Cardiac Review, An Issue of Critical Care Nursing Clinics - E-Book

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This issue of Critical Care Nursing Clinics, Guest Edited by Bobbi Leeper, MN, RN, CNS M-S, CCRN, at Baylor University Medical Center, provides review of Cardiac topics for the practicing nurse. Article topics include: Spectrum of Acute Coronary Syndromes; Mechanical Complications of AMI; Glucose Control in the Cardiovascular Patient; Pulmonary Hypertension; Pulmonary Problems in the Patient with Cardiovascular Disease; Stroke Coronary Artery Bypass Surgery; Surgery on Thoracic Aorta; Heart Valve Surgery; Complications of Cardiac Surgery; Electrolyte Disorders in the Cardiac Patient; and Cardiogenic Shock.

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Published 28 December 2011
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Cardiovascular Review, Vol. 23, No. 4, December 2011
I S S N : 0899-5885
d o i : 10.1016/S0899-5885(11)00064-5
C o n t r i b u t o r sCritical Care Nursing Clinics of North America
Cardiovascular Review
GUEST EDITOR: Bobbi Leeper, MN, RN, CNS, CCRN, FAHA
Cardiovascular Services, Baylor University Medical Center, 3500 Gaston Avenue,
Dallas, TX 75246, USA
CONSULTING EDITOR: Janet Foster, PhD, RN, CNS
ISSN 0899-5885
Volume 23 • Number 4 • December 2011
Cardiovascular Review, Vol. 23, No. 4, December 2011
ISSN: 0899-5885
doi: 10.1016/S0899-5885(11)00065-7
Contents
Contributors
Forthcoming Issues
Preface
Acute Coronary Syndrome
Acute Coronary Syndrome: New and Evolving Therapies
Coronary Artery Bypass Surgery
A Journey Through Heart Valve Surgery
Cardiogenic Shock
Pulmonary Issues in Acute and Critical Care: Pulmonary Embolism and
Ventilator-induced Lung Injury
Electrolyte Disorders in the Cardiac Patient
Pulmonary Arterial Hypertension
Comprehensive Care of Adults with Acute Ischemic Stroke
Diabetes and Cardiovascular Disease
IndexCardiovascular Review, Vol. 23, No. 4, December 2011
ISSN: 0899-5885
doi: 10.1016/S0899-5885(11)00066-9
Forthcoming IssuesCardiovascular Review, Vol. 23, No. 4, December 2011
ISSN: 0899-5885
doi: 10.1016/j.ccell.2011.10.002
Preface
Barbara “Bobbi” Leeper, MN, RN-BC, CNS M-S, CCRN
Bobbi.Leeper@baylorhealth.edu,
Cardiovascular Services, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX
75246, USA
Barbara “Bobbi” Leeper, MN, RN-BC, CNS M-S, CCRN Guest Editor
This issue of Critical Care Nursing Clinics provides a comprehensive review and
update of some of the signi0cant cardiovascular disease patient issues we are dealing
with today. We know that cardiovascular disease is a major health problem not only for
the United States but globally, representing a signi0cant 0nancial burden. The content
in this issue addresses clinical practice related to the patient with cardiovascular
disease. The issue begins with a review of acute coronary syndromes and a brief review
of the atherosclerotic process followed by important aspects for the management of
angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation
myocardial infarction. The next article brings us forward with new and evolving
therapies for acute coronary syndromes. For those patients who require a surgical
intervention, there is an overview of coronary artery bypass surgery, which is helpful for
those who do not routinely care for these patients. Heart valve surgery is discussed
beginning with where we are today and transitioning to invasive transcatheter aortic
valve replacement, which is likely to become standard practice as technology evolves.
General topics that are always a challenge when caring for the patient with
cardiovascular disease are cardiogenic shock, pulmonary issues focusing on pulmonary
embolism and ventilator-induced lung injury, electrolyte disorders, and glucose control.
