Cardiovascular Notebook
Cardiovascular Notebook
Cardiovascular Notebook
Inside:
• Module Outline
• Lesson Objectives
• Lesson Summary
• Lesson Resource Files
• Lesson Practice Pearls
2
Module Outline
Module 2 - Care of the Patient with Cardiovascular Disorders
• Conduction System
Introduction
In this lesson, we will discuss the structures and functions of the heart. We will review the conduction system, the circulatory
system, electrophysiology of the heart, and the cardiac cycle. Finally, we'll discuss cardiac output and autoregulation.
Heart Muscle
• Has 3 layers (epicardium, myocardium, and endocardium) and a surrounding sac called the pericardium
• Location: In the mediastinum, above the diaphragm, and is surrounded on both sides by lung
• Shape: Resembling triangle, with base parallel to the right edge of the sternum
Heart Chambers
• The right side of the heart is a low pressure system and the left side is a high pressure system and each side has an atrium
and ventricle.
• Here is the Right Atrium (RA,) Right Ventricle (RV,) Left Atrium (LA,) Left Ventricle (LV,) and the Medial Wall separating the
RV and LV.
Valves
• The heart contains the two atrioventricular valves (AV) and two semilunar valves as well as the Chordae Tendineae and
the Papillary Muscles
• AV valves are Tricuspid Valve and Mitral Valve
• Semilunar valves are Pulmonic Valve and Aortic Valve
• Chordae Tendineae and Papillary Muscles work together to prevent valve leaflets from turning inside out.
SA and AV Nodes
• SA Node is the major pacemaker of the heart. It keeps intrinsic heart rate at 60100 bpm
• The AV Node receives impulse from atria and slows it down before sending to ventricles. This slowing is done in order to
allow time for ventricular filling from the atrial contraction. Is capable of generating its own impulse if doesn’t receive one
(Automaticity.) Intrinsic rate is 40-60 bpm.
Bundle of His
• Bundle of His is point where impulse divides into the right and left bundle branches and further proceeds on to the Purkinje
fibers
• A blockage in a bundle branch shows up on an ECG
• Bundle of His and Bundle Branches can together act as an escape pacemaker for the heart with an intrinsic rate of 20-40
bpm.
Coronary Arteries
• There are two main ones.
• They supply oxygenated blood to the heart.
• The main or “dominant” one of the two is usually the right coronary artery.
Coronary Venous
• Two thirds of coronary blood flow occurs during diastole.
• Coronary arteries dilate up to fourfold to increase the supply of oxygen if/when there is an increased need.
Capillaries
• Capillaries:
• Tiny, one-cell thick vessel networks
• Responsible for the exchange of cellular nutrients and the removal of cellular waste products
• Veins:
• Act as volume reservoirs to the circulatory system
• Return blood to the heart
• About 50% of blood volume is in the veins
Introduction
In this topic we look at myocardial cells, the contracting unit of the myocardium. We look at a single contraction from
beginning to end.
Myocardial Cells
• Myocardial cells are responsible for the contracting action of the heart.
• Cardiac muscle is composed of muscle fibers made up of myofibrils, each myofibril a series of sarcomeres. Sarcomeres
are made up of protein filaments myosin (thick) and actin (thin.)
• Contraction produced as myosin’s “cross bridges” reach out and pull actin in toward the sarcomere’s center.
• Contraction produced as myosin’s “cross bridges” reach out and pull actin in toward the sarcomere’s center.
• The release of calcium at the beginning of a contraction, and the attaching of calcium to troponin, allow these cross bridges
to form and the contraction to occur. By contrast, the uptake of calcium then causes a relaxation of the cardiac muscle.
Cardiac Output
• Is L/min of blood ejected from the heart over a single minute
• Normal range is 4-8 L/min
• Is heart rate times stroke volume
• Cardiac index is CO divided by the patient’s body surface area
Starling’s Law
• Describes the relationship between contractility and overall cardiac function
• The longer the stretch on the myocardium (the more you stretch a rubberband, for example,) the stronger the contraction
(the harder it snaps.)
Starling’s Curve
• Describes the principle governing the balance between preload and afterload, the principle being the dependent
relationship between increased stretching and increased pressure of the myocardial fibers: The greater the stretch of the
muscle or cross bridging of the actin and myosin, the greater the force of contraction, up to the point of too much stretch,
then decompensation occurs. After the curve peaks, CO drops, the overworked heart yields, and a steady decline in the
curve occurs. Result is patients become fatigued with accompanying peripheral hypotension, dyspnea, pulmonary
congestion, and edema.
Stroke Volume
• The amount of blood (mL) pumped by the ventricle with every systolic contraction/beat
• Normal range is 50-100 mL/beat
• To understand the hemodynamics of the heart one must understand how SV is affected by preload, afterload, and
contractility
Preload
• Is the volume of blood in the ventricle at the end of diastole
• The most important component of SV
• Is affected by many things: absolute blood volume, how well the blood volume is distributed throughout the body, the atrial
contribution, ventricular function, and ventricular compliance.
• Right and left ventricular preloads are measured differently
Afterload
• Is the resistance to ventricular ejection; in other words, the tension or resistance in the arterial system that the ventricle
must overcome in order to eject the blood into the systemic circulation. Put even more simply, how hard the heart has to
work to pump the blood into the pulmonary or systemic circulation.
• Right and left ventricular afterloads are measured differently: PVR and SVR
• Is affected by many things from vascular volume to the presence of ventricular outflow obstructions
Contractility
• The ability of the heart to pump or the force with which the heart contracts
• Is determined by the vigor of the ventricular wall contraction
Introduction
In this topic we explore how the important role played by the autonomic nervous system in heart function. The autonomic
nervous system, which includes the sympathetic and parasympathetic nervous systems, controls the heart and blood
vessels. We also look at the roles played by chemoreceptors, baroreceptors, and the kidney in heart function.
Renal Perfusion
• The kidneys play an important role in regulating blood pressure: If blood pressure drops, a decrease in perfusion of the
kidney occurs. This drop, in turn, stimulates the renin-angiotensin mechanism in order to restore adequate blood flow.
Ultimately, both blood pressure and blood flow to the kidneys are increased
• Playing a role in the restoration of blood pressure: renin, angiotensinogen, angiotensin I, angiotensin II, antidiuretic
hormone (ADH,) and aldosterone
Indicative Reciprocal
Type Artery Complications Associated
Leads Leads
AV blocks, ↓ HR Papillary muscle
Inferior RCA II, III, aVf I, aVL, V5, V6 rupture, ↓ BP, N/V, hiccups
Septal LAD V1, V2 II, III, aVF VSD
2nd degree Type 2 block, RBBB, LAHB,
Anterior LAD V3, V4 II, III, aVF Complete Block
Lateral LCx, LAD I, aVL II, III, aVF Ventricular Aneurysm
Apical LAD, RCA, LCx V5, V6 II, III, aVF Ventricular Aneurysm
RVI RCA V3r, V4r RV failure, AV block
V1, V2
Posterior RCA, LCx None reciprocal AV blocks, bradychardia
15
Cardiac output (CO) is defined as the volume of blood ejected from the heart over 1
minute, and is referred to in liters per minute. Normal CO ranges from 4 to 6 L/min.
