What does vagal stimulation do?
Vagal stimulation causes bradycardia, hypotension, heart block, or other dysrhythmias
Can be used to decrease heart rate in something like SVT
What causes vagal stimulation?
Vagal maneuvers like the Valsalva maneuver
bearing down
blowing into a straw
carotid massage (but that is only for a doctor to do)
face in ice cold water
What are nursing implications related to vagal stimulation?
educate the patient on vagal stimulation maneuvers like the Valsalva maneuver if they need to bring down a rapid heartrate
this should also be documented and reported to the physician if used in emergent scenarios like SVT
the nurse cannot preform a vagal maneuver like the carotid massage
Drugs that can increase vagal stimulation
Adenosine, beta blockers, statins, and ace inhibitors
Drugs that can inhibit vagal stimulation
Atropine, scopolamine, anticholinergic drugs
R on T phenomenon
The superimposition of an ectopic beat on the T wave of a preceding beat
What is the significance?
pt has Vtach and it becomes unstable
can go into VFib
Nursing care for cardiac catheterization
Before the procedure the nurse will assess the patient’s physical and psychosocial readiness for the procedure
they will give information about what it will feel like and what will be happening during the procedure
after the procedure the nurse should restrict the patient to bedrest, the insertion site must be kept straight
vitals should be monitored every 15 min For 1 hour, then every 30 min. For 2 hours or until stable and then every 4hr
Assess insertion site for drainage, assess peripheral pulses,
Digoxin MOA
Positive ionotropic- increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart
Negative chronotropic- stimulates the PSNS, which slows electrical conduction, and decreases HR
Digoxin nursing care
assess apical HR before administration
teach patient to report signs of dig toxicity
Digoxin Patient education
Signs of dig toxicity
nausea
vomiting
diarrhea
paresthesia
confusion
visual disturbance
Common side effects
facial flushing
SOB
chest pain
Antacids interfere with the absorption
Post operative care for heart transplant
Lots of medications will be administered: immunosuppressants, anti-proliferatives,
Education on risk of rejection, increased risk of cancer
Troponin: what it measures, what’s normal, what does an increase and/or decrease indicate
myocardial muscle protein released into bloodstream with injury to myocardial muscle
Troponin T <0.1ng/mL
Troponin I <0.03ng/mL
Elevation indicates myocardial injury or infarction
CPK: what it measures
When muscle tissue is damaged, CPK leaks into your blood
before providers used Trops to assess for HF, this was used
it is not reliable because it does not apply specifically to cardiac muscle
BNP: what it measures, what’s normal, what does an increase indicate*
Peptide produced and released by the ventricles when they stretch when the patient has fluid overload as a result of HF
<100 pg/mL
increase indicates HF
PT/INR: what it measures, what’s normal, what does an increase and decrease indicate
Measures the activity of prothrombin, fibrinogen, and factors V, VII, and X
most reliable way to monitor anticoagulant status in warfarin therapy
0.8-1.1 if they are not using anticoagulants
Increase indicates that Warfarin therapy is successful and there is a risk for prolonged bleeding
Decrease indicates that blood is clotting quicker and the pt is at risk for thrombi/emboli
aPTT: what it measures, what’s normal
measures how well blood is coagulating
used during heparin therapy, aPTT must remain in therapeutic range
usually 1.5-2.5x normal control levels
Mean arterial pressure, what must it be
the arterial BP necessary to maintain perfusion of major body organs, such as the kidneys and brain
at least 60 mm Hg
usually 60-70 mm Hg
Treatment of pericarditis
pericardiocentesis to remove fluid and relieve pressure on the heart
antibiotics
pericardial drainage
NSAIDs for pain
Corticosteroids when NSAIDs don’t work
Colchicine twice a day for 3 months to prevent pericarditis recurrence
Pericarditis and symptoms
Inflammation or alteration of the pericardium, the membranous sac that encloses the heart
