CARING FOR PATIENTS W/ CARDIOVASCULAR

DISORDERS: PART I
ASSESSING THE CARDIOVASCULAR SYSTEM
TOPIC A: ASSESSING SYMPTOMS
Signs & Symptoms:
Chest pain most often associated with CV system pathology
Other common s/sx: dyspnea, nocturia, cough, fatigure, syncope, dependent edema & leg pain

Quantifying Pain
Have the patient quantify (or measure) their pain on a scale of 0-10. If the patient is cognitively impaired, use an objective
scoring system to assess for pain.
Qualifying Pain
Patients often describe cardiac pain using words such as: dull, aching, squeezing, pressure, heaviness, tightness, radiating, or
localized to describe the discomfort.
o Don't coach the patient unless they are not able to find words to describe what they are feeling.
Cardiac chest pain: Note that cardiac pain is typically sternal, left of sternum, or epigastric and not well localized. It may be associated
with dyspnea, diaphoresis, nausea, vomiting, or palpitations.
Cardiac pain is often triggered by exertion, strong emotion, or exposure to heat or cold.
Pain may improve with rest or NTG, but if it lasts longer than 20 minutes this signals a greater likelihood of infarction.
Don't forget to ask patients with chest pain about a prior history of coronary artery disease (CAD) or diagnosis of LV
Hypertrophy. When the situation allows, always identify risk factors for CAD.
Causes of Dyspnea:

TOPIC B: AUSCULTATING
Patient position: first listen supine, next (if possible) position pt on their left side or sitting forward in order to move the heart closer to
the chest wall which may allow you to hear sounds that were obscured when the heart was further away
Anatomical Landmarks:

Aortic Area: located at second ICS, R sternal border

Pulmonic Area: located at second ICS, L sternal border
Erbs Point: used to listen for murmurs, at the third ICS, L sternal border
How to locate: to locate 3rd ICS, find the sternal notch at the base of the neck
Move 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 L or R of the sternum, you will feel a hollow, which is the second ICS
Below that is a rib, then the third ICS, then the fourth ICS, and then the fifth ICS
Tricuspic Area: located at the 4th ICS, L sternal border
Mitral Area: mitral or apical area, located at the fifth ICS, L midclavicular line

S1 and S2: normal heart sounds (lub and dub) occur in sequence with each heartbeat
S1 associated with closing of the AV valves and S2 with the closer of the semilunar valves
S1 best heard at mitral area; S1 and S2 best heard at aortic and pulmonic areas
S1: associated with closing of the tricuspid and mitral valves
May want to palpate carotid pulse once you have identified the S1 sound
o Should hear S1 just prior to feeling a pulsating (pulsation identifying systole) in the carotid artery
o S1 marks the end of diastole and the beginning of systole
o Best heart at mitral area
o lub of lub dub
S2: associated with closure of the pulmonic and aortic valves
S2 marks the end of systole and the beginning of diastole
If palpating the carotid artery, you would hear S2 just after the upstroke of the carotid pulsation or just after systole has
occurred
 dub of lub dub
S3: a soft sound, closely follows S2
occurring during the early part of diastole, S3 indicates that blood is rapidly flowing into an already full R ventricle, causin
vibration
May be normal in pts under 30
After 30, S3 often associated with L side HF; the heart is unable to sufficiently propel blood out of the ventricle during systole,
creating a chronically overfilled ventricle
Sounds like lubb-DUB-ta similar to the cadence and accent of the word Ken-TUC-ky
S4: occurs late in diastole, when the atria actively contract to complete filling of the ventricle immediately prior to S1 (AV valve
closure)
S4 due to noncompliant ventricle
Noncompliance may be due to ventricular wall hypertrophy, ischemic heart disease, infiltrative disease processes, or an
increase in ventricular volume
Referred to as atrial gallops, S4 sounds like ta lubb DUB similar to the cadence and accent of the word Ten-nes-SEE
Summation Gallop: beast heard at 5th ICS, L sternum, occurs when all four heart sounds are present
S3 and S4 merge, creating an audible rhythm that resembles the sound of a galloping horse
Summation gallops generally occur with HR > 100 bpm
w/ HR <100 bpm, S3 and S4 may be heard as distinctly separate sounds
Summation gallop is often detected in the presence of HF
Resembles sound of galloping horse

Murmurs:
Murmurs are produced by increased or turbulent blood flow and are best heard at Erb's point.