Determinants of CO are heart rate and stroke volume. Stroke volume is the volume of
blood ejected from the left ventricle with each ventricular contraction. The equation is
CO = heart rate x stroke volume. Therefore, if either the heart rate or the stroke volume
increases or decreases on the right side of the equation, CO on the left side will
increase or decrease accordingly.
The cardiac index relates the cardiac output to the patient's body surface area. To
measure the cardiac index, divide CO by the patient’s body surface area.
17
Stimulates Adrenal
Glands
Stimulates Posterior
Pituitary
18
Practice Pearls
Heart Muscle
Normally the cavity between the pericardial layers contains 10 – 30 mL of serous fluid.
A pericardial effusion occurs if additional blood or fluid collects in this space. If the
amount of fluid continues to increase and cardiac chamber filling is impeded, cardiac
tamponade results.
Valves
The valve leaflets form a parachute that helps prevent prolapse of the leaflets into the
atria during ventricular contraction. The closing of the valves produces the "lub-dub"
sounds heard when the heart is auscultated using a stethoscope.
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Coronary Venous
Patients with cardiovascular disease (CVD) or coronary artery disease (CAD) have fixed
lesions that cannot dilate to meet the increase demands. The disparity in supply and
demand can lead to angina, coronary dysfunction, and infarct.
Capillaries
In shock, the precapillary sphincters dilate and postcapillary sphincters constrict in an
attempt to supply cells with more needed nutrients due to reduced blood supply.
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Contractility
Two terms used to describe contractility are inotropy and inotropic state. Positive
inotropy strengthens the action of the heart muscle, whereas negative inotropy lessons
the contractility of the muscle.
Lesson 2
Assessing the Cardiovascular
System
Included in this Lesson:
• Cardiovascular Assessment
• Auscultation
Introduction
In this lesson we discuss assessing the cardiovascular system. Your accurate assessment of the critically ill patient’s
cardiovascular system allows you to quickly identify any alterations that may complicate the patient's recovery. A complete
assessment focuses not only on the heart—but on the arterial and venous systems as well—and includes an interview,
physical exam, and diagnostic testing.
Initial Interview
• Depth of interview depends on how critically ill patient is.
• Speaking patients should be asked for certain information.
• A family history may be helpful.
Symptoms
• Most common symptoms in cardiovascular system pathology include chest pain, shortness of breath, nocturia, cough,
fatigue, syncope, dependent edema and leg pain
• Your assessment becomes even more important in patients that cannot speak/communicate their symptoms to you.
Chest Pain
• The most frequent cardiovascular complaint
• Not just degree of pain but a detailed description of pain necessary
Dyspnea
• Can be indicative of cardiovascular problems or respiratory problems; important to identify the correct origin. This includes
questions about frequency and duration of episodes, what makes it worse, and accompanying symptoms.
Physical Assessment
• Provides objective data to confirm information obtained in interview
• Three modes of assessment: inspection, auscultation, and palpation
General Appearance
• The “assessment/physical assessment” portion looks at the patient’s general appearance.
• You’ll be examining / looking for acute distress, peripheral cyanosis, central cyanosis, pallor, consciousness, and posture
Cardiovascular Assessment
• After noting the patient’s general appearance, you now move to “cardiovascular assessment” where you focus on the
heart.
Precordial Movement
• Part of the cardiovascular assessment is to look for any precordial movement. This involves exposing and inspecting the
chest wall.
Palpation
• Next is palpation of the chest, done in order to locate the apical pulse as well as to assess for the presence of thrills, lifts,
or heaves.
• Needs to be done systematically such that the base, apex, precordium, and sternal borders are all included.
Introduction
Recall that the assessment of the patient includes three modes of assessment: inspection, auscultation, and palpation. In
this topic we look in detail at auscultation.
Auscultation
• Is an important cardiovascular assessment tool so it’s important to do it correctly. This includes:
• Eliminating noise
• Focusing on the sounds
• Using the right stethoscope
• Doing the auscultation directly on skin and not through a gown
• Doing the listening over several different patient positions
• Giving the patient specific breathing instructions
The Stethoscope
• Important to understand that wile some sounds are heard best with the diaphragm of the stethoscope, while others are
best heard best using the bell of the stethoscope.
• This doesn’t mean use one with one sound and the other with the other; rather, it serves as a reminder that to get the most
complete auscultation possible, you will use both – diaphragm and bell - in all areas of the precordium.
Auscultation Points
S1 S2 Heart Sounds
• The first heart sound (S1) results from the closing of the tricuspid and mitral valves (which separate the atria from the
ventricles) and is heard best at the fourth to fifth ICS to the left of the sternum and at the fifth ICS, left midclavicular line.
• The second heart sound (S2) results from closure of the pulmonic and aortic valves and is heard best at the second ICS to
the right and left of the sternum.
S3 Heart Sounds
• S3 sounds, S4 sounds, and murmurs may be heard in patients with cardiovascular diseases. (S3 can also be heard in
children and adults under the age of 30 and may also occur during exercise, with anxiety, or in the presence of anemia.
However, if none of these are the case and you hear an S3 sound, consider it pathologic, and not simply physiologic.)
• The presence of an S4 heart sound is abnormal and is due to a noncompliant ventricle.
• This noncompliance may be due to ventricular wall hypertrophy, ischemic heart disease, infiltrative disease processes, or
an increase in ventricular volume.
S4 Heart Sounds
Summation Gallop
• The sound of a galloping horse, made when all 4 heart sounds are present. (The S3 and S4 sounds merge to create the
“gallop” sound.)
• Is often detected in the presence of heart failure.
Murmurs
• Produced by increased or turbulent blood flow
• Often implies significant disease of heart valves, great vessels, or septal defects
Murmur Classification
• Classified along many lines:
• Timing
• Pitch
• Quality
• Location
• Pattern
• Radiation
• Skill at identifying improves with time and exposure to patients with murmurs
Murmur Location
• Murmur location is done using the standard auscultatory landmarks.
Murmur Intensity
• How loud the murmur is
• Graded from I (barely audile in a quiet room) to VI (very loud; audible even without stethoscope to the chest with palpable
and visible thrill)
Introduction
Here we look at the assessment of arterial circulation.
Assessment
• Arterial Circulation is assessed by looking at the following:
• Palpation of pulses
• Skin color and temperature
Palpating Pulses
• Palpation of pulses is the first step of Arterial Circulation assessment.
• Pulses may be palpated at a number of anatomical locations but in the critically ill patient, only upper and lower extremity
distal pulses, (radial, dorsalis pedis, and posterior tibial) are routinely evaluated.
Abnormal Pulses
• Different types, each indicating something different:
• Thready pulses
• Bounding pulses
• Pulsus paradoxus
Palpating Locations
• When a pulse is not palpable in the radial and dorsalis pedis, it is important to systematically assess pulses beginning
distally and moving toward the central circulation until a pulse is palpable.
Arterial Blockage
• A blocked artery is a medical emergency, requiring immediate intervention.
• Interventional cardiovascular procedures and surgeries place critically ill patients at risk for this.
• Signs/symptoms include the 4 Ps: Pulselessness, Pain, Pallor, and Paralysis
Introduction
Here we explore blood pressure and learn about blood pressure’s importance in screening and trending cardiovascular
function as well as the importance of knowing the patient’s pre-illness blood pressure.
Introduction
Here we look at the venous system; the final segment of our cardiovascular exam.
Venous System
• Although most assessment books and resources spend a great deal of time describing how to approximate central venous
pressure by visualizing the right internal jugular vein, this vein is often difficult to visualize.
