Exam 2 Flashcards
Atrium vs ventricle walls
Atrium have thin walls, easy to stretch
LV has thick wall
Dysrhythmias
disorders of the formation or conduction (or both) of the electrical impulse within the heart
Atrium contracts first, then ventricle to maximize blood flow
If not in sync, arrhythmia and low CO
2 possible problems that can arise in conduction disorders
Pacemaker doesnt put a signal regularly (generation of signal
Or blockage in conduction pathway
ECG
A voltmeter that records the electrical voltages (potentials) generated by depolarization of the heart’s cells
12 lead ecg reflects electrical activity in LV
Right sided heart damage
flip ECG leads
QRS
depolarization of ventricle
Atrial repolarization hides in here
Wide is considered >3 squares (0.06-0.12 seconds is normal)
T wave
Repolarization of ventricle
Usually the same deflection (direction) as QRS
P wave
Depolarization of atrium
<0.2 seconds (<3 small boxes wide)
<1.5-2.5 small boxes tall (for chest and limb leads respectively)
What delays time for filling of the ventricles
AV node
V1
4th intercostal at right border of sternum
V2
4th intercostal at left border of sternum
V3
Midway between V2 and V4
V4
Mid-clav line in 5th intercostal
V5
Anterior axillary line on the same horizontal level as V4
V6
Midaxillary line on same horizontal level as V4 and V5
Shouldn’t see this if looking straight at patient
LL and RL
Above ankle and below torso
AVR, AVL, and AVF
Augmented view limb leads
Calculated
Last line of ecg
lead 2, used to check rhythm issues (patterns)
Why multiple leads?
If we see ST elevation or depression in one lead, we want to be able to confirm and check with other leads
EKG changes in one lead and not another could be due to artifact, so we want at least two
Frontal plane leads
View the heart from the front of the body as if it were flat
Six leads view the heart in the frontal plane
Leads I, II, and III: standard limb leads
Leads aVR, aVL, and aVF: augmented limb leads
Which leads look inferior
II, III, aVF
Which leads look septal
V1 and V2
Which leads look anterior
V3, V4
Which leads look lateral
I, aVL, V5, V6
5 lead ecg
White on top right
Green on bottom right
Brown on tummy
Black on top left (smoke)
Red on bottom left (fire)
SA node
60-100 BPM
Primary pacemaker
If SA node fails to send out signals—Caused by cardiac arrest/infarction, muscles die and SA node is killed so it can’t send signal
AV node
secondary pacemaker
40-60 BPM
Ventricular pacemaker
30-40 BPM
Too slow to provide cardiac output, get them a pacemaker!
How many boxes in 6 second strip
30
Formula for HR
1500/number of small boxes
Directions of p waves
Positive in lead I and II in NSR (points up)
Negative in lead aVR in NSR
Biphasic in lead V1
PR interval
Indicates AV conduction time
Beginning of the P wave to the QRS complex
Measures 0.12-0.20 seconds (3-5 small boxes)
Prolonged PR interval=1st degree heart block
QRS breakdown
Q wave: the first negative deflection after the P wave
R wave: the first positive deflection after the P wave
S wave: first negative deflection after the R wave
Small box on ecg
0.04 seconds
U wave
small rounded wave follows T wave. Less prominent than the P, QRS, and T waves. Only sometimes present.
Causes of sinus brady
lower metabolic rate: sleep, athletic training, hypothyroidism
Vagal stimulation: vomiting, suctioning, severe pain, bearing down
TAKE COLACE STOOL SOFTENER
Idiopathic sinus node dysfunction
Increased intracranial pressure
Coronary artery disease (e.g. MI of the interior wall)
Women’s cycle
Resolving the causative factors might be the only treatment needed.
Medications that cause sinus brady
calcium channel blockers, amiodarone, beta-blockers
Atropine for sinus brady
If the bradycardia produces signs and symptoms of clinical instability (e.g., acute alternative of mental status, chest discomfort, syncope, or hypotension): Atropine: 0.5 mg given rapidly as an IV bolus every 3-5 minutes to a max dose of 3 mg
Causes of sinus tachy
Physiologic or psychological stress
Varies depending on menstrual cycle
Medications that stimulate the sympathetic response; stimulants; and illicit drugs
ALCOHOL INCREASES HR BECAUSE BP GOES DOWN
Enhanced automaticity of the SA node/or excessive sympathetic tone with reduced parasympathetic tone (to improve stress level and increase influence of parasympathetic, deep breathing, meditation
Autonomic dysfunction: POTS-increase in heart rate greater than 30 bpm without hypotension when moving to a standing position
Prolonged sinus tachy can cause
Tired heart
Low myocardial supply → myocardial ischemia → possible heart attack
Persistent sinus tachy treatment
synchronized cardioversion is the treatment of choice (reset the heart)
Vagal maneuvers: carotid sinus massage, gagging, bearing down, forceful and sustained coughing, and applying a cold stimulus to the face.
Administration of adenosine (narrows the QRS)
Wide QRS: procainamide, amiodarone, and sotalol
Catheter ablation (done in EP lab)
Sinus dysrhythmia
HR changes based on respirations (faster on inspiration, slower on expiration)
Does not cause any significant hemodynamic effect and not typically treated
Pattern! Irregular but there’s a pattern
Defined as regularly irregular
Atrial dysrhythmia: PAC causes
caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety, hypokalemia, hypermetabolic states, or atrial ischemia, injury, or infarction
QRS comes earlier than it’s supposed to
Atrial dysrhythmia: PAC treatment
treat the underlying cause (potassium levels, anxiety, etc)
Atrial dysrhythmia: aflutter treatment
vagal maneuvers, adenosine.
Treated with antithrombotic therapy, rate control, and rhythm control in the same manner as afib
How is aflutter described
Described with atrial to ventricular ratio (how many p waves per r wave)
Afib
Most common heart dysrhythmias
uncoordinated atrial electrical activation: rapid, disorganized, and uncoordinated twitching of atrial musculature.
Irregular
Causes of afib
Older people with structural heart disease, inflammatory or infiltrative disease, coronary artery disease, hypertension, congenital disorder, and heart failure.
DM, obesity, hyperthyroidism, pheochromocytoma (a rare, usually non cancerous (benign) tumor that develops in cells in the center of an adrenal gland.), pulmonary hypertension and embolism, obstructive sleep apnea, and acute moderate to heavy ingestion of alcohol
Symptoms of afib
Symptoms of heart failure
Hemodynamic collapse
Pulse deficit (hard to find)
Myocardial ischemia
Thrombi
Treatment of afib (meds)
Antithrombotic: aspirin, warfarin (not given as much, new ones given so they don’t have to get levels checked so much), Pradaxa, Xarelto, Eliquis, Savaysa.