The latest information about caring for a patient with pulmonary hypertension is
provided as well as information about comprehensive care of adults with ischemic
stroke. Many facilities are seeking certi0cation for stroke. This article provides key
information related to that process.;
It is hoped that the readers of this issue will 0nd content within that will help them
in some aspect of their practice, whether they are pursuing certi0cation, looking for
articles to help with orienting new sta to a cardiac ICU, or searching for
evidencedbased practices. There's something in this issue for almost every nurse caring for a
patient with cardiovascular disease.Cardiovascular Review, Vol. 23, No. 4, December 2011
ISSN: 0899-5885
doi: 10.1016/j.ccell.2011.10.001
Acute Coronary Syndrome
a,*Barbara Leeper, MN, RN-BC, CNS M-S, CCRN
Bobbi.Leeper@baylorhealth.edu, Alaina M. Cyr, BSN, RN,
b,c bCAPA, NE-BC , Christa Lambert, BSN, RN, CEN , Kimberlee
bMartin, RN
a Cardiovascular Services, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX
75246, USA
b The Heart Hospital Baylor Plano, 1100 Allied Drive, Plano, TX 75093, USA
c College of Nursing, The University of Texas at Arlington, 411 South Nedderman Drive,
Arlington, TX 76019, USA
* Corresponding author
Keywords
• Acute coronary syndrome • Coronary • ST-segment elevation myocardial infarction •
Angina • Heart • Cardiac
At present, cardiovascular disease a, ects 82.6 million Americans, with more than 8
million Americans experiencing a myocardial infarction (MI) annually. More than
1800,000 will succumb to the e, ects of cardiovascular disease. Although the death rate
attributable to cardiovascular disease has declined, it is still the primary cause of death
1in the United States, accounting for approximately 34% of all deaths. According to the
American Heart Association, an American dies from cardiovascular disease every 39
1seconds. A recent policy statement from the American Heart Association predicted
40.5% of the population in the United States will have some form of cardiovascular
2disease, including hypertension, coronary heart disease, heart failure, or stroke.
Mortality from cardiovascular disease is estimated to reach 23.4 million by the year
2030. Annually in the United States, an estimated $165.4 billion in direct and indirect
2costs of cardiovascular disease are realized, with projections of $818 billion in 2030.
Hospital emergency departments are inundated on a daily basis with patients
presenting with a variety of symptoms. Patients presenting with cardiac symptoms are
in need of rapid assessment, diagnosis, and treatment. The following content describes
the spectrum of acute coronary syndrome (ACS), management of ACS, and secondary
prevention strategies.Overview of Atherosclerosis
Acute coronary syndrome (ACS) represents a spectrum of the atherosclerotic process
including unstable angina, non-ST-segment elevation MI (NSTEMI), and ST-segment
elevation MI (STEMI). It is associated with increased risk of acute myocardial infarction
3(AMI) and cardiac death. These life-threatening disorders are a major cause of
emergency care and hospitalization in the United States.
Although other conditions may lead to the development of angina, the most
common cause is atherosclerosis. Atherosclerosis is a disease of the medium and large
arteries. The earliest manifestation of atherosclerosis begins in childhood and is
characterized by the presence of fatty streaks in the walls of the arteries. The
atherosclerotic process begins with injury to the endothelial cells lining the artery.
In; ammation ensues, with the accumulation of lipids, cholesterol, calcium, and cellular
debris within the intima of the vessel wall. Over time, this process leads to the buildup
of these materials protruding into the lumen of the coronary artery, forming an
advanced lesion called “> brous plaque” that usually appears in early adulthood and
4progresses with age. Unless the plaque ruptures, the patient can remain asymptomatic
for a long time. If the plaque ruptures, the platelets become activated and aggregate at
the site of the rupture. The intrinsic clotting cascade is activated, resulting in the
formation of a thrombus at the site that may cause either > xed occlusion of the vessel or
intermittent occlusion. Over time, the thrombus is resorbed and the plaque continues to
enlarge. This process may be repeated several times until there is signi> cant obstruction
of the coronary artery leading to the onset of symptoms.