Edema
• An abnormal accumulation of fluid in the interstitial spac which can be indicative of right-sided heart failure, renal failure,
low plasma albumin, or increased capillary permeability due to activation of the inflammatory response.
• Identify best spot for measurement and then mark it so that other caregivers are consistently using the same spot.
Pitting Edema
• An indentation that remains in the skin after pressure is applied to the edematous tissue
• Many methods for describing it exist but best is describing how long it takes for the tissue to return to baseline (i.e., “Skin
returned to baseline after one minute.”)
Have the patient turn their head to the left side. As you look at the patient locate the top
of the clavicle where it intersects with the sternum. This is where the
sternocleidomastoid muscle attaches to the sternum and serves as an anterior
landmark for locating a soft tissue triangle within which the internal jugular vein lies. The
clavicle forms the bottom of this triangle.
Note the external jugular vein. It lies slightly posterior to the 3rd side of the soft tissue
triangle. Look for soft palpations within this triangle extending up towards the jaw. Make
sure you are not visualizing the carotid pulse which is located close by but is situated
more towards the front of the neck. Palpate the carotid if necessary to differentiate its
location.
Most textbooks describe a somewhat complex method of measuring the internal jugular
pressure using a centimeter ruler and straightedge to measure the height of the highest
pulsation. However, this type of assessment is not really feasible, especially in a critical
care setting. A simpler approach is to place the head of the bed at 30 degrees. Have the
patient turn their head to the opposite side, observe for the internal jugular pulsations
and determine if they extend more than 2-3 finger breaths above the clavicle. If so,
assess for other signs and symptoms of fluid volume overload.
If the JVD is absent when the patient is lying flat, they are hypovolemic. Tangential
lighting may be required to help visualize the internal jugular veins. The correct method
for utilizing tangential lighting to enhance visualization of the internal jugular vein is
demonstrated on the slide.
A comprehensive physical examination and clinical education site for medical students
and other health care professionals can be found at:
http://medicine.ucsd.edu/clinicalmed/heart.htm
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Practice Pearls
Initial Interview
The modifiable risk factors for cardiovascular disease are:
• Smoking
• High blood pressure
• High blood cholesterol
• Diabetes
• Being overweight or obese
• Physical inactivity
Palpation
Changes in apical impulse: Lateral and downward displacement results from left
ventricular enlargement. Upward displacement is seen with ascites, pregnancy, obesity,
and in short stature. Medial displacement, (meaning towards the midline of the body),
occurs in chronic obstructive pulmonary disease or with a mediastinal shift due to a left
pleural effusion or tension pneumothorax. It can also occur in tall, thin people.
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Auscultation
To ascultate the chest of a patient requiring an intra-aortic balloon pump, place the
pump on standby when auscultating as long as pausing the pump does not cause
hemodynamic stability or there are no other contraindications to doing so.
Auscultation Points
To locate the second ICS, find the sternal notch at the base of the neck. Move your
fingers downward until you feel a bump on the sternum. This is the angle of Louis. If you
slide your fingers slightly downward and to the left or right side of the stenum, you will
feel a hollow, which is the second ICS. Below that is a rib, then the third ICS, etc.
Murmur Classification
Systolic murmurs include: Mitral Regurgitation, Physiologic, and Aortic Stenosis:
Systolic. You can remember this with the acronym MR. PASS. Diastolic murmurs
include: Mitral Stenosis, Aortic Regurgitation: Diastolic, and can be remembered by the
acronym MS. ARD.
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Pitting Edema
Anasarca is generalized edema and is seen in severe heart failure, hepatic cirrhosis,
and nephritic syndrome.
Lesson 3
Management of Acute
Coronary Syndromes
Included in this Lesson:
• Assessment of Chest Pain
• ST Elevation MI
• Non ST Elevation MI
• Complications
• Nursing Considerations
Introduction
It is critical for you as a nurse to be able to recognize and respond to patients experiencing an acute coronary syndrome;
coronary heart disease being the leading cause of death in the United States. In this lesson we learn how to identify and
manage a patient with an acute coronary syndrome. Specifically we learn:
ACS Defined
• Acute Coronary Syndrome
• A term given to the spectrum of clinical symptoms compatible with acute myocardial ischemia of one of these sorts:
unstable angina, ST elevation MI, and non-ST elevation MI
• A generic/broad term used only in a prediagnostic setting; after medical evaluation/diagnosis it will defined further as one of
these: unstable angina, ST elevation MI (often called “STEMI”) or non-ST elevation MI (often called “NSTEMI.”)
Pathophysiology
• Primary mechanism of ACS is the development of atherosclerosis in which plaque is formed within the arterial lumen
Etiology
• An imbalance in myocardial oxygen supply and demand (specifically demand being higher than supply) can result in
symptoms of ACS. Elements affecting this supply and demand are:
• Preload • Contractility
• Afterload • Heart rate
Oxygen Supply
• With CAD, atherosclerosis narrows the coronary artery lumen. As the occlusion increases, it will take less and less physical
activity by the patient to trigger pain. (This sensation of pain from physical activity usually begins once the lumen has
narrowed to only 50% its original size.)
Diagnosis
• A patient interview, physical exam, laboratory tests, CXR, and 12-lead ECG are used to determine whether it is unstable
angina, a non-ST elevation MI, or an ST elevation MI.
Types of Angina
• There are many types, characterized by the duration and intensity
• Stable Angina • Anginal Equivalent
• Unstable Angina • Silent Ischemia
• Prinzmetal’s Angina • MI Associated Angina
Interview
• Important to use the right questions with patients in order to get the information you need to successfully differentiate
angina from noncardiac chest pain
• Anginal pain has certain symptoms:
• Onset that’s sudden
• Location in precordial or substernal areas
• Diffuse and may radiate to the arm, jaw, shoulders or back
• Often described as pressure, tightness, squeezing, heaviness, aching, or indigestion
Physical Exam
• May provide little information if the angina is stable
• More severe signs typically seen with unstable angina, NSTEMI, and STEMI
Obtaining an ECG
• Should be obtained as soon as possible in patients presenting with symptoms. Standard of care for patients presenting to
the emergency department is to have an ECG completed and reviewed within 10 minutes of their arrival of ACS
• The ECG taken must be reliable; i.e., electrodes must be properly placed using standard anatomical locations. Follow 5-
step process.
ECG Leads
• Knowing the electrical activity recorded by each lead is helpful:
• Leads I, aVL, V5 and V6: Record the activity on the LV’s lateral surface
• Leads I and aVL: Record activity on LV’s high lateral surface
• Leads V5 and V6: Record activity on LV’s low lateral surface
• Leads II, III, and aVF: Record activity on the inferior surface of the left ventricle
• V1 and V2: Record activity of the interventricular septum
• V3 and V4: Record activity on the LV’s anterior surface
Ischemia
• Ischemia produces T-wave inversion and/or ST depression. This may occur transiently or may persist.
Myocardial Injury
• Myocardial injury results in ST-segment elevation.
• To be considered significant, the amount of elevation should be 1 mm or larger, and it should be this size in two leads
which look at the same area of the heart (i.e., Leads II and III, both of which look at the inferior surface of the left ventricle.)
