Adult Nursing 3: Exam 1

BLUE: EXTRA NOTES

RED: LECTURE NOTES
Cardiac Dysrhythmia Review

Dysrhythmia
Disorder of the formation or conduction of the electrical impulse within the heart
● Irregularity causes disturbances in:
o Heart Rate, Heart Rhythm, or BOTH
● Hemodynamic effects
● Regular rate and rhythm required to circulate oxygenated blood and life-sustaining nutrients to body
organs
o THINK about HR/rhythm: We worry about blood flow and oxygenation (something is wrong)
▪ If not regulated → the patient will have a negative outcome
o The best thing to do is an EKG for the patient
● Diagnosed by analyzing the electrocardiogram
● Named according to site of origin

Normal Electrical Conduction

Review of Cardiac Conduction System

SA Node Internodal Pathways AV Junction, AV node, Bundle Branches Purkinje Network
Bundle of His

Firing rate of Transfer impulse from Slows impulse Two main branches Spreads impulse
60-100 bpm the SA node throughout Intrinsic firing rate of (left and right) throughout the
the atria to the AV 40-60 bpm transmit impulses to ventricles
junction the ventricles Intrinsic firing rate of
20-40 bpm
 We don’t like less than 60, more than 100.

In the Normal Heart

● Electrical impulses cause and is followed by the mechanical contraction of the heart:
o Electrical Stimulation = Depolarization
o Mechanical Stimulation = Systole
o Electrical Relaxation = Repolarization
o Mechanical Relaxation = Diastole

Influences on HR and Contractility******

 ● Sympathetic Nervous System Stimulation - FIGHT OR FLIGHT
o Increases HR (positive chronotropy)
o Increases conduction through AV node (positive dromotropy)
o Increases force of myocardial contraction (positive inotropy)
● Parasympathetic Nervous System Stimulation - REST AND DIGEST
o Reduces HR (negative chronotropy)
o Reduces AV conduction (negative dromotropic)
o Reduces force of myocardial contraction (negative inotropy)

The Electrocardiogram
● EKG/ECG is a graph tracing of the electrical activity of the heart (Not the mechanical activity)
● Information obtainable from an EKG rhythm strip analysis: SATA**
o Heart rate? Yes
o Rhythm/regularity? Yes
o Impulse conduction time intervals? Yes
o Pumping action? No
o Blood pressure? No
o Cardiac Output? No
● What else does the EKG reflect?
o Ischemia  ST DEPRESSION [WHEN THE MUSCLE IS LACKING OXYGEN]
o Infarction  ST ELEVATION
o Electrolyte disturbances
o Drug toxicity – QT could say drug toxicity
o Enlarged cardiac chambers

EKG Waveforms/Segments/Intervals
● P wave
● PR interval***
● QRS complex
● ST segment (should normally be isoelectric)
• Elevated at your level → THINK MI
● T wave

P Wave
Represents the electrical impulse starting in the SA node and spreading through the atria (rounded and upright)
● Atrial muscle depolarization (atrial contraction)
● <0.11 seconds in length
→ THERE SHOULD BE 1-2 SMALL LITTLE BOXES
End of P start of Q
PR Interval
Measured from the beginning of the P wave to the beginning of the QRS complex
 Movement of electrical activity from atria to ventricles
 Represents time needed for sinus node stimulation, atrial depolarization and conduction through the AV
node
● 0.12-0.20 seconds in length
→ THERE SHOULD BE at least 3 SMALL LITTLE BOXES, or up to 1 BIG BOX MAX
● 1 small box = 0.04 [ 0.04 x 3 = 0.12]
● 1 big box = 0.20

QRS Complex
Represents ventricular depolarization (vent. contraction)
o 1st negative deflection: Q wave
o 1st positive deflection: R wave
o 1st negative deflection after the R wave: S wave
o <0.12 seconds in length
→ THERE SHOULD BE 3 SMALL LITTLE BOXES MAX
● 0.04 x 3 = 0.12 (max)

ST Segment
Represents early ventricular repolarization
● Time from ventricular depolarization (contraction) and repolarization (relaxing)
● Lasts from the end of the QRS complex to the beginning of the T wave
● Normally isoelectric → meaning it will stay on the line
o Analyzed above or below the baseline
  P through R = Atria issues
 R and beyond = Ventricular issues
 Anything ST whether its elevation/depression/segment = MI **

ECG done 5-10 min fast

Systematic read left to right

T Wave
Represents ventricular muscle repolarization (relaxation)
● Normal T wave = upright, lasting 0.16seconds
● Resting phase - when the cells regain a negative charge
● Follows the QRS complex; usually in the same direction as the QRS
● Refilling with blood, Relaxing, Repolarizing
Systematic Analysis of ECG
1. Identify P wave: is there a p-wave before every QRS?
1. Is the P wave Consistent? Upright? Before every QRS complex?
2. IF no P wave, the ECG is not normal.
2. Determine each PR interval: Consistent? Irregular but with a pattern? Irregular?
3. Identify the QRS: Duration consistent? Shape consistent?
4. Evaluate the ST segment: Isoelectric? Depression vs. Elevation? Peaked?
5. Identify the T wave: Upright? Inverted?
6. Identify ventricular rate and rhythm (R-R):
1. Is the R-R consistency regular or irregular?
2. Determine HR by: 6 second method OR big box method

**KNOW THIS PICTURE**

 1 tiny box = 0.04 sec
 5 tiny boxes= 1 big box
 1 big box = 0.20 sec
 5 big boxes = 1.00 sec

Heart Rate Determination

● Regular
o 1- minute strip contains 300 large boxes (1500 small boxes)
o Count number of small boxes within an RR interval and divide 1,500 by that number
● Irregular
o Less accurate method:
o Top of ECG paper is marked at 3-second intervals (15 large boxes horizontally)
o Count the number of RR intervals (not QRS complexes) in 6-seconds and multiply that number by
10

Heart Rate Determination

Heart Rhythm Determination

 ● RR interval used to determine ventricular rhythm
● PP interval used to determine atrial rhythm
● If intervals are the same: regular rhythm
● If intervals are different: irregular rhythm

Normal EKG

Abnormal EKG

 Elevation in 2nd row- patient is having an MI **

Cardiac Dysrhythmia Management and Pacemakers

Normal Sinus Rhythm

 Determine this to practice. MUST know what is normal to find out what is abnormal!!
 Normal: 60-100 bpm – uniform throughout/nice (measure point A to B)

Sinus Bradycardia
HR<60 bpm
● Sinus node creates impulse at slower than normal rate
 ● Characteristics of NSR but a slower rate
● Etiology: ALWAYS THINK CARDIAC, THEN RESPIRATORY
o Sleep
o Athletic training
o Hypothyroidism
o Vagal stimulation
• Vomiting, suctioning, pain**
o Medication
• CCB, amiodarone, beta-blockers – these cause HR to be lower
o Increased intracranial pressure
o CAD/Acute MI
o Hypoxemia
o Altered mental status
o Acute decompensated heart failure
• Clinical Manifestations
o SOB, Altered LOC, Hypotension
o EKG changes (ST segment changes PVC’s)
→ State boards wants you to call another nurse when needed
• Management  ONLY IF INDICATED/SYMPTOMATIC
o Resolve causative factors
o Atropine 0.5 mg IV every 3-5 minutes****
• Maximum dose of 3 mg
• Atropine is an antiarrhythmic drug (also known as an anticholinergic)
• It antagonizes acetylcholine receptors
• This will reverse the PNS essentially, increasing the HR
o Emergency transcutaneous pacing (have crash cart on bedside, pt on monitor as well just in case
patient needs to be paced). Atropine is given but comes back down
o Catecholamines - These are hormones of the SNS (epi, norepi)

Sinus Tachycardia
HR: 100-120
● Sinus node creates impulse at faster than normal rate
● Does not start or stop suddenly- it is gradually over time
● Etiology
o Physiologic stress
o Acute blood loss, anemia, Shock –
• blood loss, heart starts working more, eventually lose so much can go into shock and
these can all cause sinus tachy
o Hyper/hypovolemia – dehydration ,losing blood, compensating
o Heart failure
o Pain
o Hypermetabolic states
o Fever
o Exercise
o Anxiety
o Medications
 • Catecholamine, Atropine, Stimulants (caffeine, nicotine), Illicit drugs (Ecstasy, cocaine)
• If med is the factor, ONCE the med wears down than the HR must come back down
● Clinical Manifestations
o Decreased filling time of heart - AS THE HR INCREASES, THE DIASTOLIC FILLING TIME DECREASES
• Reduces cardiac output
• Syncope
• Hypotension
• Acute pulmonary edema
• If the rapid rate persists and the heart cannot compensate for the decreased
ventricular filling, the patient may develop pulmonary edema
● Management
o Abolish the cause!!!
→ MUST FIND THE UNDERLYING CAUSE FOR TREATMENT (keep asking yourself why is this
happening??)
→ Our goal is to get rid of the cause
→ a lot of times they start with fluids for sinus tachycardia (because we think of dehydration) - so the
DR will order some fluids such as normal saline
o Synchronized cardioversion (hemodynamic instability)
o Vagal maneuvers
• Carotid sinus massage, gagging, bearing down against a closed glottis (as if having a
bowel movement), forceful and sustained coughing, and applying a cold stimulus to the
face (such as immersing the face in ice water)
o Adenosine (antiarrhythmic) Increase parasympathetic stimulated, causing slower conduction
through the AV node and blocking the reentry of the rerouted impulse SVT 150
o SOTALOL, AMIODARONE, LIDOCAINE
o Give fluids unless they are on restriction
o Narrow QRS?
• Beta-blockers (rare)
• Calcium-channel blockers (rare)
o Wide QRS?
• Adenosine (SVT HR 150 not 120)
• In tachycardia, it slows AV node conduction time, interrupts AV node reentry
pathways
• Sotalol ( class II & III antiarrhythmic/ beta blocker)
• Amiodarone ( class III antiarrhythmic)
o Patients with hypovolemia → Increased fluid/sodium (POTS) [increase fluid and sodium intake, or
use of salt tablets if necessary]

Atrial Flutter
*SAWTOOTH*
Conduction defect in the atrium and causes a rapid, regular atrial impulse
• Creates atrial rate between 250-400 times/minute
• (Ventricular rate 75-150)
• Not all impulses conducted to ventricle: therapeutic block at AV node
• 2:1, 3:1, 4:1 (Ratio of p waves to QRS complex)
• Regular atrial activity
 • P wave= “saw tooth” appearance (NOT CONSISTENT)
• HR > 100 bpm- “Uncontrolled”
• HR > 150 bpm- “Rapid ventricular rate”
• Etiology- Respiratory or Cardiac May or may not have these symptoms
o COPD
o Pulmonary HTN
o Valvular disease
o Thyrotoxicosis: excess of thyroid hormone in the body
o Open heart surgery
• Clinical Manifestations
o Chest pain
o Dyspnea
o Hypotension
o Either seen, or patient reports it. REPORT THE CM TO BEGIN MANAGEMENT!!!
• Management
o STABLE: drug therapy
o UNSTABLE: electrical cardioversion (NOT defibrillation)
o Use of vagal maneuvers
o Trial administration of adenosine, which causes sympathetic block and showing conduction
through the AV node
o Meds FOR FLUTTER (to slow ventricular response RATE ):
• Beta blockers *
• Calcium channel blockers *
• Digitalis * digoxin know dig level signs and symptoms of dig toxicity
• Anticoagulant (risk for clots)