The plaque may be described as stable or unstable. The stable plaque does not
rupture but continues to increase in size, eventually reducing blood ; ow and leading to
the development of angina. The unstable plaque is also referred to as a vulnerable
plaque that is prone to rupture. Triggers for plaque rupture have been found to have a
circadian rhythm, occurring more often in the morning. Plaque rupture is also
associated with seasonal variation, speci> cally in the winter, and is often associated
with emotional stress or exertion.
Signs and Symptoms
The patient begins experiencing symptoms when the coronary artery becomes so
narrowed that blood supply is insuA cient to meet the metabolic demands of the cardiac
muscle cells, causing ischemia of the myocytes. The symptoms often begin with
exertion, which can be in the form of emotional or physical stress. The typical signs and
symptoms may include discomfort in the jaw, neck, one or both arms, chest tightness or
heaviness, and complaints of shortness of breath. It is important for the clinician todi, erentiate the signs and symptoms associated with angina from those associated with
AMI. Refer to Box 1 for additional signs and symptoms associated with angina and
AMI. A patient experiencing angina will usually have resolution of the discomfort with
termination of exertion or after administration of nitroglycerin. The patient
experiencing an AMI will have discomfort or pain lasting longer than 20 minutes that
usually is not relieved by nitroglycerin. Other signs may include diaphoresis, nausea
and vomiting, tachycardia, and shortness of breath. Patients may also report a feeling of
3impending doom or general feeling of not being well. Women in the throes of
experiencing an MI may not have complaints of chest discomfort. Instead, they are
likely to have more subtle symptoms such as fatigue and indigestion. The symptom of
dyspnea should not be overlooked. Studies have shown self-reported dyspnea in patients
undergoing stress perfusion testing was an independent predictor of cardiac and total
mortality. The risk of sudden cardiac death was increased fourfold even when patients
5had no prior history of coronary artery disease.
Box 1 Signs and symptoms associated with angina and AMI
Anginal Equivalent:
Resolve with rest OR nitroglycerin
Pain or discomfort
Jaw
Neck
Ear
Arm
Epigastric
Shortness of breath
Acute MI:
Symptoms last longer than 20–30 minutes
Typical
Tightness
Chest pain or pressure
Squeezing
Heaviness
Usually lasts longer than 20–30 minutes
Usually unrelieved by nitroglycerin
May radiate
Down one or both arms
Jaw
Neck
Back
Shoulder(s)Possible associated signs and symptoms
Dyspnea
Diaphoresis
Nausea
Vomiting
Light-headedness
Syncope
It is important to keep in mind that not all patients with myocardial ischemia
3experience chest discomfort. The Framingham Study revealed that in as many as half
of all patients experiencing an MI the symptoms may be clinically silent and
6unrecognized by the patient. A study looking at patients in the National Registry of
Myocardial Infarction (NRMI) found that nearly one-third of patients with con> rmed
MI had symptoms other than chest pain when presenting to the hospital. When the
investigators looked at those MI patients without chest discomfort, the patients were
7more likely to be older, female, and have diabetes or heart failure or both. The
investigators found MI patients without chest pain delayed longer before going to the
hospital (mean, 7.9 hours vs 5.3 hours). They were less likely to be diagnosed with an
MI on admission (22.2% vs 50.3%) as well as receive evidence-based interventions
including thrombolysis or a percutaneous coronary intervention (PCI), aspirin (ASA),
7beta blockers, or heparin. Patients with “silent” MIs were 2.2 times more likely to die
during their hospital stay, with an in-hospital mortality rate of 23.3% when compared
to 9.3% for those with a “symptomatic” MI. Clinicians should be cautious to avoid
8allowing the severity of pain to be a factor in evaluating patients with ACS.
