Exam 2 Flashcards
Cardiac Output Calculation
Heart Rate x Stroke Volume
Normal Range: 4 - 6 L/min (at rest)
Measure of contractility
Preload
Volume entering ventricles allows stretch and enhances force of contraction
Fluid volume
Right Ventricle: Central Venous Pressure, Blood Pressure, Heart Rate
Left Ventricle: Pulmonary Artery Pressure
Contractility
Force of muscle contraction itself
Myocardial Strength
Cardiac Index, Cardiac Output
Afterload
Pressure LV needs to overcome to eject blood
Systemic vascular resistance, valve compliance, viscosity of blood, aortic compliance
Stroke Volume is composed of…
Preload
Contractility
Afterload
Flow is determined by…
Pressure
Resistance
Volume
Principle of Hemodynamic Assessment
Pressure does not always equal flow
HTN can be a result of atherosclerosis
Cardiac Output
Volume of blood ejected by left ventricle per minute
Normal is 4-8 liters/minute
Cardiac Index
Adjustment to cardiac output made for body size
Normal is 2.5-4 liters/minute/m2
CO/BSA
Measure of contractility
Stroke Volume
Volume ejected each beat
Normal is 60-120 ml/beat
SYSTOLIC BLOOD PRESSURE
Measure of contractility
Ejection Fraction
Percentage of blood ejected from the left ventricle
Normal is 55-60%
Right Ventricle Preload Indirect Assessment
Jugular Venous Distention
Hepatojugular Reflex
Peripheral edema
Weight gain
Left Ventricle Preload Indirect Assessment
Chest x-ray
BNP
Lung sounds
S3
Blood pressure
Urine output
Weight gain
Direct Right Ventricle Preload Assessment
Central Venous Pressure (right atrial pressure)
Direct Left Ventricle Preload Assessment
PA Diastolic
PCWP (left atrial pressure)
Left Ventricle Afterload Assesment
Diastolic BP
Pulse pressure
Systemic Vascular Resistance
Right Ventricle Afterload Assessment
Causes: hypoxemia, PEEP, pulmonary HTN
Direct Assessment: Pulmonary Vascular Resistance, PA Systolic
Blood Pressure Formula
Cardiac Output x Systemic Vascular Resistance
Low Blood Pressure
Due to low cardiac output
Heart rate slow/fast
Preload low/high
Contractility low
Low Systemic Vascular Resistance
Vasodilation
Pulse Pressure < 35 with Tachycardia
Early sign of inadequate blood volume
Blood pressure 88/64 = Pulse Pressure of 24 (constricted)
Pulse Pressure > 35 with Tachycardia
Early sign of vasodilatory state
BP 82/30 = Pulse Pressure of 52 (dilated)
Vasoconstriction
Increased vascular tone
Compensation for low stroke volume
Shock states
Vasodilation
Decreased vascular tone
Abnormal pathology
Anaphylaxis, altered neurological control
Systemic Vascular Resistance Formula
MAP – CVP/CO x 80
Normal: 900 - 1400 dyns/sec/mm
Afterload for the left ventricle
Pulmonary Vascular Resistance Formula
MPAP – PAOP/CO x 80
Normal: 100 - 250 dyns/sec/mm
Afterload for the right ventricle
Principles of Hemodynamic Monitoring
Don’t just look at the numbers, look at the client
Single readings are not as significant as trends of data
Use the patients own normal for a reference
Invasive Monitoring
Pressure line with transducer
Heparinized solution
Phlebostatic reference point (4th intercostal space, midaxillary line)
“Zeroing” the system
Arterial Pressures
First check Allen’s test
Sharp upstroke with systole
Dicrotic notch at diastole
Problems: infection, accidental blood loss, impaired circulation to extremity
Mean Arterial Pressure
[Systolic + (2x Diastolic)] / 3
Normal: 70 - 105 mmHg
Perfusion Pressure
“Invasive” Cardiac Output Measurements
Thermodilution boluses
Continuous thermodilution measurements
Esophageal doppler
“Noninvasive” Cardiac Output Measurements
Arterial waveform assessment
PiCCO2
Computation of Cardiac Index
Cardiac Output / Body Surface Area
Mixed Venous Oxygen Saturation (SvO2)
MEASUREMENT OF O2 SATURATION IN VENOUS BLOOD
INDICATOR OF O2 BALANCE
Factors: CO, Hgb, SaO2, tissue oxygen metabolism
NORMAL: 60-80%, usually 70-75%
If SvO2 decreases more than 10% for more than 3-5 minutes, troubleshoot factors
Steps for Investigating Clinically Significant Changes in SvO2
- Assess the patient
- Examine the oxygen supply to the patient
- Evaluate cardiac functioning (VS, CO, CI)
- Check patient’s most recent Hgb level
- Consider nursing activities (repositioning)
- Resolve the clinically significant change before resuming other nursing cares
Central Venous Pressure
Normal range: 2 - 5 mmHg, 3 - 8 cm water
Affects PRELOAD
PA Systolic
Normal range: 20 - 30 mmHg
PA Diastolic
Normal Range: 5 - 10 mmHg
PAP Mean (PAPm)
Normal Range: 10 - 15 mmHg
Pulmonary Artery Pressure (PAOP)
Normal Range: 5 - 12 mmHg
Contractility
Ability to contract
Cardiac glycosides increase effectiveness
Excitability/Irritability
Ability to respond to an impulse
Stimulated by isoproterenol, epinephrine
Depressed by lidocaine, procainamide, quinidine
Conductivity
Allowance of transmission of impulse
Slow/delay through AV node (Digoxin)
Automaticity
Ability to create an impulse
Atropine and epinephrine increase impulse
Refractoriness
Inability to respond to another impulse
Indications for Antidysrhythmic Medications
Ventricular rate rapid with cardiac output reduced
Minor dysrhythmias threatening to develop into major (PVCs)