• Early signs of ST elevation MI or STEMI:
• Hyperacute T waves
• Loss of the ST segment as the ST segment and the T wave become fused together
Q Waves
• The first negative deflection of a QRS complex
• Produced by infarction
• May be seen in NSTEMI but more frequently result from STEMI
Introduction
Here we explore the goals of therapy in ACS and look at the specific therapeutic interventions used.
Goals of Therapy
• Therapeutic interventions:
• Restricting activity • Performing interventional therapies
• Administering pharmacologic agents • Educating the patient
Activity
• Activity restrictions are based around ischemic symptoms.
• Since immobility comes with its own set of complications, mobilization as early as reasonably possible is encouraged.
Drug Therapy
• Paramount to caring for patients with ACS
• Includes:
• Oxygen
• Nitrates
• Anticoagulants, antiplatelets, antithrombins, and GP IIb IIIa platelet receptor inhibitors
• Beta blockers
• ACE Inhibitors or Angiotensin receptor blockers (ARBs)
• Calcium channel blockers (in select patients)
• Fibrinolytic agents (used only in the presence of STEMI)
Oxygen Therapy
• Supplemental oxygen used only in these cases:
• Arterial O2 saturation is less than 90%
• Patient is exhibiting respiratory distress
• Patient is at high risk for hypoxemia
• Need for continued oxygen therapy should be reevaluated six hours after patient presentation
Nitroglycerin
• A cornerstone of treatment for ischemic heart disease because it reduces preload and dilates coronary arteries
• First administered sublingually (spray or tablet) and if 3 doses like this don’t
relieve pain, continuous IV administration is considered Involves monitoring requirements
•There are certain steps to take to help patient avoid building up a tolerance.
• Nitrates in all forms should be avoided with these patients/situations:
• Patients with an initial systolic BP less than 90 mm HG or those who have had a drop in systolic BP of 30 mm Hg
or greater from their baseline
• Patients with marked bradycardia (less than 50 bpm) or tachycardia (greater than 100 bpm)
• Patients who have taken a phosphodiesterase inhibitor for erectile dysfunction within 24 hours (48 hours for
tadalafil)
• Patients suspected of having a right ventricular infarct
• When hypotension secondary to nitrates prohibits the administration of beta-blocking agents
Morphine Administration
• Morphine sulfate is the analgesic agent of choice for treating pain due to ST elevation MI.
• Is also used in treating pain related to unstable angina and non-ST elevation MI if ischemic symptoms persist or recur even
after anti-ischemic therapy.
Platelet Activation
• Since a key contributor to ACS is thrombus formation, many of the pharmacologic agents used for ACS prevent platelet
aggregation.
• Different ones work in different phases of/on the clotting cascade (the cascade of events that makes up clotting) and
therefore several different antiplatelet and anticoagulant drugs are administered at the same time. Each of these does
something specific:
• Aspirin • Heparin 2 • GPIIb IIIa 1
• Clopidogrel 1 • Heparin 3 • GPIIb IIIa 2
• Clopidogrel 2 • LMW Heparin
• Heparin 1 • Bivalirudin
Other Medications
• Other medications used to manage patients with ACS are Beta Blockers, Calcium Channel Blocker, and ACE Inhibitors.
Mechanical Interventions
• Are interventions used to clear the involved coronary artery of occlusion
• Includes PTCA, stent placement, atherectomy, and rotablator
Introduction
In this topic we will explore the fact that while some elements of caring for ACS patients are the same one patient to the
next, some elements are different.
Myocardial Infarction
• Is the irreversible death or necrosis of myocardial tissue due to an inadequate coronary blood supply
• The amount of damage or necrosis (irreversible cell death) caused by an MI depends on several factors:
• Duration of the occlusion (i.e., necrosis begins within 20 minutes of the cessation of blood flow through the
coronary artery)
• Which coronary artery is blocked
• Degree of collateral blood flow to the affected area of the myocardium
Fibrinolytic Therapy
Contraindications of Fibrinolytic Therapy
• Fibrinolytics (fibrinolytic therapies) work directly on the fibrin in a clot, causing it to lyse or break apart.
• Patients must be carefully screened before using these.
• There are many contraindications associated with fibrinolytic therapy.
True Posterior MI
• There are no leads directly monitoring the posterior wall of the left ventricle.
• Posterior MIs can be misinterpreted as anterior ischemia.
Posterior MI
• Be suspicious of posterior MI when leads V1-V3 and/or V4 show tall R waves with ST depression and an upright T wave.
Confirm that it is, in fact, posterior MI by using additional leads V7-V9 as well. ST segment elevation in leads V7V9 will
confirm posterior MI.
Introduction
In this topic we will explore the fact that while in many ways NSTEMI and Unstable Angina (UA) are closely related
conditions, in some ways they differ.
Introduction
Here we will look at complications that can occur when caring for ACS patients, and the possible nursing interventions.
Complications of MI
• Include, but are not limited to dysrhythmias, pump failure, infarct extension, thromboembolic phenomena, pericarditis, LV
aneurysm, ventricular septal defect, and valve malfunction
Dysrhythmias
• The most common complication of MI
• The use of beta-blockers as a standard of care decreases the risk of dysrhythmias due to SNS
Heart Failure
• Spans the continuum from mild dysfunction to cardiogenic shock
• Often due to the change in structure (and therefore in function) of the myocardial cells due to infarction
Thromboembolic Phenomenon
• May occur in patients with atrial fibrillation, mural wall thrombus, and akinetic wall segment
• May include the development DVT, PE, and ischemic stroke
Pericarditis
• The result when full thickness MI produces local pericardial inflammation with fluid, fibrin, and cellular exudates
• Anterior wall MIs are the most common culprit for early pericarditis.
Introduction
Here we look at the nursing care for patients with MI.
Patient Management
• The 8 main aspects of caring for MI patients are:
• Assessment • Monitoring
• Heart Sounds • Oxygen Administration
• Chest Pain • Neurological
• Cardiac Monitoring • Bleeding Risk
Patient Management
• Nursing care for MI patients revolves around these 2 main elements:
• Ongoing focused clinical assessment • Use of appropriate interventions
Patient Education
• Start should start as soon as the patient is stable
• Include the patient’s family or significant other
• Focus the education on evidence-based post STEMI and non-STEMI treatments such as the importance of:
• Smoking cessation
• Adhering to medication regimens
• Beginning an exercise program.
Introduction
Here we explore the elements of invasive and noninvasive cardiovascular procedures. Noninvasive procedures include
stress testing, stress echocardiography, myocardial perfusion imaging, and coronary CT scanning. Invasive procedures
include coronary arteriography, cardiac catheterization, PCI, pacemakers, and cardiac surgery.
Cardiac Catheterization
• Cardiac Catheterization with Angioplasty is one of the more invasive procedures for diagnosing the severity of heart
damage
• Because it provides direct visualization of the coronary artery anatomy, it is considered the gold standard for diagnosing
and localizing coronary artery disease.
PCI
• May be performed during the cardiac catheterization procedure if warranted
PTCA
• Percutaneous Transluminal Coronary Angioplasty (PTCA) and stent placement are commonly performed together to
improve the long-term patency of the artery.
Pre-procedure Preparations
• Taking a history • Cardiac and pulmonary assessments
• Review renal function tests • Medications
• Educate and prep the patient • Diabetic meds
• Pulse check
Post-Procedure Care
• Includes vigilant monitoring of vital signs, access site, distal circulation, cardiac rhythm, and patient recovery from sedation
Circulation Checks
• Checking for presence and quality of pulses, extremity warmth and sensation, and motor function
IV Fluids
• Maintain IV fluid and pharmacologic infusions as ordered
• Fluid therapy important to prevent renal dysfunction and because contrast media acts as an osmotic diuretic.
