S3E2 Flashcards
Cardiac risk factors
Males
Age related
African American
Alcohol use/abuse
Obesity
Glucose intolerance
Diabetes
Inactivity
⬆️ lipids
Stress
⬆️cholesterol
Hypertension s/s
HA
Dizziness
Fatigues
Palpitations
SOB
CAD risk factors
Former smoker
Obesity
Hx of htn
Inactivity
Hx of Diabetes
Stress
⬆️ lipids
Age
African / Native American
Fm hx
Disease that consist of plaque and fat buildup or blockage and may damage major blood vessels
Coronary artery disease
P wave
atrium depolarization
.06-0.12
PR interval
p wave to pqrs complex
0.12-0.2
QRS interval
time ventricle depolarization
<.12
ST
isometric; time between ventricular Contraction and repolarization; diastole
T-wave
relax; depolarization ventricular
QT interval
time for entire depolar/repolar of ventricles
Normal sinus rhythm
60-100, all normal
Sinus Bradycardia
<60, all else normal
Tx for Sinus Bradycardia
stop, hold reduce meds
Rapid Iv push atropine
Atropine no work? Transcutaneous pacing
Dopamine/epi infusion
Permanent pacemaker
Sinus tachycardia
101-180, all other normal
Tx for Sinus tachycardia
underlying cause
Pain? Pain relief
Vagal maneuver
IV b-Blockers
Calcium channel blockers IV/PO diltiazem
Unstable? Synchronized cardioversion
MI clinical manifestations
Pain → “heavy,” “persistent,” “crushing
Located: substernal, epigastric area radiate to the neck, lower jaw, arms/back
With activity or rest, asleep or awake
Last greater than 10 minutes
More severe than chronic angina pain
Unstable Angina Clinical manifestations
New?
Occurs at rest or activity
longer duration
effortless
> 10 min
SOB
nausea
dizziness
palpitations
heaviness
tightness
radiating pain jaw to neck to arm
isn’t relieve with typical measures
Women: upset stomach/upper back pain
Unstable angina Risk factors
Former smoker
Obesity
Hx of htn
Inactivity
Hx of Diabetes
Stress
⬆️ lipids
Age
African / Native American
Fm hx
Unstable angina Nursing managements
Onset of pain
Location
Duration
Characteristics
Aggravating factors
relief?
radiation?
Treatment go to ACS
ACS Risk factors
Former smoker
Obesity
Hx of htn
Inactivity
Hx of Diabetes
Stress
⬆️ lipids
Age
African / Native American
Fm hx
ACS Clinical manifestations
Think unstable angina, STEMI, & NSTEMI
New? Occurs at rest or activity, longer duration, effortless, > 10 min, SOB, nausea, dizziness, palpitations, heaviness, tightness, radiating pain jaw to neck to arm, isn’t relieve with typical measures.
Women: upset stomach/upper back pain
Assessments for ACS
s/s
Pt hx of pain
Risk factors
Health hx
ACS labs, exams, tests
EKG
Troponins (T=<0.1, I=<0.03)
Cardiac cath
CKMB
Lipids
CRP (c-reactive protein=marker for inflammation)
BNP (brain
Chemistries
coags
CBC
CXR
Echo (heart US)
Tee ( Tranesogial echo)
Stress test
ACS goal and nurse management’s
Goals: Pain relief & increased cardiac output! Pain relief, Quick & appropriate treatment, Preserve the heart muscle
Continuous telemetry
VS w/SpO2 → frequently, q1hr
Serial 12-lead EKGs
Serial cardiac biomarkers → troponins
Bed rest, limit activity for 12-24 hrs
Oxygen
UA/NSTEMI → heparin infusion,asa, clopidogrel
○ Cardiac cath
STEMI → reperfusion therapy (PCI or thrombolytics)
Pt. teaching → risk reduction, expectations, medications, labs, follow up appt, activity
Anxiety
Monitor all lab work
ACS surgical interventions
Cardiac catheterization
● PCI → balloon angioplasty
○ Stent placement
○ Nursing management p. 839
● Coronary artery bypass graft (CABG)
○ Can be done via sternotomy or
minimally invasive
Post cath lab nurse management
Monitor insertion site
Monitor bleeding or hematoma
Check all pulse involved in the artery line
Bed rest for the appropriate time length
VS
Dysrhythmia
Kidney levels
Head to toe asses
Cardiac
Plum
Neuro
Extremity perfusion
Pain
Tele monitoring
NSTEMI nursing management
-aspirin
-heparin infusion prior
-May undergo cardiac catheterization within 12-72 hours → Gold standard to identify and localize the arterial disease
-🚫 Thrombolytic therapy
STEMI cath lab key points
-90 minutes to PCI = percutaneous coronary intervention
-Emergent PCI
-Open the blocked artery within 90min
-We are “intervening” in order to restore perfusion
○ Balloon angioplasty
○ Intracoronary stents
-Thrombolytic therapy
○ Done when there is not access to a
cardiac cath lab
-Some sort of treatment is needed otherwise the STEMI will continue to evolve
Sudden Cardiac Death Risk factors
● CAD w/prior MI
● LV dysfunction
● Structural heart disease
○ LV hypertrophy
○ Myocarditis
○ Hypertrophic cardiomyopathy
● Changes in conduction system
○ Prolonged QT syndrome
○ Wolff-Parkinson-White syndrome
Sudden Cardiac Death Clinical manifestations
-Angina
-palpitation
-dizzy
● V-fib
● May have symptoms within 1 hour of SCD
Sudden Cardiac Death Nursing management
Determine underlying cause → Acute
MI?, Undiagnosed CAD?