Atrial Fibrillation****
*RISK FOR CLOTS*
Rapid, disorganized and uncoordinated twitching of atrial muscle (ATRIA QUIVERING)
● NO CLEAR P WAVES BC OF RAPID QUIVERING OF ATRIA MUSCLE (quivering can cause clots)
○ R TO R INTERVALS ARE IRREGULAR
○ IF P wave is missing, the heart is NOT paced. P wave paces the heart.
○ Fibrillation means it is shaking, blood pulls and blood that pulls tends to clot and forms micro-
emboli which tends to move ***
● Paroxysmal or chronic (patient lives with it)
● Rapid ventricular response; loss of atrial kick (25-30% of cardiac output)
● Atrial rate 300-600 BPM
● Ventricular rate: 120-200 bpm
● Paroxysmal: recurrent; with sudden onset and termination
● Persistent: continuous
● Permanent: persistent = decision made not to restore or maintain NSR
● Etiology
o Post-operative period after CABG
o Valvular disease
 o Inflammatory disease (pericarditis)
o HTN
o CAD, cardiomyopathy
o Heart failure
o Hyperthyroidism
o Pulmonary HTN and embolism
o OSA (obstructive sleep apnea)
o “Holiday heart”
o Subarachnoid hemorrhage
→ This is a common rhythm for elderly patients
• Clinical Manifestations [ALL DUE TO LOW O2]
→ causes a loss in AV synchrony (the atria and ventricles contract at different times), the atrial kick (the
last part of diastole and ventricular filling, which accounts for 25% to 30% of the cardiac output) is also
lost
o Pt has palpitations/SOB/fatigue  12 lead ECG (to validate a-fib)
• Ask yourself, WHY are they in a fib? Do whatever it takes to find out why.
o Palpitations
o Fatigue
o SOB
o Exercise intolerance
o Hemodynamic collapse
→ Auscultation with an irregular rate that will quicken and slow down
• Diagnosis
o LOOK AT thyroid levels to rule out. They can be in tele floor thinking its cardiac because they are
not checking their thyroid levels.
→ MUST DO ONE because you can’t assume someone is in Afib you must validate this
→ DETERMINE THE UNDERLYING CAUSE (the why and possible reasons as to why the patient is in Afib
o Depends on cause and duration, patient age, symptoms and co -morbidities
o 12-lead EKG
o Echocardiogram
o Thyroid, renal and hepatic function labs
o CXR
o Exercise test
o Holter monitoring
• Management
→ patients with atrial fibrillation are at an increased risk of heart failure, myocardial ischemia, and
embolic events such as a stroke
o STABLE OXYGEN/MEDS
o UNSTABLE OXYGEN/CARDIOVERSION
o Rhythm control vs. rate control
o Hemodynamically unstable?
• Electrical cardioversion if < 48 hours
• >48 hours: TEE to confirm mural wall thrombus (CAN SHOCK A CLOT)  give
anticoagulants
• If absent: Heparin prior to cardioversion
• High risk of embolization of atrial thrombi if cardioverted if AF duration > 48
hours
• Coumadin x 4 weeks after cardioversion
• Amiodarone, Sotalol, Propafenone prior to cardioversion
o Pharmacologic cardioversion
• Tikosyn, Ibutelide = required patient hospitalization
 o HR control
o Beta blocker
• Contraindicated with bronchospasm
o Calcium channel blocker (THINK OF A-FIB)
• Contraindicated with impaired ventricular function AV block (Know med names)
Lidocaine, Sotalol, Amiodarone, Digoxin
o IV amiodarone or digoxin
• Dig can be given, but not right away- other stuff are tried first. With dig we have too
look out at potassium
o Antithrombotic therapy indicated for all patients with AFib
o Heparin therapy until INR therapeutic with Coumadin
• Xarelto, Pradaxa**** anticoagulant

→ IRREGULAR RATE (which makes it dangerous) - IT MUST BE TREATED

● The P wave is missing (this is our pacer - which is pacer our heart regularly) this is why we do not use
the word sinus since our sinus is missing (P wave) it is quivering and shaking the blood will pool and clot
and this can form a microemboli which tends to move
● The rate is disorganized and the patient can be at risk of a clot the rate is jumping (the number will
jump from 60’s to 80’s to 100’s)

Premature Atrial Contractions *DIDN’T TEACH THIS*

Single, ECG complex occurs when an electrical impulse starts in the atrium before the next normal impulse of
the sinus node
AN EARLY AND DIFFERENT P WAVE MAY BE SEEN
● Atrial bigeminy, trigeminy
● Interrupts the sinus rhythm
● Etiology
o Caffeine
o Alcohol
o Nicotine
o Anxiety
o Hypokalemia
o Stretched atrial myocardium (Hypovolemia)
o Hypermetabolic states
o Atrial ischemia, injury or infarction
● Clinical Manifestations
o Clinical Manifestations:
• “Skipped beat”
• Etiology
• Caffeine intake
• Hypokalemia
● Management
• Treat the underlying cause
• If infrequent: no treatment necessary
 • If > 6 per minute: treat underlying cause
• Such as reduction of caffeine intake, correction of hypokalemia

AV Nodal Re-entry Tachycardia (AVNRT)

Impulse conducted in the AV node that causes the impulse to be rerouted back into the same area over and over
again at a very fast rate
P WAVES ARE VERY DIFFICULT TO DISCERN
● Causes fast ventricular rate
● Abrupt onset and abrupt cessation
● QRS normal duration
● Atrial rate 150-250 (P waves??)
● Ventricular rate 120-200
● Etiology
o Caffeine
o Nicotine
o Hypoxemia
o Stress
o Coronary artery disease
o Cardiomyopathy
● Clinical Manifestations
o Reduced cardiac output
o Restlessness
o Chest pain
o SOB
o Pallor
o Hypotension
o Loss of consciousness
● Management
o Treatment aimed at breaking reentry of impulse
• Catheter ablation is the initial treatment of choice and is used to eliminate the area that
permits the rerouting of the impulse that causes tachycardia
o Vagal maneuvers
• Carotid sinus massage (contraindicated with carotid bruit)
• Gag reflex
• Breath holding
o Adenosine: Real fast IV push!!!!!!!
o CCB: verapamil, Cardizem
• Unstable: cardioversion
• Amiodarone, Diltiazem to prevent reoccurrence
o If P-waves not identified may be called Supraventricular Tachycardia (SVT)
• Indicates only that it is NOT ventricular tachycardia
o SVT can be
• Atrial fibrillation
 • Atrial flutter
• AV nodal reentry tachycardia
• Vagal maneuvers/Adenosine help slow rhythm to allow visualization of P waves
→ PATIENT IS GIVEN ADENOSINE (fast push medication which will cause asystole and it brings down the HR it
has a half life of 3 seconds)

Premature Ventricular Complex (PVC) (ONE)

Impulse that starts in a ventricle and is conducted through the ventricle before the next normal sinus impulse
• QRS is 0.12 seconds or longer; shape abnormal, bizarre
● More recent research shows that the following are NOT precursors to VT:
o More frequent than 6/minute
→ Patient can start going into V-tach
o Multifocal
o Occur two in a row
o Occur on the T wave
● Clinical Manifestations
o Patient may feel nothing or may say that the heart “skipped a beat”
● Etiology
o Cardiac ischemia/infarction
o Increased workload on the heart (heart failure/tachycardia)
o Digitalis toxicity
o Hypoxia
o Acidosis
o Electrolyte imbalance
o Healthy people: caffeine, nicotine, alcohol
● PVC Patterns
o Ventricular Bigeminy
▪ Occurs when every other beat is a PVC

o Ventricular Trigeminy
▪ Occurs when every third beat is a PVC

o Ventricular Quadrigeminy
▪ Occurs when every fourth beat is a PVC
o Ventricular Couplets
▪ Two PVC’s occurring together without a normal complex in between
● PVC: Management
o PVC’s are usually not serious
o IF Frequent and persistent  PVC’s may be treated with amiodarone or lidocaine or sotalol,
QBOLUS DRIP FORMAT
o Long-term therapy not usually indicated
o IF PVC IS NOT TREATED  PT WILL END UP WITH V TACH !!!!!
Ventricular Tachycardia (VT)
● Three or more PVC’s in a row → IS A MEDICAL EMERGENCY BECAUSE THE PATIENT IS NEARLY ALWAYS
UNRESPONSIVE AND PULSELESS
● Rate exceeds >100 BPM (100-250)
● Manifestations: LOW cardiac output = LOW oxygen (lethargy, syncope, palpitations, anxiety, chest pain)
● Etiology
○ Same as PVC
○ At risk for Lethal VT
■ Larger AMI
■ Lower ejection fraction
● Characteristics → WIDE AND CONSISTENT QRS COMPLEXES
o Ventricular rate: 100-200 BPM
o QRS: Duration > 0.12, abnormal
o P wave: difficult to detect, so the atrial rate and rhythm may be indeterminable
o PR interval: very irregular, if P waves are seen
● Management
o Determination of stable vs. unstable required for treatment
 o Stable
▪ Continuing assessment
▪ 12-lead EKG (DONE FIRST) THEN GIVE MED
▪ Antiarrhythmic medications (Procainamide, Amiodarone)
▪ Supportive care
● Management for Symptomatic Patient ******* KNOW THIS SLIDE
o Unstable with a Pulse:
▪ Cardioversion
o Unstable without a Pulse:
▪ CPR
▪ Defibrillation
▪ Precordial thump
▪ Implantable cardioverter defibrillator (ICD) for ejection fraction < 35%
▪ IV magnesium for Torsades de point (Polymorphic)
▪ Amiodarone IV
● Those with an ejection fraction greater than 35% may be managed with this
medication
● Never leave this patient alone
APIXABAN (elequis)