Symptoms
substernal precordial pain that radiates to the left side of the neck, shoulder, or back
aggravated by inspiration, coughing, and swallowing
pericardial rub
ST elevation
Patient with pericarditis, positioning for comfort
Sitting upright and leaning forward will help with the pain
Drugs that reduce preload
Diuretics and Nitrates
Drugs that reduce afterload
ACEIs, ARBs, and ARNI (Sacubitril/Valsartan)
Drugs that enhance contractility
Digoxin, Milrinone, and Beta blockers
Risk factors for endocarditis
IV drugs use
Valve replacement
Systemic alterations in immunity
Structural cardiac defects
Endocarditis and symptoms
Microbial infection of the endocardium
Symptoms
fever associated with chills, night sweats, malaise, and fatigue
anorexia and weight loss
cardiac murmur
petechiae
splinter hemorrhages
Osler nodes (on palms of hands and soles of feet)
Janeway lesions (flat, reddened macular on hands and feet)
Roth spots (hemorrhagic lesions that appear as round or oval spots on the retina)
Treatment and precautions for endocarditis
Nonsurgical
IV antimicrobials for 4-6 weeks
Surgical
removing infected valve
repairing or removing congenital shunts
repairing injured valves and chordae tendineae
draining abscesses in the heart
Precautions
Standard precautions
Contact with infected person’s blood should be avoided
Mitral valve stenosis and symptoms
Thickening of the mitral valve due to fibrosis and calcification, the valve leaflets fuse and become stiff
valve opening narrows, preventing normal blood flow from the LA and LV
Symptoms
mild stenosis pts are asymptomatic
with progression…
dyspnea on exertion
orthopnea
PND
palpitations
dry cough
hemoptysis
pulmonary edema
apical diastolic murmur
symptoms of RVF
Risks of prosthetic valves and treatments for these risks
Thromboembolism - anticoagulant therapy
Structural valve dysfunction - repair or replacement of the valve
Endocarditis - most commonly treated with antibiotics, sometimes surgery is needed
Mitral valve regurgitations and symptoms
Inability of the mitral valve to close completely during systole, which allows the backflow of blood into the LA when the ventricle contracts
LA and LV dilate and hypertrophy
Symptoms
fatigue and chronic weakness
anxiety
atypical chest pain
palpitations
Later Symptoms
dyspnea on exertion
orthopnea
Risks associated with mitral valve regurgitation!
Adventitious sounds heard with mitral valve regurgitation
high pitched murmur at the apex, with radiation to the left axilla
S3
What is an S3 gallop indicative of
Heart failure
Dilated cardiomyopathy and symptoms
Most common type of cardiomyopathy, inability of the heart to pump effectively due to enlargement (dilation) and weakening of the ventricles
Symptoms caused by decreased CO
dyspnea on exertion
decreased exercise capacity
fatigue
palpitations
dysrhythmias or heart block
S3 and S4 gallops
moderate to severe cardiomegaly
Causes of dilated cardiomyopathy
alcohol abuse
chemotherapy
infection
inflammation
poor nutrition
Hypertrophic cardiomyopathy and symptoms
Inability of the heart to pump blood effectively due to asymmetric thickening (hypertrophy) of the ventricles and disarray of the myocardial fibers
some die with no symptoms
athletes who die suddenly probably had this
Symptoms
syncope
dyspnea on exertion
dizziness
palpitations
angina
mild cardiomegaly
S4 gallop
Causes of hypertrophic cardiomyopathy
mitral valve structural abnormalities
Autosomal dominant gene
Restrictive cardiomyopathy and symptoms
Rarest types of cardiomyopathy, inability of the heart to pump effectively due to restrictive filling of the ventricles because they are stiff
Symptoms
symptoms of LVF
symptoms of RVF
or symptoms of both
Restrictive cardiomyopathy causes!
primary disease
endocardial disease
myocardial disease
sarcoidosis
amyloidosis
Diagnosis of cardiomyopathies!
EKG
echo to look at overall heart function
cardiac catheterization (biopsy)
X-ray
Intervention for dilated cardiomyopathy
Increase CO with
diuretics
vasodilating agents
cardiac glycosides
Intervention for hypertrophic cardiomyopathy!
medications
diuretics
Ace inhibitors
Intervention for restrictive cardiomyopathy!