Heart rate control medications: goal→ resting heart rate is less than 80 bpm. Beta-blocker or verapamil, diltiazem
Pharmacologic cardioversion: amiodarone.
Cardioversion for afib
Electrical cardioversion: for those hemodynamically unstable (e.g., acute alteration in mental status, chest discomfort, hypotension) and does not respond to medications
Old people have small brains so be careful when they fall
Junctional dysrhythmias
40-60 beats/min (above is junctional tachycardia)
AV node as the pacemaker
Components of ECG with junctional dysrhythmia (AV node is pacemaker)
Location of P wave varies
P waves may be:
Inverted and before, during, or after QRS
Absent (hiding in QRS)
PR interval: short
QRS: normal
Treatment of junctional dysrhythmia
May produce s/s of reduced cardiac output
Treatment same as sinus bradycardia
(Atropine, dopamine, epi)
PJC treatment
Treat underlying conditions (CAD or other abnormalities)
Catheter ablation
Meds and lifestyle mods
PJC meds
beta-blockers, calcium channel blockers, and other antiarrhythmics
Lifestyle mods for PJC
reducing or eliminating triggers (avoiding caffeine, alcohol, and nicotine, as well as managing stress and getting adequate sleep)
Junctional tachy
60-120 BPM
SVT
P waves not clear
Afib, a flutter, or junctional tachycardia can all be called SVT
QRS: normal (tight and narrow, once it’s wide, that means something is wrong with the ventricles)
Treatment for SVT
Adenosine–6mg rapidly: always follow with NS bolus
Warn patient: chest pressure, feeling faint
PVC
Initiated by Purkinje fibers–“skipped beat” and felt as palpitations in the chest (irregular pulsations)
Bigeminy: every other complex
Trigeminy: every third complex
If persistent what do we give for PVC
Amiodarone
Vtach
three or more PVCs in a row, occurring at a rate exceeding 100 bpm.
Assess the patient!!
Emergency: unresponsive and pulseless
Patients with larger MIs and lower ejection fractions are at higher risk of lethal VT.
Types of VT
stable monomorphic VT (do not have acute MI or severe HF): continuing assessment
Symptomatic monomorphic VT: cardioversion
Pulseless VT: defibrillation
Treatment of vtach
ejection fraction <35%: implantable cardioverter defibrillator
ejection fraction>35%: amiodarone
vfib
most common dysrhythmia in patients with cardiac arrest
rapid disorganized ventricular rhythm>300/min
Heartbeat and treatment of vfib
no atrial activity is seen
absence of an audible heartbeat, a palpable pulse, and respirations
cardiac arrest and death are imminent if not corrected
early defibrillation is critical to survival
Treatment of asystole
high quality CPR with minimal interruptions and identifying underlying and contributing factor (do not shock the patient)
Heart block
AV block
delayed or failed conduction of supraventricular impulses through the AV node (atrium) to the ventricles (atrium contracts, ventricles don’t contract appropriately)
PR interval is a measure of conduction between the initial stimulation of the atria and the initial stimulation of the ventricles
PR interval is used to identifying the degree (type) of block present
1st degree heart block
Long
PR interval >0.2 seconds (5 small boxes)
PR interval measurement is constant (all same length!)
Not so serious, you can get by
Second degree type 1 heart block
Wenckebach
Atrial contractions but no ventricular, can’t stimulate the QRS contraction
PR interval becomes longer with each succeeding ECG complex until there is a P wave not followed by a QRS. The changes in the PR interval are repeated between each “dropped” QRS
Atrium takes longer and longer to communicate, eventually the ventricle doesn’t receive a signal (QRS drops)
This pattern repeats itself
Regularly irregular!
2nd degree type 2 heart block
Second degree type II:
PR interval constant (length varies can be less than 0.2 or longer than that)) for those P waves just before QRS complexes
Third degree heart block
Complete
Two impulses (pacemakers!!) stimulate the heart.
PR interval: very irregular
More P waves
Than QRS complexes
Ps and Rs on their own, no coordination
PP is the same, and so is RR
P wave to R wave ratio is off: More p waves
Pacemaker for ventricles is intrinsically much slower, which is why there’s fewer R waves
Medical management of heart blocks
increase HR and maintain CO
Stable, no symptoms: no treatment (usually 1st degree, treatment in third degree)
The initial treatment of choice is an IV bolus of atropine, although it is not effective in second-degree AV block, type II, or third-degree AV block.
Acute dysrhythmias may be treated with medications or with external electrical therapy (emergency defibrillation, cardioversion, or pacing).
Chronic management of heart block
pacemaker for bradycardias and ICDs for chronic tachydysrhythmias [vtach or vfib])
Adjunctive modalities and management of heart block
cardioversion and defibrillation: to depolarizes myocardial cells (to terminate a tachydysrhythmia)
Indications of a successful response are conversion to sinus rhythm with adequate perfusion
Cardioversion vs defibrillation
cardioversion: deliver SYNCHRONIZED current (50 jules, aligns with patient’s rhythm, meaning they need to have a rhythm)
defibrillation: the delivery of the current is immediate and UNSYNCHRONIZED (VT/VF, irregular rhythms)
Defibrillation
Used in emergency
treatment of choice for v fib and pulseless VT
not for those who are conscious or have a pulse
use more voltage than used in cardioversion
give epinephrine or vasopressin after defibrillation
Synchronized cardioversion
a shock is timed to delivered during ventricular depolarization (QRS complex, when ventricles contract)
not to delivery the shock during vulnerable period of the T wave repolarization (when heart is relaxed)
is used to treat rhythms that have a clearly identifiable QRS complex and a rapid ventricular rate (SVT, monomorphic VT)
not for disorganized rhythms (polymorphic VT, VF)
Instructions for elective cardioversion
May need to take anticoagulants for a few weeks before the procedure.