Pathologic Causes
Murmurs often imply significant disease of heart valves, great vessels, or septal defects.
Physiologic Causes
Murmurs that occur for physiologic reasons are referred to as innocent or benign. They commonly occur during pregnancy,
anemia, or transiently during exercise as a result of increased blood flow.
Auscultation Tips
In addition to Erb's point, murmurs may be heard over the individual valve locations and the sound may radiate along the
path of blood flow.
Systolic v. Diastolic murmurs:
First determine if the murmur is new or pre-existing
Then determine where it is best heard
Next, determine if it occurs during systole or diastole
o Systolic: if murmur is heard when the pulse is felt
o Diastolic: if murmur is heard when pulse is not felt
Finally identify if it is causing hemodynamic compromise
Classifying murmurs:
Providers document murmur details to help classify them. Recognizing quality, pitch, intensity, and patterns are advanced
skills that take time to develop and refine with increased exposure to various murmurs.
In time and with practice you will be able to recognize the following aspects of murmurs:
o Timing: Is it systolic or diastolic?
o Pitch: Is it high or low pitched?
o Quality: Is it blowing, harsh, musical, or rumbling?
o Location: Where is it best heard?
o Pattern: Is it crescendo, decrescendo, or holosystolic?
o Radiation: What is the direction of the sound? Does it radiate towards the back, up the neck, or to the axilla?
Pericardial friction rubs:
Pericardial friction rubs are best heard at the fifth ICS, left sternal border.
Pathophysiology
o Caused by inflammation of the pericardium
o Occur in up to 25% of MIs, often following cardiac surgery
o May be associated with fever, sharp chest pain, and an elevated white blood cell count
Audio Description
o Rough, scratching, squeaking sound, or like two pieces of leather rubbing against each other
Auscultation Tips
o Heard best with diaphragm with the patient leaning forward, in full expiration
o May sound like a murmur (important to learn to differentiate them)
Pericardial Rub Versus Pleural Rub
o Pericardial rubs occur with heart beats.
o Pleural rubs occur with the respiratory cycle, and may occur at various locations on the chest wall.

DIAGNOSING ACUTE CORONARY SYNDROME (ACS)

TOPIC A: DIFFERENTIATING ACS PAIN
Characteristics of ACS Pain:
S/SX of STEMI

MI: Myocardial infarction (MI) is defined as the irreversible death or necrosis of myocardial tissue due to an inadequate coronary
blood supply. MI is nearly always due to a thrombus in the coronary artery. Irreversible cell death begins within 20 minutes of the
cessation of blood flow through the coronary artery.

Etiologies of Fatal MIs:

Amount of Damage to Myocardial Area: The amount of damage or necrosis depends on whether the occlusion is complete or partial,
the duration of the occlusion, where in the coronary artery the blockage occurred, and the amount of collateral blood flow to the
affected area of the myocardium.
Progression of Cellular Damage:

Types of Angina:
Angina is categorized by its duration, intensity, or cause.
It is important to know the types of angina, because they have different symptoms and require different treatments.
For example, stable angina is separated from other types of angina in its severity, in that what triggers it is predictable, and
because treatment that relieved it in the past continues to be effective.
Stable angina and variant angina are not considered part of ACS.
Stable Angina:
Cause & Pattern:
o Caused by atherosclerosis
o Predictable onset, severity and duration at a consistent level of exertion or stress
Triggers:
o Physical or emotional stressors that increase myocardial oxygen demand
o Factors that decrease oxygen delivery to tissues such as smoking, dysrhythmias, hypoxemia, anemia, or hypotension
Duration: predictably relieved with rest and/or nitroglycerin (NTG)
Unstable Angina (UA)
Cause & Pattern:
o Caused by atherosclerosis with thrombus that partially occludes the lumen
o Does not follow predictable onset and relief pattern of stable angina
o Increasing in frequency
o May be more sever or prolonged than the patients prior angina symptoms
Triggers:
o Occurs with less provocation than stable angina, or at rest
MI-Associated Angina
Cause & Pattern:
o Caused by atherosclerosis and thrombus completely or nearly completely occluding the lumen
o Symptoms are generally more sever, last longer than UA, and are not relieved with NTG and rest
o If not relieved within 20-30 minutes of onset, myocardial injury and/or infarction is very likely
Triggers:
o May have no identifiable trigger
Variant Angina (Prinzmetals Angina)
Cause & Pattern:
o Due to coronary artery spasm, which narrows arterial walls and slows or blocks blood flow
o Usually occurs at rest, often in the early hours of the morning
o Can occur both in people who have CAD and in those who dont
Treated chronically with nitrates and CCBs to vasodilate the arteries and inhibit spasm
Triggers:
o No identified triggers
Did You Know?
Indicators of Chronic Ischemic Myocardial Disease

TOPIC B: IDENTIFYING ISCHEMIA AND INFARCTION

12 Lead ECG Tracing:
Any pt presenting with s/sx of ACS coupled with T wave inversion, ST depression, hyperacute T waves, ST elevation, or new or
developing Q waves should be reported to the provider immediately as suspicious for ACS
T to P Interval/Baseline:
o Before looking for changes related to ACS, establish the baseline against which ST changes should be measured
T to P interval represents electrically silent period for atria and ventricles and is considered isoelectric
Since there is no electrical activity during this time, the T to P interval provides an accurate baseline against
which to compare the ST segment, looking for either ST depression or ST segment elevation