Major dysrhythmias have developed which may become fatal
Objectives for Antidysrhythmic Medications
To restore normal sinus rhythm
Abolish abnormal rhythm
Prevent reoccurrence of dysrhythmia
Control ventricular rate
Nursing Implications for Antidysrhythmic Medicaitons
Know toxic vs. therapeutic serum levels
Administer at even intervals to maintain blood levels
Check apical HR for a full minute (hold if < 60 or > 120)
Check blood pressure (hold if < 100 systolic or 30mmHg drop in previous reading)
Vaughan Williams Classification of Antidysrhythmic Medications
Based on the medications’ effects on the CELL ACTION POTENTIAL
Class I Antidysrhythmic Drugs
Sodium channel blockers in fast action potentials
Slows impulse conduction in atria and ventricles
Delays repolarization
(Quinidine, Procainamide, Lidocaine, Phenytoin)
Quinidine Use
Long-term suppression of atrial and ventricular dysrhythmias
Adverse Effects of Quinidine
Diarrhea
Cinchonism
Cardiotoxicity
Signs of Quinidine Toxicity
Widening of QRS
Prolonged QT interval
Drug Interactions for Quinidine
Doubles digoxin levels (risk for digoxin toxicity)
Administer slow IVP
Monitor serum levels
Procainamide Use
Long term suppression of atrial and ventricular dysrhythmias
Adverse Effects of Procainamide
Hypotension
SLE syndrome (70%)
Blood dyscrasias
GI symptoms
Cardiotoxicity
Signs of Procainamide Toxicity
Widened QRS
PROLONGED QT INTERVAL
Administration of Procainamide
Bolus 20 mg/min slow IVP
Maximum dose 600mg
Infusion 2-6 mg/min
Actions of Lidocaine
Slows conduction
Reduces automaticity
Accelerates repolarization
Used for ventricular dysrhythmias
Adverse Effects of Lidocaine
Drowsiness
Lidocaine Toxicity
Early signs: confusion, agitation
Late signs: seizures
Administration of Lidocaine
NEVER with epinephrine
50-100 mg IV bolus
1-4 mg/min IV drip
Short half life
Class II Antidysrhythmic Drugs
BETA ADRENERGIC BLOCKERS
Slows SA node automaticity, conduction through AV node, decreases myocardial contractility
CARVEDILOL AND METOPROLOL
Propranolol Actions
Nonselective alpha-blocker
Decreased SA node automaticity
Decreased AV conduction
Decreased myocardial contractility
Uses for Propranolol
SVT
Recurrent VT, VFib
Adverse Effects of Propranolol
Hypotension
AV block
Heart failure
Sinus arrest
Bronchospasms
Administration of Propranolol
1-3 mg/5 min slow IVP
Watch cardiac monitor during administration
Class III Antidysrhythmics
Potassium channel blockers
Delay depolarization and refractoriness of fast potentials
Anti-fibrillatory action
Amiodarone
Uses of Amiodarone
Ventricular and supraventricular tachydysrhythmias
Action of Amiodarone
Delays repolarization
Prolonged serum half-life
Do not give with bradycardia because this drug slows down the heart rate
Adverse Effects of Amiodarone
Hypotension
Bradycardias
Signs of Amiodarone Toxicity
Pulmonary toxicity
Paradoxical dysrhythmias
SA and AV blocks
Photophobia and blindness
Blue-gray skin
Administration of Amiodarone
150 mg IV infusion over 10 minutes
Enhances digoxin levels
Monitor liver enzymes, serum level, pulmonary status, and ocular funduses
Class IV Antidysrhythmics
Calcium channel blockers
Reduced SA node automaticity, delayed AV conduction, reduced myocardial contractility
Verapamil, diltiazem, nicardipine
Calcium channel blockers relax the smooth muscle
Verapamil Uses
Paraoxysmal SVT (SVTs that occur out of nowhere and then disappear; not sustained)
Actions of Verapamil
Reduced SA automaticity
Delayed AV conduction
Reduced myocardial contractility
Adverse Effects of Verapamil
Hypotension
Constipation
Bradycardias
Headache
Administration of Verapamil
3-10 mg slow IVP over 5 minutes
Monitor cardiac rhythm for response
Diltiazem Uses
Slow ventricular rate of SVTs
Contraindication of Diltiazem
CHF or heart failure
Adverse Effects of Diltiazem
AV blocks
Heart failure
Headache
Administration of Diltiazem
.25 mg/kg slow IVP
IV infusion 5-15 mg/hour
Uses of Digoxin
SVT
Heart failure
Slows AV node conduction, increased vagal stimulation, increased myocardial contractility
Slows the contraction of the heart muscles and makes the beats more effective
Adverse Effects of Digoxin
Prolonged PR interval
AV blocks
Nausea, vomiting, cramping
Visual disturbances (halos, based on hyperkalemia)
Signs of Digoxin Toxicity
Premature beats (PACs, PVCs)
AV blocks, prolonged PR interval
Nausea, vomiting, diarrhea
Halos seen around lights
Hyperkalemia
Administration of Digoxin
Loading dose: 1-1.5 mg slow IVP
May repeat bolus every 6-8 hours
MONITOR SERUM LEVELS
NOTE TIME OF CARDIOVERSION
MONITOR POTASSIUM
MANY DRUG INTERACTIONS
Adenosine Use
Paroxysmal SVT
WPW syndrome
Decreases SA automaticity
Adverse Effects of Adenosine
Sinus bradycardia
Bronchospasms
Hypotension
Facial flushing
Transient adverse effects, flatline for 3-6 seconds
Administration of Adenosine
6 mg rapid IVP with 10 mL flush –> next dose is 12 mg
No longer a priority drug in ACLS
Monitor cardiac rhythm
Uses of Ibutilide
Recent onset (< 90 days) of atrial fibrillation atrial flutter
Prolongs action protential
Adverse Effects of Ibutilide
Sustained ventricular tachycardia, PVCs