Patient Education
• Activity restrictions
• The need to prevent undue stress on the access site
• After sheath removal, showing the patient how to hold pressure on the groin area (if utilized as the access site) if s/he
needs to cough
• Instructing the patient to report any chest pain or anginal equivalent immediately
Complications
• Abrupt vessel closure • Pseudoaneurysm
• Restenosis • Vessel Occlusion
• Overt bleeding • Impaired renal function
• Covert bleeding
• Leads I, aVL, V5 and V6 record electrical activity on the lateral surface of the left
ventricle.
• Leads I and aVL monitor the high lateral surface of the left ventricle, whereas Leads
V5 and V6 monitor the low lateral surface.
• Leads II, III, and aVF record the electrical activity on the inferior surface of the left
ventricle.
• V1 and V2 record electrical activity of the interventricular septum.
• V3 and V4 monitor the anterior surface of the left ventricle.
• Some sources include V1-V4 as anterior leads while others call all V leads anterior
leads.
55
CK
740 615 442
(Normal: 35-230)
CK MB
54.1 25.8 20.8
(Normal: 0-7.9)
CK MB%
7.3% 4.2% 4.7%
(Normal: 0-1.9%)
Troponin I
9.44 4.02 3.78
(Normal: 0-0.3)
Franks, George M 72
Dr. Gail Hunter
Acct # 00045678349
MR 24-06-33
59
Infarction produces Q waves and may be seen in NSTEMI but more frequently result
from STEMI.
A Q wave is the first negative deflection of a QRS complex. Q waves are significant if
they become wider or if new Q waves appear where there were no Q waves in the past.
Q waves occur normally as an indication of septal depolarization in many leads
including I, aVL, V5, and V6. In some patients, small Q waves will also be seen in leads
II and aVF.
Normal Q waves are very small and very narrow. Pathologic Q waves, indicative of MI,
are generally at least 1 small box wide on the 12 lead ECG tracing.
Q waves seen in leads that did not have Q waves previously or leads where the Q wave
is widening or deepening is also indicative of an acute process. Q waves may occur in
the presence of ST elevation, which indicates that the infarction is acute.
Once present, pathological Q waves may remain and will be seen on subsequent ECG
tracings as a permanent reminder that infarction has occurred.
60
Practice Pearls
Types of Angina
Unstable angina is not promptly relieved by rest or nitroglycerin.
Physical exam
If the patient has a pulmonary artery catheter in place, you may see giant "V" waves on
wedge tracings, indicating regurgitation of blood into the atrium with systole.
Case Presentation
Reperfusion therapy is a general term used to describe any therapeutic intervention
aimed at removing the barrier to coronary artery blood flow and perfusion of the
myocardium with oxygenated blood. This can be accomplished with either the
administration of a Thrombolytic or with an Percutaneous Coronary Intervention (PCI).
Reperfusion therapy will be discussed a little later in the lesson.
Q Waves
You may see 12 lead ECGs printouts that say “infarct, age undetermined.” This usually
indicates the infarct is not acute and is sometimes referred to as an old MI.
62
Nitroglycerin
When administering heparin and nitroglycerin concurrently, the nitroglycerin may block
some of the antithrombin effects of the heparin. Should the nitroglycerin be
discontinued, the effects of the heparin may be enhanced resulting in elevations in
aPTT and ACT values increasing the risk of bleeding.
Posterior MI
Some ECG machines are equipped to record 15 lead ECGs, which include two
posterior leads. Check with your facility to determine if your equipment has this
capability.
64
Patient Education
The American Heart Association is an excellent resource for current educational
materials related to ACS.
65
• Hypertension
• Cardiomyopathy
Consequences of Hypertension
• Is a major risk factor for coronary artery disease, myocardial infarction, heart failure, and stroke
• Can cause direct injury to the vascular system
• Can cause an increase in myocardial oxygen demand
• Increases the work of the left ventricle, causing left ventricular hypertrophy
• Left ventricular hypertrophy can cause myocardial ischemia and left ventricular diastolic dysfunction (a cause of
heart failure)
• Left ventricular hypertrophy, if left untreated, may lead to left ventricular dilatation and systolic dysfunction (a
cause of heart failure)
Introduction
In this topic we will examine heart failure whereby the heart becomes unable to pump enough oxygenated blood to meet the
metabolic needs of the body. It is a complex clinical syndrome whereby the ventricle becomes impaired and can no longer
fill properly or eject optimally.
Statistics
• Patients with heart failure present with one or both of the following:
• Dyspnea and fatigue
• Extracellular fluid retention
• About 5 million Americans live with heart failure today.
• 550,000 new cases are diagnosed each year.
• 300,000 patients die each year of heart failure-related causes.
• 50% of those diagnosed with heart failure die within 5 years of their diagnosis.
Compensatory Mechanisms
• Activated to restore cardiac function to normal after acute heart failure (and the associated decrease in cardiac output and
in blood pressure)
• Includes activation of the sympathetic nervous system (SNS) and the renin-angiotensin system, ventricular hypertrophy,
and dilation.
• Knowledge of these is essential to adequately assess the patient and understand the goals of treatment.
• Most patients with heart failure will present with a decreased exercise tolerance due to dyspnea or fatigue.
• The exercise intolerance could also be due to the fact that many heart failure patients also have coexisting conditions such
as pulmonary disease.
• Diagnostic tests that help determine the presence of heart failure include:
• Chest X-ray • Electrocardiogram
• Echocardiogram • Cardiac Catheterization
Fluid Status
• Functional status is assessed by the rating systems discussed earlier, so we now turn to fluid status. Extracellular fluid
volume status is difficult to assess, with the most reliable sign being jugular venous distention and others being edema,
organ congestion, and weight.
__________________________________________________________________________________________
__________________________________________________________________________________________
Laboratory Values
• Using lab values to monitor potassium levels is very important since
• Diuretics can cause hypokalemia which, in turn, can increase the risk of digoxin toxicity in patients also on digoxin
• Some of the other heart failure medications (like ACE inhibitors, angiotensin II receptor blockers, and aldosterone
antagonists) can predispose patients to hyperkalemia.
• Using lab values to monitor renal function and anemia is also important.
Dysynchrony
• Common in heart failure patients
• Cardiac Resynchronization Therapy (CRT) is helpful in patients with moderate to severe heart failure and in those with
bundle branch block (typically left bundle branch block) who are symptomatic despite optimal medical therapy.
Introduction
In this lesson we discuss cardiomyopathy, a disease of the heart muscle that primarily affects the myocardial layer of the
heart.
Definition
Cardiomyopathy refers to a group of disorders which:
• Are associated with the mechanical and/or electrical dysfunction of the myocardium
• Are either confined to the heart or are part of a generalized systemic disorder
• Often lead to cardiovascular death or progressive heart failure-related disability
Classification of Cardiomyopathy
• Standard classifications equal primary and secondary however have evolved to also include mixed (genetic and
nongenetic) and acquired
• You can also classify cardiomyopathies in a functional manner, describing the ventricular changes:
• Dilated cardiomyopathy • Restrictive cardiomyopathy.
• Hypertrophic cardiomyopathy
Introduction
In this lesson we look at valvular heart disease which affects about 5 million Americans.