Digoxin withheld for 48 hours before the procedure (to ensure the resumption of sinus rhythm with normal conduction)
No food or drinks at least 4 hours before the procedure
Can be chosen to be done to correct afib
Transcutaneous pacing
use electrical stimulation through pacing pads positioned on a patient’s torso to stimulate contraction of the heart
=temporary external pacing or noninvasive pacing
indication: symptomatic bradycardia unresponsive to atropine therapy or atropine is not available
painful, skin burns, tissue damage
Get put on a sedative because it’s painful
Indications of pacemaker
Symptomatic bradycardia (slow ventricular rate)
Symptomatic heart block (also slow rate)
Two components of pacemaker
Electronic pulse generator (intrinsic/house pacemaker)
Pacemaker electrodes (conduction pathway)
Pacemaker is externally programmable
Single chamber (unipolar) pacemaker:
One lead placed in atrium or ventricle
Produce large spic on the ECG
Sensing and pacing in the chamber where the lead is located
More likely to be affected by electromechanical interference
Dual-chamber (bipolar) pacemaker
One lead located in the atrium and one in the ventricle
Sensing and pacing in both chambers mimicking the normal heart function
Less affected by electromechanical interference
This is the one we see more
NASPE-BPEG code (first)
Paced
A: atrium
V: ventricle
D: dual
NASPE-BPEG (second)
Sensed
A: atrium
V: ventricle
D: dual
NASPE-BPEG (third)
Response to pt’s HR
I: inhibited (when heart beats normally, the pacemaker does not function)
T: triggered
D: dual
AAI pacemaker
sinus node dysfunction–no conduction disturbance in the AV node, atrium to ventricle is fine so we can only use one lead since this conduction is fine
DDD pacemaker
AV conduction disturbance
With complete heart block, we use DDD because it needs to sense both chambers
Pacing
Stimulation of the chamber–mimic normal heart conduction
Produce a spic on ECG
Inhibited response on pacemaker
response of the pacemaker is controlled by the activity of the patient’s heart. only function when pt’s heart not beat up to programmed rate (usually below 60)
Triggered response with pacemaker
response when it sense intrinsic heart activity (triggered by each p wave)
Capture with pacemaker
the heart has responded to the stimulus by producing an appropriate complex
Failure to capture
may occur with a low battery or poor connection, doesn’t send out impulse strong enough for contraction. The pacemaker is discharging the impulse; however, there is no responding cardiac contraction
Pacemaker says hey heart! Contract! And heart says nope
Pacemaker therapy prep
Check pt has a patent IV, and that the defibrillator, emergency cart and appropriate medications are available
Obtain consent–make sure patient is capable to make decision and witness the signature, doctor’s job to educate and answer questions
Obtain vital signs and ECG rhythm strips prior to insertion. connect to 12 lead ECG and continuously monitor before, during, and after
Anesthetize the area locally
Portable chest x-ray is required to confirm placement
Nursing management of pacemaker insertion
monitor the insertion site for bleeding, hematoma, and infection
Complications of pacemaker insertion
Movement and dislocation of the lead (don’t lift arms or heavy objects for a while)
Bleeding and hematoma
Ventricular ectopy or VT from wall stimulation
Infection leading to cardiac tamponade
Hemothorax, pneumothorax
Hiccups: may indicate that the generator is pacing the diaphragm
Pacemaker syndrome
Pacemaker syndrome
most common in VVI–pacemaker is only in ventricle
Fatigue, chest discomfort, SOB, activity intolerance, and postural hypotension, they feel worse than before. Teach pt to report this to the doctor
Electromagnetic interference with pacemaker
Never exposed to MRI because it may alter and erase the program memory
At security gates at airports, government buildings, or other secured areas request a hand search (no wand detection device directly over the pacemaker)
Household appliances (eg, microwave ovens) should not cause any concern
AICD
Detects and terminates life-threatening episodes of tachycardia or fibrillation, especially those that are ventricular in origin, so vtach and vfib
Risks that make you candidates for AICD
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Arrhythmogenic right ventricular dysfunction
Idiopathic prolonged QT syndrome
Vtach and vfib are huge risks in these so get an AICD!
CPR with AICD
Normal to feel tingling if you are touching patient when AICD delivers a shock
Not to place defibrillator paddles directly over the device
Patient with a permanent pacemaker with defibrillator or AICD should have the device checked after defibrillation
(check battery or if rate changed, needs to be replaced if so)
EP study
invasive cardiac catheterization
Evaluates and treats dysrhythmias
Includes cardiac cath and catheter ablation
Take fluid out and bring it to lab to check for bacteria, treats bc we’re removing fluid and also diagnoses
Patient is conscious but lightly sedated
Cardiac cath
performed in a specially equipped cardiac catheterization lab by an electrophysiologist
Catheter ablation
destruction of the causative cells
Radiofrequency–thermal injury and cellular changes
Extremely cold temperature
EP study nursing care
Similar to those associated with cardiac catheterization:
Restriction of activity
Duration 2-6 hours (if treatment is indicated)
Procedure is not painful but can be tiring. It may also cause feelings that were experienced when the dysrhythmia occurred in the past
Which valves are similar
Tricuspid and mitral are similar in terms of location (in between atrium and ventricles
Aortic and pulmonic are also similar because they both send blood out of the heart
Chordae Tendineae
fibrous tissue that anchor valve leaflets to papillary muscles of the ventricles, white stringy thingies
Holds onto the valves
Heart muscle can die or chordae tendineae can rupture
Regurgitation
when valves do not close completely when they are supposed to close.
Stenosis
when valves do not open completely when they are supposed to open (something is stuck)
Anterior vs posterior leaflet
anterior leaflet: longer
posterior leaflet: shorter
Mitral valve prolapse
Enlargement of one or both of the leaflets of mitral valve.
When leaflet is too long it can buckle onto ventricle itself, can’t close completely (regurgitation issue)
annulus often dilates; chordae tendineae and papillary muscles may elongate or rupture.
A portion of one or both mitral valve leaflets balloons back into the atrium during systole–blood regurgitates from the left ventricle back into the left atrium
Needs to close during systole (systolic murmur)
Clinical manifestations of MVP
Most never have symptoms
A few have fatigue, SOB, lightheadedness, dizziness, syncope, palpitations, chest pain, or anxiety
Assessment and diagnostics of MVP
Extra heart sound–mitral click
A murmur of mitral regurgitation may be heard if the valve opens during systole (systolic murmur) and blood flows back into the left atrium.
Echocardiography for structure problems is used to diagnose and monitor progression of MVP
Controlling symptoms of MVP
Eliminate caffeine and alcohol, stop using tobacco products.
Antiarrhythmic medications
Chest pain: nitrates or calcium channel blockers or beta-blockers
HF management
Severe: mitral valve repair or replacement
Endocarditis r/t MVP
At risk for endocarditis because of the extra long tissue (bacteria on it)
Women diagnosed with mitral valve prolapse without mitral regurgitation or other complications may complete pregnancies with vaginal deliveries
Antibiotic prophylaxis is recommended for high-risk patients before and after dental procedures–Amoxicillin, not everyone needs it, just depends on condition
Mitral regurgitation
By itself, this is a pathology
Blood flowing back from the left ventricle into the left atrium during systole.
Due to the thickness and fibrosis of the chordae tendineae pulls on to leaflets so they can’t close tightly
systolic murmur
Causes of mitral regurgitation
Developing countries: rheumatic heart disease
Developed countries: degenerative changes of the mitral valve as people get older
Clinical manifestations of mitral regurgitation
Often asymptomatic
Acute mitral regurgitation: usually from a MI–manifests as severe CHF (heart failure management can be used here as well as with MVP)
Most common: Dyspnea, fatigue, and weakness, not enough blood pumped to body because it flows back into the left atrium
S/s are similar to MVP
Big risk for clots!!