○ Cardiac cath
○ PCI
○ CABG
● Assess for dysrhythmias
● Holter monitor
● ICD → to prevent recurrence
● Medications such as amiodarone
● Education → disease, anxiety,
depression, emotional support
Inflammatory cardiac disease Pathophysiology
Inflammation of heart muscles and lining of the heart area
-Infective Endocarditis (IE)
-Acute Pericarditis
-Myocarditis
-Rheumatic Fever & Rheumatic heart
disease
Infective endocarditis Pathophysiology
-Disease of the endocardium& heart valves
-When blood flow allows organisms to contact& infect previously damaged heart valves or heart surfaces
Infective endocarditis clinical manifestations
**new or worsening systolic murmur
**Vascular signs
□ Black lines in nail beds
□ Petechiae
□ Osler’s nodes (panful, tender,
red pea-size lesions on the
fingertips or toes)
Non specific and involve multiple systems
Fever
Chills
Weakness
Fatigue
Anorexia
Infective endocarditis nursing assessment
□ CO
□ s/s infection
□ Fever
□ joint pain
□ Fatigue
□ head to toe assessment
□ Skin
□ Pain
□ ADLs
Infective endocarditis patient education
***May need home care for IV abx&prior to dental procedures
□ Help reduce infection &
recurrence of IE
□ Rest periods
□ Good oral hygiene and regular
dental appointments
□ Continuing antibiotics per
orders
□ s/s of infection
□ When to contact HCP
□ Risk factors of IE
□ S/s of stroke
□ Pulmonary edema & HF
IE: take prior to dental procedures
Antibiotics
IE: new or worsening _______
Murmur
IE: painful lesions/nodes on fingertips and toes
Oslers
IE: disease of the inner most layer of the heart
IE
IE: can break off and cause emboli
Vegetation
IE: may need this if infection here
Valve replacement
IE: occurs from vessel damage (vasculitis)
Black lines
IE: a risk factor for this disease
IV drug abuse
Rheumatic fever Pathophysiology
Inflammatory disease caused by strep A that can involve all layers of the heart
□ Heart
□ Skin (subq nodules)
□ Joints (muscle and joint aches)
□ CNS
Rheumatic heart disease Pathophysiology
Chronic scarring and deformity of heart valves resulting from abnormal immune response to streptococcus (RF)
-mitral and aortic valves are most affected
-Affects children and young adults
vegetation
deposits of fibrin and blood cells in areas of erosion → thickening of valve leaflets → calcification → stenosis! → cannot close properly → regurgitation
Rheumatic fever & heart disease clinical manifestations
Aschoff’s bodies
Rheumatic fever & heart disease nurse management
-head to toe assessment
□ skin for rashes and nodules
-monitor for fatigue, impaired cardiac function, pain and infection
-optimal positioning for relief of painful joints
-provide adequate rest
-early detection and immediate treatment for group A strep can prevent RF
-educate on full course of medication/treatment and disease progression/management
-Reach out if experiencing :
® Excessive fatigue
® Dizziness
® Palpitations
® Unexplained wt gain
® Exertional dyspnea
may need prophylactic abx upon discharge
□ minimum 5 years
□ some need lifelong
RF/RHD: lead to scar tissue in myocardium
Aschoffs bodies
RF/RHD: can be caused by this
Strep A
RF/RHD: this can lead to valve regurgitation
Vegetations
RF/RHD: aschoffs bodies can lead to this…rheumatic ________
Pericarditis
RF/RHD: disease: chronic scarring & deformity of heart valves
RHD
RF/RHD: may need this lifelong
Antibiotics
RF/RHD: inflammatory disease that can involve all layers of the heart
Rheumatic fever
RF/RHD: teach patient that this can develope
Valve disease
Pericarditis Pathophysiology
Inflammation of the pericardial sac, often with fluid accumulation
-Common causes
Unknown viral
Bacterial (pneumococci, staph, strep,
TB, septicemia)
Fungal
Viral-hepatitis, mumps, adenovirus,
HIV
Acute MI
Cancers
Medication reactions
RF
Pericarditis Clinical manifestations
Pericardial friction rub
-Scratching, grating, high
pitched sound as friction between
roughened pericardial and epicardial
surfaces
-Heard lower left sternal border
with pt leaning forward
-Progressive, severe, sharp chest pain
-Worse with deep inspiration & when lying flat
-Referred pain to trapezius muscle
-Dyspnea
Pericarditis complications
Cardiac tamponade
Pericardial effusion
Pericarditis complications s/s
□ Chest pain
□ Confusion, anxious, restless
□ ⬇️ CO
□ Muffled heart sounds
□ Narrowed pulse pressure
□ Tachycardia
□ ⬆️RR
Pericarditis nurse management
○ Manage pain and anxiety
