Critical care: Exam III
Pacemaker cells & automaticity
- Electrical signals generated by pacemaker cells
- Cells can generate stimulus w/out outside stimulation- it called automaticity
Cardiac Cycle: Composed of 2 activities
- Electrical (caused by automaticity)
- Mechanical (muscular) known as a contraction
Mechanical (muscular) activity is known as a ________
Contraction
A perfect electrical signal doesn't always mean there is a ______.
pulse
Cardiac cycle: Two phases of electrical activity:
Depolarization= active
Repolarization= resting
Cardiac cycle: Two mechanical responses
Systole
Diastole
The heart gets it blood during ________ the rest of the body gets it from _______.
diastolic / systolic
Cardiac Cycle:
Depolarization =
systole = contraction
Cardiac Cycle:
Repolarization =
diastole = resting or filling phase
Cardiac Cycle:
Electrical activity precedes_____ ______
mechanical activity
Cardiac Cycle:
Electrical + mechanical =
cardiac contraction
Cardiac action potential:
Cardiac muscle cells generate an electrical current =
cardiac action potential
Cardiac action potential:
- Cardiac muscle cells generate an electrical current = cardiac action potential
- Sinoatrial node (SA node)
- Exchange of electrolytes
- Depolarization
- Repolarization begins
Cardiac action potential:
Depolarization:
- Na outside cell; K inside the cell
- Change cell permeability
- Na enters cells; K leaves cells
- Ca slowly enter cells
- ATP (adenosine phosphate) needed to move electrolytes back to resting state
Depolarization:
Na+ is _____ the cell
outside
Depolarization:
K+ is ________ the cell.
inside
Depolarization:
Ca+ ____ _____ the cell
slowly enters
Depolarization:
_____ _________ needed to move electrolytes back to resting state
ATP (adenosine phosphate)
Muscular Contraction:
- Depolarization leads to contraction
- Repolarization leads to resting & fill of ventricles from atria
- ECG is evidence of electrical activity, not contraction!
Cardiac Conduction Pathway
- SA node
Intraatrial & intermodal pathways to AV node - AV node
- Bundle of His
- Left & right bundle branches; fascicles
- Purkinje fibers
Cardiac Conduction Pathway
SA node
- Depolarization begins- atria fills
- Atrial contraction or atrial kick
Cardiac Conduction Pathway
AV node
- Delays impulse to ventricles; allows for filling
- Back-up pacemaker- hopeful to get if sinus node goes out.
You lose atrial kick when in __ ___.
A. Fib
Inherent Rates:
SA node=
60-100 beats/min
Inherent Rates:
AV node =
40-60 beats/min
Inherent Rates:
Ventricles (Purkinje fibers) =
15 to 40 beats/min
12 lead ECG:
Impulses toward electrode
* Positive QRS complex
12 lead ECG:
Impulses away from electrode
* Negative QRS complex
Cardiac Monitoring:
Continuous monitoring via
three-lead or five-lead systems- not a 12 lead EKG
Cardiac Monitoring:
- Record & interpret 6-second strip every 4hrs
- Monitor ST segment
- Monitor dysrhythmias
- Daily 12-lead ECG for cardiac patients- this is not always true...
ECG graph paper: Uses
- Used to standardize tracings
- Vertical boxes measure voltage/amplitude
- Horizontal boxes measure time
Graph paper: Big box is how many seconds?
0.2
Graph paper: Small box equals how many seconds?
0.4
P Wave
Atrial depolarization
- Normally indicates firing of the sinoatrial node
- Not to exceed 3 boxes high
QRX Complex
-Ventricular depolarization
- Q wave first negative deflection after P wave
- R wave first positive deflection after P wave
- S wave negative waveform after R wave
-Not everyone has a traditional QRS- doesn't mean anything is wrong.
Pathological Q waves:
- 0.04 seconds in width
- More than one fourth of the R-wave amplitude
- Indication of a MI
PR interval
- Atrial depolarization/delay in AV node
- Beginning of P wave to beginning of QRS complex
- 0.12 to 0.20 seconds
- Shorter interval= impulse from AV junction
- Longer interval = 1st° AV block
Which should be between 0.12 to 0.20 seconds?