Prolonged QT interval
Administration of Ibutilide
1 mg/50 cc over 10 minutes IV infusion
0.01 mg/kg over 10 minutes
Antidysrhythmic-Antidysrhythmic Drug Interactions
Mechanism: Additive
Result: Pro-arrhythmic, may cause dysrhythmias
Antidysrhythmic-Anticoagulant Drug Interactions
Mechanism: Anticoagulants displaced from protein binding sites
Result: More pronounced anticoagulant effects
Antidysrhythmic-Phenytoin Drug Interactions
Mechanism: Phenytoin displaced from protein binding sites
Result: More pronounced Phenytoin effects
Antidysrhythmic-Sulfonylurea Drug Interactions
Mechanism: Sulfonylurea displaced from protein binding sites
Result: More pronounced sulfonylurea effects
Critical Thromboembolic States
CVA
MI
PE
DVT
Intrinsic Pathway Clotting Cascade
Activated by Factor XII
Blood comes in contact with foreign substance or damage endothelium in blood vessels
Extrinsic Pathway Clotting Cascade
Activated by Factor VII
Blood is exposed to substances released in response to tissue damage
Indications for Coumadin
PE, DVT treatment/prophylaxis
CVA prophylaxis in atrial fibrillation or valve replacement
Takes 8-14 days to reach full effect
Contraindications for Coumadin
Pregnancy
Recent or active hemorrhage
Recent surgery/trauma
Properties of Coumadin
Vitamin K antagonist
Effectiveness monitored by INR (target is 2-3)
Binds extensively to plasma proteins (lots of interactions)
Reversal: Vitamin K, Fresh Frozen Plasma
Dabigatran (Pradaxa)
Direct thrombin inhibitor (new alternative to Coumadin)
Fixed, more predictable dosing, minimal monitoring
History of compliance is necessary
Vitamin K not used for reversal–only FFP
Used for CVA prevention in AFib
Aspirin
Inhibits platelet aggregation
Inhibits COX enzyme
81 mg x4 in acute MI
Active stroke/MI prophylaxis
Clopidogrel (Plavix)
Irreversibly inhibits ADP, a promoter of platelet binding
600mg in AMI
Plavix plus aspirin given before coronary intervention and continued for a year
Integriln
Reversibly binds to GPIIb/IIIa platelet receptors and inhibits platelet aggregation
Bolus of 180 mcg/kg, then 2 mcg/kg/min infusion prior to and after PTCA
Reopro
Inhibits BP IIb/IIa platelet receptors and inhibits platelet aggregation
0.25 mg/kg bolus, then 10 mcg/min until PCI, and after
Heparin
Alters antithrombin III, stopping the clotting cascade
Prevents further thrombi in thrombotic events (DVT, PE, MI)
Weight-based protocols–bolus, then continuous drip
PTT monitored every 6 hours
Reversed with protamine sulfate
Contraindications: pregnancy, bleeding, epidural
Heparin Induced Thrombocytopenia
Occurs in up to 5% of clients receiving heparin therapy
Body forms antibodies to heparin-complexes, then attracts platelets
Vessel occlusion more likely than bleeding
Must discontinue heparin and use lepirudin
Symptoms of Heparin Induced Thrombocytopenia
MI: dyspnea, chest pain
CVA: headache, impaired speech
Peripheral: pain, pallor, mottling, decreased motor function
Fibrinolytics
“Clot busters” used only in emergencies (PE, AMI, CVA)
Reopens affected arteries
Very risky, extensive criteria for administration
Administration of Fibrinolytics
CT prior to administration to rule out hemorrhage
TPA, streptokinase, retavase
Frequent neuro monitoring, vitals
No arterial sticks
Contraindications of Fibrinolytics
Post CPR, recent surgery, recent trauma, BP greater than 180
Fall/injury precautions
CPR post administration usually fatal
Alpha Adrenergic Receptors
Located in vessels of skin, kidney, intestines
When stimulated, peripheral vasoconstriction of arteries occurs
Beta 1 Adrenergic Receptors
Located in cardiac tissue
When stimulated, heart rate increases, cardiac conduction and contractility increases
Beta 2 Adrenergic Receptors
Located in vascular and bronchial smooth muscle tissue
When stimulated, vasodilation and peripheral arteries and bronchodilator occurs
Sympathomimetic Agents
Stimulate adrenergic receptors, stimulated cardiovascular effects
Effects vary on the receptor stimulated and the dose delivered
Catecholamines
Naturally Occurring Catecholamines
Dopamine
Epinephrine
Norepinephrine
Synthetic Catecholamines
Dobutamine
Phenylephrine
Isoproterenol
Cause extensive tissue damage if extravasation occurs
Requires transdermal/subcutaneous injections of PHENTOLAMINE
Dopamine
Stimulates alpha and beta receptors, as well as dopamine receptors
Low doses: dopamine receptors stimulated, renal and mesenteric perfusion increases, urine output increases
Moderate doses: heart contractility increases, CO increases, HR increases
High doses: vasoconstriction
Epinephrine
Stimulates both alpha and beta receptors
Lower doses: effects beta receptors, increasing HR, contractility, and vasodilation
Higher doses: alpha receptor stimulation is predominate, resulting in vasoconstriction (increased afterload)
Increases workload of the heart (not good in MI)
Norepinephrine
Similar to epinephrine, but does not stimulate beta-2, so no vasodilation
Lower doses stimulate beta-1, increasing contractility
Higher doses create vasoconstriction
Preferable vasoconstrictor in MI, tachycardia
Vasopressin