ST Segment Depression & T Wave/Ischemia

o ST Segment Depression and T wave inversion are produced by ischemia, and may occur transiently during UA, or
may persist, indicating non-STEMI
ST depression and T wave inversion may become ST elevation (injury) as ischemia progresses
Symmetrical precordial T wave inversion of 1-2 mm or more strongly suggests acute ischemia
ST depression of 0.5 mm (1/2 small box) on the 12-lead ECG tracing that is seen with symptoms and
resolves when the pt is asymptomatic is highly indicative of severe CAD
ST depression may occur in multiple lead groups indicating that the pt has diffuse disease involving more
than one coronary artery
 ST Segment Elevation/Injury
o Myocardial injury results in ST-segment elevation
o Significant elevation is defined as 1 mm (1 sm box high on ECG tracing) or greater in two anatomically contiguous
leads (looking at the same area of the heart)
Hyperacute T waves are considered an early sign of STEMI and should be treated as a STEMI
Loss of the St segment as the ST segment and the T wave become fused together is another early sign of
STEMI
Other causes (beyond MI) for ST segment elevation include L ventricle aneurysm, L ventricle hypertrophy,
early repolarization, pericarditis, and ventricular-paced rhythms

Reciprocal Changes
o When ST segment depression occurs on an ECG that is also demonstrating ST elevation, it may be due to reciprocal
changes in leads monitoring the L ventricle from the wall opposite to the injured myocardium
o An angiogram may be the only way to know for certain if ST depression on an ECG showing ST elevation is due to
reciprocal changes or if there is also occlusion of another coronary artery resulting in ischemic changes

Normal & Pathologic Q Waves

o Q wave is the first negative deflection of a QRS complex
o Normal Q waves are very small and very narrow
Q waves occur normally as an indication of septal depolarization in many leads, including I, aVL, V 5 and V6
In some patients, small Q waves will also be seen in leads II and aVF
o Pathologic Q waves indicate MI and are at least one 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 are also indicative of an acute process
Q waves seen in the presence of ST elevation, which indicates that the infarction is acute
Pathological Q waves are permanent and will indicate prior infarction on subsequent ECGs

Systemic ECG Review:

Step 1: Look for T wave changes (inversation and hyperacute)

Step 2: Look for ST segment changes (elevation or depression)

Step 3: Look for Pathologic Q waves

Associating Leads with Heart Walls

Left Main Coronary Artery Infarction:
Posterior Wall:

Posterior MI Indications:
When to suspect a posterior MI:
o ECG Readings
Clinicians should be suspicious of posterior MI when leads V1V3 and/or V4 show tall R waves with ST
depression and an upright T wave.
o Direct Visualization
If you need to directly visualize the electrical activity of the posterior wall of the left ventricle, use
additional leads, V7V9, to look for ST elevation.
Did You Know?

12-Lead ECG Summary

TOPIC C: INTERPRETING BIOMARKERS
Cardiac biomarkers, sometimes called cardiac enzymes, are a group of enzymes and proteins that are released as
a result of cardiac cell injury or death.
Cardiac biomarkers are measured in the blood to diagnose the presence and extent of myocardial damage. Ideal
biomarkers are sensitive, cardiac-specific and reliable.
Cardiac Biomarkers

Rise & Fall of Biomarkers

Cardiac Biomarker Frequency

Normal Ranges for Cardiac Biomarkers:
Normal ranges may vary based on the hospital's equipment and the reagents used. These ranges are often
considered normal:
o CK
Total Male 55-170 units/L
Total Female 30-135 units/L
o CK-MB
Less than 10 ng/mL or less than 3% of total CK
o Troponin
Cardiac troponin I less than 0.03 ng/mL
Cardiac troponin T less than 0.2 ng/mL
TOPIC D: MYOCARDIAL OXYGEN SUPPLY & DEMAND

Oxygen Balance:
Preload:

Contractility:
Contractility affects oxygen demand.
Contractility, or cardiac muscle squeeze during systole, consumes approximately 70% of the oxygen supply
delivered to the myocardium.
o Oxygen consumption of the myocardium is high, compared to the body's overall oxygen extraction ratio
of 25%40%.
Anything that increases sympathetic stimulation, such as exercise or activation of the fight-or-flight response,
increases contractility, resulting in an increased demand for oxygen from a blood supply that is already extracting
a large percentage of the oxygen delivered.
Afterload:
Changes in afterload affect oxygen demand.
What is afterload?
o Afterload is the force, or resistance, that the ventricle must overcome to eject its preload.
What happens when afterload increases?
o Increases in afterload require the ventricles to work harder to overcome the pressure in the aorta and
pulmonary artery, in order to open the aortic and pulmonic valves.
This increases the demand for oxygen.
How can we decrease oxygen demand?
o Decreasing the myocardial oxygen demand is largely accomplished using pharmacologic agents that
optimize preload, heart rate, afterload, and contractility.