QRS interval
ST segment
PR interval
PR interval
Longer PR interval means-
1st° AV block
QRS interval
- Ventricular depolarization
- 0.06 to 0.10 seconds
- Various configurations
-
Wide: slowed
conduction
- Bundle branch block (BBB)
- Ventricular rhythm
What does a wide QRS interval mean?
Slowed conduction:
- Bundle Branch Block (BBB)
- Ventricular rhythm
QRS interval should be between
0.06-0.10 seconds
ST segment
Look for depression or elevation:
- ST elevation= Myocardial injury
- ST depression= reciprocal changes- digoxin, and ischemia
What is myocardial injury necrosis determined by?
The time that it is fixed
T Wave
Ventricular repolarization
- Follows a QRS complex
- Bigger than a P wave
- No greater than 5 small boxes high
- Inversion indicates ischemia to myocardium
What does T wave inversion indicate?
Ischemia to myocardium
How tall should the T wave be?
No greater than 5 small boxes high
QT interval:
-Beginning of QRS complex to end of T wave
-0.32 to 0.50 seconds
-Varies w/heart rate
Which interval varies with heart rate?
QT interval
The QT should be between how many seconds?
0.32-0.50
U wave:
- Sometimes seen after T wave
- Unknown origin
- May be normal
- May indicate hyopkalemia
What might the U wave indicate?
Hypokalemia
Where is the U wave seen?
After the T wave (sometimes)
Rhythmicity:
- Regularity or pattern of heart beats
- PP intervals
(atrial)
- Is regular when distance between PP intervals is equal
- RR intervals (Ventricles)
- Is regular when distance between RR intervals is equal
QRS equals
Ventricular
P wave equals
Atrial
Rhythmicity:
When are PP intervals (atrial) regular?
When the distance between PP intervals is equal
Rhythmicity:
When are the RR intervals (Ventricles) regular?
When the distance between RR intervals is equal
Calculating Heart Rate
-Irregular- count for a full minute
-Calculate atrial PP and Ventricular rates RR
Normal Sinus Rhythm
- Regular rhythm
- Rate 60-100 beats/min
- Normal P wave in lead II
- P wave before each QRS
- Normal PR, QRS, and QT intervals
Which rhythm has the following:
60-100 beats/min
Normal P wave
P wave before each QRS
Normal PR, QRS, and QT intervals
Sinus rhythm
Sinus Tachycardia
- Sinus rhythm w/a rate of 100-150 beats/min
*Normal P wave, P before each QRS & normal PR, QRS, QT intervals- sinus
Sinus Tachycardia: causes
Stimulants, exercise, fever & alterations
Sinus Tachycardia: Assess for
Symptoms of low cardiac output:
- Hypotension
- ↓ urine output
- Chest pain
- Confusion
- Edema
- Weakness & fatigue
- Rapid breathing-> abnormal ABGs
- ECG changes- abnormal hear rhythm
* These are just to name a few, there are plenty more
Sinus bradycardia
- Sinus rhythm w/rate less than 60 beats/min
Sinus bradycardia: Causes
*Vagal, drugs, ischemia, ICP, and normal in athletes.
Sinus bradycardia: Produces
* Various hemodynamic responses
Do we treat sinus bradycardia?
NO, do not treat unless patient is symptomatic
A symptom of ↓ cardiac output that is an indication of ↓ coronary artery perfusion is:
- Cyanosis
- Chest pain
- Dyspnea
- Decreased urine output
2- Chest pain
What assessments indicate that the patient is not tolerating the low heart rate?
- Syncope
- Hypotension
- ↓ urinary output
This is just to name a few :)
Why might prolonged tachycardia result in heart failure?
Tachy causes ↓ cardiac output
Sinus Arrhythmia
Sinus rhythm
Rate varies w/respirations
Rarely affects hemodynamic status
Sinus Arrhythmia
Rate varies w/respirations:
- Inspire= increase
- Expire= decrease
With sinus arrhythmia, the rate varies w/respirations. When the patient exhales the rate _____.
decreases
With sinus arrhythmia, when the patient inhales the what happens to the rate?