Assessment and diagnostic findings of mitral regurgitation
Systolic murmur: high-pitched, blowing sound at the apex that may radiate to the left axilla
May have irregular pulses
Echocardiography is used to DX and monitor
Medical and surgical management of mitral regurgitation
medical management: same as for HF (goal: reduce afterload)
surgical management: mitral valvuloplasty (trim and fix) and valve replacement
Mitral stenosis
DIASTOLIC murmur
Valve is supposed to open but doesn’t
Obstruction of blood flowing from the left atrium to the left ventricle due to the narrowing of the mitral valve orifice/opening
Pulmonary congestion in which valve disorder and why
Mitral stenosis
blood can’t move so it gets stuck in left atrium and then backs up into the lungs, right side heart failure, reduced cardiac output
Clinical manifestations of mitral stenosis
Dyspnea on exertion (DOE)
Enlarged left atrium (due to thin atrial walls)–create pressure on the left bronchial tree, resulting in a dry cough or wheezing. (also leads to afib)
May have hemoptysis from congested lungs, palpitations, orthopnea, paroxysmal nocturnal dyspnea, repeated respiratory infections
Assessment of mitral stenosis
Weak and irregular pulse in the presence of afib
Low-pitched rumbling diastolic murmur
May have s/s of HF
Medical management of mitral stenosis
Anticoagulants, beta-blockers, digoxin, or CCB.
Avoid strenuous activities, competitive sports, and pregnancy
Usually old age so these aren’t issues
Also seen in child bearing age!! Fibrosis can cause mitral valve to stick together, not related to age. Fibrotic changes of mitral valve. Can’t take anticoagulants during pregnancy
Surgical intervention of mitral stenosis
percutaneous transluminal balloon valvuloplasty
great outcome
Good for child-bearing age women
Catheter goes into right atrium, then needs to locate mitral valve, wire needs to poke a hole between left and right atrium and move down to find stenotic mitral valve. Balloon stretches and opens the mitral valve, remains open and is a cure
Problem is that the wall may not heal properly
Not as good for elderly because it’s usually due to calcification and this will not prevent recalcification
Also mitral valve replacement
Aortic regurgitation
Diastolic murmur
This valve needs to close during diastole so blood stays in ventricle
Flow of blood back into the left ventricle from the aorta during diastole.
The left ventricle dilates in an attempt to accommodate the increased volume of blood.
Usually asymptomatic
Mitral valve and aortic valve during systole and diastole
During diastole, mitral valve opens and aortic closes
Opposite for systole
What do you see in pts with aortic regurgitation and what type or murmur
Some may be aware of a forceful heartbeat especially in the head or neck.
Marked arterial pulsations visible or palpable at carotid or temporal arteries
High-pitched, blowing diastolic murmur at the third or fourth intercostal space at the left sternal border.
Widened pulse pressure
What to avoid in aortic regurgitation
Avoid physical exertion, competitive sports, and isometric exercise
Sodium and fluid restriction
Management of aortic regurgitation
Afterload reduction
Valve replacement or valvuloplasty
Surgery is recommended for any patient with left ventricular dilation, regardless of the presence of absence of symptoms. Keeps dilating and leads to dilated cardiomyopathy. Diagnosed with echocardiogram
Aortic stenosis
Very commonly seen and easy to hear in little old ladies with calcified aortic valves
Aortic valve doesn’t open
Murmur in aortic stenosis
loud, harsh systolic murmur heard over the aortic area and may radiate to the carotid arteries and apex of the left ventricle. Low pitched, crescendo-decrescendo, rough, rasping, and vibrating.
Prevention of aortic stenosis
focused on controlling risk factors for proliferative and inflammatory responses: diabetes, HTN, HL, avoid tobacco products.
Surgical replacement
Commissurotomy
procedure performed to separate the fused leaflets. (surgeon puts their finger in the stenotic valve to open it up)
Closed vs open valvuloplasty
Closed: balloon valvuloplasty (can be used for mitral stenosis or aortic stenosis [Usually due to calcification so it’ll become stenotic in a few months again])
Open: open commissurotomy
Who is balloon valvuloplasty beneficial for
Beneficial for mitral valve stenosis in younger patients with complex medical conditions
Contraindications for balloon valvuloplasty
Those with left atrial or ventricular thrombus (Wire can dislodge clots)
Severe valvular calcifications
Thoracolumbar scoliosis (Hard to move wire around when everything is not straight)
Rotation of the great vessels
Cardiac conditions that require open heart surgery
Complications of mitral balloon valvuloplasty
Mitral regurgitation
Bleeding from the catheter insertion sites
Emboli
Atrial septal defect (wire poking a hole in atrial-septum wall, healing may not happen and lead to this)
Complications of aortic balloon valvuloplasty
Aortic regurgitation
Bleeding from the catheter insertion sites
Emboli
Ventricular perforation, rupture of the aortic valve annulus, ventricular dysrhythmia, mitral valve damage
Not as effective as mitral valve procedure because rate of stenosis is high
Valvuloplasty
Repair of a cardiac valve
No need for anticoagulation
Only mitral valve can be repaired well; other valves are better to be replaced
When is replacement better than repair of valves
When valvuloplasty is not a viable alternative: when the annulus or leaflets of the valve are immobilized by calcifications (elderly), severe fibrosis, or fusion of leaflets, chordae tendineae, or papillary muscles
valvuloplasty-Annuloplasty
repair of the valve annulus.
If chordae tendineae rupture, you can suture them together
Mechanical valve replacement
More durable
Less likely to be infected
Need anticoagulants
Tissue valve replacement
Less likely to generate thromboemboli and long term anticoagulation is not required
Bioprosthesis, homograft, and autograft for tissue valve replacement
Bioprosthesis: from pigs, cows, or horses.
Homografts: human valves
Autografts: patient’s own pulmonic valve
Types of cardiomyopathy
dilated cardiomyopathy (DCM) most common
hypertrophic cardiomyopathy (HCM)
restrictive or constrictive cardiomyopathy (RCM)
arrhythmogenic right ventricular cardiomyopathy (ARVC)
Clinical manifestations of cardiomyopathy
Regardless of type and cause, cardiomyopathy may lead to severe heart failure, lethal dysrhythmias, and death.