Oxygen Supply:
Arterial Oxygen: made up of both dissolved oxygen in the blood (PaO2) and oxygen carried by hgb molecules
(SaO2)
Increasing Oxygen Supply: supply may be increased by administering oxygen and maintaining adequate levels of
hgb
CAD Narrows Artery: with CAD, atherosclerosis narrows the coronary artery lumen
o When lumen narrows significantly, any increase in demand can result in insufficient delivery of oxygen
and tissue ischemia
Occlusion Increases: as occlusion increases, a further reduction in the blood flow occurs, resulting in myocardial
ischemia at lower levels of activity
Potential Infarction: when myocardial oxygen demand exceeds supply, infarction may occur
Vasoactive Medications:
NTG: causes smooth muscle vasodilation and reduces preload
 o Low Dose Effects:
At low doses (< 100 150 mcg/min), its primary effect is venous dilation (preload reduction)
o Higher Dose Effects:
At doses > 150 mcg/min, arterial vasodilation is also seen, resulting in a slight reduction in
afterload
Phenylephrine (Neosynephrine): selective alpha 1 receptor agonist that cause arterial vasoconstriction (increases
afterload) without an associated increase in HR
Dopamine (Intropin): immediate precursor of norepinephrine and epinephrine
o Low Dose Effects:
At infusion rates of 0 10 mcg/kg/min, beta adrenergic receptors are activated, increasing
contractility and leading to increased cardiac output and variable systemic vascular resistance
(SVR)
The HR may increase, especially in patients with low preload
o Higher Dose Effects:
Higher doses ( 10 20 mcg/kg/min ) are contraindicated in ACS because the increase in SVR will
increase myocardial oxygen consumption
Dobutamine (Dobutrex): potent inotrope with moderate vasodilatory properties, increasing contractility and
decreasing afterload without a significant increase in HR
o Indicated for decompensated HF and cardiogenic shock
Milrinone (Primacor): phosphodiesterase inhibitor, with properties very similar to dobutamine
o Effects: will cause a decrease in mean pulmonary artery pressure (PAP), pulmonary artery occlusion
pressure (PAOP), and SVR without increasing HR
Nitroprusside (Nipride): dilates both arterioles and venules, resulting in a reduction in preload and afterload
o Might be used in combo with dobutamine or dopamine for a pt in cardiogenic shock until and intra-aortic
balloon pump can be placed

TREATING STEMI, NON-STEMI, AND UA PATIENTS

TOPIC A: TREATING STEMI PATIENT
ACS Protocol:
 Any patient presenting with chest discomfort or other symptoms of ACS should be immediately triaged and evaluated
utilizing a chest pain protocol.
In a case where symptoms had resolved and then there is new onset of significant symptoms, selected elements of the ACS
protocol need to be repeated.
o Focus on the things that are already in place, and implement actions for patient diagnostic information that may
have changed.
Immediate care should include:
o 12-lead ECG completed and reviewed within 10 minutes
o Cardiac biomarkers
o Medications to improve myocardial oxygen supply and demand, and to alleviate pain
Treatment Goals

When to administer supplemental oxygen:

Administer supplemental oxygen to patients presenting with ACS if:
o SpO2 is less than 90%.
o Patient is exhibiting respiratory distress.
o Patient is at high risk for hypoxemia.
Supplemental oxygen may increase coronary vascular resistance, so administer with caution
Nitrates in pt w/ ACS:
Nitroglycerin (NTG) reduces preload and to a smaller extent reduces afterload, and dilates coronary arteries. Consider
continuous intravenous NTG if, after three sublingual doses, the pain has not been relieved.

Morphine for pt w/ ACS:

Morphine is used because it:
o Decreases pain, which may decrease afterload and myocardial oxygen demand
o Decreases anxiety, which helps attenuate the effects of increased sympathetic nervous system stimulation (elevated
heart rate and systemic vascular resistance)
o Increases venous capacitance, which is helpful in decreasing preload and myocardial oxygen demand
Treating & Preventing Thrombus | Medications:
Managing Serious Bleeding:
All medications that treat thrombus carry a risk for bleeding. There are limited options that may reverse anticoagulant
effects:
o Protamine sulfate may be used to reverse heparin and, less effectively, LMWH. Protamine carries a small risk of
anaphylaxis.
o Anecdotal reports show Factor VII may reverse bleeding due to bivalirudin. Bivalirudin's half-life is 20-25 minutes in
patients with normal renal function.
o There are no drugs to reverse clopidogrel, prasugrel, or ticagrelaor. If a patient's platelets are not functional due to
one of these medications, platelet transfusion may be effective and can be given, even if the patient has a normal
platelet count.
o The half-life of GP IIb/IIIa antagonists vary by agent; stopping tirofiban or eptifibatide will significantly restore
platelet binding function within 2-4 hours. Abciximab has a 12-hour half-life, and platelet transfusion may be needed
if significant bleeding occurs.
Monitoring patient Response:
PT
INR
aPTT
Platelet count
Thrombin clotting time (TCT)
Activated clotting time (ACT)
Thromboelastography (TEG)
ACS Medications:
Beta Blockers:
o Uses:
Block sympathetic nervous system stimulation
Decrease afterload by causing arterial vasodilation
Slow the HR to allow increased diastolic perfusion time, which increases blood flow through the coronaries
to improve myocardial oxygen supply
Decrease contractility, which decreases myocardial oxygen consumption
Decrease incidence of ventricular dysrhythmias
Prevent ventricular remodeling, retaining a more normal systolic function
o Dosing Notes:
 Start within 24 hours, unless contraindicated
Pts should be discharged on BBs unless contraindicated
Notify provider if pt will miss multiple doses, as they prevent L ventricular remodeling an improve long
term mortality
Ventricular remodeling: changes in the geometry and contractile patterns in the hear; these are
compensatory changes early after myocardial infarction tha ultimately lead to HF
o Contraindications:
SBP < 90
Cardiogenic shock
Severe bradycardia
Second or Third degree AV Block
HF on presentation
ACE Inhibitors
o Should be started within 24 hours of presentation, especially for pts with:
HF, particularly if EF less than 40%
Large anterior MIs or pulmonary congestion in the absence of hypotension
Stable CKD
Hx of bilateral renal artery stenosis
o ACE inhibitors work to prevent remodeling of myocardium, and reduce preload and afterload, decreasing the
workload of the heart
Angiotensin Receptor Blockers (ARBs)
o Some pts do not tolerate ACEIs since they prevent breakdown of bradykinin, resulting in a dry, hacking cough
Calcium Channel Blockers
o CCBs are not routinely prescribed for pts with ACS
o May be useful for pts who are intolerant of beta blockade or those with vasospastic disease and HTN, since they
block vascular smooth constriction and can decrease HR
Reperfusion:
Emergent PCI
o Catheter passed through vasculature to the site of coronary obstruction, and intervention are applied to disrupt the
thrombus and dilate the coronary lumen
o Most effective reperfusion therapy, but not all hospital can provide emergent PCI
Fibrinolytic Agents
o IV meds used to cause thrombus to lyse (used if PCI not quickly available)
Urgent CABG
o Surgical placement of grafts performed to bypass significantly narrowed or occluded coronary arteries
o Indicated in pts with STEMI whose coronary anatomy is not suitable for PCI, or those post-PCI with recurrent
ischemia, cardiogenic shock, or severe HF
o CABG more commonly used after recovery from ACS, as indicated by extent of CAD
Fibrinolytics:

Criteria
o Fibrinolytic therapy should be administered to patients presenting with STEMI with symptom onset within the
previous 12 hours, if urgent PCI is not available.
o ASA, heparin, and a P2Y12 receptor inhibitor are given in conjunction with fibrinolytics to help maintain a patent
vessel once the thrombus is dissolved.
 o Fibrinolytics may be given as late as 24 hours after symptom onset if pain persists in patients who meet the criteria;
but the earlier they can be given in the course of the infarction, the more likely they are to be effective at lysing the
thrombus.
o When a fibrinolytic agent is to be administered, the time from arrival to the facility to actual injection of the
medicine should be no longer than 30 minutes.

Contraindications to Fibrinolytic Therapy:

Due to its systemic action, carefully screen patients before initiating fibrinolytic therapy.
Absolute contraindications include:
o Any history of intracranial hemorrhage
o Ischemic stroke, significant closed head injury, or facial trauma within the previous three months
o Severe uncontrolled HTN
o Suspected aortic dissection
o Active known bleeding or bleeding diathesis (excluding menstruation)
o Known structural cerebral vascular lesion or malignant intracranial neoplasm
Relative contraindications to fibrinolytic use will be screened by the provider. Communicate any information you know about
the patient that may constitute a bleeding risk.
V1: best identify ventricular ectopy
V3: assess for reinfarction
V5: assess for lateral reinfarction
Management of STEMI Pt:

Discharge Plan:
Patient Education:
Patient education is an important opportunity to identify risk factors for secondary prevention and to give instructions for
what symptoms to report and when to call 911.
Modifiable Risk Factors
o Secondary prevention is focused on improving modifiable risk factors including:
Diet
Physical activity
Cigarette smoking
Obesity
HTN (therefore, medication compliance is critical)
Diabetes mellitus (glucose management through diet, medications, and exercise can improve outcomes)
Dyslipidemia (can be impacted through diet and exercise, but also treated medically)
Symptoms to Report
o When to Contact the Provider
Patient discharge education should include symptoms to report to the provider. These symptoms include:
Chest pain
Dyspnea
Dizziness
Unusual sweating
Unusual fatigue
Chest discomfort that moves into arms, jaw, back, neck, or abdomen
o When to Call 911
Make special note of symptoms that may indicate MI and the need to call 911 if these occur. These include:
Chest pain that is more severe and is not relieved with NTG and rest
The same symptoms experienced with the current M

TOPIC B: TREATING NON-STEMI AND UA PATIENTS

Non-STEMI or UA Diagnosis
Types of UA:
Thrombus that only partially or temporarily blocks an artery causes UA.
o Rest Angina
Occurs at rest and lasts longer than 20 minutes
o New-onset Severe Angina
Has been present for less than two months and causes marked limitation of ordinary activities
o Increasing Angina
Has been previously diagnosed but occurs more frequently, lasts longer, or produces symptoms with less
and less exertion

Treatment Pathways:

Areas where Tx for STEMI and non-STEMI differ:

 The timing of the administration of some medications differ, in particular GP IIb/IIIa antagonists may be provided
early in the hospital course, not only as adjunct to PCI.
Patients presenting with non-STEMI are generally NOT candidates for emergent reperfusion therapy. Instead,
when a patient with non-STEMI has ongoing, unrelieved chest pain, hemodynamic instability, or rhythm
disturbances, they may be taken immediately to the catheterization lab for angiography and possible PCI.
Fibrinolytic therapy is not indicated in non-STEMI.
Management of Non-STEMI and UA Pts:

COMPLICATIONS
TOPIC A: PULMONARY EDEMA
Myocardial Dysfunction
TOPIC B: RVMI
Occluded RCA
30%50% of patients with an inferior wall MI will have right ventricular (RV) infarction as well.
RV infarctions seldom exist alone; they are almost always seen with an inferior infarct. The coronary artery
involved is usually an occluded RCA.
Other Effects of RCA Blockage

RVMI on ECG:
ST segment elevation in RV4: 1 mm ST segment elevation in RV4 is considered to be diagnostic for R ventricular infarction

T wave in RV4: a convex or domed shape on the T wave in RV4 usually signals injury is occurring
Leads RV3-RV6: Any ST elevation in RV3-RV6 suggest RVMI
Pathological Q waves: signal that necrosis has occurred to a significant area of myocardium; absence of appreciable R
waves (R wave progression) in V leads is equivalent to Pathological Q waves

Diagnostic Tests:
Echo:

Repeated cardiac biomarkers

Chest XR

BNP

Pathophysiology
Results of Impaired RV Stroke Volume

Effects of Decreased LV Preload

Management of RVMI
In addition to volume loading the RVMI patient to create sufficient preload so that RV output can provide sufficient LV
preload, there are several other considerations that make management of RVMI different from left ventricular myocardial
infarctions (LVMIs).
Beta Blockers
o Beta blockers should be used with caution for a patient with RVMI, because they decrease heart rate and
slow conduction through the AV Node. These patients are already at risk for bradycardia and AV block,
and beta blockers can exacerbate both of these.
NTG
o For a patient with RVMI, NTG should be given with great caution, if at all. A significant reduction in
preload will significantly impair the RV stroke volume, as the infarcted RV cannot compensate. The
resulting decrease in RV output means limited LV preload, and decreased LV output.
Reperfusion Therapy
o Reperfusion therapy should be initiated at the earliest signs of RV dysfunction. Complete recovery over a
period of weeks to months is a rule in a majority of patients, suggesting RV "stunning" rather than
irreversible necrosis has occurred.
Pacing
 o Common dysrhythmias seen with RVMI include sinus bradycardia, atrial fibrillation, and AV block, which
may require temporary pacing. Maintaining AV synchrony optimizes ventricular filling and output, so dual
chamber pacing may be needed. AV blocks with wide QRSs are due to damage below the AV node and do
not respond to atropine, which is the usual first treatment for symptomatic bradycardia
TOPIC C: CARDIOGENIC SHOCK AND IABP (EXTRA ICU ONLY CONTENT ON IABP)
Pathophysiology of Cardiogenic Shock

Tx for cardiogenic shock:

Interventions aimed at improving a component of cardiac output: contractility, rate, afterload, or preload.
Fluid Management:

Inotropic Support

Oxygenation
Electrolyte Imbalances

Intra-Aortic Balloon Pump (IABP)

An intra-aortic balloon pump (IABP), also called balloon pump, is a short-term mechanical device that assists the
heart by reducing afterload (which facilitates unloading of the LV) and increasing coronary artery perfusion by
increasing the augmented diastolic pressure in the aortic arch to improve coronary artery perfusion pressure.
The IABP consists of two parts:
Balloon inserted into the aorta
Machine outside the body to inflate and deflate the balloon in synchrony with the heart
Because it is easy to insert, the IABP is the most widely used form of mechanical circulatory support.

IABP therapy indications include:

Cardiogenic shock
 High risk or failed PCI patients
Failure to wean from CPB
LV failure or coronary artery rupture during PCI
Contraindications for IABP therapy include:
Aortic Regurgitation
Severe aortic disease
Severe peripheral vascular disease in the affected limb
TOPIC D: OTHER COMPLICATIONS
Dysrhythmias: Dysrhythmias are the most common complication of MI.
Etiology
o Dysrhythmias are often the result of ischemia to the myocardium and conduction system, resulting in
cellular dysfunction and disruption of the normal cardiac action potentials.
Dysrhythmias can also result from:
o Increased sympathetic nervous system (SNS) stimulation
o Proarrhythmic effects of medications
o Irritability of the injured myocardium
Occurrences
o Dysrhythmias occur most frequently while the infarct is evolving and are often self-limiting.
The dysrhythmias range from benign to life-threatening, such as:
o Sinus bradycardia or tachycardia
o Atrial fibrillation and flutter
o Supraventricular tachycardia
o AV heart blocks
o Bundle branch blocks
o PACs and PVCs
o Ventricular tachycardia and fibrillation
Treating Dysrhythmias:

Pathophysiology of Papillary Muscle Rupture

Objective Findings for Papillary Muscle Rupture

Use of IABP: An IABP may help improve perfusion to the coronary arteries, alleviating ischemia.
The device may also significantly decrease afterload, facilitating unloading of the LV as well.
Some patients may be able to tolerate vasodilator therapy better after the IABP has been inserted.
Achieving Target Temperature Management:
 CARING FOR PATIENTS W/ CARDIOVASCULAR
DISORDERS: PART II
CARDIOVASCULAR PATHOLOGIES & ELECTROPHYSIOLOGY: ELECTROPHYSIOLOGY
TOPIC A: LONG QT SYNDROME (LQTS)
Long QT Syndrome:
LQTS is a cardiac repolarization disorder that prolongs the QT interval.
QT interval prolongation increases risk of torsades de pointes (TdP).
LQTS can cause sudden cardiac death (SCD).
LQTS can be acquired or congenital, though congenital is rare.

Causes of Acquired LQTS: Meds are the most common causes of acquired LQTS; not all meds in a category prolong QT, but the most
common culprits are in the following categories

Risk factors for Acquired LQTS:

Normal vs. Prolonged QT Interval:

Monitoring QTc:
Routine cardiac rhythm assessment includes measuring and documenting the QT interval, and calculating the QTc.
The QTc is an essential measure when monitoring any patient.
Monitoring Systems: Depending on your hospital protocol and equipment, you may measure QTc manually or use on-screen
calipers and a QTc calculator.
Bazett's Formula: Bazett's Formula is the most commonly used QTc calculation.

Treating Acquired LQTS:

TOPIC B: CARDIOVERSION
Cardioversion Procedure:
Overview: during cardioversion, electrical energy is synchronized with the ECG rhythm and delivered to the heart
o Must be delivered during ventricular depolarization
o Energy delivered during the T wave (ventricular repolarization) can potentially cause VF
o Cardioversion may be emergent or scheduled depending on pts stability

Patient Prep:
o Ensure K and Mag are within normal limits (WNL)
o If pt is on anticoagulation, verify this is within therapeutic range
o Ensure chest is dry. Clip extra hair to ensure proper electrode contact
o Set pt expectations:
Inform pt shock is painful, like a kick to the chest
Assure them they will receives meds to lessen pain & reduce anxiety
o Gather defib, emergency meds, suction, sedation & sedation reversal agent, O2 and intubation equipment
o Establish SpO2 monitoring, Use end tidal CO2 (EtCO2) monitoring per hospital protocol
o Transesophageal echocardiogram (TEE) may be performed immediately prior to scheduled cardioversion
to evaluate for atrial thrombus
Equipment Prep:
o Electrode Pads Placement:
Place defib electrode pads on pts chest
Anterior-posterior placement: L anterior precordial area & L posterior infrascapular area
Anterior placement: second intercostal space to the R of the sternum and 5th intercostal
space, midaxillary line to the L of the sternum
If paddles are used instead of patches, use conductive medium/gel
Do not place electrode pads/paddles over the pulse generator ina pt with a permanent
pacemaker or ICD
o Defibrillator:
On the defibrillator:
Select monitoring lead that displays a large R wave
Activate synchronization mode, and ensure R waves are flagged
Procedure:
o Step 1: Charge Defibrillator
Set energy level as ordered by the provider (typically 50-100 joules, depending on the rhythm).
Charge defibrillator
o Step 2: State All clear
State all clear and verify no personnel are touching the patient, bed or anything attached to the
pt
o Step 3: Discharge Defibrillator
Discharge defibrillator. Maintain pressure on the buttons until you observe delivery of the
synchronized shock
o Step 4: Evaluate Rhythm
 If the heart has not returned to a normal rhythm, additional shock is required. Verify the
synchronization feature remains activated before delivering each additional shock
Post-Procedure:
o Assess hemodynamics
Assess cardiac rhythm, HR, BP, RR, and LOC. Palpate pulse to verify rhythm is perfusing
o Provide O2
Provide O2 to maintain SpO2 greater than 92%
o Monitor post-sedation recovery
Follow institution protocol for post-sedation recovery
TOPIC C: DEFIBRILLATION
Definition:
Defibrillation is the delivery of electrical energy to the myocardium to terminate life-threatening ventricular
dysrhythmias (VF and pulseless VT).
o The electrical energy depolarizes all cells in the heart simultaneously.
o This stops the dysrhythmia and allows the sinus node to resume function as the normal pacemaker of the
heart.
o Electrode pads or paddles may be used.
While similar in process to cardioversion, defibrillation is different in important ways.
o During cardioversion, the "Synchronize" button is used, and the shock button is held until the shock is
delivered in synchrony with the next R wave.
o Defibrillation shocks are not synchronized with the QRS. Each procedure uses different amounts of
electrical energy.
In an emergency:
o Do not delay defibrillation if a defibrillator is immediately available.
o Administer CPR until a defibrillator arrives.
Electrode Pads vs. Paddles:

Procedure: Defibrillation should occur in a set series of steps

 STEP 1: Ensure patient's ECG rhythm is visible

Ensure pt's ECG rhythm shows on the defibrillator monitor & that the Sync feature is OFF

STEP 2: Set the energy level & charge

Set the energy to the desired joules, & press the charge button

STEP 3: State "All clear"

When ready, state "All clear" and verify no one is touching the pt, bed, or anything attached to the patient

STEP 4: Discharge defibrillator

Press the shock button to discharge the defibrillator. The shock will be delivered immediately.