It increases
Sinus arrest or Exit block (same thing)
- Sinoatrial node fails to initiate impulse
- Causes: vagal, heart disease, and drugs that slow heart rate
- Heart rate can be normal to slow
- Irregular rhythm
- Can decrease cardiac output
What causes a sinus arrest or exit block?
Sinoatrial node fails to initiate impulse
What contributing factors can cause sinus arrest/exit block?
Vagal, heart disease, and drugs that slow heart rate
What is the HR like in sinus arrest/exit block?
Can be normal or slow
Atrial dysrhythmias
Increased automaticity in the atrium
Generally have P-wave changes
Atrial dysrhythmias: Causes due to psychosocial or medical mismanagement
- Stress
- Digitalis toxicity
- Alcohol
Atrial dysrhythmias: Physiological causes
- Electrolyte imbalances
- Hypoxia
- Atrial injury
- Hypothermia
- Hyperthyroidism
- Pericarditis
Premature Atrial contractions
- Early beats initiated by atrium
- P waves and PR interval may vary
- Noncompensatory pause
- P wave may be found in T wave
Premature Atrial contractions: Strip presentation
* Narrow QRS
* Has a P wave
* Compensatory pause after a PAC
Nonconducted premature atrial contractions:
Pause noted on rhythm strip
Premature P wave
May alter cardiac output
Which contraction has a premature P wave & may alter cardiac output?
A nonconducted premature atrial contraction
Wandering atrial pacemaker
- Varying configurations of P waves
- At least 3 different P-wave shapes must be seen
- Heart rate not >100
- PR interval varies
- Irregular rhythm
What causes 3 different P wave shapes, is irregular on a strip and has a heart rate equal to or less that 100 beats/min
Wandering atrial pacemaker
Multifocal atrial tachycardia
- Almost identical to wandering atrial pacemaker
- Heart rate exceeds 100 beats/min
- Common in COPD patients
Which type of tachycardia exceeds 100 beats/min, common in COPD patients and is almost identical to Wandering atrial pacemaker?
Multifocal atrial tachycardia
Multifocal atrial tachycardia has abundant _ ___ & is ____than QRS
P waves/faster
Atrial flutter
- Ectopic foci in atria, heart disease
- Classic "sawtooth" pattern in leads II, III, and aVF
- Atrial rate fast & regular (250-350 beats/min) with AV block
- Degree of conduction varies; may be 1:3 or 1:4, etc
Atrial fibrillation
Erratic impulse formation in atria
No discemible P wave
Irregular ventricular rate
Aberrant (abnormal) ventricular conductions can occur
Results in loss of atrial kick
High risk for pulmonary or systemic emboli
Hemodynamic monitoring : Regulation of blood flow
- Heart rate
- Strength of contraction
- Blood vessels diameter
- Degree of turbulence
- Pressure
Pressure = ______ x ____________
flow / resistance
Pressure
Force exerted on the liquid
* mm Hg
Flow: amount of fluid moved over time
* L/min or mL/min
Resistance: Opposition to flow
Cardiac output:
Volume of blood ejected from heart/min
Cardiac output = ____ x ____ ______
HR / Stroke volume (volume of blood ejected w/each beat)
* 4 to 8 L/min
Ejection fraction
Fraction of blood ejected w/each beat
* Normal 60% to 70%
Preload:
Degree of muscle fibers stretch before systole
* Volume of blood in ventricle prior to contraction (LVEDV/LVEDP)
Preload: Frank-Starling law
* Increased stretch = volume
* Stretch is within physiological limits
- Example= balloon
Afterload:
- Pressure or resistance against flow
- Related to lumen size & viscosity
- Example: Opening a door against wind
After load: Related to lumen size & viscosity
Systemic vascular resistance
- Force overcome by the left ventricle upon contraction
Pulmonary vascular resistance
- Force overcome by the right ventricle upon contraction
Contractility:
Force of ventricular contraction
How well the heart is pumping
Systemic Vascular Resistance (SVR):
- Peripheral vascular resistance
- Diameter of blood vessels
Arterial BP= CO x SVR
Cardiac output versus index
- Index is better assessment; based on body size
- CI= CO ÷ body surface area
- Calculated on the computer after entering patient's height & weight.
