High Acuity Exam 1

Calculating a MAP

-[SBP + (2 x DBP)] / 3
-Normal value: 70-100
-< 60 results in insufficient organ perfusion (kidneys, gut, brain)

Factors Affecting Preload

Increased preload
-Increasing circulating volume
-Increasing venous return
-Drugs
-Vasoconstrictors (pressors)

Reduce preload
-Drugs
-Diuretics, vasodilators, nitrates
-Hypovolemia
-Mitral stenosis
-Cardiac tamponade
-Constrictive pericarditis

Factors Affecting Afterload

-Blood viscosity
-Arterial pressure (resistance)

Systole

Closure of the AV valves and the opening of the pulmonic and aortic valves

Diastole

-Return to the resting state
-Filling

Contractility

How hard the heart squeezes

Factors Affecting Contractility

Increased
-Positive inotropic agents
-Dopamine
-Digoxin
-Calcium

Decreased
-Negative inotropic agents
-B blockers
-Calcium channel blockers
-Hypoxia
-Hypercapnia
-AMI
-Shock

Coronary Supply

-Supply blood to the myocardium
-3 major coronary arteries

Automaticity

Ability to initiate impulses

Excitability

Ability to respond to stimuli

Conductivity

Ability to transmit an electrical impulse

Depolarization

-Electrical activation of myocardial cell
-Due to electrolyte changes in and around cell
-(Na+, K+, Ca+)
-Occurs slightly before muscle contraction

Repolarization

-Electrical recovery of myocardial cell
-Electrolyte levels normalize due to Na+/K+ pump
-Prepares cell to accept next impulse and depolarize

Sinoatrial Node

-Normal pacemaker of heart
-Initiates an impulse
-Located in RA near SVC
-Adolescents and adults
--60-100 intrinsic HR

Atrioventricular Node

-Delays impulse from atria
-Allows for ventricular filling
-Protective mechanism against rapid supraventricular impulses
-Located in the floor of the Right Atrium, near tricuspid valve

Junctional Tissue

-Serves as back up pacemaker
-Tissue in lower AV node, above the bifurcation of the bundle of His
-\>3 years old 40-60

Ventricular Tissue

-Back up pacemaker
-\> 12 years old 20-40 HR

Perkinje System

-Rapidly conducts impulses to ventricular subendocardial layers
-Distal to the bundle branches
-Terminal Conduction System

The P Wave

-First wave of the cardiac cycle
-Represents Atrial depolarization
-Characteristics:
--Precedes the QRS
--Round & upright

Abnormal P Waves

-Peaked, notched, or enlarged
--Atrial hypertrophy
--COPD, PE, valve disease or heart failure, congenital heart defects

-Inverted
--Retrograde or reverse conduction from the AV node

-Varying
--Impulse from different sites
--Irritable atrial tissue
--Damage near SA node

QRS Complex

-Represents Ventricular depolarization
-Characteristics:
--Measured from the onset of ventricular activity to the end of ventricular depolarization
--May not have all 3 waveforms but it is still referred to as the QRS complex

QRS Duration

< 0.12

Abnormal QRS

-Widened \>0.12 seconds
--Intraventricular conduction delay

-Absent
--AV block or ventricular standstill

T Wave

-Ventricular repolarization
-Vulnerable period in the cardiac cycle
-Characteristics:
--Follows S wave
--Round & smooth

Abnormal T Wave

-Bumpy
--There may be a hidden P wave in it

-Tall, peaked, or pointed
--Hyperkalemia
--Myocardial ischemia
--Myocardial injury
--Pericarditis

-Inverted
--Myocardial Ischemia

PR Interval

Beginning of P wave to beginning of QRS complex

PR Interval Duration

0.12-0.20 seconds

Abnormal PR Interval

-Shortened interval
--Impulse did not originate in SA node

-Prolonged interval
--Conduction delay through atria or AV junction

-Variable
--Conduction delays or blocks

ST Segment

-From end of QRS complex to beginning of T wave
-Early Ventricular Repolarization

Abnormal ST Segment

-Depression
--Myocardial ischemia or digoxin toxicity

-Elevation
--Myocardial injury

QT Interval

-Ventricular depolarization and repolarization

QT Interval Duration

Less than or equal to 0.12

Abnormal QT Interval

-Prolonged
--Medications
--Congenital conduction-system defect

-Shortened
--Digoxin toxicity
--Hypercalcemia

Normal Sinus Rhythm

-Atrial and ventricular depolarization occurs in an orderly and organized manner, over a normal, constant period, as evidenced by the PR interval and the QRS width.
-Rate
--\> 12 years (60-100)
-P wave precedes each QRS
-PR Interval constant
-PR Duration (0.12-0.20)
-QRS duration: Constant (< 0.12)