● UNTREATED VTACH CAN LEAD TO  V-FIB  DEATH

Polymorphic and Monomorphic Ventricular Tachycardia

*****DIDN’T WRITE DOWN WHAT HE SAID HERE****

Ventricular Fibrillation
Rapid, disorganized ventricular rhythm (>300 bpm) waves all over the place
• Causes ineffective quivering of ventricles
o Rhythm is extremely irregular, without a specific pattern
• No atrial activity
 • Irregular and undulating waves without recognizable QRS complex
• Electrical impulses initiated by multiple sites
• Etiology  think cardiac or electrolyte imbalance !!!!
o Most common: CAD and resulting AMI
o Untreated or unsuccessfully treated VT
o Cardiomyopathy
o Valvular heart disease
o Pro-arrhythmic medications
o Acid-base and electrolyte disorders
o Electrical shock
• Clinical Manifestations
→ is always characterized by the absence of an audible heartbeat, palpable pulse, and respirations
o NO CARDIAC OUTPUT = NO OXYGEN TO THE BODY
o Fatal dysrhythmia
o Pulseless- → NO PULSE?? CPR AND THEN WE DEFIBRILLATE AND THEN WE WILL GIVE
EPINEPHRINE FOR 3-5 MINUTES
o Amiodarone
• Apneic
o No coordinated cardiac activity
• Cardiac arrest and death imminent if VF not corrected
• Management
→ there is no coordinated cardiac activity, cardiac arrest and death are imminent is the dysrhythmia is not
corrected
o Check for pulse, no pulse start CPR right away until defibrillator arrives (switch every 5 cycles)
o CPR until defibrillator arrives
o ** DE-FIB THE V-FIB **
o Immediate Defibrillation
o 5 cycles of CPR alternating with defibrillation
o Epinephrine every 3-5 minutes
o One dose of vasopressin instead of epinephrine (every 10min)
o Anti-arrhythmic
• Amiodarone
• Lidocaine
• Magnesium IV
o Intubation/airway management
Patient is up and awake and then goes into V-fib all of a sudden this is a v-fib arrest and we would use
hypothermia protocol which would cool the patient down and correct any electrolyte imbalance
o Hypothermia protocol (TO COOL THEM DOWN)
• Mild hypothermia in comatose adults (32-34 °C)
• Induction started as soon as circulation is restored
• Maintained 12-24 hours
• Nursing Management
o Monitor appropriate level of cooling
o Medication administration and monitoring (sedation, paralysis)
o Monitoring and prevention of seizures, shivering
o Monitor electrolyte imbalance
o Correct hypotension
o Treat infection
o Monitor and treat hyperglycemia
Ventricular Asystole
“Flatline”
• ABSENT QRS complex, may be P waves for a short duration
• Confirmed in two different leads
• No heartbeat, no palpable pulse, no respirations
• Etiology
o If related to blood volume, you can get them back
o H= hypoxia stuff
o T= trauma stuff
o Assessment of H’s and T’s (these are the reason why we go into asystole)
• Hypoxia
• Hypovolemia
• Hydrogen ion (acid-base imbalance)
• Hypo/hyperglycemia
• Trauma
• Toxins
• Tamponade
• Tension pneumothorax
• Thrombus
• Management
o CANT CARDIOVERT BECAUSE THERE IS NO ELECTRICAL ACTIVITY
o High-quality CPR!!!!
• Can be run for up to 1hr if young and healthy (in elderly 2 rounds and that’s it)
o Minimal interruptions
o Identify underlying factors
o Intubation
o Establish IV access
o Epinephrine bolus (repeat 3-5 minutes)
o Vasopressin
o Call code

Conduction Abnormalities
● General Information
o Identify underlying rhythm
o Assess PR interval – IMPORTANT
o AV blocks occur when the conduction through the AV nodal or His bundle is decreased or
stopped)
 ▪ Medications (CCB, BB)
▪ Myocardial ischemia/infarction
▪ Cardiomyopathy
▪ Increased vagal tone
● Clinical Manifestations
o Vary with resulting ventricular rate and severity of underlying disease process
o Asymptomatic
o Hemodynamic instability (according to the book - first-degree AV block rarely causes any
hemodynamic effect, the other blocks may result in hemodynamic instability)
▪ Decreased perfusion to vital organs (brain, heart, kidneys, lungs, skin)
o Treat the patient not the monitor
o Treatment based on hemodynamic effect of the rhythm

Classifications of AV Blocks
• First-degree AV block
• Second-degree AV block Type I (Wenckebach)
• Second-degree AV block Type II
• Third-degree AV block
• BEST WAY TO FIGURE OUT AV BLOCKS IS BY PR INTERVALS***

First Degree AV Block – LONG PR INTERVAL

Occurs when all atrial impulses are conducted thorough the AV node into the ventricles
● LOOKS like normal sinus, but the PR intervals are different!!!
● Characteristics
○ Rate is slower than normal
○ P wave is in front of the QRS
■ P wave is regular
○ PR interval → ABNORMALLY LONG PR INTERVAL
■ > 0.20 seconds
■ PR interval is constant

Second-Degree AV Block Type 1 (Wenckebach)

Repeating pattern in which all but one of a series of atrial impulses are conducted through the AV node into the
ventricles
● Characteristics
○ PR INTERVAL BECOMES LONGER WITH EACH SUCEEDING COMPLEX UNTIL IT EVENTUALLY
DISAPPEARS
○ P wave- In front of the QRS; shape is dependent on the underlying rhythm
○ PR interval → INTERVAL IS LENGTHENING WITH EACH BEAT (termed as cyclic)
■ PR interval becomes longer with each succeeding ECG complex until there is a P wave
not followed by QRS. The changes in the PR interval are repeated between each
“dropped” QRS, creating a pattern in the irregular PR interval measurements
○ QRS: normal or abnormal
 ■ DROPPED QRS COMPLEX AFTER LENGTHENING

Second-Degree AV Block Type II (HAS NO CYCLIC LENGTHENING)

Only some of the atrial impulses are conducted through each AV node into the ventricle
● Characteristics → DROPPED QRS COMPLEX RANDOMLY
● PR interval are the same here, constant, but eventually one is missing
○ Ventricular rate is lower than the atrial rate
○ P wave: in front of the QRS
■ Present and regular
○ PR interval
■ PR interval is constant for those P waves just before the QRS
○ R wave: irregular
○ QRS: normal or abnormal

Third-Degree AV Block
LIKE A BAD RELATIONSHIP, EVERYONE DOING THEIR OWN THING NOT TALKING TO EACH OTHER, NO SENSE
No atrial impulse is conducted through the AV noted into the ventricles
• Two impulses stimulate the heart
• One stimulates the atrial (P wave)
• One stimulates the ventricle QRS)
• “AV dissociation”
• PR interval: very irregular, DOING THEIR OWN THING
• IN EXAM, third degree block the rate is always in the 20s-30s (so if rate is higher in exam its not 3 rd
degree)
• ****IF LEFT UNTREATED, PATIENT CAN DIE*****
Management of Conduction Abnormalities
● Treatment based on cause and degree of stability (TREAT UNDERLYING CAUSE)  still assess and check
for pulse
● Directed towards increasing heart rate to maintain normal cardiac output
○ No treatment if stable: just eliminate the cause
■ Withhold medications
● Permanent pacemaker insertion (if you can’t stop medications)
● Transcutaneous pacing (temporary)
○ For a symptomatic patient and this can be done at the bedside ASAP
→ such as a patient with a low blood pressure and has a low HR we would need this!
● Initial treatment of choice: Atropine (not effective in second-degree AV block type II or third-degree AV
block)
● CPR
● BASICALLY, assess, check for pulse, provide crash card to bedside if symptomatic (anticipate they might
need pacemaker since HR is too low).
● REMEMBER, it is a temporary pacemaker (transcutaneous pacing) not permanent [pay att in exams if it
says permanent or temporary]

** TAKE HOME POINT **

• It is IMPERATIVE, AT ALL TIMES, to observe and treat the patient based on his or her clinical
presentation regardless of the rhythm being observed on the EKG monitor.
• Ask yourself: “How is this rhythm clinically significant to my patient?”

Nursing Process: The Care of the Patient with Dysrhythmia:

● Diagnosis:
○ Decreased cardiac output*** most important
■ Hypotensive and low HR- this would be low C.O
○ Anxiety
○ Deficient knowledge
● Nursing Interventions: (TO DO)
○ Evaluate BP, pulse, rhythm
○ Evaluate rate and depth of respirations
○ Auscultate breath sounds
○ Assess for syncope, dizziness  PATIENT IS UNSTABLE DO SOMETHING
○ Obtain 12-lead ECG
○ Medication administration
○ Assess for factors which contribute to dysrhythmia
○ Minimize anxiety, provide assurance
○ Maximizes self-management
○ Empathy
● Collaborative Problems/Potential Complications
○ Cardiac arrest
○ Heart failure
○ Thromboembolic event, especially with atrial fibrillation
EXAM TIPS**
 What interventions (TO DO) to be done for Patient SOB? Raise HOB, then give oxygen
o IT IS ASKING FOR AN INTERVENTION
 Anything test says pt is dizzy and in syncope = patient is unstable, DO SOMETHING!!!!!!!

Cardioversion and Defibrillation

 • Used to treat tachydysrhythmia
• Delivers an electrical current that depolarizes a critical mass of myocardial cells
• When cells repolarize; the SA node is usually able to recapture its role as heart’s pacemaker
• *READ UP ON THIS A LITTLE BIT* to familiarize

Defibrillator Technology
• Used for cardioversion and defibrillation
• Electrical current delivered through the skin
• AED
• Safety measures
• Good contact must be maintained between pads and patient skin
• No one is to be in contact with the patient or with anything touching the patient when the
defibrillator is discharged
• See chart 26-5, p. 716

Electricity
● Cardioversion – PT CAN BE AWAKE
○ Delivery of “timed” electrical current to terminate a tachydysrhythmia
○ Synchronized with the ECG to impulse is discharged during ventricular depolarization (QRS
complex)
○ Sedation required if elective
○ ABC monitoring
→ Indications of successful response are conversion to sinus rhythm, adequate peripheral pulses, and adequate
blood pressure
● Defibrillation
○ Treatment of choice for V-fib and pulseless V-tach, pulseless
○ NOT used for patients who are conscious or with a pulse
○ Medications utilized to make it easier to convert:
■ Epinephrine/Vasopressin
● Epinephrine is given after initial unsuccessful defib to make it easier to convert
dysrhythmia to a normal rhythm, also can increase cerebral and coronary
artery blood flow
■ Amiodarone/Lidocaine/Magnesium (antiarrhythmics)
● Given if ventricular dysrhythmias persists
○ Continuous CPR UNTIL PULSE IS REGAINED
→ when a pulse is regained - look to see what rhythm the patient is in - if the patient is in v-tach shock the
patient!

Pacemaker → regular cardiac rhythm

An electronic device that provides electrical stimuli to the heart muscle that consists of two components: an
electronic pulse generator and pacemaker electrodes which are located on leads or wires
● Types
○ Permanent
○ Temporary (only used in hospital settings)
● Indications
○ Slower-than-normal impulse
○ Symptomatic AV or ventricular conduction disturbance
○ Control of tachydysrhythmia that do not respond to medication
○ Heart failure (Biventricular pacing)
● Leads carry impulse created by generator (pacemaker) to the heart
○ The generator contains the circuitry and batters that determine the rate (measured in beats per
minute) and the strength or output (measures in milliamperes [MA]) of the electrical impulse
delivered to the heart
 ○ Endocardial leads or epicardial wires
→ leads are threaded by fluoroscopy through a major vein into the heart
■ Endocardial: right atrium and ventricle
■ Epicardial: lightly sutured onto the outside of the heart and brought through the chest
wall during open heart surgery
● ALWAYS TEMPORARY AND ARE REMOVED BY A GENTLE TUG A FEW DAYS
AFTER SURGERY
● Energy source is common household battery (elective replacement indicator [ERI])
● Paces the atrium and/or ventricle when no activity is sensed for a period of time.
● Single chamber vs. dual chamber
Think about this, what do you need to know as a NURSE about pacemakers? If you are taking care of a patient
with a pacemaker, what do you NEED to KNOW??
- Infection**
- Hematoma**
- Emboli**

Implanted Transvenous Pacemaker

Transcutaneous Pacemaker

FROM BOOK:
● Transcutaneous Pacing can cause significant discomfort (burning and involuntary muscle contraction) and
is intended to be used only in emergencies for short periods of times, this pacing requires hospitalization.
● Following this pacing, the skin under the electrode should be inspected for erythema and burns.
● Not indicated for pulseless bradycardia

Atrial Pacemaker
Ventricular Pacemaker

→ Pacer spike that Is *** capturing ***

● If it is not working → LOOK AT THE PATIENT FIRST (HE SAID THIS)

Complications and Pacemaker Use

● Infection
o Prophylactic antibiotic and antibiotic irrigation of the subcutaneous pocket prior to generator
placement has decreased the rate of infection
● Pneumothorax/Hemothorax
o The use of sheaths that are marketed as “safe” reduces this risk
● Bleeding or hematoma formation
o This can usually be managed with cold compresses and discontinuation of antiplatelet and
antithrombotic medications
→ small amount is NORMAL and this is okay because it is expected
→ MODERATE AND LARGE IS ABNORMAL
● Dislocation of the lead
● Skeletal muscle or phrenic nerve stimulation
o The occurrence of this complication is avoided by testing during device implantation
● Cardiac tamponade
o This condition can be recognized by the change in QRS complex morphology, diaphragmatic
stimulation, or hemodynamic instability
● Pacemaker malfunction
● Twiddler syndrome
o May occur when the patient manipulates the generator, causing lead dislodgement or fracture of
the lead
● Pacemaker syndrome
o Hemodynamic instability caused by ventricular pacing and the loss of AV synchrony
● Ventricular ectopy/tachycardia
o From irritation of the ventricular wall by endocardial electrode

FROM BOOK
● Type of pacemaker generator and settings selected depend on the patient's dysrhythmia, underlying
cardiac function, and age.
○ In the initial hours after placement, the most common complication is dislodgement of the
pacing electrode.
■ Minimizing patient activity can prevent this complication.
 ○ Malfunction can be indicated by bradycardia and s/s of decreased cardiac output (diaphoresis,
postural hypotension, syncope); malfunction is diagnosed via ECG

Question on exam example: If patient had a pacemaker placed 24hrs ago, it is significant for the nurse to assess
for BLEEDING/INFECTION (not small amount), it is warning if it is moderate/abnormal/large/hematoma.