Hemodynamic monitoring: Noninvasive modalities
- Noninvasive blood pressure
- Assessment of jugular venous pressure
- Assessment of serum lactate levels
Hemodynamic monitoring: Invasive modalities
- Arterial pressure monitoring
- Pulmonary artery pressure monitoring
- Right atrial pressure monitoring
Components of invasive hemodynamic monitoring
- Invasive catheter
- Noncompliant pressure tubing
- Transducer & stopcocks
- Flush system
- Bedside monitor
Accuracy in hemodynamic monitoring: Level
Level = phlebostatic axis
* Fourth intercostal space, midaxillary line
* Approx. level of right atrium.
Accuracy in hemodynamic monitoring: Zero reference
- Negate atmosphere pressure
- Zeroing stopcock is leveled at phlebostatic axis & "zeroed"
Accuracy in hemodynamic monitoring: Dynamic response testing
Square wave test
Arterial pressure monitoring:
Invasive technique to monitor arterial blood pressure
Arterial pressure monitoring: Sites
- Radial artery
* Allen's test prior to insertion to verify collateral circulation in the extremity
* Issues related to predictability of Allen's test
2. Brachial artery
3. Femoral artery
Arterial pressure monitoring: Equipment
- Pressurized flush solution w/transducer
- Pressure at 300 mm Hg
- Why does this need to by high?
- A-line catheter (angiocath)
Arterial pressure monitoring: Major Complications
Thrombosis
* Clot if flush not used appropriately
Embolism
* Air entering system/clot dislodgment
Hemorrhage
* Loose connections/catheter dislodgement
Infection
RAP/CVP Monitoring
Right atrial pressure (RAP)- catheter in right atrium
* Proximal port of pulmonary artery catheter
Central venous pressure (CVP)- catheter in superior or inferior vena cava
* Triple lumen
Values are similar & terms interchanged
RAP/CVP
- Direct measurement of pressure in right atrium
- Right ventricular preload or right ventricular end diastolic pressure (RVEDP)
- Normal value
- 2 to 6 mm Hg
- Recorded end exhalation as a mean value
Nursing implications RAP/CVP
- Zero/ balance
- Waveform analysis
- Respiratory variation and PEEP
- Patient position- Head of bed between 0 & 60°
- Correlate values w/assessment
- Monitor for complications
Complications of RAP /CVP
- Infection
- Pneumothorax or hemothorax
- Carotid puncture
- Heart perforation
- Dysrhythmias
Pulmonary artery catheter
Flow directed catheter
* Inserted via subclavian, internal jugular, or femoral vein
* Balloon tipped
* Multiple lumens
Variations
* SvO2 catheter
* Continuous cardiac output (CCO)
Insertion of PA catheter: Position
Proper position of patient
- Trendelenburg common
- Towel roll between shoulder blades
Insertion of PA catheter:
- Inserted w/balloon deflated, selected inflation to "float" catheter into PA
- Waveform changes as catheter progresses
- Check for proper "wedging" for PAOP
- Chest x-ray
Pulmonary artery catheter: Measurement capabilities
- PA systolic
- PA diastolic
- PAOP/PCWP/PAWP
* Inflated balloon flows into wedge position in pulmonary capillary measuring pressure
- Cardiac output/Index
- Thermodilution CO
- Proximal injectate port
Nursing implications: Measure pulmonary artery pressure
- Pulmonary artery occlusive pressure (PAOP) reflects left ventricular end-diastolic pressure
- In many patients the PADP can be substituted for PAOP measurements if values are similar
- Record amount of air to inflate balloon- no more than 1.5 mL
Complications of PA catheters
- Infection
- Dysrhythmias
- Air embolus
- Thromboembolism
- PA rupture
- Pulmonary infarction
TdCO Method
Procedure:
- Inject solution within 4secs
- Increased accuracy at end expiration
- Check waveform
- Repeat at least three measurements
- Average values within 10% of each other
- Calculate CO and cardiac index (computer does this)
CCO Method
Continuous monitoring via specialized PAC
* Copper filament at distal catheter end
* Pulses of energy at intervals warms blood
