Cardiovascular Study Guide for the CCRN

Acute Peripheral Vascular Insufficiency

Acute peripheral vascular insufficiency is the event in which a peripheral blood vessel is blocked by either plaque occlusion or emboli. Systemic atherosclerosis causes significant narrowing of arteries distal to the arch of the aorta. The most common symptom of peripheral vascular disease is intermittent claudication. The blockage may occur in the arterial or venous vessels.

Arterial insufficiency will manifest as intermittent claudication to severe and constant pain. Pulses may be weak or absent. Skin turgor and color will be decreased and the patient will have thickened nails. Necrotic ulcers may be present, especially in the lower extremities or feet. A majority of arterial occlusions are due to atherosclerosis.

Venous insufficiency will manifest as intermittent to constant aching or cramping. Pulses will be palpable. Skin will have some discoloration, usually brownish in color, especially around the ankles and anterior tibia. Ulcers, when present, are often superficial, irregular, and noted commonly on the lateral malleolus and anterior tibia. The patient may also experience moderate to severe edema. A majority of venous obstructions are due to thrombosis.

Arterial/Venous Occlusion

Sudden occlusion of a blood vessel can occur due to traumatic or non-traumatic events. Traumatic events include vessel crushing or rupture whereas non-traumatic events include embolism, vasospasm, and swelling. Once perfusion of the distal vessel is stopped, ischemia, cellular death, and necrosis ensue. Risk factors include age, tobacco use, diabetes, hyperlipidemia, and hypertension.

Diagnosis

When assessing for vascular occlusion, the nurse will monitor for the 6 Ps. These are: pain (excruciating not relieved), pulselessness, poikilothermia (inability to regulate body temperature), paresthesias, pallor, and paralysis (late sign). Diagnosis can be confirmed with ultrasound, angiography, and physical exam. Common blood work completed includes coagulation studies, CBC, BMP, and creatinine phosphokinase (CK). The goal of therapy is to reestablish blood flow and remove (or manage) the clot.

Acute Venous Thromboembolism

The most common acute venous thromboembolisms are deep vein thrombosis (DVT) and pulmonary embolism (PE). Risk for these embolism formations is significantly increased after invasive procedures and with decreased mobility and inflammation. Virchow’s triad includes the risk factors of blood stasis, injury to endothelium, and hypercoagulability.

Symptoms

Patients with acute venous thromboembolism may complain of continuous aching or throbbing in the affected extremity, positive Homan’s sign (pain in calf when foot is dorsiflexed), unilateral erythema and edema, dilation of vessels, and cyanosis (PE).

Diagnosis and Treatment

Patients with these symptoms will undergo several diagnostic studies, including ultrasound, D-dimer testing (which checks serum blood for cross-linked fibrin derivatives), CT scan, pulmonary angiogram, and ventilation-perfusion lung scan (PE). If an acute venous thromboembolism is identified, the patient will be started on IV antithrombin medications such as heparin or tPA. The patient will also be provided an analgesic for pain.

Surgical removal of the clot or placement of an IVC filter (DVT) may be implemented to prevent the breaking and movement of the clot. The patient should have frequent extremity, circulation, and neurological examinations to monitor for dislodgement of the embolism. The risk for stroke is high during the treatment of these large clots. The patient will also need to be on bed rest with elevation of the affected limb.

Prevention is a large part in avoiding consequences of acute venous thromboembolism. All patients at high risk for DVTs or PEs should be prescribed sequential compression devices or compression stockings, be evaluated for anticoagulant use, and have frequent ambulation or range of motion exercises performed if ambulation is limited.

Carotid Artery Stenosis

The carotid artery provides the brain with its primary supply of blood from the heart. This artery bifurcates into the external carotid and internal carotid arteries. The location of the bifurcation is a common site of plaques. As these plaques slowly build, they begin to narrow the vessels, causing stenosis (atherosclerosis) and decreased cranial blood flow. Although surrounding vessels attempt to compensate to aid in circulation, any sudden occlusion of the carotid arteries can cause permanent brain damage and death. Occlusions most often occur due to thromboembolism. Risk factors for carotid artery stenosis include hypercholesterolemia, hypertension, smoking history, and increased age.

Symptoms and Causes

Carotid artery stenosis is often asymptomatic. For those that do experience symptoms, severe pain, anxiety, hemiparesis, confusion, aphasia, and diplopia may occur. Diagnosis with a duplex ultrasound, CT, and MRA angiogram can be used to determine the location and of blockage. Pharmacologic treatment of carotid artery stenosis includes anticoagulants, thrombolytics, antihypertensives, and cholesterol-lowering statins. Carotid endarterectomy is recommended in greater than 60% of cases.