The mortality rate is highest for African Americans and older adults
Dilated cardiomyopathy
Most common form
Dilated left ventricle without hypertrophy (thin and dilated, floppy and large, can’t pump as well, clots can occur and low cardiac output from diminished contractility)
Low EF
Causes of dilated cardiomyopathy
pregnancy
ischemia
heavy alcohol intake (damaging to heart muscle)
viral infection
chemotherapeutic medications
Chagas disease (parasite)
20-30% idiopathic
Genetic factors may be involved: first degree blood relatives screening
Pathophysiology of cardiomyopathy
Dilation of the ventricles without simultaneous hypertrophy and systolic dysfunction
Complete recovery is rare
Diminished contractile elements (can’t pump the blood out)
Diffuse necrosis of myocardial cells (fatal)
Clinical presentation of dilated cardiomyopathy
Poor systolic function: low EF
Increasing end-diastolic pressure
Increasing pulmonary and systemic venous pressures
Altered valve function (usually regurgitation, when the wall stretches, the chordae tendineae can’t close the leaflet tightly)
Thrombi formation
Treatment of dilated cardiomyopathy
Limited activity based on functional status
Salt and fluid restriction
Meds
Heart transplant
LV reduction surgery
DCM meds
Ace inhibitors, diuretics
Digoxin to help with contractility
hydralazine/nitrate combination
Anticoargulation PRN (EF<30%, hx of embolic event)
Implantable defibrillators
AVOID CA CHANNEL BLOCKERS LIKE VERAPAMIL (pulmonary edema from vasodilation)
Hypertrophic cardiomyopathy
Good EF but low CO
Rare, with family history:
12-18 years of age: echocardiograms every year
18-70: echocardiograms every 5 years
Patho of hypertrophic cardiomyopathy
Thickening begins during early adolescence and stops when growth has finished
Heart muscle increases in size and mass: especially along the septum
Reduced size of the ventricular cavities
Takes longer for the ventricles to relax after systole
Cardiac muscle cells disorganized, oblique, and perpendicular to each other, decreasing the effectiveness of contractions and possibly increasing the risk of dysrhythmias
Manifestations of hypertrophic cardiomyopathy
Cardiac arrest (high demand of blood, not enough supply, cardiac arrest)
Sustained V-tach and V-fib: most likely mechanism of syncope/sudden death
Angina, syncope, palpitations, and left heart failure
Treatment of hypertrophic cardiomyopathy
No treatment unless there’s symptoms
Avoid dehydration (avoid diuretics, teach teens about hydration)
BB
Limited physical activity to avoid dysrhythmia
Implanted pacemaker (biventricular)
Nonsurgical septal reduction therapy (alcohol ablation)
Restrictive cardiomyopathy
Diastolic dysfunction caused by rigid ventricular walls that impair diastolic filling and ventricular stretch
Systolic function is usually normal (can contract but can’t dilate/stretch to accomodate blood)
S/S of restrictive cardiomyopathy
Venous congestion, jugular venous distention, hepatomegaly, ascites (signs of right sided heart failure)
Due to rigid myocardium: decreased ventricular filling, decreased CO→ weakness and fatigue
3 things associated with restrictive cardiomyopathy and what med to avoid
May be associated with amyloidosis, sarcoidosis, hemochromatosis
Avoid: nifedipine to maintain contractility
Arrhythmogenic right ventricular cardiomyopathy
Right ventricle replaced with chaotic mix of heart muscle, fibrous tissue, and fat
Right ventricle dilates and develops poor contractility
Arrhythmia: palpitations or syncope
Ventricular tachycardia originating in the right ventricle
Sudden death among young athletes
Screening of arrhythmogenic right ventricular cardiomyopathy
first-degree blood relatives should be screened with 12 lead ECG, Holter monitor and echocardiography
surgical management of cardiomyopathy
mechanical assist devices and total artificial hearts: Left ventricular assist devices (LVAD) (battery and controls are outside and everything else is inside)
How is an LVAD used
a “bridge to recovery” for patients who require temporary assistance for reversible ventricular failure
a “bridge to transplant” for patients with end-stage heart failure until a donor organ becomes available
“destination therapy” for patients with end-stage heart failure who are not candidates for or decline heart transplantation
IABP for cardiomyopathy
temporarily (1 week or so) (waiting for the heart transplant)
deflated during systole; inflated during diastole
reduces afterload
increases myocardial perfusion/function
Surgical management of cardiomyopathy
Heart transplant
balancing rejection and infection
postoperative function depends on the heart being implanted within 4 hours of harvest from the donor
Indications of heart transplant
Cardiomyopathy
ischemic heart disease
valvular disease
rejection of previously transplanted hearts
congenital heart disease
Balancing rejection and infection in HT
Immunosuppressants:
tacrolimus (Prograf)
cyclosporine
mycophenolate mofetil (CellCept)
azathioprine (Imuran)
corticosteroids (prednisone)
What can immunosuppressants cause
increase arterial injury and inflammation
osteoporosis
weight gain, obesity, diabetes, dyslipidemias, hypotension, renal failure, and CNS, resp, and GI disturbance
Survival rates for HT
1 year survival rate: 81-95%
10 year survival rate: 50-70%
Total artifact hearts
replace both ventricles
long-term results disappointing
Complication of VAD and total artificial hearts
Bleeding disorders
Hemorrhage
Thromboemboli
Hemolysis
Infection
Renal failure
Right-sided heart failure
Multisystem failure
Mechanical failure
Heart failure epidemiology
one of the fastest growing heart conditions in the U.S.