Unstable Angina
Unstable angina is present when there is progression from a stable coronary artery
disease state to an unstable disease state. There are three classi> cations of unstable
angina: (1) angina at rest; (2) new onset angina (<2 _months29_3b_="" and=""
_28_329_="" increasing="" angina="" that="" increases="" in="" _intensity2c_=""
3_duration2c_="" or="" _frequency2c_="" all="" of=""> Unstable angina can progress
to NSTEMI and STEMI if left untreated. Unstable angina does indicate a reduction in
the blood ; ow in the coronary arteries typically caused by a rupture of atherosclerotic
9 11plaque, leading to thrombus formation. – Studies have shown the average patient
experiencing unstable angina delays seeking medical attention as much as 2 hours after
3symptom onset. A common reason stated by patients for treatment delay is that they
expected to have severe crushing chest pain, which is in contrast to what they actually
3were experiencing.Unstable angina is diagnosed after STEMI and NSTEMI are ruled out in patients
presenting with signs or symptoms of myocardial ischemia. The electrocardiogram
(ECG) in patients with unstable angina may demonstrate transient ST-segment
depression that develops during the ischemic episode and resolves when the patient's
symptoms subside. The cardiac biomarkers will remain within normal limits in patients
with unstable angina.
NSTEMI
NSTEMI results when the coronary artery is partially occluded causing myocardial cell
death. This type of MI occurs more frequently than STEMI. These patients will
demonstrate a minor elevation of their cardiac biomarker. Their ECG will demonstrate
3,10,12abnormal ST-segment depression or prominent T-wave inversion or both. Fig. 1
is an example of a NSTEMI. Patients with a NSTEMI will not go on to develop
STsegment elevation on their ECG.
Fig. 1 NSTEMI. Note the prominent T-wave inversion in leads V2 through V5 and leads
I and avL indicative of an anterior lateral infarction. This ECG was recorded on a
68year-old woman within 6 minutes of arriving at the emergency department.
STEMI
STEMI occurs when there is an abrupt and complete occlusion of the coronary artery
causing acute ischemia. STEMI is the most serious form of ACS with the highest rate of
13mortality. The classic > nding on the ECG is ST-segment elevation (Fig. 2). The
cardiac biomarkers are elevated above normal, and in some cases can be linked to the
timing of the acute closure of the vessel.Fig. 2 STEMI from a 54-year-old man upon presentation to the emergency
department. Note the elevated ST-segments in leads II, III, and avF.
Management of ACS
Patients arriving at the emergency department triage desk should be rapidly assessed
for signs and symptoms of ACS and immediately taken to a room. A 12-lead ECG should
be obtained quickly and interpreted in a timely manner. This is vital to identi> cation of
14patients in need of reperfusion treatment. Guidelines recommend obtaining an initial
ECG within 10 minutes of presentation and continuous ECG monitoring for patients
13with suspected STEMI.
Cardiac biomarkers should be drawn and sent to the laboratory as soon as possible.
The biomarkers are useful for diagnosing/correlating with time of symptom onset.
When the cardiac myocytes are ischemic for a sustained period of time, the cell
membranes lose their integrity and macromolecules will di, use out into the circulation
and eventually become detectable. The common biomarkers used in clinical practice
include the serum troponin I and T, and creatine kinase MB (CK-MB). The CK-MB is the
> rst to rise, usually within 3 to 6 hours of symptom onset. It is followed by troponin I
and T. Evaluation of serum troponin I is very cardiac speci> c and one of the best
indicators for myocardial injury. Troponin I begins to rise within 3 to 6 hours after
15symptom onset and peaks at 12 hours. One of the advantages of troponin I for
diagnosis of AMI is that it will remain elevated for as long at 5 to 10 days after the MI.
This is useful for diagnosing an MI in patients who may delay coming to the hospital for
as long as 3 to 4 days.