Risk of carotid endarterectomy includes increased incidence of post-procedure stroke due to plaque dislodgement and increased blood flow to the narrowed vessels. Non-invasive approaches include carotid stents/angioplasty. This disease is progressive and recurrence is high. Nurses are responsible for patient teaching regarding medication administration and appropriate lifestyle changes.

Carotid Endarterectomy

The practice of carotid endarterectomy can be used to help remove plaques that become occlusive to the vessel. In this procedure, the carotid arteries are clamped, then opened, so that the plaques can be removed. Shunts may be placed inside the vessel to ensure blood supply is maintained after the procedure is completed.

Nurses should monitor for these possible complications from this procedure:

• Hematoma— respiration difficulty, increased effort, swelling

• Hypertension— first 48 hours post-op, increased neurologic changes, hematoma

• Hypotension— resolves in 24 to 48 hours, may indicate MI

• Hyperperfusion syndrome— inadequate vasoconstriction of vessels dilated from long diminished blood flow, may cause hemorrhage edema identified by severe unilateral headache relieved by raising head

• Hemorrhage— fatal to severe impairment

• Stroke— risk of dislodged plaque forming embolus

Quick suspicion and provider notification is important to prevent long-term consequences from these possible complications. Nurses should perform frequent respiratory, cardiac, and neurologic assessments after the procedure. They should be concerned for any increased bleeding risk and immediately notify the providers if the patient experiences a severe headache.

Fem-Pop Bypass

The femoral-popliteal or Fem-Pop bypass is a treatment for severe femoral artery disease. In this disease, plaque buildup or arteriosclerosis occurs in the large lower vessels of the leg. The blockage(s) may cause intermittent claudication, lower leg pain, and tissue injury. Sometimes, this procedure will be used in the event of an aortic aneurysm to restore lower extremity perfusion. In the Fem-Pop bypass procedure, another vessel—usually the saphenous vein or synthetic graft—is taken and sewn above and below the blocked vessel to bypass the blockage and restore circulation to the lower part of the extremity.

An alternative option to the Fem-Pop bypass is an embolectomy to remove the clot. In the event of an aortic aneurysm, the operating team may first try to repair the vessel with a vascular or Dacron graft. However, depending on the extent of vessel damage and the location, a Fem-Pop bypass may still be the preferred intervention. Nursing considerations following any of the previously listed interventions include controlling blood pressure to protect the patency of the grafts, vascular circulation assessment, monitoring the integrity of the dressings, and frequent neurologic function and renal function assessments.

Compartment Syndrome

Compartment syndrome occurs when there is an increase of pressure within a grouping of muscles, nerves, and blood vessels. It usually occurs after a fracture (usually a long bone) or crushing syndrome. It may also occur with rhabdomyolysis. Signs of compartment syndrome include intense pain, decreased sensation, paresthesia, firmness at site, pallow, and pulselessness (late sign).

Risks

Without treatment, decreased or absence of blood flow to the distal tissues will cause tissue injury and death. Diagnosis of this syndrome includes assessment of the tissues and intra-compartmental pressure measurement. Treatment goals are decompression of the inflamed tissues with restoration of perfusion with a fasciotomy.

Assessment

Nurses should closely monitor patients at high risk for compartment syndrome, including those with circumferential burns, long-bone fractures, new casts, and large open wounds, including open abdomen closures. For those patients who received perfusion-restoring fasciotomies, nurses should monitor closely for continued distal perfusion, infection risk, and neurologic intactness of the affected extremity.

Medications

Several medications can be used to prevent and treat acute peripheral insufficiency. Two common medication classifications that are used to improve perfusion and reduce the risk of vascular occlusion include anticoagulant agents and smooth muscle relaxants.

Anticoagulant Agents

Anticoagulants help to prevent clot formation. Patients are often prescribed these medications in response to or prevention of thromboembolism, MI, or stroke. Nurses should monitor for increased risk of bleeding for patients on these medications. Prior to invasive procedures, patients may be asked to stop this medication for a specific amount of time.

• Aspirin: prophylaxis; do not give to children or adolescents as it poses an increased risk of Reye’s syndrome

• Warfarin (Coumadin®): blocks the body’s uptake of vitamin K; patients need routine blood work to monitor for anticoagulant effects; antidote to overdose is vitamin K administration

• Heparin: primarily used for IV anticoagulation; monitored labs include aPTT or anti-Xa; monitor for adverse reaction of heparin induced thrombocytopenia (HIT); antidote to overdose is protamine sulfate.