Antidiuretic hormone
Stimulates vascular smooth muscle
Adjunct to norepinephrine infusion in septic shock
Dobutamine
Predominantly Beta-1 effects (increases CO by increasing contractility)
Also stimulates Beta-2, resulting in mild vasodilation
Not used for HTN
Useful in heart failure, post-op heart surgery to increase CO without vasoconstriction
Phenylephrine
Blocks histamine, stimulates only alpha receptors, causing vasoconstriction and increasing SVR
Decreases HR–useful in tachycardia, used often in euro events to increase blood pressure and cerebral perfusion
Milrinone
Phosphodiesterase inhibitor
Inotrope and vasodilator–increased contractility plus decreased afterload
Can cause hypotension
Useful in heart failure and post-open heart surgery
Vasodilators
Arterial or venous
Decreases preload, afterload, or both
Increases CO and decreases workload of the heart
ACE Inhibitors
Vasodilation occurs by stopping Renin-Angiotensin-Aldosterone System
Used in heart failure to decrease SVR and PAOP (LV preload and afterload)
Nitroglycerin
Both arterial and venous dilation, but more pronounced venous effect
Dilates coronary arteries
Used in angina
Decreases preload, relieving pulmonary congestion in heart failure
Side effects: hypotension, tachycardia, HEADACHE
Nitroprusside
Potent arterial vasodilator (decreases afterload)
Works quickly and aggressively, short half-life
Contains thiocyanate to prevent toxicity
Nipride can increase blood pressure if high afterload is causing decreased CO, and causes hypotension
Nicardipine
Calcium channel blocker
Arterial vasodilator, no effect on preload
Used for hypertensive emergencies only
Beta-Blockers
Decrease HR and BP by dilating arteries and veins
Decrease the workload of the heart
Unstable Angina
Character of Pain: New onset or change in pattern or pain
Enzymes: Normal
EKG Changes: Normal or ST depression
NON-STEMI
Character of Pain: Can develop at rest
Enzymes: Elevated
EKG Changes: Normal or may have ST depression
STEMI
Character of Pain: Can develop at rest
Enzymes: Elevated
EKG Changes: ST elevation
Chronic Stable Angina
Episodic pain lasting 5-15 minutes
Precipitating factor present
Relieved by rest or nitroglycerin
Unstable Angina
New onset angina
Chronic stable angina that increases in frequency, duration, or severity
Occurs at rest without precipitation
Unrelieved by rest or nitroglycerin
INFERIOR WALL INJURY
Right coronary artery
Right ventricle involvement, SA and AV node dysrhythmias
II, III, and AVF leads
ANTERIOR WALL INJURY
Left anterior descending artery
Left ventricle pump failure, CHF, cardiogenic shock
Normal Range for Creatine Kinase
55-170 IU/L
CK is released when any muscle is damaged
Normal Range for CK-MB/CK
< 5% CK
Normal Range for Troponin I and Troponin T
0 - 0.4 ng/mL
Chest Pain Medications to Know
Aspirin
Heparin
Nitroglycerin
Beta Blockers (Metoprolol)
Clopidogrel
Glycoprotein IIb/IIIa Inhibitors
Fibrinolytics (Streptokinase, Alteplase, Retaplase, Tenectaplase)
Statins
Risk Factors for Chest Pain
Family history
Smoking
Diabetes, lipid disorder, hypertension, PVD
Previos CVA or TIA
Severe obesity
Ischemia
Outer region of infarcted myocardial area
Viable tissue
T wave inversion
Injury
Middle layer of tissue, potentially viable
ST segment elevation
Infarction
Area of necrosis
Pathological Q waves, lack of depolarization of affected area
Replaced by scar tissue
How to Manage LDL
Eat fresh fruits and vegetables
Ingest 20-30 grams per day of fiber
Use unsaturated vegetable oils instead of butter, coconut oil, lard
Reduce or avoid coconut or chocolate
Blood Pressure Guidelines
Check blood pressure daily at the same time
Lopressor (Metoprolol) doses should be taken 12 hours apart
Restrict sodium
Limit alcohol consumption
Progressive aerobic exercise
Cardiac Catheterization Lab Guidelines
Going within 90 minutes, no fibrinolytics
Going between 90-180 minutes, half-dose of thrombolytics
Going later than 2 hours, full dose of thrombolytics
Contraindications to Fibrinolytic Therapy
Systolic > 180, Diastolic >110
Closed head/facial trauma, recent trauma, active bleeding (except menses)
Pregnancy
Active peptic ulcer, serious systemic disease
Signs for Reperfusion due to Effective Fibrinolytic Therapy
Relief of chest pain
Ventricular dysrhythmias
ST segments return to baseline
Increase in cardiac enzymes
Fibrinolytic Associated with Allergic Reactions
Streptokinase
ER Priorities for Chest Pain
VS and pulse oximetry
O2 therapy
ECG monitor
Chewable ASA 324 mg PO
STAT 12 lead ECH
Nitroglycerin SL 1st dose
STAT cardiac enzymes
2 peripheral IVs 18-20 G
Cautions with Aspirin
Allergies
Gastric bleeding
Bronchospasms
Alternative for Aspirin due to Allergies
Plavix
Eptifibatide
Glycoprotein IIb-IIIa inhibitor
Keeps clots from forming on catheters
Rationale for Metoprolol
Vasodilator
Decrease workload of the heart
Decrease myocardial oxygen demand
Post-Cardiac Catheterization Complications Associated with PTCA
Bleeding from femoral insertion site
Peripheral ischemia
Prior to removing femoral sheath, what nursing intervention will protect from occlusion of femoral artery?