STEP 5: Resume CPR.

Resume CPR for two minutes before rhythm & pulse check. Continue emergency ACLS procedures as indicated by cardiac rhythm, BP, and LOC

Conclusion:
Defibrillation is the emergency intervention with the greatest chance of restoring a normal rhythm in a patient
with pulseless VT or VF. Any delay in providing defibrillation decreases the chance of success.
If a defibrillator is immediately available, defibrillate without delay.
If a defibrillator is not immediately available, perform CPR until one reaches the bedside, then defibrillate.
 CARING FOR PATIENTS W/ CARDIOVASCULAR
DISORDERS: PART III
CARDIOMYOPATHIES
TOPIC A: DILATED CARDIOMYOPATHY

Pathophysiology:

Etiology:
Compensatory Mechanism: SNS Activation

Compensatory Mechanism: RAAS Activation

Symptoms Associated with HF

Assessment:
TOPIC B: HYPERTROPHIC CARDIOMYOPATHY (VIGNETTE)

TOPIC C: STRESS-INDUCED CARDIOMYOPATHY (VIGNETTE)

Pathophysiology & Etiology

Takotsubo

Risk Factors

Assess patient:

Treatment

Contraindicated treatments:

Recovery Process

TOPIC D: RESTRICTIVE CARDIOMYOPATHY

Restrictive cardiomyopathy is the least common type of cardiomyopathy and accounts for a very small population of
patients. It is characterized by a rigid myocardial wall that decreases the expansion of the chamber walls during
ventricular filling. This impairment is referred to as a noncompliant ventricle and results in diastolic dysfunction.
Etiology:
Pathophysiology:

Signs & Symptoms

Assessment:
Treatment Goals:

Treatment Priorities:
Meet Patient Needs:
Ambulate: encourage ambulation as tolerated
Elevate legs: position patient, and elevate legs when OOB to limit edema
Maintain Diet: educate pts on the benefits of a low sodium diet and weight control
Provide stockings: compression stockings
Reduce stress: counsel & educate pts on stress reduction
Surgical Options:
 HEART FAILURE
TOPIC A: SYSTOLIC HF: ASSESSMENT (SCENARIO)

TOPIC B: SYSTOLIC HF: TREATMENT (SCENARIO)

TOPIC C: SYSTOLIC HF: COMPLICATIONS (SCENARIO)

TOPIC D: DIASTOLIC HF
Diastolic dysfunction results in a stiff ventricle with impaired relaxation, preventing optimal filling of the ventricle
Etiology

Diastolic Dysfunction
Pathophysiology

Cardiogenic Pulmonary Edema:

Just like in systolic HF, patients with diastolic HF presenting at the more severe end of the spectrum may have
acute decompensated HF and pulmonary edema.
Cardiogenic pulmonary edema usually results from an acute cardiac event, which further impairs the already
limited cardiac function.
The heart is unable to effectively pump blood forward and blood backs up toward the lungs.
This process is not the result of diffuse pulmonary disease; however, if left untreated, it can lead to long-term
pulmonary complications.
Symptoms & Physical Activity:
Patients with diastolic HF become symptomatic because exertion induces tachycardia.
Tachycardia results in a decrease in diastolic fill time and a significant decrease in ventricular preload, and
therefore, in stroke volume.
Symptoms may progress to pulmonary interstitial fluid overload, as well as signs of inadequate tissue perfusion.
Flash pulmonary edema can develop if a patient becomes ischemic, worsening the compliance of the ventricle.
Signs & Symptoms:
Assessment:

Treatments:
Response to Treatment:

Conclusion: caring for patients with diastolic and systolic HF is similar, with the main differentiator being fluid
management. Diastolic HF patients should be provided with lower doses of diuretics to control symptoms of fluid
overload, as it is critical to maintain adequate preload.
TOPIC E: RIGHT-SIDED HF
Right-sided HF usually results from prolonged left ventricular failure. When the LV cannot efficiently move blood forward,
volume continues to back up toward the lungs, resulting in pulmonary vascular congestion and edema. This significantly
increases the afterload on the RV, causing the RV to fail.
Etiology:
Assessment:

Assessment Findings:

Diagnostic Tests

Treating the Cause of RV Failure:

Response to Treatment

Conclusion:
Right-sided HF can be a consequence of long-standing left-sided HF, and that the findings of fluid overload seen in
right-sided HF are sometimes also seen in left-sided HF.
Treatments are in part targeted toward rectifying the cause of the right-sided HF, and patients should be
monitored for potential complications of decreased cardiac output and atrial fibrillation or flutter.
TOPIC F: PATIENT EDUCATION (SCENARIO)