Implantable Cardioverter Defibrillator (ICD)

A device that detects and terminates life-threatening episodes of tachycardia or fibrillation (especially
ventricular)
● Delivers a programmed charge with detection of arrhythmia
○ If pace goes up a lot, machine will shock!
○ Has at least a right ventricular lead that is implanted intravenously and can sense intrinsic
electrical activity and deliver an electrical impulse
○ Generator is the size of a book of matches that is implanted in a subcutaneous pocket, usually in
the upper chest wall
○ Are designed to respond to at least two criteria: a rate that exceeds a predetermined level and a
change in the isoelectric line segments.
→ When the dysrhythmia occurs, rate sensors require a set duration of time to sense the
dysrhythmia. Then the device automatically charges; after a second “look” confirms the
dysrhythmia, it delivers the programmed charge through the lead to the heart
● At risk populations
○ Survival of sudden cardiac death syndrome
■ EF < 35%
■ Nonischemic dilated cardiomyopathy
■ Symptomatic, refractory AFib
● Nursing interventions and complications similar to pacemaker insertion
○ Try pharmacology first (least invasive first before cardioversion)
○ Nursing Interventions:
■ Patient’s HR and rhythm are monitored by the ECG
■ Cardiac output and hemodynamic stability are assessed to identify the response to
pacing and the adequacy of pacing
■ Incision site is observed for bleeding, hematoma formation, or infection - which may be
evidenced bys welling, unusual tenderness, drainage, and increased warmth
○ Complications:
■ Surgery-related infection
■ Technical aspects of the equipment such as premature battery depletion and dislodged
or fractured leads
● **KNOW TEE AND EJECTION FRACTION** 50-75
● He said: “know as a nurse to answer….. what???” didn’t hear him.
→ When it triggers it resets the heart, this is not first line treatment (we want to control those with medications
first before doing this!)

Nursing Process: The Care of the Patient with an ICD

● Assessment
o Device function; ECG
o Cardiac output and hemodynamic stability
o Incision site
o Coping
o Patient and family knowledge
o WHEN SOMETHING IS GOING NEW INSIDE BODY THEY ARE AT RISK FOR INFECTION
● Diagnosis
Risk for infection → BECAUSE YOU ARE PUTTING SOMETHING IN THE BODY - ALWAYS ASSESS
FOR THIS
o Risk for ineffective coping
Knowledge deficit → ALWAYS ASSESS KNOWLEDGE AND READINESS TO LEARN
● Goals
o Goals include absence of infection, adherence to self-care program, effective coping, and
maintenance of device function.

FROM BOOK:
● Must assess the function of the device throughout its lifetime and especially after changes in medications,
antiarrhythmic agents, beta-blockers, and diuretics may increase the pacing threshold. Corticosteroids and
alpha-adrenergics may decrease the pacing threshold; and the opposite occurs when a patient stops these
meds.

OVERALL → TAKE CARE OF THE PATIENT FIRST - ASSESS THE PATIENT FIRST REGARDLESS OF WHAT IS GOING ON
WITH THE PATIENT
● Try the less invasive first!

→ Know about TEE and ejection fraction and the nursing care surrounding both

Hemodynamic Monitoring

Hemodynamic Monitoring
Critically ill patient requires continuous assessment of the cardiovascular system to diagnose and manage
medical conditions
→ Doing whatever it takes to stabilize patient
 ● Achieved via direct pressure monitoring systems
○ Central venous pressure (CVP)
○ Pulmonary artery pressure (PAP)
○ Intra-arterial blood pressure (Arterial line)
→ Know these and the goal is to know how these devices function
● Nursing care
○ Ensure system is set up and maintained properly
■ The pressure monitoring system must be kept patent and free from air bubbles
○ Ensure stopcock is at level of atrium (this landmark is referred to as the phlebostatic axis) before
pressure measurements obtained
○ Establish zero reference point
■ This process is accomplished by placing the stopock of the transducer at the phlebostatic
axis, opening the transducer to air, and activating the zero function key on the bedside
monitor
*Stroke volume is affected by contractility*

Complications
● Uncommon
o Pneumothorax [always monitor for this]
o Infection
▪ The longer a catheter is in place (after 72 to 96 hours), the greater the risk for infection
▪ Catheter-related bloodstream infections are the most common preventable
complication
▪ See care bundle, page 687
o Air embolism
▪ Can be introduced into the vascular system if the stockpocs attached to the pressure
transducers are mishandled during blood drawing, administration of medications, or
other procedures that require opening the system to air
→ Any device placed in patient near heart/chest, pneumothorax is big risk ***
 anything going INTO the patient think “SIGNS OF INFECTION” always think emboli can happen

Hemodynamic Monitoring: What does it measure?

● Hemodynamic monitoring measures:
o Heart chamber pressures
o Cardiac output – volume of blood ejected x HR
o Preload (VOLUME) – in the ventricles when heart is resting. Drug for preload drug for volume
o Afterload (PRESSURE/RESITANCE)- what are you pushing it against. Left ventricle. CAD, HF.
o Contractility
▪ Ability of the heart to pump
▪ Positive inotrope can affect contractility such as digoxin
Stroke volume is affected by contractility
 Diuretics affect VOLUME
 Antihypertensives, vasodilators, ace inhibitors affect RESISTANCE
Cardiac output increases with stress, epinephrine.

Cardiac Output = Stroke Volume x HR

● Cardiac Output  ALWAYS THINK URINE OUTPUT WHICH IS 30ML/HR
● Measures Right Atrium Pressure
o Total amount of blood ejected by the ventricle in liters per minute
o Resting adult: 4-6L/min
o Varies based on metabolic need
 → Change in LOC: LOW CARDIAC OUTPUT!
→ Good cardiac output is good for tissue perfusion
→ Decreased cardiac output → must have VS and some indication the patient has a low cardiac output
● Stroke Volume - determined by preload, afterload, and contractility
SIDE NOTE: preload (degree of ventricular stretch), afterload (resistance to ejection of blood from the
ventricle, contractility (refers to the force generated by the contracting myocardium - more forceful =
blood ejected)
o Total amount of blood ejected by the ventricle per heartbeat
o Resting adult: 60-130 mL
 know labs: WBC, HCT, HB, ICP, ETC (cant know how to treat without these labs)

Effect of Heart Rate on Cardiac Output (CO)

● CO responds to changes in metabolic demands of tissues associated with stress, physical exercise, illness
○ To compensate: CO enhanced by increases in SV and HR
● HR affected by CNS and baroreceptor activity
● Baroreceptors: aortic arch, right and left carotid arteries
○ Chronotropy  THINK OF HR
○ Inotropy  POSITIVE inotrope will INCREASE contractility HF patient
■ Atropine, CCB, and beta blocker will decrease HR
■ Digoxin
○ Dromotropy  electrical conduction

Baroreceptor Activity During Hypertension

● Increased BP (hypertension)  increased parasympathetic activity  decreased BP and HR

Baroreceptor Activity During Hypotension

● Decreased BP (hypotension) - decreased parasympathetic activity  increased BP and HR

Stroke Volume
● Determined by
o Preload - Volume
o Afterload- Resistance
o Contractility

Preload and Afterload

● Preload  has to do with VOLUME
o Degree of stretch of ventricular cardiac fibers at end of diastole (relaxation phase- where the
ventricles are filling with blood)
o Volume of blood at end of diastole = preload
● Afterload  has to do with RESISTANCE/PRESSURE (think ventricles)
o Resistance to ejection of blood from the ventricle
→ Pressure the ventricles must work against to open the SL valves so blood can leave the ventricle and go out to
the lungs or the rest of the body
o Resistance to left ventricular ejection: Systemic vascular resistance (SVR)
→ Left side of the heart gets blood to the body
o Resistance to right ventricular ejection: pulmonary vascular resistance (PVR)
→ Right side of the heart gets blood to the lungs

Preload
Increased Preload Decreased Preload
 Increased by increasing the return of circulating blood
volume to the ventricles  in order to INCREASE
PRELOAD  you need BLOOD PRODUCTS
INCREASE PRELOAD - GIVE FLUIDS
-CAN GIVE VASOPRESSOR
• Blood products
• Crystalloids (Saline, DW5) loses integrity
• Colloids (Large particles) Albumin
 if DR orders to give CHF pt NS at 500ml/hr  QUESTION the order because you cannot give too much fluid to
pt.
 to increase preload we can give vasopressors
 to decrease preload we can use diuretics (Lasix/bumix) or vasodilators (nitroglycerin)
Acute Stage monitor BP and urine output every HR
Afterload
Increased Afterload
Afterload is increased due to arterial vasoconstriction
Leads to decreased stroke volume
• Increased resistance to ejection
Contractility: The Force Generated by the Contracting Myocardium
Enhanced Contractility
Circulating catecholamine's (epi/norepi)
Decreased by reduction in volume of blood returning
to the ventricles
DECREASE PRELOAD - CAN GIVE A VASODILATOR
-SUCH AS NITRO (sublingual, patch, can be given IV,
and spray) monitor BP
• Diuresis – Furosemide, Bumetanide Monitor
urine output immediately if kidneys working.
• BUN, CREATINE, POTASSIUM
• 10-20, 0.74-1.35- 3-5
• High potassium gets pt. on the monitor
• HYPERKALMIA TALL PT WAVE ON ECG WIDEN
QRS COMPLEX, PROLONGED INTERVALS.
• Hypo inverted t wave
-Patient in CHF, what would you do with preload?
Decrease it
-What would you monitor? Intake and output, vital
signs, and electrolytes
• Venodilating agents
• Sodium Nitropusside Nipride monitor BP and
urine output (sodium nitruposside
• Excessive blood/volume loss (dehydration)
-Assess for dehydration- Dry mucous membrane,
poor skin turgor, etc.
Decreased Afterload
Afterload is decreased due to arterial vasodilation
Leads to increased stroke volume
• Decreased resistance to ejection
Reduced Contractility
Hypoxia (good choice for respiratory) - we should
assume this patient has limited perfusion
● What would we check? SPO2 monitor
● Early sign of hypoxia - restlessness and
 confusion
-Restlessness - we would do an ABG