Accurate w/head of bed up to 45°
Monitoring O2 delivery and consumption
- Calculated values
- Obtained via monitoring catheters
- SvO2- mixed venous oxygen saturation via specialized PAC
- ScvO2- central venous oxygen saturation via specialized central line
Monitoring O2 delivery and consumption: Normal values
- SvO2- 60% to 75%= adequate balance between supply and demand
- ScvO2- 65% to 85%= adequate balance between supply and demand
Monitoring O2 delivery and consumption: High values
High values= tissues not able to use oxygen
Monitoring O2 delivery and consumption: Low values
Low values= oxygen demand exceeds delivery
Trends in hemodynamic monitoring
- Esophageal Doppler
* Thin silicone probe placed in the distal esophagus
* Evaluates descending aortic blood flow
- Pulse contour cardiac output
Effects of respiratory variation
- Right atrial pressure variation
- Systolic pressure variation
- Arterial pulse pressure variation
- Stroke volume variation
Heart murmur
- Caused by a turbulence of blood flow through the valves
- Rumbling, blowing, harsh, or musical in sound
- Identify location, sound, loudness, and intensity & whether other heart sounds are heard.
Coronary artery disease (CAD)
* Progressive narrowing of coronary arteries by atherosclerosis
- Coronary heart disease
- Atherosclerotic heart disease
Pathophysiology of CAD
- Injury to epithelial cells in intima
* Platelet aggregation
* Migration of monocytes
* Lipoproteins enter intima
2. Fatter streak
- Monocytes develop into macrophages
- Lipid-rich "foam cells" develop
3. Atheroma
4. Damage to intima- liberates platelet-derived growth factor
5. Proliferation of smooth muscle cells
6. Fibrous cap forms
* From connective tissue & low-density lipoprotein (LDL)
7. Fibrous cap often ruptures
- Thrombus
- Clotting cascade initiated
8. Adhesion: platelets bind to receptors
9. Activation: platelets change shape & activate receptors
- Release: thromboxane A2 & serotonin
- Activate glycoprotein IIb/IIa receptors
10. Aggregation: platelets clump together
Drugs administered to stop the platelet aggregation process
- Aspirin
- Glycoprotein IIb/IIIa inhibitors
- Heparin
- enoxaparin (Lovenox)
- Warfarin- coumadin
Risk factors for CAD:
- Age:
* Men > 45
* Women > 55
- Family history
- Cholesterol
* High LDL
* Low levels of HDL
- Smoking
- Hypertension
- Inactivity
- Overweight
* Diabetes
CAD History
- Risk factors
- Prior hospitalizations
- Shortness of breath, chest pain
- Medications
- Erectile dysfunction meds if considering nitroglycerin
- Psychosocial history
- Include stressors
CAD diagnostic studies
- 12 lead ECG
- Holter monitor
- Exercise tolerance test (stress test)
- Chest x-ray
- Echocardiography
- Transesophageal echocardiography
- Diagnostic heart scans
- Single photon emission computed tomography
- Magnetic resonance imaging
- Electrophysiology study
CAD diagnostic studies: Stress test
AKA- Exercise tolerance test
- Exercise to increase demand on heart
- Stressed via drugs if patient cannot tolerate exercise (e.g., adenosine)
- Monitoring vital signs, ECG
*Tries to induce symptoms of patients complaints*
CAD diagnostic studies: Echocardiography
Ultrasound to visualize cardiac structures
CAD diagnostic studies: Diagnostic heart scans
- Technetium-99m stannous pyrophosphate
- Thallium-201
- Multigated blood pool study
Cardiac catheterization & arteriography:
Catheter (Right or Left)
- Heart pressures (similar to PA catheter)
- Cardiac output
Arteriography
- Visualize blood vessels
Post catheterization care
- Bed rest; head of bed no higher than 30°
- Monitor bleeding; newer collagen agents for hemostasis may be used
- Monitor pulses
- Antiplatelet drugs after the procedure (usually after interventions such as PCI)
- May be discharged in 6 to 8hrs; depends on diagnosis & procedures done in catheterization laboratory.