Management of Patients With ACS
Management of ACS begins at the initial point of contact with a health care provider
13and should be based on predetermined written protocols. The management of ACSincludes pain relief, early reperfusion, use of antiplatelet therapy and anticoagulants,
controlling the risk factors, and secondary prevention. There are similarities in the
management of patients with ACS, but there are also di, erences. Each is discussed in
the following section.
Unstable Angina/NSTEMI
The management of patients experiencing unstable angina/NSTEMI should have two
immediate goals including the immediate relief of chest discomfort and prevention of
serious adverse outcomes. The achievement of these goals includes the initiation of
antiischemic therapy, antithrombotic therapy, and invasive procedures. Patients with
ongoing symptoms should be admitted to a coronary care unit for closer monitoring and
3ready access to PCI. Those who are asymptomatic after interventions have been found
to do well on cardiac telemetry units with continuous ECG monitoring.
The standards indicate the administration of oxygen as well as restricted activity
levels will increase oxygen delivery to the myocardium and reduce cardiac workload.
Morphine is administered intravenously and titrated according to response to provide
pain relief. The typical dosage is 2 to 4 mg intravenously (IV) with increments of 2 to 8
mg IV repeated at 5- to 15-minute intervals. Morphine works directly on the nervous
system to reduce anxiety and lessen the autonomic responses such as diaphoresis
associated with MI. In addition, morphine has a slight e, ect on dilation of the coronary
16arteries to increase oxygen supply to the cardiac tissue.
Anti-ischemic therapy includes the administration of nitroglycerin IV, sublingually,
or by nasal spray. Nitroglycerin dilates the venous bed and increases venous pooling,
thus reducing venous return (preload) to the heart. This contributes to a further
reduction of myocardial work, restoring the balance between oxygen delivery and
oxygen demand. Nitro spray is short acting with e, ects lasting up to 30 minutes. The
16sublingual route is preferred owing to the avoidance of metabolism in the liver.
Nitrates should not be administered if the systolic blood pressure is less than 90 mm Hg
or to patients who have received a phosphodiesterase inhibitor for erectile dysfunction
13in the last 24 to 48 hours.
Antiplatelet medications work to prevent thrombus formation and reduce the risk
of subsequent MI, stroke, and death. Currently, aspirin and clopidogrel are the most
17often used antiplatelet medications. Aspirin is recommended for all patients
presenting with signs and symptoms of ACS. Patients should be given 325 mg of aspirin
orally upon presentation of chest discomfort if there are no contraindications. Having a
patient chew the aspirin allows for a more rapid buccal absorption. Aspirin inhibits the
formation of thrombus by inhibiting thromboxane A production. The administration of2
aspirin as a > rst-line treatment decreases the rate of cardiovascular death by up to onehalf. The ongoing usage of aspirin is recommended for patients who have su, ered a
13,17cardiac event if there are no contraindications.
The use of clopidogrel, in addition to aspirin, is part of the standard regimen for
NSTEMI patients. Clopidogrel works to block adenosine diphosphate receptor sites,
preventing platelet aggregation. Adenosine diphosphate is produced by platelets and
18attaches to receptor sites on the surface of platelets to promote platelet aggregation.
Another class of platelet inhibitors is the glycoprotein IIbIIIa inhibitors. These
primarily include abciximab (Reopro) and epti> batide (Integrilin). These medications
may be initiated before a PCI, and in some cases are continued for several hours after
16the interventional procedure. Their primary e, ect is to inhibit platelet aggregation
and prevent abrupt vessels closure, especially after a stent has been deployed.
Anticoagulation is a > rst-line therapy for NSTEMI and unstable angina.
Anticoagulation therapy is utilized in STEMI in conjunction with other interventions.
Anticoagulants include heparin and enoxaparin, a low molecular weight heparin.