#1 reason for hospitalization of patients age 65 and older
More hospitalizations from heart failure than for all forms of cancer combined
About 550,000 new cases per year
Prevalence is high
Hospital Admissions for Acute HF are Rising Due to:
Noncompliance with diet and drugs (low fluid and salt)
Inevitable progression of disease
Rising incidence of chronic heart failure (population aging, improved survival with acute MI [revascularization])
Poor application of chronic heart failure management guidelines
Incomplete treatment during hospitalization
Heart Failure
inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients
Preload
amount of blood in the ventricle at the end of diastole
venous return of blood
compliance of ventricular (hypertrophy; fibrotic tissue after MI)
Afterload
amt of resistance to the ejection of blood
EF
R/t contractility
percentage of blood volume in the ventricles at the end of diastole that is ejected during systole; a measure of contractility
Systolic heart failure
Impaired contraction of the heart
More common than diastolic heart failure
Low EF
Example: left-sided systolic heart failure
Diastolic HF
Impaired filling of the heart
Stiffened and noncompliant heart muscle like restricted cardiomyopathy
Normal EF
HF etiology
CAD
HTN
Cardiomyopathy
Valvular disorder
Renal dysfunction with volume overload
Diabetics: high risk
Pulmonary hypertension (pressure inside lungs is too high so RV needs to work harder to balance the pressure, eventually leading to RVHF
Patho of HF
In reaction to the stretch of heart muscles body releases: natriuretic peptides (NPs)
ANP and BNP
BNP most accurate in identifying CHF (>100), works to lower BP and afterload
Elevated with heart related congestion
Vascular remodeling
Vascular remodeling in HF
Heart compensates for the increased workload to increase the thickness of the heart muscle (ventricular hypertrophy)
Enlarged myocardial cells become dysfunctional and die early–leaving the other normal myocardial cells struggling to maintain CO
A “vicious cycle”
Ace inhibitors
First line of defense in mild HF
Relieves s/s and decreases morbidity and mortality
What to watch for in ACE inhibitors
Angioedema (rare allergic reaction, go to hospital for treating)
Annoying dry cough
Hyperkalemia
ARBS
For HF
have many of the same benefits as ACE inhibitors
alternatives for those cannot tolerate ACE inhibitors
similar side effects
Valsartan (diovan) and losartan (cozaar)
SE of ARBs
hyperkalemia
hypotension
renal dysfunction
Nitrates
For HF
isosorbide dinitrate
may be another alternative for those who cannot take ACE inhibitors
venous dilation–lowers preload
Hydralazine
For HF
lowers systemic vascular resistance and left ventricular afterload
smooth muscle arterial vasodilator
good for those with poor kidney function
Beta blockers
For HF
reduced the stimulation of the sympathetic nervous system
given in addition to ACE inhibitors, diuretics, and digitalis (increases contractility)
may prevent the onset of symptoms of HF
Things to know about BB
pts may feel worse at the beginning and then feel better, big reason for noncompliance
Reduced sympathetic nerve stimulation so they feel tired, impotence
Diuretics for HF
watch for dehydration
loop first: furosemide (Lasix slow IV push), bumetanide (Bumex) (increase potassium excretion)
thiazide (increase potassium excretion)
Spironolactone (Aldactone): potassium-sparing diuretic
SE of diuretics for HF
electrolyte imbalances
symptomatic hypotension
hyperuricemia (gout)
ototoxicity
cardiorenal syndrome: not a SE just something to watch for, resistant to diuretics
Digitalis
does not result in decreased mortality rates
digoxin: increase the force of myocardial contraction and slows conduction through the AV node
digoxin toxicity
vision changes first (yellow halos)
anorexia, nausea, vomiting, fatigue, depression, and malaise
changes in heart rate or rhythm; onset of irregular rhythm
ECG changes: (sagging ST)
What to watch with digoxin
Monitor serum potassium level because the effect of digoxin is enhanced in the presence of hypokalemia and digoxin toxicity may occur
A serum digoxin level is obtained if the patient’s renal function changes or there are symptoms of toxicity
CHF exacerbation treatment
IV diuretics
fluid restriction
pt may want to dangle his/her legs, helps them breathe better
oxygen
use of positive inotropes: (such as: Amiodarone)
Reduce anxiety
Positive inotropes for CHF
short term
balancing the good (improved cardiac output, stroke volume) against the bad (increased myocardial oxygen consumption)
long-term use: worsen mortality
Most common cause of CAD
atherosclerosis–repetitious inflammatory response to injury of the artery wall over many years
Atherosclerotic lesions most often form where the vessels branch
Nonmodifiable risk factors for CAD
Family history of CAD
Age: 45 for male, 55 for female
Gender: male
Race: African Americans
Modifiable risk factors of CAD
HL
Cigarette smoking, tobacco use
HTN
Diabetes
Metabolic syndrome
Obesity
Physical inactivity
Angina pectoris
Most common manifestation of myocardial ischemia is the onset of chest pain.
burning, bursting, constricting, grip-like, heaviness, pressing, squeezing, strangling, suffocating, a band across my chest, a weight in the center
Associated factors of angina pectoris
physical exertion–O2
exposure to cold–vasoconstriction
eating a heavy meal–decreased blood flow to the heart muscle
stress or emotion-provoking situation–catecholamines–increase blood pressure, heart rate, and myocardial workload
Stable angina
Predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin
Nitroglycerin for stable angina
relaxes smooth muscle–dilating primarily the veins and to a lesser extent, the arteries
reduce preload (venous pooling) and afterload–lower the workload of the heart
0.3-0.6 mg SL q5min up to 3 times; use at first sign of angina
not for those with severe bradycardia or tachycardia
Unstable angina
attacks that increase in frequency and severity
not relieved by rest and administering of nitroglycerin
should be treated at the closest ED
Treatment of angina
Nitrates: Nitroglycerin
BB: Metoprolol
CCB: Amlodipine, Cardizem
Antiplatelet medications: Aspirin, Plavix
Anticoagulants: Heparin, Lovenox
Reperfusion procedures: PCI procedures and CABG
ECG changes in ischemia
T-wave inversion
ST-elevation
Or development of an abnormal Q wave.
ST elevation will return to normal, but Q wave alterations are usually permanent.
ACS Assessment and diagnostic findings
Obtain ECG within 10 minutes from the time a patient reports pain or arrives in ED.
Through ECG and lab tests (serial cardiac biomarkers) to clarify whether the patient has
Unstable angina, NSTEMI, and STEMI
Unstable angina: no ST elevation, no abnormal biomarkers
NSTEMI: no ST elevation, with elevated cardiac biomarkers
STEMI: ST elevation and elevated cardiac biomarkers
Cardiac biomarkers for ACS and MI
CK-MB: for heart muscle
Troponin I and T: Only in myocardium
Myoglobin
CM-MB for ACS and MI
Indicates an acute MI
Increased within a few hours
peaks in 24-48 hr
Troponin I and T for ACS and MI
Indicates a recent MI
elevated within a few hours during acute MI
remains elevated for as long as 2 weeks
Myoglobin in ACS and MI
Peaks within 12 hours
An increase in myoglobin is not very specific in indicating an acute cardiac event; however, negative results used to rule out an acute MI
Goals in medical management in ACS and MI
Managing myocardial oxygen supply with demand
minimize myocardial damage
preserve myocardial function
prevent complications
Immediate treatment for MI
MONA
Morphine, oxygen (first), nitro, aspirin
In ICU/CCU, IV beta-blockers (watch for cardiogenic shock, long-term therapy can decrease future cardiac events)
Morphine for ACS/MI
potent narcotic analgesic and anxiolytic
vasodilation and can lower heart rate and systolic blood pressure
reducing myocardial oxygen demand
Adverse effects of morphine
respiratory depression; nausea and vomiting (20% of patients); hypotension
Aspirin and clopidogrel (plavix) for ACS/MI
antiplatelet and anticoagulant therapies are important components of ACS patient management because of exposure of a ruptured plaque’s contents triggers activation of the coagulation cascade
Emergent Percutaneous Coronary Intervention (PCI):
percutaneous transluminal coronary angioplasty: evaluate coronary artery blood flow and open the occluded coronary artery and promote reperfusion to the area been deprived of oxygen
STEMI patients can be taken directly to cath lab for PCI
better outcome than thrombolytics
with good results in elderly
door-to-balloon time: 60 min-90 min
Thrombolytics for ACS/MI
fibrinolytic therapy (IV alteplase [Activase[, reteplase [r-PA], and tenecteplase [TNKase])
Given if not able to do PCI or do PCI on time
must be given as early as possible (within 3-6 hours onset of pain)
door to needle time–30min
given to those with ECG evidence of acute MI (STEMI)
fibrinolytic therapy for ACS/MI
dissolve all clots
watch for bleeding
must have at least two IV lines
minimize the number of times the patient’s skin is punctured
Contraindications of fibrinolytic therapy for ACS/MI
had recent surgery (even minor surgery) or
hemorrhagic stroke or
prolonged CPR
Pregnancy
Post MI Hypothermia
hypothermia treatment for unconscious adults who experience cardiac arrest (including cardiac arrest due to vfib) and who receive CPR within 10 minutes
start within 60 minutes after circulation is restored (ASAP)
Complications of acute MI
electrical complications (very common)
embolic complications
inflammatory complications
ischemic complications
electrical complications post MI
very common
bradydysrhythmias (sinus bradycardia most common)
tachydysrhythmias
AV blocks
bundle branch blocks
sudden cardiac death
embolic complications post MI
stroke
deep vein thrombosis
pulmonary embolism
inflammatory complications post MI
pericarditis
ischemic complications post MI
angina
reinfarction
infarct extension: a myocardial infarction that has spread beyond the original area, usually as a result of the death of cells in the ischemic margin of the infarct zone
Medications post MI
BB
aspirin
Ace inhibitor
Percutaneous Transluminal Coronary Angioplasty–PTCA
Purpose of PTCA: improve blood flow within a coronary artery by compressing the atheroma.