Aspirate 5-10 cc of blood from sheath
Length of Bedrest Following Removal of Femoral Sheath
Flat in bed for 6-8 hours
Chest Pain Following Cardiac-Catheterization
Prep for cardiac surgery
Nitroglycerin intravenous drip
HDL Cholesterol Sources
Omega-3 fats (fish oil)
Dark chocolate
Nuts
Berries
Proper Lipitor Schedule
Take at bedtime to maximize the effects on the liver
Acute Coronary Syndrome
Thrombotic episode
Risk of acute myocardial infarction
Diagnosis: unstable angina, NSTEMI, STEMI
Electrical Interventions for Cardiac Conditions
Defibrillation
Cardioversion
Pacemakers
Implanted Cardioverter
Defibrillators
Radiofrequency Ablation
Cardiac Resynchronization Therapy
Defibrillation
Delivery of electrical current
Unsynchronized countershock
Asynchronous countershock
Sufficient intensity to depolarize cells
Used for VTACH and VFIB
Opportunity for heart’s natural pacemaker to take control
Asynchronous Countershock
Delivery of current no relationship to cardiac cycle
Manual Defibrillation
Place paddles/pads on chest
Professional interprets rhythm
Controls delivery of shock
Automated External Defibrillator
Place pads on chest
Computer interprets rhythm
Computer gives instructions to deliver shock
Steps for Defibrillation
Turn on machine
Place paddles/hold paddles on chest
CHARGE machine
CLEAR the area, look 360 degrees
Press shock
Assess patient
CPR
Cardioversion
Delivery of electric shock; scheduled or emergency procedure
Patient is lightly sedated; IV line, ET tray available
Synchronized: timed to avoid relative refractory period of cardiac cycle (T wave, peak to end)
Machine identifies and released shock in safe period
Rhythm Necessary for Cardioversion
Rhythm needs to have clearly identifiable QRS complex
Narrow QRS tachycardia
AFib, Atrial Flutter
Monomorphic Ventricular Tachycardia
Pacemakers
ELECTRONIC DEVICE THAT DELIVERS CONTROLLED ELECTRIC SIMULATION TO THE HEART THROUGH ELECTRODES IN ORER TO CONTROL HEART RATE
Indications for Pacemaker
Decrease or absent cardiac output
Failure of heart to initiate or conduct an intrinsic electrical impulse at a rate adequate to maintain organ perfusion
Bradyarrhythmias, AV block, sick sinus syndrome, tachycardia
Components of Pacemaker
Pacing pulse generator
Pacing lead systems (bipolar, unipolar)
Temporary Pacemaker
External (transcutaneous)
Transvenous
Epicardial
Permanent Pacemaker
Pacing mode: asynchronous, synchronous, rate modulated
Asynchronous Pacemaker
Delivers a pacing stimulus at a FIXED rate, regardless of the occurrence of spontaneous myocardial depolarization
Occurs in non-sensing modes
Synchronous Pacemaker
Delivers a pacing stimulus only when the heart’s intrinsic pacemaker fails to function at a predetermined rate
Five-Letter Pacemaker Codes
Chambers paced
Chambers sensed
Response to sensing
Rate modulation
Multisite pacing
Chamber of the Heart Paced
ATRIAL
VENTRICULAR
DUAL
AAT, VVI, DDD
Complications of Pacemakers
Related to insertion, subcutaneous implantation of generator, displacement of catheter electrode
Pacer Malfunction: failure to pace, failure to sense, failure to capture
Implanted Cardioverter Defibrillators
Used for tachycardias/fibrillations unresponsive to medication
Atrial and/or ventricular tachycardias
Used to terminate life-threatening ventricular dysrhythmias
Functions of ICD
Monitors heart rate and rhythm, detects abnormal rhythm
Tiered therapy: 1) anti-tachycardia pacing, 2) cardio version, 3) defibrillation; if systole, ventricular pacing
Delivers 25 Joule shock up to 3 times in a row
S-ICD
Subcutaneous Implantable Converter Defibrillator
Electrode placed just under the skin over sternum
Eliminates potentially serious short/long term risks with venous/cardiac electrode placement
Patient Teaching for Pacemaker
Check pulse daily at the same time (report if less than set rate)
Restrict arm movement for 2 weeks after insertion
Avoid contact sports
Keep ID card of pacemaker
Avoid large magnetic fields (MRI, arc welders, electrical substations)
Patient Teaching for ICD
Pre-insertion assessment of patient’s dysrhythmia
Acceptance of life extender
What to do if ICD shock occurs
Family education: CPR, unanticipated shock when in contact during shock
No driving, avoid strong magnetic fields
Radiofrequency Ablation
Percutaneous catheter interventions
Electrophysiology study: cath lab, isolate foci, stimulate dysrhythmias, ZAP it
Cardiac Resynchronization Therapy
Ventricular Conduction Delays
Atrial Pacing
