pulsation in the neck or abdomen, palpitations, headache, anxiety, lethargy, weakness, and jaw or chest pain/pressure.

• Moderate symptoms include increasing dyspnea with exertion, dizziness, vertigo, confusion, and a choking feeling.

• Severe symptoms may lead to pulmonary edema, syncope, fluid retention in the lungs (evidenced by rales), and heart failure.

In the event the patient presents with these symptoms and has a pacemaker, evaluation of the impulses, location of the electrodes, and mechanical manipulation may be indicated to correct this syndrome.

Pacemakers on ECG

Pacemakers can stimulate the atria, ventricles, or both, depending on the setting. When a pacemaker fires an electrical stimulus, a small vertical line called a pacer spike should be observed on the ECG. Pacemakers that are only stimulating the atria should have a pacer spike before the P wave. This rhythm is referred to as A paced. Pacemakers that are only stimulating the ventricles should have a pacer spike before the QRS complex. This rhythm is referred to as V paced. Pacemakers that stimulate both the atria and ventricles should have two pacer spikes, one before the P wave and one before the QRS. This rhythm would be referred to as AV paced.

Just like any medical device, pacemakers can malfunction. The ECG is key for detecting these issues, which allows providers to intervene as needed. Below are the most common malfunctions observed on ECG:

• Failure to pace is when the pacemaker does not fire when it should. This is evidenced by decreased or absent pacer spikes where they should be present.

• Failure to capture is when the pacemaker fires, but the heart does not respond. This is evidenced by appropriate pacer spikes, but no P wave or QRS complex following.

• Failure to sense is when the pacemaker does not accurately detect the intrinsic cardiac activity, which leads to asynchronous pacing. This is evidenced by pacer spikes at wrong times. If the pacer fires during the T wave, known as theR-on-T phenomenon, it can induce life-threatening arrhythmias, such as v-fib or torsades de pointes.

Many of these malfunctions are related to the pacemaker settings, such as output and sensitivity being too high or low, which can be adjusted by a medical provider. Hardware issues can also occur, including depleted battery, lead displacement, and internal damage. If the patient is pacemaker dependent and the device is not functioning properly, stabilizing measures such as temporary transcutaneous pacing may be needed until troubleshooting can occur. Pacemakers can directly cause arrhythmias such as pacemaker-mediated tachycardia, and indirectly contribute to other arrhythmias, as having a foreign device in the heart can sometimes aggravate underlying rhythm disturbances, such as atrial fibrillation.

Implantable Cardioverter Defibrillator (ICD)

An ICD is an implanted device slightly larger than a pacemaker, but it works similarly. Many devices combine a pacemaker and an ICD into one device. The difference between the two is that an ICD sends an energy shock that can reset an abnormal heart rhythm. A pacemaker is often used for bradycardias, while an ICD is used for tachycardias or fatal rhythms such as ventricular fibrillation.

Hypertensive Crises

A hypertensive crisis is an acute and life-threatening condition characterized by a marked elevation in blood pressure. It may lead to severe organ damage if untreated. Nurses must be quick to recognize the risk factors and early signs of this condition. Common risk factors include hypertension, endocrine, and renal disorders, especially pheochromocytoma. A hypertensive crisis may also occur in the event of aortic aneurysm dissection, pulmonary edema, subarachnoid hemorrhage, stroke, eclampsia, or medication non-compliance. Symptoms of hypertensive crisis include basal headache, blurred vision, chest pain, nausea, vomiting, shortness of breath, seizures, ruddy pallor, and anxiety.

Types

There are two classifications of hypertensive crisis. This includes hypertensive emergency and hypertensive urgency. In a hypertensive emergency, the patient will experience acute hypertension (1.5 x 95th percentile) with readings of >220 systolic and 120 mmHg diastolic. This condition must be treated immediately to prevent long-term organ damage. Patients generally are more symptomatic, including chest pain, shortness of breath, and can show signs of a stroke, such as confusion, unilateral weakness, vision changes, slurred speech, etc.

In hypertensive urgency, the acute hypertension must be treated within a few hours, but the vital organs are not in immediate danger. Readings are usually >180 mmHg systolic and >120 mmHg diastolic. These patients are generally more asymptomatic or have mild symptoms, most commonly a headache.

Treatment

Pharmacological treatment of acute hypertension and hypertensive crisis include the implementation of vasodilators (Cardene®, nitro, etc.) and diuretics. Alpha-adrenergic blockers, labetalol (Normodyne®), and phentolamine (Regitine®), may be used to dilate peripheral arteries and veins to reduce cardiac afterload, thus decreasing the blood pressure response. Calcium channel blockers may be used to dilate the arterial vessels and decrease the patient’s heart rate. In acute hypertension, nifedipine (Procardia®) and nicardipine (Cardene) will be considered. Nifedipine should not be prescribed in older adults as it may increase their risk for hypotension and MI.

To help reduce the patient’s heart rate, diltiazem (Cardizem®) and verapamil (Calan®, Isoptin®) may be used. Side effects of calcium channel blockers include lethargy, flushing, edema, ascites, and indigestion. Goals of blood pressure lowering for hypertensive urgency include ⅓ reduction in six hours, ⅓ reduction in the following 24 hours, and ⅓ reduction over two to four days whereas in hypertensive emergency, the goal is to control the blood pressure immediately. Also anticipate blood work such as a BMP and diagnostic imaging to assess for any organ damage.

Nursing Interventions

To improve cardiac outcomes, these include raising the head of the bed to 90 degrees, supplemental oxygen administration, frequent neurologic assessments, and providing medication compliance education. Nurses should monitor for side effects of any of the medications prescribed and continue to record changes in blood pressure to ensure adequate treatment. Assess for hypotension that can happen when overcorrecting hypertension.