• Dalteparin (Fragmin®) and Enoxaparin (Lovenox®): used in DVT prophylaxis, unstable angina, MI, and cardiac surgery

• Bivalirudin (Angiomax®): used for prophylaxis and in the event of HIT

Glycoprotein IIB/IIIA inhibitors also prevent clot formation by blocking the platelet binding cascade. These are most commonly used in addition to anticoagulant therapy, especially after invasive cardiac procedures (percutaneous coronary intervention) and in acute coronary syndrome. Do not administer these medications in patients with current bleeding or decreased platelet counts.

• Abciximab (ReoPro®): decreases platelet binding for 48 hours

• Eptifibatide (Integrilin®): decreases platelet binding for six to eight hours

• Tirofiban (Aggrastat®): reduced dosage indicated for those with renal function concerns; decreases platelet binding for four to eight hours

Smooth Muscle Relaxants

Smooth muscle relaxants help to decrease vascular resistance by dilating both arterial and venous peripheral vessels. Side effects of these medications include hypotension and headaches. The most common medications in this classification include: sodium nitroprusside (Nipride®), nitroglycerin (Tridil®), and hydralazine (Apresoline®).

Acute Pulmonary Edema

Acute pulmonary edema occurs when there is excess fluid in the lungs, causing a buildup of fluid in the alveoli, decreasing the oxygen movement through the lungs, and subsequently increasing respiratory effort. It most often occurs in light of congestive heart failure but can also occur in patients with pneumonia, toxin exposure, adverse drug reactions (cocaine, heroin, aspirin), chest trauma, and high elevation.

Symptoms

Onset of this condition is usually sudden, with symptoms such as extreme shortness of breath, feeling of suffocating or drowning that is worse when lying down, wheezing, cold/clammy skin, anxiety, tachycardia, cyanosis, and frothy pink sputum.

Diagnosis and Treatment

Patient exam may identify abnormal heart sounds, lung rales, tachycardia, and tachypnea. Diagnostic testing of this condition includes ECG, echocardiogram, and chest x-ray. Pulse oximetry testing should be implemented to monitor for hypoxia. Treatment includes placing patients in high Fowler’s position with 100% oxygen administered via face mask or nasal cannula to achieve a PO2 of greater than 60%. In some cases, positive end-expiratory pressure (PEEP) by way of BiPaP or intubation may be indicated to help open the airways, recruit the alveoli, and help with redistribution of the liquid within the lung. Diuretic medications help to alleviate extra fluid from the body. Pain should be controlled with analgesic medications such as morphine sulfate 2 to 8 mg IV every two to four hours to decrease preload and anxiety. If not treated in an efficient manner, pulmonary edema may result in death.

Ruptured or Dissecting Aneurysm

Aneurysms are the weakening or enlarging of an arterial wall. They may be caused by cardiac disease (hypertension and arteriosclerosis) or by anatomical/genetic defects (connective tissue disorders, Marfan syndrome, Ehlers-Danlos disease). They are often asymptomatic. Aneurysms can happen along any artery; however, the most common locations include arteries of the brain, heart, and descending aorta (abdomen). Without immediate treatment, a ruptured aneurysm has a high mortality rate.

Diagnosis

Diagnostic testing for aneurysm includes x-ray, CT, MRI, cardiac catheterization, and transthoracic echocardiogram. With this testing, aneurysms can be classified by their location and severity. The DeBakey classification system uses anatomic location as the key identifier to the type of aneurysm. In this system, three types of abdominal aneurysm exist. Types I and II are considered thoracic aneurysms. In Type I, the aneurysm begins in the ascending aorta but may extend all the way to the descending aorta. Type II is restricted to just the ascending aorta. Type III is restricted to the descending aorta and is considered an abdominal aneurysm.

Treatment

The goal in treating aneurysms is early diagnosis and preventing rupture. After the aneurysm ruptures, the risk of mortality increases significantly. Rupture prevention measures include anti-hypertensives such as beta-blockers (esmolol) or alpha-beta-blocker combinations (labetalol) to reduce the force of blood leaving the heart; surgical repair (especially in Types I and II); and if necessary, intubation and ventilation with sedation to control hemodynamics and anxiety/pain.

If deemed necessary, one of two surgical procedures will be performed: open repair or endovascular repair. In open repair, a patient is placed on cardiopulmonary bypass and the section of damaged vessel is removed and replaced with a graft. In endovascular repair, the affected part of the aorta is stented to prevent further damage to the weakened vessel. The nurse should monitor for and educate patients regarding potential complications (now and in the future) such as myocardial infarction, acute renal injury, hemorrhage, and future or re-rupture of the affected vessel.