Atrial Arrythmia Suppression
Anti Tachycardia pacing
Ventricular Conduction Delays
Lack of synchrony between RV and LV, biventricular pacing (wires in each ventricle)
Atrial Pacing
Three pacing leads RA, RV, and LV; optimize synchrony for CO
Atrial Arryhthmia Suppression
Bi-atrial pacing RA and LA, pace at higher rate than intrinsic sinus rate, then decrease rate to allow SA node to control
Goal of Pacemakers
To stimulate normal physiologic cardiac depolarization and conduction
Nursing Management of Pacemakers
Assessing and preventing pacemaker malfunction, protecting against micro shock, surveillance for complications, and patient education
Nursing Management of ICDs
Assessing for dysrhythmias, monitoring for complications, and patient education
Treatments for Bradycardia
Give oxygen
Meds: Atropine, Epinephrine, Dopamine
Transcutaneous Pacing
Treatments for Tachycardia
Remove the stimulus (anxiolytics, pain medications)
Beta blocker, calcium channel blocker
Undersensing Pacemaker
Failure to sense
Pacemaker continues to fire regardless of what the heart is doing
Oversensing Pacemaker
Pacemaker is hyper vigilant of heart rhythm and pays attention to all activity
Need to decrease sensitivity of the pacer; increase the millivolts
Failure to Capture
Problem with the heart
Heart is not picking up the pacer influence; need to increase the milliamps on the pacemaker
Hypovolemic Shock
Loss of intravascular fluid volume
Reduced preload
Cardiogenic Shock
Pump-Contractility
Distributive Shock
Afterload
Neurogenic, anaphylactic, septic
Obstructive Shock
Caused By: PE Cardiac Tamponade Constrictive Pericarditis Tension Pneumothorax
Treatment: Fix the cause
Shock
Acute, widespread process of impaired tissue perfusion
Imbalance between cellular oxygen supply and demand
Leads to cellular dysfunction and death
Nursing Diagnoses for Shock
Ineffective tissue perfusion
Impaired cardiovascular function
Stages of Shock
Compensatory
Progressive
Refractory
Progression through stages varies on patient’s prior condition, duration of initiating event, response to therapy, correction of the underlying causes
Pathophysiology of Shock Syndrome
Initial: decreased CO leads to threatened tissue perfusion
Compensatory: homeostatic mechanisms attempt to maintain CO, BP, and perfusion; mediated by SNS
Neural Response
SNS Compensatory Response
Increased HR, contractility, arterial and venous vasoconstriction, shunting of blood to vital organs
Hormonal Response
SNS Compensatory Response
Activation of Renin response (Ang II –> vasoconstriction, release of aldosterone and ADH for sodium and fluid retention)
Stimulation of anterior pituitary to produce glucocorticoids
Stimulation of adrenal medulla to release epi and norepi
Chemical Response
SNS Compensatory Response
Tissue perfusion switches from aerobic to anaerobic (increases lactic acid, acidemia)
Systemic release of inflammatory mediators (impairment of microcirculation, SIRS)
Assessment of Compensatory Shock
Increased HR and contractility Vasoconstriction Clammy skin Fight/flight response Anxiety/fear Decreased urine output Hypoactive bowel sounds
Interventions for Compensatory Shock
Identify cause of shock
Continuous assessment
Begin fluid replacement
Progressive Stage of Shock Syndrome
Compensatory mechanisms begin to fail
Switch from aerobic to anaerobic metabolism (increased lactic acid)
Increased vascular permeability, tissue edema, and decline in tissue perfusion
SIRS
Irreversible damage begins
Assessment of Progressive Stage of Shock
Decreased BP Increased capillary permeability Crackles in lungs Heart rate > 140 bpm Confusion, coma Anuria
Interventions for Progressive Stage of Shock
Aggressive fluid replacement Colloids Continuous assessments and documentation Vasoactive drugs TPN Family support
Refractory Stage of Shock
Shock syndrome
UNRESPONSIVE TO AGGRESSIVE INTERVENTIONS
ALI, AKI, Multi Organ Dysfunction Syndrome (MODS)
Interventions for Refractory Stage
Continue interventions
Be attentive to family needs
Continue to speak to the client
MAP
SBP + 2(DBP) / 3
Average pressure in arteries during cardiac cycle
CVP
Measured in right atrium
Right heart preload
PAS
Pulmonary Artery Systolic pressure
PA pressure measured in the pulmonary artery
Right heart afterload
PAD
Pulmonary Artery Diastolic pressure
Pa pressure is measured in the pulmonary artery
Non-occlusive measure of left heart preload
PCWP/PAOP
Pulmonary Capillary Wedge Pressure/Pulmonary Artery Occlusive Pressure