Laboratory tests
- CBC- Hemoglobin & Hematocrit (H&H)
- Potassium
- Magnesium
- Calcium
- Sodium
* Want labs to be w/in normal ranges, if not must fix!
Cardiac enzymes
* CK (total)
2 to 6hrs; peak 18 to 36hrs
* CK-MB (cardiac specific)
4 to 8hrs; peak 18 to 24hrs
* Troponin I and T
As early as 1hr after injury
* Myoglobin
30 to 60 minutes after injury
Cardiac enzymes: CK-MB
4 to 8hrs- after injury
peaks: 18 to 24hrs
Cardiac enzymes: Troponin I and T
As early as 1hr after injury
Cholesterol in CAD
HDL- considered GOOD
LDL- is BAD
LDL target levels (NIH)
* No CHD & fewer than 2 risk factors
- 160 mg/dL
* No CHD & 2 or more risk factors
- 130 mg/dL
* CAD
- <100 mg/dL
↑ Cholesterol treatment
- Diet: Low cholesterol, low salt
- Exercise: aerobic
- Medications: Lipid-lowering agents
- Various types: weigh advantages & disadvantages of each
Medications for hyperlipidemia
* HmG CoA reductase inhibitors; slow production: most effective:
- Statins
* Bile acid resins bind & are excreted via bowel
- Cholestyramine
- Colestipol
* Nicotinic acid; inhibits LDL synthesis & increases HDL; many side effects
* Fibric acid derivatives; increase VLDL clearance
- Gemfibrozil
Hyperlipidemia: Medications Affecting Platelets
- ASA
- Others: dipyridamole, ticlopidine, and clopidogrel
Chest pain
- Classic symptom
- Often midsternal
- May radiate to arms, jaw, or back
Angina
Myocardial ischemia: demand higher than supply
Types of Angina: Stable
Chronic, exertional= Effort, classic
T-wave inversion on ECG
Treatment: rest & nitroglycerin
Types of Angina: Unstable
Crescendo (starts off mild, then increases)
- More often & severe, less relief
* May see ST elevation on ECG
* Treatment: Rest and nitroglycerin; drugs affecting platelets; revascularization
Types of Angina: Variant
Prinzmetal's (vasospasms)
* ST elevation during pain episodes
* Treatment: Calcium channel blockers
Nursing management: Angina
Maintain cardiac output
Pain relief
Self-care; risk-factor modification
Nursing management of the patient w/angina is directed toward
A. Immediate administration of nitrates
B. Assessment of history of previous angina episodes
C. Assessment & documentation of chest pain episodes
D. Administration of prophylactic lidocaine for ventricular ectopy
C. Assessment & documentation of chest pain episodes
Acute myocardial infarction (AmI)
- Ischemia w/myocardial cell death
- Imbalance of oxygen supply & demand
- Causes
- Atherosclerosis
- Emboli
- Blunt trauma
- Spasm
Acute myocardial infarction (AmI): Types
- Q wave: total occlusion of coronary artery w/ thrombus
- Non Q wave: partial occlusion of coronary artery
Collateral circulaion
Assessment of AMI
~ Midsternal chest pain
- Severe, crushing, and squeezing pressure
- May radiate
- Unrelieved w/nitrates
~ Pale & diaphoretic
~ Dyspnea & tachypnea
~ Syncope
~ Nausea & vomiting
~ Dysrhythmias
Describing factors of AMI midsternal chest pain:
- Severe, crushing, and squeezing pressure
- May radiate
- Unrelieved w/nitrates
Diagnosis of AMI
- Signs & symptoms- often atypical symptoms in women
- 12 lead:
- ST elevation followed by Q wave (Q wave myocardial infarction)
- ST depression (non-Q-wave myocardial infarction)
- Elevated cardiac enzymes
- CPK-MB
- Elevated serum troponin I/T, myoglobin
Which finding on the ECG is most conclusive for infarction?