Measure of success is an improvement in blood flow and a residual stenosis of less than 30%
Used for angina, ACS, and to open blocked CABGs
What may a patient feel with PTCA
chest pain and the ECG may display ST-segment changes when the balloon inflated inside of the coronary artery
Intracoronary stent implantation=Coronary artery stent
A metal mesh that provides structural support to a vessel at risk of acute closure.
placed to overcome “restenosis”
coated with medications to minimize the formation of thrombi or scar tissue within the stent
Meds for coronary artery stent
must be on aspirin and clopidogrel
Clopidogrel: up to 1 year following drug-eluting stents
Complications of PCI
coronary artery dissection, perforation, abrupt closure, or vasospasm
acute MI, serious dysrhythmias, cardiac arrest
bleeding at the insertion site, retroperitoneal bleeding, hematoma, and arterial occlusion (receive anticoagulant during the procedure)
acute kidney injury from the contrast agent
Chance of restenosis and mortality rate after PTCA
20-30% restenosis after 6 months
mortality 0-2%
Post procedure care of PTCA
remain flat in bed and keep the affected leg straight until the sheaths are removed and then for a few hours afterward to maintain hemostasis.
Sheath removal and the application of pressure on the vessel insertion site may cause the heart rate to slow and blood pressure to decrease (vasovagal response)
The patient is instructed to monitor the site for bleeding or development of a hard mass indicative of hematoma.
Bleeding!!! Circulation!!! Immobilization!!!
Major indications for CABG
alleviation of angina that cannot be controlled with medication or PCI
treatment for left main coronary artery stenosis or multivessel CAD
prevention of and treatment for MI, dysrhythmias, or heart failure
treatment for complications from an unsuccessful PCI
Who is CABG less frequently performed in and why
women
Smaller vessels
higher risk of complications
CABG is the preferred treatment for pt with
severe triple-vessel CAD
ventricular dysfunction
diabetes
For a pt to be considered for CABG
the bypassed coronary arteries must have more than 70% occlusion (50% if in the left main coronary artery)
artery must be patent beyond the area of blockage
Why are arterial grafts preferred over venous
Arteries do not develop atherosclerotic changes as quickly and remain patient longer.
right and left internal mammary arteries are recommended for CABG
radial and gastroepiploic arteries
3 most commonly used veins for CABG
First: the greater saphenous vein
Second: lesser saphenous vein
Third: cephalic and basilic veins
Adverse effects of vein removal
edema in the extremity from which the vein was taken
edema can diminish over time
within 5-10 years, atherosclerotic changes often develop in saphenous vein grafts
What type of blood vessels are usually used in CABG
many CABG procedures are performed with a combination of venous and arterial grafts
internal mammary arteries may not be long enough to use of multiple bypasses
CABG Cardiopulmonary bypass
extracorporeal circulation
mechanically circulates and oxygenates blood for the body while bypass the heart and lungs
allows surgeon to complete the grafting in a motionless, bloodless surgical field
Temperature during CABG cardiopulmonary bypass
During the procedure, hypothermia is maintained at a temperature of about 28C.
Reduce the body’s basal metabolic rate, and decrease the demand for oxygen
Off pump CABG
standard median sternotomy incision
performed with CPB
beta-adrenergic blocker used to slow the heart rate
myocardial stabilization device to hold the site still
less incidence of stroke and complications
On pump CABG
graft patency rate is higher and long-term mortality may be lower
Complications of CABG
Hemorrhage (hypovolemia)
dysrhythmias
MI
Postop assessment for CABG
neurologic status
cardiac status
respiratory status
peripheral vascular status
renal function
fluid and electrolyte
pain
Maintaining cardiac output
Neuro status after CABG
Impaired cerebral perfusion
hypoperfusion or microemboli during or following cardiac surgery may produce injury to the brain
brain function depends on a continuous supply of oxygenated blood
the brain does not have the capacity to store oxygen and must rely on adequate continuous perfusion by the heart
Maintaining CO after CABG
Renal function is related to cardiac output.
Urine output of less than 1ml/kg/h may indicate a decrease in cardiac output or inadequate fluid volume
CABG postop care (bleeding)
chest tube should have less than 200 mL/h drainage during first 4-6 hours
CABG postop care (postcardiotomy delirium)
transient perceptual illusions
visual and auditory hallucinations
disorientation
paranoid delusions
Physiologic factors that contribute to CABG postcardiotomy delirium
long periods of extracorporeal circulation,
arterial hypotension during surgery, emboli, and low postoperative cardiac output.
Age, and the type and severity of heart impairment are also factors.
Delirium is fostered by sensory overload (or deprivation) in the recovery room and intensive care unit, and by staff tension.
delirium resolves after the pt is transferred from the unit
Hemodynamic monitoring
Direct pressure monitoring system
Flush system for hemodynamic monitoring
IV solution (may include heparin or only NS)
tubing
stopcocks
flush device: provides continuous and manual flushing
Pressure bag for hemodynamic monitoring
maintained at 300 mmHg of pressure
must have fluid in the tubing to transduce pressure
Pressure bag should ensure the system to deliver 3-5 ml of solution per hour to prevent clotting and backflow of blood into the pressure monitoring system
Transducer for hemodynamic monitoring
to convert the pressure coming from the artery or heart chamber into an electrical signal
Amplifier (monitor) for hemodynamic monitoring
increases the size of the electrical signal for display on an oscilloscope.