Measured in pulmonary artery with balloon up
Left heart preload
SVR
Force left ventricle must overcome
Left heart afterload
PVR
Force right ventricle must overcome
Right heart afterload
Assessment and Diagnosis of Shock Syndrome
Shock state
Clinical manifestations
Global indicators
Hyperlactemia
Medical Management of Shock Syndrome
TISSUE PERFUSION PULMONARY GAS EXCHANGE CO and hemoglobin levels Fluid administration Blood Vasoconstrictor agents Nutritional supplementation Glucose control
Nursing Management of Shock Syndrome
Patient status
Explaining procedures and routines
Supporting the family
Encouraging the expression of feelings
Facilitating problem solving and shared decision making
Individualizing visitation schedules
Involving the family in the patient’s care
Establishing contacts with necessary resources
Causes of Hypovolemic Shock
Hemorrhage
Dehydration
Burns
3rd spacing
Diuresis (DI)
Excessive diarrhea
Class I Hypovolemic Shock
15% of fluid volume (750mL)
Class II Hypovolemic Shock
15-30% of fluid volume (750-1500mL)
Class III Hypovolemic Shock
30-40% of fluid volume (1500-2000mL)
Class IV Hypovolemic Shock
> 40% of fluid volume (>2000mL)
Absolute Hypovolemia
Loss of fluid from intravascular space
Relative Hypovolemia
Vasodilation produces increase in vascular capacity relative to circulating volume
Interventions for Hypovolemic Shock
LARGE BORE IV ACCESS
FLUID REPLACEMENT WITH CRYSTALLOIDS (Lactated Ringers, NS)
Hetastarch or Dextran IV solutions
COLLOIDS (albumin)
MODIFIED TRENDELENBURG
MILITARY ANTI-SHOCK TROUSERS
RAPID IV FLUID INFUSER
Noninvasive Hemodynamics
SVI (Stroke Volume Index)
Change of SVI with 250mL infusion over 3-5 minutes
If > 10% – fluid responder
If < 10% – non responder
Leg Raise Noninvasive Test = 250mL
Cardiogenic Shock
PUMP FAILURE
LOSS OF CONTRACTILITY
MYOCARDIAL INFARCTION
CARDIOMYOPATHY
CARDIAC TAMPONADE
DYSRHYTHMIAS
Interventions for Cardiogenic Shock
OXYGEN THERAPY
REDUCE CARDIAC WORKLOAD
MORPHINE SULFATE
HEMODYNAMIC MONITORING
VASODILATORS (NITROGLYCERIN, NITROPRUSSIDE)
DOBUTAMINE, DOPAMINE
ANTIDYSRHYTHMIC MEDS
INTRA-AORTIC BALLOON PUMP
WATCH FOR FLUID OVERLOAD
Benefits of Intra-Aortic Balloon Pump
Decreased afterload
Increased coronary artery perfusion
Contraindications for Intra-Aortic Balloon Pump
AORTIC VALVE INSUFFICIENCY
SEVERE PERIPHERAL VASCULAR OCCLUSIVE DISEASE
PAST AORTIC GRAFTS
AORTIC ANEURYSM
IABP Timing
1: Use arterial or aortic waveform
2: Inflation after dicrotic notch (beginning of diastole)
3: Compare diastolic peak to systolic peak pressures
4: Deflation prior to systole (note end-diastolic pressure)
5: Compare systolic peaks between unassisted and assisted systolic peaks
Monitoring IABP Therapy
WATCH URINE OUTPUT
CHECK LEFT RADIAL PULSE
CHECK PEDAL PULSES
MONITOR HR, MAP, PCWP
MONITOR EXTREMITIES FOR PULSES, COLOR, SENSATION
Nursing Interventions for IABP
PREPARE FAMILY
ASSESS NEED FOR RESTRAINT
REVERSE TRENDELENBURG
MONITOR IABP MACHINE FUNCTION AND TIMING
ANTICOAGULATION THERAPY
WEANING
Prognoses for IABP Therapy
WEANING AND RECOVERY
DETERIORATION AND DEATH
IABP DEPENDENCY AND HEART TRANSPLANT
Ventricular Assist Devices
Designed to support or replace a failing natural heart with flow assistance
Nursing Management of VADs
Monitor for hemodynamic changes and for complications
Complications include bleeding, infection, thromboembolism, and device failure
Distributive Shock
NEUROGENIC (SPINAL CORD INJURY, SPINAL ANESTHESIA)
ANAPHYLACTIC
SEPTIC
ADRENAL CRISIS
Assessment of Neurogenic Shock
Loss of sympathetic tone
Dry, warm skin
Bradycardia, confusion
Risk of thrombophlebitis
Poikilothermic
Interventions for Neurogenic Shock
Spinal cord immobilization
Glucose if hypoglycemic
IV fluid therapy
Vasoactive drips
Elastic stockings, elevate legs, pneumatic stockings
Anticoagulation therapy
Characteristics of Anaphylactic Shock
RAPID ONSET
PRESENCE OF ALLERGEN
HISTAMINE AND BRADYKININS
BRONCHO/LARYNGEAL SPASMS
INCREASED CAPILLARY PERMEABILITY
TACHYCARDIA
HYPOTENSION
Prevention of Anaphylactic Shock
Assess allergy history
Watch closely after first doses of new drugs
Interventions for Anaphylactic Shock
Ensure airway (ET tube, tracheostomy)
100% O2
Epinephrine IVP or DRIP
Antihistamine (diphenhydramine)
Steroids
Glucagon or Ipratroprium if patient takes beta-blockers
Sepsis
Life-threatening organ dysfunction due to a dysregulated host response to infection
Septic Shock
Subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality
Persisting hypotension requiring vasopressors to maintain MAN > 65 and serum lactate > 2 mmol
Sepsis-Induced Hypotension
BP < 90 mmHg Systolic
Or reduction of > 40 mmHg from baseline
Multiple Organ Dysfunction Syndrome
Homeostasis cannot be maintained without intervention
Intrinsic Factors Associated with Septic Shock
Extreme of age
Coexisting conditions (malignancies, burns, AIDS, diabetes, substance abuse)
Malnutrition
Extrinsic Factors Associated with Septic Shock
Invasive devices
Drug therapy
Fluid therapy
Surgery and trauma
Immunosuppressive therapy
End Result of All Shock
Ineffective tissue perfusion and impaired cellular metabolism
Sequential Organ Failure Assessment
Respiration: PaO2/FiO2 ratio
Coag: Platelets
Liver: Bilirubin
CV: BP, MAP, need for vasopressors
CNS: GCS
Renal: Cr, UO
qSOFA
SBP < 100 mmHg
RR > 22/min
Mental Status: GCS < 15
Positive score if two or more indicators present
Septic Shock Pathophysiology
Inflammatory response (mediators released; tumor necrosis factor, interleukin, chemokines, prostaglandins, platelet activating factor)
Sepsis results in systemic inflammatory response with excessive coagulation in microvasculature
Tissue oxygenation becomes critical
Pro-Inflammatory Responses
Initial response or result to infection
Prostaglandin, leukotriene, production/release
Coagulation cascade
Complement cascate
Implications of persistent pro-inflammatory state (thrombi, DIC, ALI)
Anti-Inflammatory Response
Compensatory attempt to regulate the pro-inflammatory response
Period of immunosuppression
Implications of persistent anti-inflammatory state (nosocomial infection, death)
2016 Sepsis Guidelines for Hemodynamics
Target MAP: > 65
Fluid resuscitation with > 30 mL/kg of crystalloids within first 3 hours
Target: normalize lactate
Echocardiography
Use dynamic over static measures to predict fluid responsiveness
2016 Sepsis Guidelines for Infection
Start with broad spectrum antibiotics
Recommend AGAINST sustained antimicrobial prophylaxis with inflammatory states with noninfectious origins
Procalcitonin levels used to stop unneeded antimicrobial therapy
2016 Sepsis Guidelines for Ventilation
Patients with ALI/ARDS should be prone
DO NOT use HFJV
NMBA < 48 hours
Use of lower TV with ALI
2016 Sepsis Guidelines for Metabolism
Early full enteral nutrition
Only test gastric residual volume in patients at high risk for aspiration or feeding intolerance
Suggest use of post pyloric feeding tubes for patients at high risk for aspiration
Summary of Shock
Patients with MAP < 60 are considered to be in shock
Management focuses on supporting oxygen delivery
Prevention of shock is a primary responsibility of nurses
Summary of Hypovolemic Shock
Results from loss of intravascular volume
Decreased CO/CI, CVP, PAOP, and Increased SVR
Manage by identifying and stopping source of fluid loss and administering fluid
Minimize fluid loss, assess therapy response, provide support, prevent complications
Summary of Cardiogenic Shock
Results from impaired ability of heart to pump
Decreased CO/CI, Increased PAOP, CVP, and SVR
Manage by identifying etiologic factors of pump failure and administering drugs to enhance CO
Limit myocardial oxygen demand, enhance myocardial oxygen supply, maintain tissue perfusion, monitor for complications
Summary of Anaphylactic Shock
Results from an immunologic antibody-antigen activation
Decreased CO/CI, right arterial pressure/PAOP, and SVR
Remove offending antigen, reduce effects of biochemical mediators, promote tissue perfusion
Administer epinephrine, facilitate ventilation, volume replacement
Summary of Neurogenic Shock
Results from loss of sympathetic tone due to interrupted impulse transmission or blockage of sympathetic outflow
Decreased CO/CI, RAP/PAOP, SVR, HR
Prevent cardiovascular instability and promote tissue perfusion
Treat hypovolemia, maintain perfusion, maintain normothermia, monitor for and treat dysrhythmias
Summary of Septic Shock
Results from initiation of SIRS due to microorganisms entering body
Decreased CO/CI, RAP, PAOP, SVR, and increased HR
Early identification of sepsis, administer fluids, give medications, provide nutrition
Summary of MODS
Results from progressive physiologic failure of two or more separate organ systems
Fluid resuscitation and hemodynamic support, prevention and treatment of infection, maintenance of tissue oxygenation, nutritional and metabolic support