Increased sympathetic activity (SNS)2 Acidosis

Medications Medications
Digoxin- Increase BP and contractility lowers hr Beta blockers
Dopamine – increases HR, increases Bp CCB
Dobutamine – Increases BP does not affect HR
→ Walk into room and patient BP is 60/30
● FIRST Assess the patient (because numbers do not determine the story)
● We want to increase contractility
○ Give fluids (even if the patient is in CHF, because we need to bring the blood pressure up)
○ Give Dopamine to bring BP up (be aware that this also increases HR)
○ What if the patient's HR is 150?
■ Dobutamine is going to be used since it does not have that much effect on HR
→ low blood pressure and high heart rate **
○ DOPAMINE BEFORE DOBUTAMINE
→ Reduce contractility (patient HR is 150 and is Afib)
● BETA blockers and CALCIUM CHANNEL BLOCKERS IV

Central Venous Pressure (CVP) Monitoring *KNOW THIS SLIDE*

Measurement of the pressure in the vena cava or right atrium
● Vena cava, right atrium and right ventricle pressures are all equal at the end of diastole; thus, CVP also
reflects right ventricle pressure = Measures right ventricular PRELOAD
● Normal CVP= 2-6 mm Hg KNOW
● Catheter is positioned in the right atrium
● Most valuable when monitored over time
→ Preferred site is subclavian vein; femoral vein is avoided
 If CVP greater than 6, not good. Hypervolemia or failure!!! Do not give more fluids.
 IF less than 2 (hypovolemia) need to give fluids!!!
→ Priority assessment for fluid on board → LUNGS (we would hear crackles)

CVP >6 mm Hg CVP < 2 mm Hg

(indicates elevated right ventricular preload) (indicates reduced right ventricular preload)

Hypervolemia Hypovolemia
Right heart failure

DO NOT GIVE THIS PT MORE FLUIDS GIVE FLUIDS TO THIS PT

Phlebostatic Axis: Left Atrium Did not go over

Pulmonary Artery Pressure (PAP) Monitoring [measures tissue perfusion]
→ measure blood volume, how effective the pump is, and measures tissue perfusion good cardiac output
determinant
● Used in critical care to assess - USED FOR CRITICALLY ILL PATIENTS (shock, open-heart surgery, poor
defusion, BP of 60/30 (which is their highest)
o Left ventricular function
o Diagnose the etiology of shock
o Evaluate response to interventions (fluid administration, vasoactive medications)
● Balloon tipped, flow-directed catheters with multiple lumens
o Balloon tipped can give a temporary reading of the pulmonary artery which gives an indication of
volume
o Distal lumen has a port that opens into the pulmonary artery
o Proximal lumen has a port that opens into the right atrium which is used to administer IV
medications
● May include specialty functions: cardiac pacing, oximetry, cardiac output measurements
● See page 656, figure 25-2
→ Complications include pulmonary artery rupture, pulmonary thromboembolism, pulmonary
infarction, catheter kinking, dysrhythmias, and air embolism
→ MONITORING DEVICE: good guideline for the medication given, how many fluids is given, can give medication
through this, can tell oxygenation
Gives guideline as to how much medication or fluid is being given.
Can tell you oxygenation.
Piece of wire/tube that goes to jugular, then sup vena cava, then right atrium, then ventricle, then artery
Trying to measure blood volume***
Gives you good idea of TISSUE PERFUSION****
 he says to just know the systolic and diastolic pressure*** highlighted.

Pulmonary Artery Pressure Device

Intra-Arterial Blood Pressure Monitoring (A-line)
→ Placed easily in the radial or femoral, gives a continuous blood pressure reading
→ Radial > over femoral because of infection control
● Obtains direct and continuous BP measurements
● Severe HTN or severe hypotension
● ABG and blood samples may be drawn frequently
● Radial artery is most common site of placement
● Allen’s test
● Nursing Interventions
o Monitor for complications:
o local obstruction/distal ischemia
o Hemorrhage
o Ecchymosis
o Dissection
o Air embolism – ANY WIRE IN A PT THINK OF THIS
o Blood loss
o Pain
o Arteriospasm
o Infection
→ Assess patient for pneumothorax when placing any type of device in lung area (atrium/ventricles/lungs)
always ASSESS!!  Patient is at high risk for pneumothorax, get a chest xray and verify the placement before
using the device
→ Patient may get an arrhythmia if placement is not correct, must report this
→ MAP (seen on a monitor) normal is between 70-105
● This can tell about perfusion it is the pressure the walls place on the ventricles of the heart before it
leaves the heart
● A MAP OVER 60 CAN MAINTAIN PERFUSION
○ LOWER THAN 60 IS A PROBLEM (we would start looking)
● Determine by ⅓ of the systolic - diastolic + diastolic
○ Ex: Pressure 100/70  systolic minus diastolic is 30, 3rd of 30 is 10, 10 plus diastolic is 80.
NORMAL!
LOW MAP = NO PERFUSION OR LIMITED PERFUSION (AKA LOWER THAN 60 IS PROBLEM)
Kaplan meds (he said to know)
● Dopamine before dobutamine
○ Dopamine: vasoconstrictive - improve cardiac output (remember this increases HR)
○ Dobutamine: Stimulates beta1 receptors on the myocardium; increases cardiac output by
increasing contractility (positive inotropy), which increases the stroke volume, especially in
clients with HF (mainly used as last resort and if pt has increased HR)
● Vasopressor: increase blood pressure – increased preload
○ Epinephrine and norepinephrine
● Vasodilators: decrease blood pressure – decrease preload/afterload
○ Nitrates and
milrinone
● Diuretics - lasix and bumex – decrease BP/preload
(monitor urine output, electrolyte imbalance such as potassium, and lung sounds)
○ Reduces the heart's workload
○ Promote diuresis
○ Decrease blood pressure

Acute Coronary Syndrome and Myocardial Infarction

→ Take care of the pain first for NCLEX purposes
→ If they came in by rescue and they were given something for the pain already then you can do a EKG
 KNOW THIS POWERPOINT GOOD!!!

Acute Coronary Syndrome UNSTABLE through full blown MI

● Emergent situation: acute onset of myocardial ischemia resulting in myocardial death if no intervention
● Unstable angina and acute myocardial infarction (AMI) are considered to be the same process but
different points along a continuum

Spectrum of ACS
● Unstable Angina (USA) – pain don’t go away, not relieved by rest. Ask when it occurs what makes it better
or worst
● Non-ST Elevation MI (NSTEMI)
● ST elevation MI (STEMI)

Pathophysiology of ACS/MI
● USA
○ Reduced blood flow in a coronary artery
○ Partial occlusion of an artery
○ Atherosclerosis/plaque rupture
● MI  ALWAYS THINK ISCHEMIA/NECROSIS
 ○ Area of the myocardium is permanently destroyed
○ Plaque rupture, thrombus formation
○ Complete occlusion (he said not necessarily true in his opinion, but for reading and book
purposes think of occlusion)
○ Ischemia and necrosis of myocardium supplied by artery
● Vasospasm
○ Sudden constriction or narrowing of a coronary artery
○ Decreased oxygen supply
○ Increased demand for oxygen
● Decreased oxygen supply
ETIOLOGY
○ Acute blood loss
○ Anemia
○ Low blood pressure
● Increased oxygen demand
ETIOLOGY
○ Tachycardia
○ Thyrotoxicosis
○ Ingestion of cocaine
■ Always at risk for an MI and we do not give beta blockers to these patients because
they do not work!

 NOT ENOUGH BLOOD FLOW- at some point your preload/contractility/afterload will be affected

EKG Patterns: Ischemia, Injury, and Infarction

→ Zone of ischemia: inverted T wave 

→ Zone of injury: elevated ST segment 
→ Zone of infarction: well pronounced Q wave

Clinical Manifestations
● Chest pain that occurs suddenly and continues despite rest and medication
● Asymptomatic or prodromal symptoms
○ Atypical chest pain
■ In women it presents differently
■ In diabetics it presents differently
 → they both do not feel what is going on inside of them - they are sometimes having a
“silently MI”
○ Typical chest pain
● May not be distinguished from unstable angina
Shoulder pain, back pain, hiccups- all s/s of Heart attack
● Cardiovascular
○ JVD
○ Chest pain not relieved by rest or nitroglycerin
○ S3 or S4
○ Palpitations
○ Hypertension/Hypotension
○ EKG changes
○ Irregular pulse
○ ST segment, T-wave changes
■ ST ELEVATION AND T WAVE INVERSION
Chest pain not relieved by rest or nitrogylecrin you will see some EKG changes such as  ST segment and
Twave changes
● Respiratory
○ SOB
○ Dyspnea
○ Tachypnea
○ Pulmonary edema
● GI
○ Nausea
○ Vomiting
■ In elderly who is vomiting - we would do an EKG on them anyway
○ Indigestion
● Skin
○ Cool
○ Clammy
○ Diaphoretic
■ Patient is symptomatic, can’t ignore this clinical manifestation!!!!!!!!!!!!
○ Pale or dusky
● Neurologic (don’t administer sedative) they have decreased cardiac output
○ Anxiety
○ Restlessness
○ Syncope
○ Headache
○ Changes in LOC
○ Dizziness
○ Lightheaded
all of these neuro CM indicate patient is not doing well
● Psychological
○ Fear
○ Impending doom- this is a nursing diagnosis for MI
○ ` Denial

Diagnostic Findings
● Presenting symptoms, regular pain assessment, HPI
● 12-lead ECG findings  look for ST and T waves
● Laboratory results – cardiac markers  TROPONIN  0 AND 0.4
→ High troponin level and normal EKG = NSTEMI
→ STEMI is when ST elevation is seen
→ Unstable angina = normal troponin, could be a precursor for MI

Electrocardiogram
 ● Should be obtained within 10 minutes from time patient reports pain or arrives in ED
● “Time is Muscle”; changes evolve (evolution of MI)
● Serial ECG: evolution of MI
○ Classic ECG changes
■ T-wave inversion
■ ST-segment elevation
■ Development of abnormal Q waves
● Can be a non-q wave MI
● Q wave stays for an old MI in the past (the wave is longer and will remain like
that) 2-3 days

T-wave Inversion
● Ischemia cases delay in myocardial repolarization, causing T wave to invert

ST Segment Elevation
● Injured myocardial cells repolarize more rapidly than normal cells, causing ST segment to elevate at least
1 mm above the isoelectric line

Abnormal Q Waves
● Develops in 1-3 days AFTER THE EVENT
● Does not exist before the event