Sinus Tachycardia Interventions

-Atrial and Ventricular Depolarization follow the normal conduction pathway so the PR interval and the QRS width are within normal limits for age
-Rhythm: Regular
-Rate: 100-160
-P Wave: Normal, precedes each QRS
-PR: 0.12 - 0.20 sec
-QRS:

Sinus Tachycardia Causes

-Compensatory Mechanism in response to:
--Anemia, Hypoxia, Hypovolemia, Hypotension, Fever

-Sympathetic Stimulation
--Exercise, Emotion, Anxiety, Pain

-Drug related
--Caffeine, Epinephrine, Cocaine,

-Theophylline
-Early sign of CHF
-Hyperthyroidism

Sinus Tachycardia Significance

-Depends on patient's underlying condition
-May be normal in infants and small children
-Increased rate may decrease filling time, which may result in a decrease in stroke volume and cardiac output.

Sinus Bradycardia

-Atrial and ventricular depolarization follow the normal conduction pathway so the PR interval and the WRS width are within normal limits
-Rhythm: regular
-Rate: < 60
-P Wave: normal, precedes each QRS
-PR: 0.12 - 0.20 sec, constant
-QRS: < 0.12 sec, constant

Sinus Bradycardia Significance

-If severe or prolonged, may cause decrease in cardiac output and syncope
-At risk for escape rhythm or beats to gain control due to long pauses

Sinus Bradycardia Causes

-Normal in healthy, young, athletes

-Vagal stimulation
--MI, vomiting, straining at stool, pharyngeal suctioning, etc.

-Medication effect
--Beta blockers, calcium channel blockers, etc.

-Increased Intracranial Pressure
-Hypokalemia
-Sick Sinus syndrome

Sinus Bradycardia Interventions

-Assess patient
-Adjust Drug Regimen
-Relieve source of Vagal Stimulation
-If symptomatic, treat with Atropine
-May require a temporary pacemaker

Sinus Arrhythmia

-Sinus node is in charge, but the rhythm is irregular, most commonly varies with respiratory cycle
-Rhythm: irregular
-Rate: 60-100 (normal)
-P wave: Normal, precedes every QRS
-PR: 0.12 - 0.20, constant
-QRS: < 0.12, constant

Sinus Arrhythmia Causes

-Common in children & often outgrown in teens
-Variation of Sinus rhythm
-Vagal stimulation

Sinus Arrhythmia Interventions

-Usually none
-R/O more serious irregular rhythm
-Minimize vagal stimulation

Sinus Pause/Arrest

-Sinus node fails to generate an impulse for one or more beats; usually reset by sinus node but escape beats/rhythms may occur
-Rhythm: Regular except for pause
-Rate: depends on underlying rhythm
-PR: 0.12 - 0.20, constant
-QRS: < 0.12, constant

Sinus Pause Significiance

-May decrease C.O.
-Observe for further signs of sinus node dysfunction
-Duration of the pause as well as the ability of a lower (escape) rhythm to respond determines the seriousness of the dysrhythmia.

Sinus Pause Interventions

-Assess the patient
-If pause \> 3 sec evaluate for pacemaker
-Atropine

Sinus Pause Causes

-Vagal Stimulation
-Carotid Sinus Massage
-Sick Sinus Syndrome
-Medications
--Digoxin, Beta Blockers, Calcium, Channel Blockers, Amiodarone
-Ischemia of the SA Node
-Pericarditis
-Hyperkalemia

Premature Atrial Complexes

-Irritable focus within the atria takes over as the pacemaker, fires early and produces an ectopic beat
-Originates outside the SA node
-Single or multiple ectopic focus
-May or may not be conducted via AV node
-Various shapes of P waves

Premature Atrial Complexes Significance

-Irritable focus in the atria
-May progress to other dysrhythmias

Premature Atrial Complexes Interventions

-Assess the patient
-Look for an underlying cause

Premature Atrial Complexes Causes

-Any factor that produces atrial irritation or atrial stretching (Mitral stenosis, CHF)
-Stimulants
--Caffeine, Stress, Nicotine, Dig, etc.
-Electrolyte Imbalance
-Hypoxia
-Aging

Supraventricular Tachycardia (SVT)

-Rhythm: regular
-Rate: \> 160
-P wave: May not be discernable
-PR: 0.12 - 0.20, Normal for age, constant, if measurable
-QRS: < 0.12, normal for age, constant

Supraventricular Tachycardia (SVT) Significance

-If rapid, may decrease cardiac output
-Angina
-Palpitations
-Anxiety
-Shortness of Breath
-Decreased Level of Consciousness
-Decreased BP
-Shock
-Pulmonary congestion
-CHF
-Acute MI