• These non-surgical treatment options in the time before surgery can be helpful:
• IV Medication • Beta Blockers
• Preload • Inotropic Support
Introduction
In this lesson we look at Abdominal Aortic Aneurysms (AAA,) considered present when the anteroposterior diameter of the
aorta reaches 3 cm.
The majority of aortic dissections involve the ascending aorta. A smaller percentage involves the aortic arch
and descending thoracic aorta. Dissections of the abdominal aorta are rare
AAA: Complications
• Rupture or occlusion resulting from dissection • Compression of nearby anatomical structures such as
• Thromoembolic ischemic events the duodenum
AAA: Treatment
• Most important treatment goal is to prevent fatal rupture • Surgery
• Smoking cessation and blood pressure control
Nursing Interventions
• Monitoring vital signs, oximetry, and ECG
• Reviewing lab values, especially hemoglobin and hematocrit, electrolytes, BUN, and Creatinine
• Managing the patient's pain
• Keeping blood pressure high enough to maintain perfusion through the graft but low enough to prevent rupture
• Monitoring the output from the NG tube and assessing bowel sounds for return of peristalsis
• In patients whose aorta was cross clamped during surgery, there are additional items to monitor for.
Surgical Treatments
• Thoracic aortic aneurysms are found in the ascending or descending thoracic aorta.
• Acute and Chronic
• “Acute” aortic dissections: Those diagnosed within two weeks of onset
• “Chronic” aortic dissections: Those diagnosed outside the two-week window
Treatment Goals
For patients with hypertension the blood pressure treatment goal should be < 140 mm
Hg systolic and < 90 mm Hg diastolic in all patients.
For patients with diabetes, heart failure, or chronic kidney disease, blood pressure
treatment goal should be lower at < 130 mm Hg systolic and < 80 mm Hg diastolic.
Patient Education
Empowering patients with knowledge is an important part of hypertension management.
Patient's need education regarding:
• lifestyle modifications
• prescribed medications
• avoid over-the-counter medications such as decongestants.
• The risk of untreated hypertension.
Patient compliance is an important part of therapy; therefore, the costs and side effects
of medications are important considerations. Self-monitoring of blood pressure by
patients has been shown to improve compliance. Patients should have monthly follow-
up blood pressure checks, with medication adjustments, until target results are
achieved. More frequent follow-up is indicated for patients with stage 2 hypertension
and for those with cardiovascular disease, renal disease, or diabetes. After blood
pressure goals are achieved, follow-up should continue at 3- to 6-month intervals. Dose
reduction of medications should be attempted after 1 year of controlled therapy.
90
ACE inhibitors are contraindicated in angioedema, pregnancy, and anuric kidney injury.
Angiotensin II receptor blockers directly block angiotensin II. Angiotensin II receptor
blockers are indicated in chronic heart failure patients who cannot tolerate an ACE
inhibitor due to cough or angioedema.
End-stage heart failure patients often decompensate frequently and may need to be
admitted for intravenous inotropic or vasodilator therapy. Patients unable to be weaned
from intravenous inotropic support may be candidates for at-home continuous inotropic
support. This measure is a final option, used only for palliative relief in end-stage
disease. Because inotropic therapy is associated with an increased risk of sudden death
and there is a lack of research supporting the benefit, intermittent inotropic therapy is
not indicated in the management of chronic heart failure.
Physicians should discuss end-of-life care issues with patients with end-stage heart
failure while they are still able to participate in the decision-making process. Hospice
care is one option for end-stage disease management that is often underutilized.
Interventions in heart failure to decrease the risk of sudden cardiac death include: beta
blockers, amiodarone, and implantable cardioverter-defibrillators (ICDs). Although not
routinely used due to its toxicity, amiodarone is one antiarrhythmic that can be tolerated
in heart failure patients if needed. ICDs are indicated in heart failure with suspected
survival and good functional status for at least one year who also meet one of the
following criteria:
• Survivors of cardiac arrest / sustained ventricular tachycardia / inducible
ventricular tachycardia on electrophysiology study.
• Ejection fraction less than 30% more than 40 days after an MI or less than
30% with no ischemic heart disease.
Patients with heart failure have an increased risk for ventricular arrhythmias and should
be assessed for exacerbating factors such as electrolyte abnormalities (low potassium
and low magnesium) and digitalis toxicity.
Patient Education
Teaching the patient and family self-management strategies is key to the effective
management of heart failure. Patient education should include the following:
• Recognition of signs and symptoms
- Activity intolerance: An activity diary can provide an objective way for
patients or families to track activity tolerance.
94
Practice Pearls
Compensatory Mechanisms
Sinus tachycardia may be one of the earliest warning signs in heart failure.
Fluid Status
Crackles may occur in the presence of rapid or acute left ventricular heart failure where
the lymph drainage system is not able to compensate for the rapid increase in volume.
Classifications
Indications
• The decision to perform cardiac surgery is based on a number of factors, the most significant being severity of the cardiac
disease and the stability of the patient’s condition.
Contraindications
• CABG not recommended for patients who do not have adequate native vessels to use as a graft
• Patients with very small coronary arteries and atherosclerosis of the aorta are also challenges in CABG.
• Risks of surgery need to be weighed against benefits for each patient.
Preoperative Assessment
• The key to minimizing any postoperative complications is a thorough preoperative assessment. This includes:
• A thorough history and physical and detailed nursing assessment
• The completion of certain diagnostic studies as part of the preoperative evaluation
DC aspirin 2-3 days a, DC clopidogrel 5-7 days a, tirofiban and eptifibadtide 4-6 hrs a, abciximab 12-14 hrs a
warfarin 4 days a, reg heparin doesn't need to be DC'd and lovenox 12-24 hrs a.
Traditional CABG
Additional Conduits
• Radial artery • Right gastroepiploic artery
Overview
Here we look at Off-Pump CABG (OPCAB,) an alternative method to performing CABG. This surgery is done without CPB
but does involve a full median sternotomy so that the surgeon has better visability to bypass the vessels that supply the
lateral and posterior walls of the left ventricle.
Technical Considerations
• During OPCAB, hemodynamics are controlled by the patient’s heart; not by the CPB system.
• Patients who have persistent instability are converted to on-pump surgery, and those requiring return to on-pump surgery
have a higher risk of mortality and other complications.
• To allow for suturing on a beating heart, medications such as beta blockers or
adenosine can be given to slow or temporarily stop the heart.
• Patient’s temperature is kept as close to normothermic as possible to prevent arrhythmias, bleeding, and postoperative
shivering.
Introduction
Here we discuss heart valve operations, about 99,000 performed each year in the U.S., most done to repair or replace the
mitral or aortic valves. Some patients have more than 1 valve that is damaged and in need of repair or replacement.
Mechanical Valves
• More durable than tissue valves, but require life-long anticoagulation with warfarin.
• Are indicated in young patients with no contraindications to anticoagulation.
• 3 primary types:
• Ball and cage
• Single leaflet tilting disc
• Bileaflet valve
Bioprosthetic valves
• Also called tissue valves
• Lower rate of mechanical failure compared to mechanical valves
• Warfarin is not required with tissue valves, but the patient will take a daily aspirin
• Particularly beneficial in
• Older patients who are not already on warfarin for another indication
• Women of child bearing age
• 2 primary types:
• Homograft (allograft)
• Heterograft (xenograft)
Valve Surgery in Mitral Stenosis: Postoperative Care And Summary of Nursing Care in Valve Surgery
• Patients experience excellent short- and long-term outcomes. Improvements felt shortly after surgery.