Heparin reduces thrombus formation by blocking thrombin production. Low molecular
weight heparin such as enoxaparin is administered subcutaneously and does not require
19,20laboratory monitoring. Bleeding is a potential complication of anticoagulation
therapy. Reducing the risk for bleeding is accomplished through weight-adjusted
dosing, modi> ed dosing in patients with renal dysfunction, or selection of an alternate
20therapy in patient at higher risk for bleeding.
Early beta blockade has been shown to reduce mortality and recurrent MIs. Beta
blockers decrease myocardial oxygen consumption. Short-acting beta blockers such as
metoprolol are used initially if there are no contradictions. Long-acting beta blockers
decrease the heart rate and contribute to reducing oxygen demands of the cardiac
muscle. Beta blockers are the only class of drugs that have been shown to reduce the
incidence of sudden cardiac death after MI. It is important that the beta blocker be
initiated while the patient is hospitalized rather than wait to start it during a follow-up
visit with the health care provider. A delay in initiation (after discharge) has been
shown to be less e, ective in reducing sudden cardiac death. Calcium channel blockers
15are used in patients who may not tolerate or have contraindications to beta blockers.
Angiotensin-converting enzyme (ACE) inhibitors should be initiated within the > rst
24 hours after an MI, particularly if the left ventricular ejection fraction is less than
40%. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II.
Angiotensin II causes peripheral vasoconstriction and is thought to contribute to the
development of hypertrophy of the myocytes adjacent to the infarcted tissue, which
may contribute to the development of a ventricular aneurysm after MI. Side e, ects of
ACE inhibitors include hypotension, cough, and angioedema. Angioedema refers to
swelling of the lower portion of the face externally or can involve the oropharynx,compromising the patient's airway. Patients should be monitored for this potentially
life-threatening side e, ect regularly. ACE inhibitors may prevent the development of
16ventricular hypertrophy and ventricular aneurysm.
STEMI
The American Heart Association/American College of Cardiology (AHA/ACC) standards
for the management of acute STEMI recommend immediate reperfusion once the
diagnosis of STEMI is made. Reperfusion strategies include the use of > brinolytics or
primary coronary intervention. Nielsen and colleagues examined the e, ects of system
21delay and timing of interventions for AMI. They found system delays contribute to
incremental increases in 30-day and 8-year mortality for both > brinolysis and primary
PCI. If primary PCI was achieved within 2 hours, mortality rates were lower when
compared to early > brinolysis. System delays for primary PCI greater than 3 hours was
associated with similar mortality when > brinolysis was administered within 1 to 2
hours. The investigators concluded primary PCI is preferred to early > brinolysis up to 2
hours after the > rst contact with a health care provider. One also must consider
21individual patient characteristics.
The AHA/ACC standards clearly state that patients presenting with STEMI to a
facility without the capability for timely intervention with PCI within 90 minutes should
13undergo > brinolysis. The > brinolytic should be administered within 30 minutes of
arrival to the emergency department. The common agents used currently include
retaplase and tenectplase. Both can be administered IV in single doses. Their ease of
administration has replaced the administration of a 90-minute infusion of atelplase for
the acute management of STEMI.
Early reperfusion through PCI reduces mortality by 25% and is the treatment of
18,19choice, as indicated previously. Mechanical reperfusion using primary PCI should
13occur within 90 minutes of presentation to the hospital (door-to-balloon time). This
usually occurs in the form of balloon angioplasty. A stent may be inserted to maintain
the patency of the vessel. Successful reperfusion has occurred when there is at least a
1350% reduction in ST-elevation. A recent report demonstrated a decline in
door-to22balloon time from a median of 96 minutes to 64 minutes from 2005 to 2010. Patients
who do not achieve successful reperfusion with PCI may need a coronary artery bypass
grafting (CABG).
Implications for Nursing
STEMI patients should be admitted to a unit that has continuous ECG and pulse
oximetry monitoring and the ability for hemodynamic monitoring such as a coronary