medications
ACEI
Beta blockers
Calcium channel blockers
Left sided heart failure causes and symptoms
Causes- hypertension, CAD, valvular disease
Symptoms-
Dyspnea
Rales
Orthopnea
Weakness
Nocturnal paroxysmal dyspnea
Increased HR
Nagging cough
Gaining weight (2-3lb/day or 5lb/week)
LVF types
Systolic HF- heart failure that results when the heart is unable to contract forcefully enough during systole to eject adequate amounts of blood into circulation
Ejection fraction <40%
preload increases with decreased contractility, and afterload increases as a result of increased peripheral resistance
Diastolic HF- heart failure that occurs when the left ventricle is unable to relax adequately during diastole (due to stiffening), which prevents the ventricle from filling with enough blood to ensure adequate CO
ventricles become less compliant over time because more pressure is needed to move the same amount of volume compared with a healthy heart
Assessment of LVF
ask about activity tolerance and ability to perform ADLs
Ask about a cough, especially nocturnal
dyspnea, orthopnea, PND
HF treatment
To increase gas exchange
ventilation assistance
To increase perfusion
CPAP
Cardiac resynchronization therapy (CRT)
Heart transplant
Ventricular Assist device
Heart reduction
Medications
Patient education for HF
MAWDS
Medications
take them as prescribed and do not run out
know the purpose and side effects
avoid NSAIDs to prevent Na and fluid retention
Activity
stay as active possible but don’t overdo it
be able to carry on a conversation while exercising
Weight
weight each day at the same time on the same scale to monitor for fluid retention
Diet
limit daily Na intake to 2-3g
limit daily fluid intake to 2L
Symptoms
note any new or worsening symptoms and notify HCP immediately
rapid weight gain (3/week or 1-2/day)
decrease in exercise tolerance lasting 2-3 days
cold symptoms lasting more than 3-5 days
nocturia
dypsnea or angina at rest
increased swellin in feet, ankles, or hands
Nursing interventions for HF
monitor for signs of acute pulmonary edema
crackles in lung bases, dyspnea at rest, disorientation, confusion
administer medications
monitor weight gain
monitor respiratory rate, rhythm, and quality every 1-4 hours
auscultate breath sounds every 4-8 hours
Right sided heart failure and symptoms
Causes-
Symptoms- SWELLING
Swelling of hands, legs, and liver
Weight gain
Edema (pitting)
Large neck veins (JVD)
Lethargic
Irregular HR (AFib)
Nocturia
Girth (Ascites)
Assessment of right sided heart failure
lower leg edema that may progress to thighs and abdomen
tight rings or shoes and weight gain
nausea and vomiting and increased abdominal girth
diet habits and extreme thirst due to Na retention
psychosocial assessment
Digoxin dosing considerations
Assess apical pulse prior to administration; HR >60 no digoxin
Monitor for dig toxicity, signs include: nausea, vomiting, diarrhea, paresthesia, confusion, or visual disturbances
Digoxin toxicity and treatment
most common cause of dig toxicity is hypokalemia or renal complications
early symptoms of digoxin toxicity are GI symptoms like nausea and vomiting
later symptoms include visual disturbances (yellow-green discoloration), palpitations, dyspnea, and syncope
treatment for dig toxicity includes: Digifab and Digibind
an immunoglobulin fragment that binds with digoxin and is considered first line treatment for digoxin toxicity causing significant dysrhythmias (severe bradyarrhythmia, 2nd or 3rd degree heart block, ventricular tachycardia or fibrillation)
Nitroglycerin MOA
nitroglycerin is converted by mitochondrial aldehyde dehydrogenase in smooth muscle cells to nitric oxide, a potent vasodilator, which activates the enzyme guanylate cyclase which converts guanosine triphosphate (GTP) to cGMP in vascular smooth muscle and other tissue. cGMP is an endogenous vasodilator of vascular smooth muscle.
Side effects and patient education of nitroglycerine
it can cause hypotension and this can cause nausea, vomiting, diaphoresis, pallor, and fainting
patient education includes the risk of orthostatic hypotension and how to get up slowly
headaches are a common side effect and should decrease with continued drug therapy
concurrent alcohol use should be avoided
patient should be educated to inform their doctor if they experience dry mouth or blurred vision.
Calcium channel blockers MOA
calcium channel blockers block the inward movement of calcium by binding to the long acting voltage-gated calcium channels in the heart, vascular smooth muscle, and pancreas
Risks associated with calcium channel blockers
lightheadedness
flushing
orthostatic hypotension
headaches
peripheral edema
worsening HF
Nursing interventions and patient education of calcium channel blockers
patients should be taught not to consume large amounts of grapefruit juice during drug therapy
how to check their pulse and that they should call their doctor if their HR is less than 50bpm
that this medication can cause orthostatic hypotension and how to move slowly when going from laying down to sitting to standing
notify their doctor if they experience rash, irregular heartbeat, dyspnea, swelling of hands or feet, pronounced dizziness, nausea, hypotension, constipation, or severe/persistent headaches.
Beta blockers MOA!