A. Q waves
B. Inverted T waves
C. Tall, peaked T waves
D. ST-segment depression
A. Q waves
Nursing goals AMI
- Maintain cardiac output
- Treat pain
- Assess for complications
- Increase activity tolerance
- Relieve anxiety
- Ongoing & discharge teaching
Complications of AMI
- Dysrhythmias
- Sudden death
- Congestive heart failure, cardiogenic shock
- Ventricular aneurysm or rupture
- Papillary muscle dysfunction
- Pericarditis
Medical management: AMI
* Pain relief: morphine, nitroglycerin
* Oxygen
* Drugs affecting platelets- ASA glycoprotein IIb/IIIa inhibitors
* Beta-blockers
* Nitrates
* ACE inhibitors
* Antidysrhythmics
Primary Angioplasty
- Get pt. to catheterization lab for emergent percutaneous intervention or stenting if facilities are available
- Better outcomes than thrombolytics
Thrombolytic therapy
- Time is muscle; 6hr window
- Several thrombolytic agents available, such as:
- Tissue plasminogen activator (t-PA)
- Streptokinase
- Retaplase
- Heparin & glycoprotein IIb/IIIa inhibitors
Interventional cardiology
* Variety of procedures
- Percutaneous transluminal coronary angioplasty (PTCA)
- Intracoronary stenting
* Drug-eluting stents
PTCA: Goal
To increase blood flow to myocardium
PTCA: criteria
- Uncompromised collateral flow
- Noncalcified lesions
- Lesions not on bifurcations of vessels
* Balloon catheter is inflated
Intracoronary Stents
- Tubes placed in conjunction w/angioplasty to keep vessel patent
- Help prevent the restenosis associated w/angioplasty
- Similar procedure as PTCA
- Anticoagulation therapy
New Interventional techniques: Nuclear
* Excimer laser angioplasty
- Xenon chloride laser
* Radiation therapy
- Beta or gamma radiation
Surgical Revascularization
- Coronary artery graft (CABG) surgery
- Minimally invasive direct coronary artery bypass (MIDCAB) surgery
- Transmyocardial revascularization (TMR)
CABG surgery
- Provides additional conduits for blood flow
- Saphenous vein
- Internal mammary artery
- Radial artery
- Arteries longer patency
Indications for CABG
- Unstable angina
- AMI
- Failure of percutaneous interventions
Risks associated with CABG
~ Increased mortality associated with:
- Left ventricle dysfunction
- Emergency surgery
- Age
- Sex (female)
- Number of diseased vessels
- Decreased ejection fraction w/congestive heart failure
Traditional CABG
- Median sternotomy or sternum split
- Excision of pericardium
- Cardiopulmonary bypass
- Myocardial preservation or cardioplegia
- Grafts
- Wean bypass; defibrillate if needed
- Mediastinal and chest tubes
- Epicardial pacing wires
- Wire sternum
Goals of CABG surgery
- Increases blood flow to myocardium
- Relieve symptoms
- Prolong survival
- Improve quality of life
Minimally invasive direct coronary artery bypass surgery: Port-access coronary artery bypass
- Cardiopulmonary bypass
- Incisions (ports)
Minimally invasive direct coronary artery bypass surgery
- No cardiopulmonary bypass
- Heart still beating
- One or two bypasses
* Heart stays beating
Cardiac surgery complications
- Low cardiac output
- Renal impairment
- Gastrointestinal dysfunction
- Impaired peripheral circulation
- Mediastinal bleeding
- Infection: very serious if sternal
- Atrial dysrhythmias
- Hypovolemia
Complications of CABG
- Dysrhythmias
- Impaired contractility; low cardiac output
- Intraoperative myocardial infarction
- Pericardial tamponade
- Respiratory insufficiency
- Pain
- Emboli; stroke
- Death
Pericardial tamponade
Fluid, pus, blood, clots, or gas accumulates in the pericardium (the sac in which the heart is enclosed), resulting in slow or rapid compression of the heart.