Supraventricular Tachycardia (SVT) Causes

-Stimulants
--Caffeine, drugs, stress, nicotine
-Medications
-Electrolyte imbalance
--Hypokalemia
-Cardiac disturbance
--Left Ventricular Failure
--Mitral Valve Prolapse
--AV Nodal dysfunction
-COPD
-Thoracic surgery

Supraventricular Tachycardia (SVT) Interventions

Assess patients' tolerance of the rhythm

If Stable
-Valsalva Maneuver
--Cough, bear down, squat, hold breath, immerse face in ice water, stimulate a gag reflex
-Carotid Sinus Massage (CSM)
-Adenosine, IV Push - Drug of Choice

If Unstable
-Prepare for Immediate Cardioversion
-Oxygen

Atrial Flutter

-Rhythm:
--Atrial - Regular
--Ventricular - may be Regular or Irregular, dependent on AV node conduction
-Rate: more than 12 years 250-350
-P wave: Called "F" waves, jagged, saw tooth pattern
-PR (FR) interval: Not Measurable
-QRS width: < 0.12, constant

Atrial Flutter Causes

Conditions that enlarge atrium and elevate atrial pressures
-Congestive Heart Failure
-COPD
-Mitral valve disease
-Acute MI
-Hyperthryoidism
-Primary myocardial disease
-Pericardial Disease

Atrial Flutter Significance

-S/S of low cardiac output if ventricular rate is high (loss of atrial kick)
-Less stable than A. Fib, it is not a benign condition
-Take a second look at sinus tachycardia with a rate \>150 - may be Atrial Flutter with 2:1 conduction
-More clinical attention needed in patients with ischemic heart disease

Atrial Flutter Interventions

-Assess the pt.
-Goal
--Control heart rate, maintain adequate cardiac output

-Cardioversion
--If patient is unstable OR if medications unsuccessful

-Medication therapy
--Calcium Channel Blockers, Beta Blockers, Amiodarone, Digoxin,

-Anticoagulation

Atrial Fibrillation

-One of the Most Common dysrhythmias in adults and
-No sign of organized atrial activity
-Conduction of impulses through the AV node is chaotic
-Atrial Kick is lost

-Rhythm:
--Atrial - Irregular, chaotic
--Ventricular -Irregular

-Rate:
--Atrial - Unable to determine
--Ventricular - Variable, dependent on AV node conduction.
· Slow -

Atrial Fibrillation Significance

-Often NO symptoms
-Irregular Pulse
-Loss of Atrial Kick
-Increased chance of thrombus formation in atria

Atrial Fibrillation Causes

Any condition that causes atrial ischemia, stretching or compression
-Hypertension
-Valvular heart disease
-CAD
-Acute MI
-Pericarditis
-Congenital Heart Defects
-CHF
-COPD
-Smoking, alcohol, caffeine, sudden emotional excitement
-Electrolyte Imbalances
-Hyperthyroidism
-Hypoxia

Atrial Fibrillation Interventions

Acute
-Beta blockers
-Amiodarone
-Ca++ channel blockers
-Cardioversion
-Anticoagulation

Subacute
-Treat reversible causes
-Cardioversion
-Anticoagulation

Chronic
-Medications
-Anticoagulation
-Ablation

Junctional Escape Rhythms

Rhythm:
-Atrial - Regular
-Ventricular -Regular

Rate:
-40-60

-P wave: Inverted, before, during(absent) or after QRS complex
-PR interval: < normal for age if measurable
-QRS width: < 0.12, constant

Junctional Escape Rhythms Significance

-Usually well tolerated
-AV junction is not as reliable as SA node as a pacemaker

Junctional Escape Rhythms Causes

-Vagal stimulation
-Ischemia (MI)
-Hypoxia
-CHF
-Post thoracotomy
-Dig toxicity
-Damage to sinus node
-Bradycardia

Junctional Escape Rhythms Interventions

-Usually none
-Identify cause and treat as needed
-Atropine or pacing
If symptomatic

Accelerated Junctional Rhythm

Rhythm
-Atrial - regular
-Ventricular - regular

Rate
-Adult: 60-100

-P wave: Inverted, before, during (absent) or after QRS complex
-PR interval: < normal for age if measurable
-QRS width:< 0.12, constant

Accelerated Junctional Rhythm Significance

-Loss of atrial kick
-Tolerated well

Accelerated Junctional Rhythm Causes

-Dig toxicity
-Excessive catecholamines
-Damage to AV node from an inferior MI

Accelerated Junctional Rhythm Interventions

-Usually, will convert spontaneously
-Hold digoxin
-Identify cause and treat

Junctional Tachycardia

-Rhythm: Regular
-Rate: \>100/min
-P wave: Inverted, before, during, or after QRS
-PR:

Junctional Tachycardia Significance

-Can decrease CO
-Loss of atrial kick
-Can cause angina, palpitations, anxiety, SOB

Junctional Tachycardia Causes

-Digoxin toxicity
-Hypokalemia
-Posterior MI
-CABG

Junctional Tachycardia Interventions

-Depending on pts tolerance
-If symptomatic treat

Premature Junctional Complexes

-Rhythm: Regular except for the ectopy
-Rate: Dependent on underlying rhythm
-P wave: May be inverted, before or after QRS or may be absent (during QRS)
-PR: If P is visible then PR is

Premature Junctional Complexes Significance

-May Progress to Junctional tachycardia
-Loss of "atrial Kick"

Premature Junctional Complexes Causes

-Digoxin toxicity
-Ischemia (acute MI), CHF, Rheumatic fever
-Medications (Quinidine, Procainamide)

Premature Junctional Complexes Interventions

-If asymptomatic - None
-Identify cause & treat if needed

Ventricular Fibrillation

-Electrical activity identical to afib but affecting the ventricles vs. the atria
-Unlike afib, no QRS complexes are discernible
-No HR measurable because no QRS waves
-Unresponsive, pulseless, and apneic
-Occurs in acute MI and myocardial ischemia and in chronic diseases such as HF and cardiomyopathy
-Can be associated with hyperkalemia, acidosis, drug toxicity

Ventricular Fibrillation Treatment

-Immediate initiation of CPR and ACLS
-Defibrillation and drug therapy (epinephrine, amiodarone)

Ventricular Tachycardia

-A very rapid heartbeat that begins within ventricles
-"Tombstone"

Ventricular Tachycardia Treatment

-Lidocaine
-Amiodarone
-Defibrillation

Natural Pacemaker of the Heart

SA node

Thrombolytic

-Given to MI patients
-Check for bleeding
-Especially in the brain (LOC)

Heparin

-Anticoagulant used to prevent the formation of clots
-Antidote is vitamin K

Mechanical Heart Events

-Systole
-Diastole
-The pumping of the heart

Acute Decompensated Heart Failure (ADHF)

-Acute exacerbation of heart failure
-Signs and symptoms of respiratory distress and poor systemic perfusion

Acute Decompensated Heart Failure (ADHF) Symptom Management

-Support oxygenation/ventilation/CO
-Identify underlying cause
-Weigh self same time every day in same amount of clothing
-Na reduction and fluid restriction
-Mild exercise

Acute Decompensated Heart Failure (ADHF) Medications

-Diuretics
-Vasodilators
-Cardioversion

Diuretics

-Decrease Na reabsorption, decreases intravascular volume, reduces preload, improves LV function, decreases pulmonary congestion
-IV preferred for faster action
-Loop (furosemide), K+ sparing (spironolactone) or thiazides (HCTZ)

Morphine

-Slight mild vasodilator and for pain

Inotropes

-Tells your heart to pump/contract more or less
-Dopamine, dobutamine, norepi, milrinone
-Short-term treatment: improved CO, BP, urine output and reduced filling pressures are the goal
-Must have continued ECG monitoring \= can cause dysrhythmias

Stable Angina/Chronic

-Pain only lasts a few minutes
-Subsides with rest
-ECG changes may be temporary but will return to normal
-SL nitro, beta-blockers, ACE inhibitors, Ca+ channel blockers
-Anticoagulants
-Anti-lipids

Unstable Angina/Acute

-New onset, occurs at rest/increasing frequency
-Pain lasts 10+ minutes
--Pain evolves -\> may change rapidly or has changed locations
-May be the first sign of CAD or may evolve from chronic angina
-Must be treated immediately
-ECG: ST depression, T wave inversion -\> ischemia

Angina Diagnostic Studies

-12 lead ecg
-cardiac biomarkers (troponin, ck)
-health hx/physical exam
-chest x-ray
-echocardiogram (measure ejection fracton, see wall abnormalities or valve failure)
-exercise stress test
-nuclear imaging (radioactive dye injected to determine where a block may be)

Hypertensive Crisis

-systolic \>180 and/or diastolic \>110
-typically happens
-hypertensive emergency
-hypertensive urgency

Hypertensive Emergency

-evidence of acute target organ damage (hypertensive encephalopathy, cerebral hemorrhage, acute renal failure, myocardial infarction, heart failure with pulmonary edema, aortic dissection)
-manifestations depend on organs involved

Hypertensive Emergency Interventions

-admit to icu
-iv drug therapy (titrated to map)
-MONITOR CARDIAC AND RENAL FUNCTION
-neurologic checks
-determine cause
-edication to avoid future crisis