Laboratory Assessment KNOW THIS SLIDE

● Tests based on cellular component that are released into the circulation when myocardial cells die
● Creatinine Kinase and Isoenzymes
 ○ CK-MM (skeletal muscle)
○ CK-BB (brain tissue)
○ CK-MB (cardiac muscle) - CARDIAC SPECIFIC
■ 0-3
■ TROPONIN. 0-0.04
■ Every 4hrsx3
○ Level increases in a few hours and peaks within 24 hours
● Myoglobin
○ Heme protein that helps transport oxygen
○ Myoglobin is found in cardiac and skeletal muscle
○ Myoglobin increases within 1-3 hours and peaks within 12 hours
○ Not specific to the event
○ Negative may rule out an acute cardiac event
● Troponin - MUST KNOW BECAUSE IT IS CARDIAC SPECIFIC (done every 4-6 hours) ** if elevated does not
always mean MI (in a septic patient is can be elevated)
○ Protein found in the myocardium
○ Regulated the myocardial contractile process
○ Three isomers of troponin (C, I and T)
○ Troponin I and T specific to cardiac muscle
○ Peaks within 1 hour but can remain elevated for up to 3 weeks
● Echocardiogram
○ Abnormal wall motion, ejection fraction

→ STEMI WILL GO TO A CATH LAB

→ NSTEMI AND STEMI WILL BOTH GET AN ASPIRIN AND BETA BLOCKER
 TROPONIN used more than CK-MB bc It shows faster and lasts longer in the system

Spectrum of ACS/MI KNOW THIS

● USA
○ Patient has chest pain (not relieved by rest and nitro)
○ Patient has clinical manifestations of coronary ischemia but ECG and biomarkers show no
evidence of AMI (negative biomarkers)
● NSTEMI
○ Elevated biomarkers but no definite ECG evidence of AMI
● STEMI
○ Patient has ECG evidence of AMI
○ Elevated biomarkers
→ ST elevation; send to cath lab; patient gets aspirin and beta blocker

Descriptors
● Type of MI
○ ST-segment elevation (STEMI)
 ○ Non-ST segment elevation (NSTEMI)
● Location of the injury
○ Anterior
○ Inferior
○ Posterior
● Point in time within process
○ Acute
○ Evolving
○ Old
→ 12-lead EKG can tell you where!
→ Patient should be placed on telemonitor on a telemetry unit if the patient needs to be transported, they
should be on a monitor at all times
→ IMCU AND ICU ARE NEVER DELEGATED TO A UAP TO BE TRANSPORTED ANYWHERE

Medical Management
● Goal:
○ Minimize myocardial damage***
○ Preserve myocardial function
○ Prevent complications
● Goal Achieved via:
○ Emergency use of Thrombolytic Medications
○ PTCA for reperfusion
○ Reduction of myocardial oxygen demand
○ Increasing myocardial oxygen supply

Goal Achievement

→ REPERFUSION IS KEY (we want to reduce oxygen demand by increasing oxygen supply) 
→ Want to stabilize afterload and preload

Treatment Guidelines
● Supplemental oxygen
● Nitroglycerin times 3 5 min apart
○ 60/30 BP → should not be given; CPR will need to be done
● Morphine decrease preload and afterload
○ Decrease the workload of the heart
● Aspirin (162-325 mg)
○ 300 mg can be given rectally
○ Antiplatelet which can keep platelets from clotting and there is an inflammatory process going on
here, so we need this to help with the inflammatory response that is occurring)
● Beta blocker
○ Do not give if patient HR is already low
● ACE inhibitor within 24 hours
● Anticoagulation with heparin and platelet inhibitors
● MONA – morphine, o2, nitroglycerin, aspirin

Be careful in exam with the dose and location given, don’t just pick morphine bc it says morphine (most are
given IV) it can say other routes in exam or say a crazy number like 20mg instead of like 1mg

Nitroglycerin
● Short term and long term reduction of myocardial oxygen consumption through selective vasodilation
○ Paste, Sublingual, IV, PO
● Nitrostat, Imdur, Nitro-bid, Nitro paste
● Acute phase nitro sublingual x3 every 5 minutes
● Give something for pain first if med has already given before coming in do ECG

Analgesia
● Morphine is drug of choice for PAIN!
● Give Narcan (NALOXONE) if respiratory rate is LOW
● IV boluses (0.9 NS)  to bring up BP
● Reduces preload and afterload (decreases workload)
● Relaxes bronchioles to enhance oxygenation
● Reduces anxiety
● Monitor BP and respiratory rate***
IF BP is low there are times you still give morphine but as a smaller dose, in the meantime give fluids to bring
up BP
times where morphine aren’t given like if you take away the respiratory drive on a hypotensive pt that is BAD

Beta Blockers
● Continued throughout hospitalization and after discharge
● Long-term therapy decreases incidence of future cardiac events
● Side effects
○ Reduces myocardial oxygen consumption by blocking beta-adrenergic stimulation of the heart
○ Lopressor, Toprol, Atenolol (less than 60 - HOLD THE MEDICATION)
● Nonselective: carvedilol, labetalol, propranolol, sotalol, and timolol
● Cardioselective: atenolol, esmolol, and metoprolol (EMA)
→ Cardiac specific vs non-cardiac specific
→ Assess HR, BP, can prolong PR interval with beta blockers
 Once started, you continue with it (long term for future cardiac event)
 Know the cardio specific beta blockers (the non-cardiac specific constrict the lungs so be cautious with
respiratory patients).

ACE Inhibitors  PRILS

● Prevent conversion of angiotensin from I to II
In absence of angiotensin II
○ BP decreases
○ Kidneys excrete sodium and fluid
○ Decreases oxygen demand of the heart
 Monitor for ANGIOEDEMA  swelling in tongue, face, etc. REMEMBER
● Post-MI
○ Decreases mortality rate
○ Prevents the onset of heart failure
○ Monitor potassium, creatinine, sodium, BP, U/O ****
→ Can increase potassium levels

Calcium Channel Blockers ZEM AND MIL

● Negative inotropic effect
● Indicated in patients not responsive to beta-blocker
● Used as primary treatment for vasospasm
○ Norvasc
○ Cardizem
○ Verapamil
○ Plendil

Treatment Guidelines
● Evaluate for indications for reperfusion therapy
○ PTCI
○ Thrombolytics Continue therapy – TPA, aleplase, Reperfusion therapy, PT on Monitor, ST
elevation more than 2 leads MONITOR BLEEDING, TELY MONITOR, VITAL SIGNS
○ IV heparin/LMWH, PTT, Platelets
○ Plavix – clopidrogel
○ GP IIb/IIIa inhibitor
○ Bed rest (12-24 hours MAX)
if exam says 3 days, it is WRONG!!2
MONITOR FOR BLEEDING
GOAL for meds reduce platelet aggravation, also aspirin rectally

Antiplatelet Medication
● Aspirin
○ Clopidrogel
● Prevention of platelet aggregation
Anti-Coagulation
● Unfractionated heparin
● LMWH
○ Platelet-inhibiting agents
○ Prevents further clot formation
(enoxaparin)- given for DVT prophylaxis 1mg SBQ distributes better 30-40 (PREVENT AND TREAT) low
molecular distributes better and don’t have to check so much
○ DVT Prophylaxis [30-40 mg] - per kg is weight based and the exact amount must be given 
● Heparin- 5k units (unfractionated) prevent dvt, ACS low molecular and high molecular
 know what labs to look at for these drugs (pTT? APTT? INR?)
PTT – 60- 70 SECONDS (Heparin and PLT 150-450) APTT 30-40 (Unfractionated Heparin) INR 2-3 (Warfrin)
 if med is mg/kg = WEIGHT BASED

Thrombolytic Therapy – actual and dissolve

● Thrombolytic agents open the artery by lysis of the thrombus in the coronary artery (Activase (alteplace)
r-PA, TNKase) For existing clots
● Thrombolysis
● Reperfusion
○ Make sure the patient is on a monitor because as the channel is opened up it can
throw a dysthymia
● Minimize the size of the infarction
● Preserve ventricular function
● Doesn’t effect the underlying atherosclerotic lesion
● Dissolves ALL clots in the body
● MONITOR FOR BLEEDING  look at CBC and H&H
● Look at systolic BP
→ 75 year old patient about to receive TPA, anything invasive should be done before such as the central line so
the patient does not bleed. Keep patient on monitor with minimal movement.
 INVASIVE procedures done BEFORE TPA
→ Assess BP and LOC – you don’t want a brain bleed
If its aspirin you still give it
**First-line therapy in facilities that lack resources to perform PCI***

Contraindications to Thrombolytic Therapy

● Active, internal bleeding
● Surgery, trauma or bleeding within 2 months
● Bleeding disorder
● Previous hemorrhagic stroke/AVM
● Severe, uncontrolled HTN
○ Make sure bp is below 160
○ If bp is too high and this med is given  at risk for BLEEDING
● Pregnancy
→ REPORT ANY SIGN OF BLEEDING IMMEDIATELY

Thrombolytic Inclusion Criteria

● Chest pain for > 20 minutes, unrelieved by NTG
● ST segment elevation in at least two leads
● < 6 hours from onset of pain
 if pain is more than 6 hrs they do not meet criteria for TPA (If chest pain was onset yesterday, no need to
provide thrombolytic)
● “Door-to-Needle Time”
● 30 minutes
Nursing Considerations
● Minimize punctures!!
● Avoid IM
● Start IV lines prior to therapy
● Avoid NIBP
● Monitor for dysrhythmias/ hypotension
● Monitor for reperfusion
○ Improvements in s/s like no more “chest pain” if that was the reason
● Monitor s/s of bleeding
○ H/H
○ Oozing, back pain
○ Changes in LOC
○ Headache
○ Rectal bleeding
how to monitor reperfusion? LOC, IMPROVED S/S (IT IS AN OUTCOME QUESTION
 CHANGE IN LOC CAN INDICATE BLEEDING- IT IS A SIDE EFFECT OF TPA

Reperfusion
● Clinical Markers:
○ Return of ST segment to baseline
○ Resolution of chest pain
○ Presence of reperfusion arrhythmias (PVC’s, AV blocks, VT, VF)
○ Rapid rise of CK-MB enzyme within 3 hours due to circulation of dead cells after reperfusion

Nursing Diagnosis
● Acute pain related to increased myocardial oxygen demand and decreased myocardial oxygen supply
● Risk for decreased cardiac tissue perfusion related to reduced coronary blood flow
● Risk for imbalanced fluid volume
● Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular
dysfunction
 MAIN DIAGNOSIS ALWAYS AT RISK FOR DECREASED CAFDIAC PERFUSION OR C.O

Nursing Process
● Goals
○ Relieve pain and/or signs of ischemia
○ Improve respiratory function
○ Promote adequate tissue perfusion
○ Reduce anxiety
○ Monitor for potential complications
● Promoting Home and Community-based care
○ Identify priorities of the patient
○ Provide adequate education about heart-healthy living
○ Facilitate the patient’s involvement in cardiac rehabilitation
○ Work with patient to develop plan to meet their specific needs
■ Ensures compliance and effectiveness

NCLEX wants you to make sure you are giving them info about the disease and in the community (resources,
groups, recommendations, social workers, case managers, etc).
Family support? Readiness to learn? Might need to go to rehab center.
 OB nurse on unit, give them GI patients
UAP don’t give them post op pts – don’t allow them to ambulate post op pt unless 24hrs post op
 LPN cant do initial assessment or discharge teaching – they can reassess and give insulin if pt diagnosis is DKA
for example – cannot do IV push
 Acute Pulmonary Edema
→ Patient having SOB, what would you do?
INEFFECTIVE CARDIAC OUTPUT
 Assess, Raise HOB, give or increase oxygen, get IV anticipating DIURETIC, EKG, tele-monitor, labs
(maybe ABG, CBC, BMP), echo, vitals, SPO2. Might need foley as “prescribed” to measure output.
 CHEST XRAY WILL TELL THE STORY***
 Right sided HF → patient has JVD, edema, splenomegaly, hepatomegaly, increased BP bc of the excesss
in fluid volume, distension
 Left sided HF → LUNGS - increase or decrease in BP (due to pump failure), dry hacking cough 
→ Sometimes these patients need a foley catheter as prescribed 
Tachycardia, tachypnea. High Fowlers
→ Patient not doing well. Any time of procedure that can be done at the bedside we must do!