• For echocardiogram results to be reliable, perform it no sooner than 72 hours after surgery.
Practice Pearls
Traditional CABG
While cardiopulmonary bypass has made it possible to perform surgery on a non-
beating heart, it is not without complications. The two most clinically important
complications of cardiopulmonary bypass are:
• Initiation of systemic inflammatory response
• Development of coagulapathies
Additional Conduits
The Allen’s test must be done to assess for patency of the ulnar artery before the radial
artery can be harvested.
When a radial artery is used as a graft, intravenous nitrates and calcium channel
blockers are used during the perioperative period to reduce the risk of spasm. Oral
medications are continued for a period of time after discharge.
Bioprosthetic valves
Antibiotic Prophylaxis Against Infective Endocarditis After Valve Surgery
Endocarditis prophylaxis is appropriate for all patients with a prosthetic valve.
Procedures requiring endocarditis prophylaxis include all dental procedures that involve
manipulation of the gingival tissue or the periapical region of teeth or perforation of the
oral mucosa.
Endocarditis prophylaxis may be used for patients with a prosthetic valve who have an
invasive procedure of the respiratory tract involving an incision or biopsy of the
respiratory mucosa. This does not include standard endoscopic procedures.
Endocarditis prophylaxis is no longer recommended for patients with a prosthetic valve
undergoing a GU or GI procedure.
• Permanent Pacemakers
In this lesson we’ll discuss cardiac pacemakers and pacemaker therapy including temporary pacemakers and permanent
pacemakers. We’ll learn the basics of pacing equipment, pacemaker terminology, types of temporary pacemakers, and how
to analyze pacemaker function and troubleshoot malfunctions. Pacemaker therapy often plays an important role in the care
of patients with cardiac disorders, pacemakers providing an artificial stimulus to the atria and/or ventricles in order to either
assist or override the patient’s native/intrinsic cardiac activity.
Pacing
• There are 3 basic indications for pacing (though others exist):
• Bradyarrhythmias
• Tachyarrhythmias
• Situations where they are placed prophylactically
Components
• Temporary pacemaker components include the temporary pacemaker, bridging cables, and electrodes.
Epicardial Electrodes
• Pacing wires placed by a cardiovascular surgeon during cardiac surgery
• Some surgeons attach only one wire to the atrium and one to the ventricle; others attach two wires to the atrium and/or two
wires to the ventricle.
• Important to know which method each surgeon uses so that you will be best able to utilize pacing therapy should it become
necessary
Transvenous Electrodes
• Pacing via one or two electrodes advanced into the right atrium/ventricle through a peripheral or central vein
• Generally have the negative pacing electrode labeled. It is sometimes referred to as the distal electrode.
Transthoracic Electrodes
• Transthoracic means through the thorax • Is usually attempted only when other temporary pacing
• Are used for ventricular pacing methods have failed
Bridging Cable
• Serves as a bridge between the pacing generator and the electrodes
• The bridging cable and the end of the pacemaker generator have negative (distal) and positive (proximal) ports labeled.
Pacing
• “Pacing” is the firing of electrical energy by the pacemaker generator.
• “Pacemaker firing” is when electrical energy is fired. The pacing light on the pacing generator will illuminate.
• “Pacing Spikes” will be visible on your EKG tracing.
• “Pacemaker Output” is the energy or electricity fired by the pacemaker. It is measured in milliamps or mA.
Capture
• To have capture, the pacemaker generator must fire electricity, the electrode must deliver the electrical impulse to the
atrium or ventricle, and the chamber must respond to the electrical stimulus.
Stimulation Threshold
• The lowest amount of energy or the lowest amount of output (milliamps) required to cause the heart to respond each time
an electrical impulse is fired by the pacemaker
• When pacing, it is important to use the least amount of energy or output required to capture the targeted chamber.
Sensitivity
• The ability of the pacemaker to see or sense the patient’s intrinsically generated (native) cardiac activity
• The clinician is responsible for setting the sensitivity for each chamber being paced. This is done by performing a
sensitivity threshold.
AV Interval
• Is only available for dual chamber pacing
Introduction
Here we take a look at permanent pacemakers.
Permanent Pacemaker
• Are similar to temporary pacemakers
• Have implanted generators consisting of a lithium battery which lasts 8-10 years and electrical micro circuitry encased in
titanium
• Endocardial or transvenous placement of pacemaker leads is the most common approach for electrode/lead insertion.
Pacemaker Modes
Introduction
Here we discuss potential pacemaker complications.
Pacemaker Complications
• Failure to pace (Failure to fire) • Undersensing
• Failure to capture • Oversensing
Failure to Pace
• When the pacemaker fails to deliver an electrical • Is often equipment related
stimulus at the preprogrammed interval • Can also be related to a sensing problem
Failure to Capture
• When the pacemaker delivers the pacing stimulus at the appropriate timing interval but it does not result in a depolarization
of the paced chamber
• On an ECG tracing, this would be seen as the absence of a P wave during atrial pacing or the absence of a QRS complex
during ventricular pacing immediately following the pacing spike.
• Both equipment and physiologic causes possible
• Requires assessing and supporting the patient, replacing the battery, increasing the mA, checking/tightening the lead
connections, and attending to identified physiologic alterations.
Sensing Malfunctions
• There are 2 types of sensing malfunctions:
• Undersensing (failure to sense): The pacemaker is not sensitive to or does not SEE intrinsic cardiac activity and
sends out pacing energy even though the patient’s heart is generating P waves and QRSs at adequate intervals
• Oversensing: The pacemaker interprets noncardiac activity as intrinsic cardiac activity, causing the pacemaker to
inhibit pacing.
Oversensing
• When the pacemaker interprets noncardiac activity as intrinsic cardiac activity, causing the pacemaker to inhibit pacing.
• Requires changing the battery and checking electrodes and connections, as with other malfunctions. Also requires treating
physiologic causes, unplugging unnecessary electrical equipment and removing it from the room, and doing a sensitivity
threshold.
Pacemaker Override
• When a permanent pacemaker is malfunctioning, you can try this as a temporary fix to maintain the patient until the
pacemaker can be assessed and reprogrammed:
• Place a magnet over the implanted generator to stop malfunctions and override the pacemaker. Generally this
puts pacemaker into an asynchronous mode at a predetermined rate of usually 100 bpm. This will stop the
malfunction and help to maintain the patient until the pacemaker can be assessed.
• This rule applies to pacemakers and not AICDs
Pacing Thresholds
Stimulation Thresholds
Determine the stimulation threshold (for each chamber as necessary):
• Set the pacing rate to approximately 10 beats above the patient's intrinsic rate.
• Gradually decrease the output until capture is lost.
• Gradually increase the mA until 1:1 capture is established. This is the stimulation
threshold.
• Set the mAs at least two times higher than the stimulation threshold. This output
setting is sometimes referred to as the maintenance threshold.
Pacing Thresholds
Setting Sensitivity
Determine the sensitivity threshold (for each chamber as appropriate).
• Gradually turn the sensitivity dial counterclockwise (or to a higher numeric
setting), and observe the pace indicator light for flashing,
• Slowly turn the sensitivity dial clockwise (or to a lower numeric setting) until the
sense indicator light flashes with each complex, and the pace indicator light
stops. This value is the sensing threshold.