Transmycardial revascularization
- Laser channels into ventricle
- Goal is to increase perfusion of heart muscle
- Relief of symptoms occurs over time
- Poor candidates for CABG Mixed results from clinical trials
Dysrhythmias
- Radiofrequency catheter ablation
- Permanent pacemakers
- Implantable cardioverter-defibrillator
Ablation
- Supraventricular tachycardia
- Interrupt electrical conduction or activity
- Radiofrequency used
- Electrophysiology
Implantable cardioverter-defribrillator (ICD)
- Used to treat survivors of sudden cardiac arrest
- Some have built-in pacemakers
- Delivers high-energy shock
- Patient education
- Emergency procedures
Heart failure
- Inability to generate adequate flow
- Systolic (impaired contractility)
- Diastolic (Impaired filling)
Heart failure: Etiology
- AMI
- Hypertension
- Idiopathic; cardiomyopathy
- Valvular disease
Left heart failure: Patho
- Decreased pumping action
- Back-up of blood from left ventricle
- Fluid build-up in lungs
- Backflow leads to right heart failure
- Fail to meet metabolic demands
- Compensatory mechanisms
* Renin-angiotensin- aldosterone system
* Sympathetic nervous system
7. Right heart failure
* Leads to system symptoms
Heart failure treatment
Improve pump function
- Diuretics
- ACE inhibitors/angiotensin receptor blockers
- Digoxin
- Beta-blockers (carvedilol [Coreg])
- BNP- nesiritide citrate (Natrecor)
Heart failure treatment: Reduce cardiac workload
- Intraaortic balloon pump
Ventricular assist device - Biventricular pacing
- Nursing interventions
Heart failure treatment: Optimization of gas exchange
- Airway
- Diuresis
- VTE prophylaxis
- Control sodium & fluid retention
Heart failure complications
Pulmonary edema
- Dyspnea
- Cyanosis
- Gurgles
- Pink, frothy sputum
- Hypoxemia
Cardiogenic shock
Inflammatory heart disease
- Pericarditis- inflammation of the pericardium
- Endocarditis- inflammation of the endocardium
Pericarditis: Etiology
- After myocardial infarction
- Uremia
- Cancers
Can lead to infusion, tamponade, and scarring
Hallmarks of Pericarditis
- Friction rub
- Pulsus paradoxus
- Initial ST elevation
Pericarditis: Procedures
- Pericardiocentesis
- Pericardial window
Endocarditis
- Endocardium continuous w/valves
- Vegetation
- Embolization
- Valvular dysfunction
Endocarditis: Diagnosis
- Echocardiogram
- Transesophageal
- Echocardiography
Endocarditis: Treatment
Antibiotics & rest
Endocarditis: Prevention
Antibiotic prescription before treatments (e.g., dentist)
- Heart valve
- History of endocarditis
- Microvascular pressure w/regurgitation
Vascular alterations: Aortic aneurysms
- Dilation or thinning of wall
- Thoracic aortic
- Thoracoabdominal aortic
- Abdominal aortic
- Treat based on size & symptoms
- False versus true
Vascular alterations: Aortic dissection
- Tear of intimal layer of the vessel
- Sudden
- Sharp
- Shifting pain
- Marfan syndrome
Signs of Marfan syndrome
- Long arms, legs and fingers
- Tall and thin body type
- Curved spine
- Chest sinks in or sticks out
- Flexible joints
- Flat feet
- Crowded teeth
- Stretch marks on the skin that are not related to weight gain or loss
Marfan syndrome:
Marfan syndrome is a genetic disorder that affects the body’s connective tissue. Connective tissue holds all the body’s cells, organs and tissue together.
Vascular alterations: Surgical treatment
- Open approach
- Endovascular approach