Right side HF (Everything getting bigger) Starts with Edema

Patient with swelling in legs- ask how LONG they have had that for
Spleen big, liver big ,JVD, high BP because there is a lot of fluid.
You could also have decrease BP because HF the pump is not working

Left side HF (Respiratory)

Lungs SOB
Shortness of breath
Tachycardia, Tachypnea 30-40 breaths a min
Crackles
BP could also be up
Dry HACKING cough, pink frothy sputum

Ask patient if they have gained weight asked patient if they have been able to sleep.
Assess perfusion: Peripheral pulses, pedals, popliteal, femoral
Patient color, temperature, hair growth, capillary refill, URINARY OUTPUT
1kg-1L of fluid
Crackles in bases in lungs and midway up drowning in their fluids. Not cleared by cough.
Agitated and Restlessness means lack of oxygenation and perfusion. Not related to Neuro. Deprived
Oxygen

Pulmonary Edema
Abnormal accumulation of fluid in the interstitial spaces and alveoli of the lung
● Life-threatening condition
● Associated with acute decompensated HF
→ can lead to acute respiratory failure and death ASSESMENT MUST BE ON POINT!  

Pathophysiology of Acute Pulmonary Edema

● Results from left ventricular failure
○ AMI or acute exacerbation of CHF
○ Non- cardiac disorders (renal failure) Dialysis patient
● Left ventricle fails => blood backs up into left atrium=> Rapid increase in atrial pressure=> increased
pulmonary venous pressure=> interstitial edema
○ “Flash pulmonary edema”-sudden HF and everything occurs “fast”
○ CONFUSION bc of lack of oxygen pt says I cant breath weak rapid pulse
 When something is ACUTE in medicine it means it is happening right now
→ when the left ventricle begins to fail, blood backs up into pulmonary circulation, causing pulmonary
interstitial edema. This may occur quickly in some patients which is a condition called “flash pulmonary edema”.
The pathophysiology is an extreme form of that seen in left-sided HF. The left ventricle cannot handle the
volume overload, and blood volume and pressure builds up in the left atrium

● Fluid within the alveoli creates a diffusion block - severely limits gas exchange
→ this results in hypoxemia,, which is often severe

→ Enlargement of the heart in CXR 

→ S3 and S4 
 S3 is for fluids and volume - it would be heard after S2 [heart has so much fluid in it so the valves cannot
close so they need to give that little extra push called GALLOP]
 S4 happens before S1 (this is due to more pressure) - get this with hypertension 
→ Echo (transmural is on the outside)
→ TEE is passed down the esophagus  (invasive, done to give you a better picture)
 Can determine EJ, valves closing and opening 
 Normal EJ is 55%-65% 
 EF < 40% not good 
→ Where is the mitral sound heard? 5th midclavicular line and this will shift in HF (she said she heard it in
midaxillary) to properly hear it you would turn the patient on the side 
→ Left sided can cause right sided; right sided can develop by itself from cor pulmonale 

Clinical Manifestations
● Decreased cerebral oxygenation
○ Confusion, anxious, restless→ stuporous
● Sudden dyspnea
● Sense of suffocation
● Cold, moist, pale
● Weak, rapid pulse
● Cyanosis/ashen (Skin/nail beds) Late signs, ashy look
● Neck vein distention
● Cough
● Breathing is rapid, noisy
● “Drowning in secretions”
 ● Decreased oxygen saturations
● Sputum→ pink, frothy sputum (Fluid within alveoli mixes with air) CLASSIC SIGN
→ If you hear crackles - have the patient cough and the cough will be moist and crackly – this is normally heard
in the bases of the lungs
 you will see cyanosis because of the lack of perfusion and decreased C.O
→ Blood not going where it needs to go (perfusion)? LOC affected and urinary output
 In exam if something is “acute” or “most” or “patient is not doing well”, the answer must always be within
15min  if it says 4hrs later do not pick that answer because they have something going on in the MOMENT

Right sided HF Left sided HF (Lungs)

Edema can occur in the legs/feet/ankles as well.  SOB and O2 stats would be low – exertional dyspnea

Everything will back up! Fatigue

JVD due to fluid backing up and pressuring
 
Ascites
 
Nocturia
 
Hepatomegaly due to the liver getting bigger
Anorexia – loss of appetite, nausea, or abdominal pain may
result from the venous engorgement and venous stasis with the
abdominal organs 
 
The feet start to swell – feet will feel cool/cold when there is
edema
 
Dependent edema: in the lower extremities
Weight gain due to retention of fluid and sodium. So, we want
to perform daily weights on the patient
 
Coughing which will irritate the mucosal of the lungs – this is a dry
nonproductive cough (worse at night)
 
Crackles in the base of the lungs
 
Orthopnea which is difficulty breathing when lying flat (need to sleep
in a recumbent position)
PND, pleural effusion, and pulmonary edema will occur because the
fluid is backed up in the pulmonary system.
 
Patient will have a decrease in renal function – oliguria will occur
 
Patient will have a cerebral anoxia à confusion, irritability, dizziness,
and lightheadedness (patient start becoming restless; a sign the
patient is getting oxygen deprived)
Tachycardiac
 
Heart sounds S3 and S4 a gallop occurring
Hallmark sign: patient will have a pink frothy sputum because the
mucosal is irritated

Assessment and Diagnostic Testing

● Physical Assessment
○ ABC evaluation TO DETERMINE SEVERITY OF RESPIRATORY DISTRESS
○ Vital signs
○ Cardiac monitor
○ IV access- 2 large
● Diagnostic
○ Electrolytes monitored weather it is right or left
○ BUN/Creatinine
 ■ Normal BUN: 10-20
■ Normal Creatinine: 0.7-1.4
○ CBC
○ CXR
■ To determine the extent of pulmonary edema
■ Heart is enlarged – apex shifts because the heart is pumping too hard, almost into axilla
(lay patient into the stethoscope and roll them) Weak thready pulses worst case could
be absent) Pallor, LATE cyanosis
■ CHECK URINE OUTPUT EVERY HOUR
○ Right vs. Left

Prevention
 Easier to prevent than treat  ASSESS EARLY, TREAT EARLY
 Assess for early indicators and treat early 
→ To recognize it early the nurse assesses the degree of dyspnea, auscultates lung fields and heart sounds, and
assess the degree of peripheral edema. A hacking cough, fatigue, weight gain, increased edema, and decreased
activity intolerance may be early indicators of developing pulmonary edema2 
 Early stages:
→ Book also mentioned pulmonary edema may be alleviated by increasing the dosage of diuretics and
by implementing other interventions to decrease preload 
o Upright position
o Legs dependent
o Eliminate overexertion- patient cannot be go upstairs or anything like that. Teach patient what to
do.
o Minimize stress
o Patient education
 Daily weights (at home and in the hospital)
 Rapid gains are fluid (a liter of fluid weighs a kilo) 
 Gradual gains are dry weight 

Medical Management
● Correct the underlying disorder
o Patient is usually on diuretics, ACE inhibitors, beta blockers
 Diuretics: decrease BP and electrolytes (decreases potassium - can educate on high
potassium foods) 
 Beta blockers: decrease BP and HR 
 Ace inhibitors: angioedema, dry cough, high potassium 
 Digoxin can be given but it is not commonly used
 they need (+) inotropic drugs to INCREASE contractility because patients with HF have a problem with
PUMP!!!*******
● Goals
○ Reduce volume overload
○ Improve ventricular function
○ Increase respiratory exchange
● Oxygen Therapy
○ Relieve hypoxemia and dyspnea
○ NRB
○ NIPPV
○ Endotracheal intubation
○ Mechanical ventilation
● Diuretics (decrease preload)
○ Loop diuretic (IV)
 ○ BP monitoring
○ U/O monitoring
○ I/O
○ Daily weights
○ Electrolytes

Medical and Nursing Management

● Vasodilators (decrease preload)  enhance symptom relief in pulmonary edema
○ IV nitroglycerin
○ IV nitroprusside – urinary output
○ Monitor BP
○ Morphine; no longer recommended (increased need for mechanical ventilation, Increase LOS,
increased mortality)
→ After giving meds; always reassess effectiveness of med
→ If morphine is given, reassess if med decreases pain; might need to go to plan B or increase medication dose
● Nursing Management
○ Upright
○ Legs dangling as long as it is not contraindicated
■ Respiratory and perfusion purposes (even if the patient has edema) - removes the fluid
by gravity away from the heart
○ Psychological support
○ Monitoring medications

Nursing Management
● Assisting with intubation
● Administer oxygen/monitor hypoxia
● Administer and monitor response to medication
○ I/O
○ VS
○ N/V
○ EKG monitoring
○ Electrolytes
● Position to promote optimal circulation
● Provide psychological support
 Nurses ASSIST with intubation or PREPARE for intubation.

Invasive Cardiac Procedures

Percutaneous Coronary Interventions (PCI)

● Invasive interventional procedures to treat CAD
○ Percutaneous transluminal coronary angioplasty (PTCA)
○ Intracoronary stent implantation

Indications for surgical intervention: PCI

 Recurrent discomfort despite medical therapy
 Ischemia during stress testing
 STEMI  Improved outcomes vs thrombolytic therapy
 NSTEMI High risk d/t persistent ischemia
Percutaneous Transluminal Coronary Angioplasty (PTCA)
 Balloon tipped catheter used to open blocked coronary vessels
o Resolves ischemia
o Improves blood flow - compresses atheroma
o May also open blocked CABG
o Performed in cardiac catheterization lab
 Catheters (Sheath)
o Radial or femoral artery (INSERTION SITE - IT IS IMPORTANT TO STUDY AND ASSESS THIS AFTER
SURGERY) 
 Catheters are then threaded through the femoral artery, up through the aorta, and into
the coronary arteries 
 Angiography/contrast agents utilized
o To identify the location and extent of the blockage 
 Inflation/deflation with subsequent stent insertion → balloon is inflated to open the vessel 
o When the catheter is properly positioned, the balloon is inflated with high pressure for several
seconds and then deflated 
o May cause CP or ST segment elevation during inflation
 Goal - NO MORE CHEST PAIN 
o Residual stenosis of less than 20%
o Increased artery lumen
o No clinically obvious arterial trauma
→ BASELINE PERIPHERAL PULSES ***
→ Need IV access that is patent  (large bore 16/18gauge)
→ Need consent BEFORE MEDICATION ADMINISTRATION 
→ Allergies (iodine) - we can premedicate the patient if they are allergic to iodine
→ Need to know NPO status (4-6 hours is acceptable for NPO liquid is 4 hours and food is 6 hours) 
→ Assess for height and weight
→ Assess vital signs 
→ Patient is on metformin hold is 24 hours before and medication can be resumed 48 hours after (always know
creatinine level and renal function) 
→ Insertion site → femoral or radial, when patient comes back, assess the site (can be given some type of
medication to take away the pain)
→ Still chest pain after the procedure? Must report because reperfusion is not where it needs to be