Beta-1 blockers
decreases HR, decreases myocardial oxygen demad
allows for more time for ventricles to fill
allows more time for oxygen demand to get to tissues
decrease preoad and afterload
decre
Risk associated with Beta blockers!
Nursing interventions and patient education for beta blockers!
ACE inhibitors/ARBs MOA
These suppress the RAS
decrease arterial resistance and arterial dilation as well as preventing sodium and water retention
Risks associated with ACEI/ARBs
adverse effects are hypotension, hyperkalemia (esp in pt with renal dysfunction), and angioedema
Nursing interventions and patient education for ACEI/ARBs
decrease potassium intake
spinach
avocado
potatoes
bananas
lentils
tomatoes
beats
broccoli
Dosing and method of administration of Adenosine
A stopcock is used with two syringes, one with adenosine and one with NS flush
Dosing starts at 6 mg IV push followed by 20mL NS
If it does not work the next dose is 12 mg IV push followed by 20mL NS
The max dose is 30mg
Emergency equipment required for adenosine use
a code cart and a physician is also necessary to have present when administering adenosine
Atropine dosing and max dose
Start with 1mg
Can try again every 5 minutes
maximum dose of 3mg
What is atropine used for?
Sinus bradycardia when the underlying cause cannot be determined
Amiodarone therapeutic effect and MOA
potassium channel-blocking effect results in increased action potential duration and a prolonged effective refractory period in cardiac myocytes
Myocyte excitability is reduced, thus hindering the continuation of tachyarrhythmias by preventing reentry mechanisms and ectopic foci
the drug's electrophysiological effects encompass a decrease in the automaticity of the sinoatrial (SA) node, a reduction in AV node conduction velocity, and the inhibition of ectopic pacemaker automaticity
Nursing care for amiodarone
continually monitor ECG rhythm during infusion
bradycardia and AV block can occur
the drug can cause serious toxicities (Lung damage and visual impairment) so it is only approved for life threatening arrhythmias
corneal pigmentation occurs in most patients, but generally does not interfere with vision
How does cocaine affect the heart?
Increases HR, BP, and myocardial contractibility
all of which cause increased myocardial oxygen demands
also causes reduced myocardial oxygen supply through coronary vasoconstriction
Increases risk for dysrhythmias
Cardioversion, when and why is it used
Synchronized countershock that may be performed with new-onset AFib
can be scheduled electively for stable AF that is resistant to medical therapy
must take anticoagulants for 3 weeks beforehand
it stops the reentry circuit and allow the sinus node to regain control of the heart
sometimes used for stable Vtach
Safety measures for cardioversion
Don’t eat for 6 hours prior to procedure
Take medication to prevent blood clots for at least three weeks prior to procedure if scheduling it electively
If the cardioversion is being used to treat A-Fib and the onset of A-fib is uncertain a transesophageal echocardiogram can be preformed to assess for clot formation in the left atrium
Defibrillation, when and why is it used
Asynchronous countershock, depolarizes a critical mass of myocardium simultaneously to stop the re-entry circuit, allowing the sinus node to regain control of the heart
pulseless V tach, Vfib
Safety measures when defibrillation is used
Do not touch patient when they are receiving the shock
Do not use alcohol to wipe the patient’s chest before the shock
loudly and clearly command all personnel to clear contact with the patient and the bed and check to see they are clear before the shock is delivered
Deliver shock and resume CPR for 2 minutes
Then reassess the rhythm and charge defibrillator again if indicated
Symptoms of VFib
faint
immediate loss of consciousness
pulseless
apneic
no BP
heart sounds are absent
within minutes
pupils become fixed and dilated
skin becomes cold and mottled
Treatment for VFib
defibrillate
CPR until AED is available
drug therapy
Indications for pacemakers
conduction disorders that are not temporary
complete heart block
hypertrophic cardiomyopathy
symptomatic sinus bradycardia
symptomatic 2nd degree heart block
sustained Vtach
systolic HF
Types of pacemakers
Transcutaneous or External-temporary pacing that is accomplished through the application of two large external electrodes
Transvenous- pacemaker is placed in a pocket between the layers of muscle and the pacemaker leads are placed in the heart, temporary
Implanted- maybe not temporary?