Nursing interventions of hemodynamic monitoring
keep the pressure monitoring system patent and free of air bubbles
the stopcock of the transducer must position at the level of the atrium (4th intercostal space): phlebostatic axis.
make sure to establish the zero reference point for it to function at atmosphere pressure
Complications of hemodynamic monitoring
Pneumothorax during the insertion
The longer the the system in place, the higher chance of infection
Air embolic can be introduced into the vascular system if the stopcocks are mishandled
hemodynamic monitoring-A Line
intra-arterial blood pressure monitoring (radial artery)
pressure should be compared with cuff pressure 2-3 times per day
Advantages of A line
real time blood pressure
ABG drawing
Who is at highest risk for impede perfusion distal to the line.
Patients with diabetes, peripheral vascular disease, hypotension, IV vasopressors, or previous surgery
Nursing interventions of a-line
Assess the perfusion of the hand (Allen test)
Circulation can also be assessed by the Doppler ultrasonography, and others.
Hemodynamic Monitoring-Central Venous Pressure Monitoring (CVP)
a measurement of the pressure in the vena cava or right atrium
Most valuable when it is monitored over time and correlated with the patient’s clinical status.
Preferred site for insertion: subclavian vein
Normal CVP
2-6 mmHg
High CVP
indicates an elevated right ventricular preload (hypervolemia or right rided HF
Low CVP
hypovolemia (dehydration, blood loss, vomiting or diarrhea, and overdiuresis)
Swan Ganz
Pulmonary artery pressure monitoring
Assessing left ventricular function
balloon-tipped, flow-directed catheters
a syringe connected to the hub and can only inflate or deflate the balloon with a capacity of 1.5ml
evaluates left ventricular filling pressures
measured by blocking the blood flow through pulmonary artery
After measuring the wedge pressure, the balloon must be deflated: may cause pulmonary artery infarction
What can swan ganz measure
Pressures:
right atrial
pulmonary artery systolic
pulmonary artery diastolic
mean pulmonary artery
pulmonary artery wedge
Nursing interventions of swan ganz
Catheter site care is essentially the same for a CVP catheter
Monitor for complications
Complications of swan ganz
Pulmonary artery rupture
Pulmonary thromboembolism
Pulmonary infarction
Catheter kinking
Dysrhythmias
Air embolism
Minimally Invasive Cardiac Output Monitoring Devices
Pulse pressure analysis
Esophageal doppler probes
Fick principle
Pulse pressure analysis
uses an arterial pressure waveform to continuously estimate the patient’s stroke volume. Limited to those with good waveform
Esophageal doppler probes
estimates CO
Fick principle
uses carbon dioxide measures for sedated, intubated, on mechanical ventilation patients
Aneurysm
a localized sac or dilation formed at a weak point in the wall of the artery.
Most common forms of aneurysms:
-saccular aneurysm
-fusiform aneurysm
Most common type of degenerative aneurysm: Abdominal aortic aneurysm (AAA)
Saccular aneurysm
…
Fusiform aneurysm
…
Thoracic aortic aneurysm
85% of all cases of thoracic aortic aneurysm caused by atherosclerosis
men age 50-70
thoracic are: the most common site for a dissecting aneurysm (separation of the wall of the vessel)
1/3 of patients with thoracic aneurysms die of rupture of the aneurysm
s/s of thoracic aortic aneurysm
Most prominent symptom: pain
Dyspnea
Couth, frequently paroxysmal and with a brassy quality
Hoarseness, stridor, or weakness or complete loss of voice
Dysphasia
Assessment and diagnostic findings of thoracic aortic aneurysm
unequal pupils (cervical sympathetic chain pressed)
dx made by chest x-ray, CT-angiogram, TEE
Medical management of thoracic aortic aneurysm without rupture
control blood pressure: systolic pressure maintained at 90-120 mmHg.
BB, hydralazine, nipride
Nipride for thoracic aortic aneurysm without rupture
continuous IV drip to emergently lower the blood pressure
advantages: rapid onset and short action of duration, and easy to titrate
Surgery for thoracic aortic aneurysm without rupture
vascular graft
open surgical repair or percutaneously
Postop for thoracic aortic aneurysm without rupture
maintain the cerebrospinal fluid pressure less than or equal to 10mmHg and to keep the mean arterial pressure greater than 90 mmHg for the first 36-48 hours postoperatively to prevent neurologic deficit
Treatment for ruptured thoracic aortic aneurysm
surgery right away!!
Abdominal aortic aneurysm (AAA)
Most common type of degenerative aneurysm
Most common cause is atherosclerosis
Common in caucasians
Affects men > women
Most prevalent in elderly
Mostly below renal arteries (infrarenal)
Patho of AAA
A damaged media layer of the vessel
Caused by congenital weakness, trauma, or disease
Risk factors of AAA
Genetic predisposition
Tobacco use
HTN
Clinical manifestations of an AAA
Only 40% of pts have symptoms
Feeling heartbeat in abdomen when laying down
May feel abdominal mass or throbbing
Thrombus may occlude a major vessel
Assessment and diagnostic findings of AAA
Pulsatile mass in the middle and upper abdomen
Do NOT perform deep palpitation of the abdomen (80% can be palpitated)
Systolic bruit may be heard over the mass
Duplex ultrasound or CT angiogram is used to determine the size, length, and location of the aneurysm
Rupture is likely with coexisting HTN and with aneurysms more than 6cm wide
Medical management of AAA
Ultrasound q6 months
Control BP (esp diastolic, high risk of rupture if >100 mmHg)
AntiHTN meds
Surgical management of AAA
Aneurysm is not repaired until it is at least 5.5cm wide
Open repair of aneurysm by resecting the vessel and sewing a bypass graft into place
Alternative for treating an infrarenal AAA is endovascular grafting
-Transluminal placement and attachment of a sutureless aortic graft prosthesis across an aneurysm
Signs of impending rupture of AAA
Severe back or abdominal pain (may be persistent or intermittent)
Localized in the middle or lower abdomen, left of the midline
Constant, intense back pain, falling BP, and decreasing hematocrit
Rupture into peritoneal cavity is FATAL
Signs of impending rupture of AAA
Severe back or abdominal pain (may be persistent or intermittent)
Localized in the middle or lower abdomen, left of the midline
Constant, intense back pain, falling BP, and decreasing hematocrit
Rupture into peritoneal cavity is FATAL