Coronary Artery Stent

● Post-PTCA treated area may re-occlude
○ RISK: Restenosis secondary to inflammatory process
 Anytime you do a procedure, always worry about vasoconstriction, clotting, and scar tissue formation
 Stent placed to prevent the above
o Metal mesh that provides structural support to a vessel at risk of acute closure. The stent is
initially positioned over the angioplasty balloon. When the balloon is inflated, the mesh expands
and presses against the vessel wall, holding the artery open. The balloon is withdrawn, but the
stent is left permanently in place with the artery 
o Stent covered by endothelium → is incorporated into the vessel wall 
 Bare-metal stent: contains no medication
 Drug-eluting stents: minimize formation of thrombi/scar within lesion
 Such as Sirolomus (Rapamune) or Paclitaxel (Taxol) 
 Antiplatelet medications (aspirin and clopidogrel) 
o One month post bare metal stent
o One year post drug-eluting
→ Why would a patient not be a candidate for a stent? Too much blockage; patient is sent back to ICU
depending on the severity 

Complications
 Coronary artery dissection, perforation
 Abrupt closure
 Vasospasm
 Acute MI
 Acute dysrhythmias, cardiac arrest
 Bleeding at insertion site – large amount address scant keep monitoring,
o DO NOT CHECK JUST THE DRESSING 
o Pull under the patient to assess bleeding 
 Hematoma
 Acute kidney injury (dye can damage kidneys)
o Avoid kidney injury by flushing it out through normal saline (give fluids) and hold meds for
48hrs
o This would be contraindicated in CHF patient and underlying kidney injury 
 If they have an underlying kidney injury, what would you do afterwards? Schedule
dialysis afterwards - this is called “coordinated care” 
→ ALWAYS MONITOR YOUR PATIENT for complications 
→ Positioning, keep extremity straight - DO NOT ELEVATED AND CAN KEEP HOB MAYBE 30 DEGREES WITH THE
EXTREMITY STRAIGHT 
→ Check the patient every 15 minutes for the first hour (up to two hours) and if stable can move to 30 minutes
(every 2 hours) 
→ 6-12 hours you want the patient up and moving around 
→ Post procedure is always assessment afterwards
Walking after 4-6 hours
MONITOR SITE FOR HEMATOMA

PTCA: Post Procedure Care

 Emergent (ACS): admit to ICU
 IV Heparin or thrombin inhibitor
o GP IIb/IIIa
 Hemostasis achieved with (Good SATA question)
o Angio-seal
o Femostop
o C-shaped clamps
 aPtt testing
 Flat in bed (no more than 15 degrees)
 Affected leg straight until sheaths removed and then post-removal
 Vasovagal
 Analgesics/sedation
 Restart Heparin if high risk for re-occlusion
 Monitor site for hematoma
 Ambulatory after procedure

→ Make sure patient is on a telemonitor 

→ Assess pain and look for dysrhythmia 
→ GET THE PEDAL PULSE BASELINE BEFOREHAND
→ Check peripheral pulses (assess for cool, clammy)
→ Compare site of insertion to the other side 
→ Can’t find a pulse? Use a doppler - document audible by doppler 
→ See bleeding and bleeding cannot be stopped? Apply pressure and use the following that is bolded
above (angio, femo, clamps)
→ Labs such as clotting profile, PTT, aPTT, and INR 
 PTT: 60-70 seconds
 aPTT: 30-40 seconds
 INR: 2-3.5
 Platelet: …

Coronary Artery Revascularization

→ THIS IS OUR GOAL 
 Indications for Surgical Intervention: CABG 
o Alleviation of angina not controlled with meds or PCI
o Treatment of left main coronary artery stenosis or multivessel CAD
o Prevention/treatment of MI, heart failure, dysrhythmias
o Complications from unsuccessful PCI
o >70% occlusion
o Other
 LV dysfunction
  Occlusion is in the vessel that takes blood to the LV and they can temporarily
on the balloon pump which will pump the heart for them (this will be put in the
cath lab if they cannot be stented) 
 Number of disease coronary vessels
 Signs/symptoms
 Previous treatment
CABG
→ It is not firstline; used when they are not able to be stented because the occlusion is too great or they stents
are not working anymore 
● Most common type of cardiac surgery
● Most common type of surgery for older adults

Traditional CABG
● Guidelines recommend internal mammary artery
○ Greater saphenous vein or lesser saphenous vein
● Median sternotomy – signs and symptoms for infection
● Chest tubes- prepare and monitor patient
● Epicardial pacer wires
● CPB (this is a lung machine- cardiopulmonary bypass)
○ Mechanically circulates and oxygenates blood while bypassing lung/heart
○ Potassium cardioplegia
○ Heparin=> protamine
○ Hypothermia
Alternative CABG Techniques
● Off pump CABG (OPCAB)
○ (still uses median sternotomy)
● Minimally invasive techniques
○ Eliminates sternotomy
○ May still require CPB required
○ Endoscopic technique using a robotic system to place bypass grafts
○ Not a candidate if multivessel disease

CABG: Preoperative Nursing Process

● Health history
● Physical exam
 ● Pre-op testing – CBC bmp ekg and type cross
● Cognitive/support systems
● Patient teaching
○ Surgical care environment
○ Surgical sites
○ Ventilator support
○ Pain medication will be readily available
● Prophylactic antibiotic 20-30 minutes pre-op to prevent infection
● Tell them about pain meds they will be on after

CABG: Intraoperative Management

● Perioperative nursing responsibilities
● Monitor for intraoperative complications

CABG: Postoperative Nursing Process (Chart 27-13 Plan of Care)

→ HEAD TO TOE ASSESSMENT - LOOK AT EVERYTHING 
● Neurologic status
● Cardiac status
● Respiratory status
● Peripheral vascular status
● ALWAYS LOOK AT PULSES
● Renal function ALWAYA
● Fluid and electrolyte status- potassium and sodium
● Pain
● Equipment- are working

Potential Complications of Cardiac Surgery (27-5)

→ Main thing to watch for is dysrhythmia first 24-48hr is most important 
● Preload alterations
● Persistent bleeding
● Cardiac tamponade – extra fluid around the heart
● Hypovolemia
● Hypotension
● Low CO
● Increased afterload
● F & E disturbances
● Impaired gas exchange
● Impaired cerebral circulation
● Fluid overload
● Hypertension
● Cardiac failure- Pump is not working.
● AMI
● AKI
● Stroke
● Hepatic failure

Cardiac Transplant

Cardiac Transplant
● Viable option for patients with end-stage heart disease
○ Advances in surgical techniques
○ Advances in immunosuppressive therapies
 ■ Cyclosporine (Neoral, Sandimmue)
■ Tacrolimus (Prograf)

Indications for Transplant

● Cardiomyopathy
● Ischemic heart disease
● Valvular disease
● Rejection of previously transplanted heart
● Congenital heart disease
→ Mostly cardiomyopathy and heart disease 
→ Not common for patient who previously rejected

Patient Presentation
● Severe symptoms uncontrolled by conventional medical therapy
● No other surgical options
● Prognosis of <2 years to live
Patient Screening
● Multidisciplinary process
○ Age
○ Pulmonary status
○ Chronic health conditions
○ Psychosocial status
○ Family support
○ Infections
○ History of other transplants
○ Compliance
○ Current health status
→ May not be a candidate even if terminally ill or patients who are immunocompromised because these
patients have a high chance of rejection 

Waitlist
● Donor heart becomes available→ recipients based on ABO compatibility, body size (donor and recipient),
age, severity of illness, length of time on waiting list, geographic locations (donor and recipient); must be
transplanted within 4 hours.

Transplant Procedure
● Orthotopic transplantation
● Three classes of medications to minimize rejection
○ Corticosteroids (Prednisone)
○ Calcineurin inhibitors (Cyclosporine, Tacrolimus)
○ Antiproliferative agents (CellCept, Imuran)
 Know these meds **
 Teaching: at risk for infection for LIFE **
 think like the nurse not the surgeon
 monitor for s/s of rejection, the meds are given in the OR so rejection doesn’t start immediately

Transplanted Heart
● No nerve connections to recipients body
● Sympathetic any vagus nerves do not affect transplanted heart
● Resting HR 70-90 BPM
● Gradual increase in exercise required
● May not experience angina/ischemia
Complications
● Accelerated atherosclerosis
● Hypertension (Cyclosporine, tacrolimus)
● Osteoporosis
● Cancer
● Weight gain, obesity
● Diabetes
● Dyslipidemia
● Hypotension
● Renal failure
● CNS, respiratory and GI disturbances
● Toxicity
→ Kidney is high risk for complications 
 a lot of these are side effects of the drugs

Psychosocial Stressors
● Better quality of life
● Survivor guilt
● Anxiety
● Depression
● Fear of rejection

Nursing Process

→ Community resources 
→ DISCHARGE INSTRUCTION IS KEY - IT IS VERY IMPORTANT
 your job as a nurse is to reduce pt anxiety (family support, give info, community resources, etc.)

Ventricular Assist Device

● Performs some or all of the pumping function for the heart
● Short and long-term devices
● Ventricular or biventricular support
 acts like a heart  doing the pumping (not everyone is a candidate)
→ Could be short term or long term
→ This is a alternative to a heart transplant 
→ Patient can go home on a VAD
→ Continuation of care for these patients, care is minute and HCP needs to know what they are doing
→ May need doppler to take a BP (do a manual blood pressure)

VAD
● Bridge to recovery
● Bridge to transplant
 ● Destination therapy
● Community, EMS and family education is imperative
● Complications
○ Bleeding disorders
○ Hemorrhage
○ Thromboemboli
○ Hemolysis
○ Infection
○ Renal failures
○ Multisystem failure

 For patients with VAD there is a team that takes care of this.
 For BP should use a doppler and manual BP taken (they don’t pump normally).

Medications
 Calcium channel blockers
o This medication class reduces cardiac cell excitability, thereby decreasing the force of contraction
of the heart muscle 
 ACE inhibitors 
o Drugs in this class control the sodium and water levels which increase urinary output and lowers
blood volume to reduce blood pressure 
 Beta blockers
o Beta blockers function in the cardiac system by reducing the heart rate - LOWER BLOOD
PRESSURE AND REDUCE HEART 
 Diuretics 
o This medication class lowers volume of blood by increasing the excretion of fluid from the body 

Lab Values
 CK-MB: 0.3
 Troponin: 0-0.4
 Lipids
o Cholesterol: < 200 mg/dL
o LDL < 100 mg/dL
o HDL > 40 mg/dL
 Blood chemistries 
o BUN: 10-20 mg/dL
o Creatinine: 0.7-1.4 mg/dL 
o Sodium: 135-145 mEq/L
o Potassium: 3.5-5.0 mEq/L
o Magnesium: 1.8-2.6 mg/dL
o Calcium: 8.8-10.2 mg/dL
o Phosphorous: 2.5-4.5
o Chloride: 97-107
 WBC: 4,500-10,500
 Platelets: 150,000-450,000
 Hgb: 15
 HCT: 45%
 RBC: 5
 Digoxin levels: 0.5-2 
o Toxicity: yellow vision and yellow halos, bradycardia, HA, dizziness, confusion, and visual
disturbances 
o Nursing management: count apical pulse for 1 full minute prior to administration (less than 60
and greater than 100 - hold dose and notify HCP, avoid giving with high-fiber foods, assess for s/s
of toxicity