Modes of pacemaker
Synchronous- demand
Asynchronous- fixed rate
Single chamber- One lead attaches to the upper or lower heart chamber
Biventricular- cardiac resynchronization therapy (CRT) device, has three leads connected to the right atrium and both ventricles. We use the biventricular pacemaker to treat people with arrhythmias caused by advanced heart failure
Dual chamber- Uses two leads, one for the upper and one for the lower chamber
What is seen on an ECG of a patient with a pacemaker? What if it’s not there?
pacemaker spike before complex
it shows output failure
must assess your patient
Post pacemaker insertion patient education
report any fever, redness, swelling, or drainage
avoid tight clothing or belts
you can take baths and showers
no sudden jerky movement for 8 weeks to allow the pacemaker to settle in place
if the surgical incision is near the shoulder, do not lift the arm over the head or lift more than 10lbs for the next 4 weeks
3rd degree heart block
impulses do not travel from atria to ventricles
AV dissociation: Ps walk out independently of QRS complexes
medical emergency
Treatment for 3rd degree heart block
Pacemaker
2nd degree heart block treatment
Find cause first
medication
if this then discontinue med
intrinsic factor
pacemaker
Mobitz Type 1/Wenckebach
PR interval becomes longer then drops a QRS
will most likely need a pacemaker
impulses from atria occasionally are blocked in AV node
Mobitz type II
PR interval remains constant then drops a QRS
will most likely need a pacemaker
impulses from atria often are often blocked in AV node
1st degree heart block
PR interval >0.20 seconds
all sinus impulses reach the ventricle
AV blocks
an interruption or delay of electrical conduction from the atria to the ventricles due to conduction system abnormalities in the AV node or the His-Purkinje system
Stable vs unstable tachycardias
Unstable tachycardia: when cardiac output is reduced to th epoint of causing serious symptoms such as: chest pain, dyspnea, weakness, syncope
Ex: torsades, ventricular tachycardia, SVT, A-Fib,
Stable tachycardia: HR within 100-149 without serious signs and symptoms; can turn into unstable tachycardia
Treatment of tachycardias!
What increases the risk of AFib?
Atrial fibrosis and loss of muscle mass
hypertension
heart failure
CAD
genetic mutations
Complications of AFib
Stroke due to the pooling of blood that occurs
Heart failure due to decreased CO
Assessment for stroke
Face
Arms
Speech
Time
Why are pts with AFib prescribed anticoagulants?
The loss of coordinated atrial contractions can lead to pooling of blood
this results in clotting
they are at high risk for PE
thrombi may form within the RA and move through the RV to the lungs
they are at high risk for embolic stroke
Patient education for AFib
clear instructions and education about medications
side effects that need to be reported
should not be stopped abruptly
teach pt and family how to take HR and BP
report signs of a change in HR
significant decrease in pulse rate
rate >100bpm
increased rhythm irregularity
SVT, cause, and symptoms
form of tachycardia that involves the rapid stimulation of atrial tissues at a rate of 100-280 bpm
Often occurs in healthy young people, especially women
P wave may not be visible, QRS is normal
Cause- re-entry mechanism in which one impulse circulates repeatedly throughout the atrial pathway, restimulating the atrial tissue at a rapid rate
Signs and symptoms
Sustained- palpitations, chest pain, weakness, fatigue, sob, nervousness, anxiety, hypotension, and syncope
If rate dose not sustain adequate BP- angina, HF, cardiogenic shock
Nonsustained or slower- asymptomatic
Treatment of SVT
Only needed if it is sustained
Adenosine, rapid IV push, never given without a physician being present, need all emergency equipment, basically a reset of the heart
Preferred treatment is radiofrequency catheter ablation
Desired outcomes: decrease ventricular response, convert dysrhythmias to a sinus rhythm and treat the cause
Vagal maneuvers- vagal stimulation of the cardiac conduction system, specifically the SA and AV node, include carotid massage and Valsalva maneuvers
Drugs: Adenosine, beta blockers, calcium channel blockers
Process for examining a rhythm strip
Determine the HR
Determine the heart rhythm
Analyze the P waves
Measure the PR interval
Measure the QRS duration
Examine the ST segment
Assess the T wave
Measure the QT interval
Cardiac action and related waveforms on ECG strip
P- atrial depolarization
PR segment- when electrical impulse is traveling through AV node, where it is delayed
QRS- ventricular depolarization
ST segment- early ventricular repolarization
T- ventricular repolarization
QT interval- total time required for ventricular depolarization and repolarization
What are shockable rhythms?
Ventricular tachycardia
Ventricular fibrillation
Torsades de Pointes