• Set the sensitivity dial to the number that was half the sensing threshold to
provide a 2:1 safety margin.
Assess the cardiac rhythm for appropriate pacemaker function:
• Capture: Is there a QRS complex for every ventricular pacing stimulus? Is there
also a P wave for every atrial pacing stimulus?
• Rate: Is the rate at or above the pacemaker rate if in the demand mode?
• Sensing: Does the sensitivity light indicate that every QRS complex is sensed?
129
Practice Pearls
Epicardial electrodes
By convention, wires exiting to the right of the sternum are atrial electrodes and those
exiting the left side of the sternum are ventricular electrodes. Some surgeons place the
ground lead beneath the sternal incision. Others make one lead longer than the other.
Anytime you are uncertain of electrode location, ask for clarification.
When not in use, epicardial pacing wires should be grounded and taped to the chest
wall. The ends of epicardial pacing wires can be placed in a glove finger, finger cot,
empty needle sheath or commercially available lead protector and secured to the
patient's chest wall with tape. Anytime epicardial wires are handled, gloves should be
worn to prevent unintentional microshock.
Capture
When atrial pacing occurs, the QRS complex is narrow (unless the patient has a
preexisting bundle branch block or other interventricular conduction defect) because
conduction occurs quickly down the normal conduction pathways. With ventricular
pacing, the QRS is wide due to cell to cell conduction which occurs much more slowly
than using the heart’s electrical conduction system.
Stimulation Threshold
The pacemaker you use may look different than these examples. Please refer to your
hospital policy and procedure manual for information on your specific temporary
pacemaker.
130
AV interval
Fusion beats: There will be times when the pacemaker initiates pacing at the same time
the patient initiates their own cardiac activity. On the EKG tracing, the paced beat will
look different than if the patient generated their own cardiac activity and it will look
different than the other paced beats. It will be a blend of these two complexes.
131
Lesson Summary
If all else fails, support the patient pharmacologically and with an external
transcutaneous pacemaker and/or CPR if needed.
132
Absolute refractory period where the cell will not depolarize no matter how strong the
period impulse
Atrial kick the atrial contraction forcing blood from the atriums into the
ventricles. Seventy percent of blood flows passively into the
ventricles. The additional thirty percent of blood flowing into the
ventricles is referred to as the atrial kick.
Baroreceptors located in the aortic arch and carotid sinus, these receptors respond
to changes in blood pressure. For example, when the arterial walls
are stretched by an increase in blood pressure, the vasomotor
center in the brain is inhibited resulting in vasodilation. The
baroreceptors also stimulate a decrease in heart rate via the vagus
nerve and the net effect is a decrease in blood pressure.
Cardiac enzymes also known as markers, these are proteins that are released as a
result of cardiac cell injury or death. They are sensitive and reliable
in indicating the degree of myocardial damage. They include
creatinine kinase (CK,) myoglobin, lactate dehydrogenase or LDH,
troponin I, and troponin T.
Cardiac Output the volume of blood ejected from the heart over 1 minute.
(CO) Measured in liters per minute. Normal CO ranges from 4 to 6 L/min.
Determinants of CO are heart rate and stroke volume. The equation
is as follows: CO=heart rate times stroke volume. Therefore, a
change in either heart rate or the stroke volume affects CO.
Cardiac tamponade when there is an accumulation of fluid in the pericardial sac which
progresses until the point in which it causes the compression of the
atria and ventricles. As the accumulations continues, there is a
decrease in cardiac filling pressures and a decrease in venous
return.
Chordae tendendea strong fibrous cords that connect the valve leaflet to the papillary
muscles
Conductivity ability of the cardiac cells to transmit the depolarization from cell to
cell
Contractility ability of the myocardial muscle tissue to contract and relax after an
electrical stimulus
Diastole also known as filling stage, this is the relaxation of the atriums or
ventricles. It usually refers to the ventricles.
Hypokinesis a decrease in the ability of the muscle to move. In the area of the
hypokinesis there will be less contraction of the myocardial muscle.
Inotropic agents used in reference to various drugs that affect the strength of
contraction of heart muscle (myocardial contractility.)
Isoelectric line This line is also referred to as the baseline and is represented by a
dotted line. Any wave above the line is called a positive deflection;
any wave below the line is called a negative deflection (or may be
referred to as inverted.)
Papillary muscles are attached to the ventricular wall and work together with the
chordae tendinae to prevent valve leaflets from turning inside out.
The valves open and close in response to pressure changes within
the chambers.
Parasympathetic originates in the medulla and is mediated by the vagus nerve. Most
nervous system of the fibers are cholinergic and secrete acetylcholine, which tends
to be inhibitory in its actions. The cardiac effects of parasympathetic
stimulation include a slowing of heart rate, decrease in the speed of
the conduction through the AV node, and slight depression in
contractility.
Pericardiocentesis the removal of fluid from the pericardial sac through a needle
Pulmonary edema the result of severe pulmonary congestion due to excess fluid in the
interstitial and/or alveolar spaces
137
Pulse pressure the pressure exerted by the blood flow during cardiac contraction. It
is reflective of stroke volume, systemic vascular resistance, and
vessel distensibility.
Pulmonary the resistance to blood flow offered by the vasculature of the lungs.
Vascular Vasoconstriction increases SVR, whereas vasodilation decreases
Resistance (PVR) SVR.
Pulsus alternans produces alternating smaller and larger pulse waves. The variability
in waveforms is a result of inconsistent stroke volume from heart
beat to heart beat.
Relative refractory the cell will depolarize only if it receives a strong stimulus
period
Repolarization the return of the membrane potential to its resting state. Potassium
moves into the cell and sodium moves out of the cell.
Sinus dysrhythmia Sinus dysrythmia occurs when the sinus node discharges
irregularly. It occurs frequently as a normal phenomenon and is
commonly associated with the phases of respiration. During
inspiration, the sinus node fires faster; during expiration, it slows.
Starling’s Law first hypothesized in 1914, this law states that, “The greater the
stretch exerted on the ventricle by the EDV, the more forceful the
heart’s contraction.”
Stroke Volume the amount of blood pumped by the ventricle with every systolic
(SV) contraction. A healthy heart will eject more than half the total
ventricular blood volume. Normal stroke volume is 60 to 130
mL/beat.
Sympathetic innervates all parts of the heart, including the atria, ventricles, the
nervous system SA and AV nodes, and all of the blood vessels. The sympathetic
fibers are adrenergic and tend to be excitatory through the release
of norepinephrine. There are three types of sympathetic receptors:
alpha-adrenergic, beta-adrenergic, and dopaminergic.
Systemic Vascular the resistance to blood flow offered by the peripheral circulation.
Resistance (SVR) Also referred to as the total peripheral resistance. Vasoconstriction
increases SVR, whereas vasodilation decreases SVR.
Tropomyosin Around the actin fibril are interwoven protein rods of troponin and
tropomyosin. They inhibit the ability of actin to connect with
myosin. At the beginning of a contraction, calcium is released and
attaches to troponin, allowing cross bridges on the myosin to attach
to the actin.
Troponin Around the actin fibril are interwoven protein rods of troponin and
tropomyosin. They inhibit the ability of actin to connect with
myosin. At the beginning of a contraction, calcium is released and
attaches to troponin, allowing cross bridges on the myosin to attach
to the actin.