○ Assess pain and distinguish from
angina
○ Bedrest with HOB up to 45 degrees
○ Anti inflammatory medications
○ Monitor for cardiac tamponade and
⬇️ CO
○ Lean forward to relieve pain
Pericarditis: an abnormal drop in systolic blood pressure during inspiration
Pulsus paradoxus
Pericarditis: inflammation here leads to certain sound
Pericardial sac
Pericarditis: can be caused by this other cardiac inflammatory process
Rheumatic fever
Pericarditis: may hear this sound on cardiac assessment
Muffled
Pericarditis: assess for this life threatening condition
Cardiac tamponade
Pericarditis: lean the patient forward to hear this
Friction rub
Pericarditis: lean the patient forward to hear this
Friction rub
Pericarditis: the type of pain that can be felt in the trapezius
Referred
Myocarditis Pathophysiology
-Focal or diffuse inflammation of the myocardium
-caused by:
○ virus
○ bacteria
○ fungi
○ radiation therapy
Early Myocarditis s/s
7-10 days after viral infection
Fever
Fatigue
Malaise
Myalgias
N/V
*Pharyngitis
Dyspnea
lymphadenopathy
Late Myocarditis s/s
development of HF
S3
Crackles
JVD
Syncope
peripheral edema
angina
Myocarditis Nursing management
○ Improve CO
○ manage s/s
○ ⬇️ cardiac workload
○ semi-fowlers
○ spacing rest and active periods
○ quiet environment
○ medication administration and
evaluation of effect
○ monitor patient level of anxiety and
provide information about the plan
○ if on immunosuppressive meds →
monitor for infection and other
complications pericarditis often
accompanies myocarditis
Myocarditis: immunosuppressive meds can lead to this
Infection
Myocarditis: nursing management to _____ the cardiac workload
Decrease
Myocarditis: decrease cardiac workload with ____&_____
Rest & activity
Myocarditis: early s/s of this disease process
Pharyngitis
Myocarditis: can accompany myocarditis
Pericarditis
Myocarditis: this disease could be caused by
Viral infection
Myocarditis: disease that causes inflammation to heart muscle
Myocarditis
Myocarditis: this process causes inflammation here
Myocardium
Valvular disorders: stenosis
constriction or narrowing
Valvular disorders: regurgitation
incompetent or insufficient closure of a valve and backward blood flow occurs
Valvular disorders: prolapse
valvular abnormality where part of the valve (leaflets) buckle back in
Valvular disorders Nursing management
○ plan for normal heart function
○ improving activity tolerance
○ understanding of disease
○ ongoing cardiac assessment
○ prevent exacerbations of HF,
pulmonary edema, thromboembolism,
recurrent RF and IE
○ monitor dysrhythmias and treat
appropriately
○ maybe undergo balloon valvuloplasty,
valve repair
○ Maintain CO and function
○ Assist with fatigue
○ Maintain Fluid balance
○ Educate: disease management
Dilated Cardiomyopathy Pathophysiology
-Primary: idiopathic involving heart muscle
-most common type
-causes HF in 20%-45% of cases
-appears with diffuse inflammation and rapid degeneration of heart fibers → ventricular dilation, impaired systolic function, atrial enlargement and blood stasis in L ventricle
Dilated Cardiomyopathy Clinical manifestations
-acute after an infection or slowly
over time
-decreased exercise capacity
-Fatigue
-dyspnea at rest
-paroxysmal nocturnal dyspnea
-orthopnea: with disease progression
-dry cough
-Palpitations
-Dysrhythmias
§ heart murmur
Dilated Cardiomyopathy nursing goals
enhance heart contractility
decrease preload and afterload
controlling Heart Failure
Dilated cardiomyopathy medications
-nitrates and diuretics-decrease
preload
-ace-inhibitors-reduce afterload
-beta-blockers-control
neurohormonal stimulation that
occurs with heart failure
-antidysrhythmics to treat
dysrhythmias
-anticoagulation therapy-reduce
embolic events
Dilated cardiomyopathy nursing management
- improve CO
-assess
=worsening or improving symptoms
=s/s of blood clot
-teach to avoid underlying causes
=EtOH
-symptom management
-possible heart transplant
-cardiac resynchronization therapy and ICD
-these patients can be very ill
-poor prognosis
Restrictive cardiomyopathy Pathophysiology
-least common type of cardiomyopathy
-a disease of the myocardium that impairs diastolic filling and stretch
-ventricles are resistant to filling and require high diastolic filling pressure to maintain CO
Restrictive cardiomyopathy Clinical manifestations
fatigue
exercise intolerance
dyspnea
may also see
angina
orthopnea
syncope
palpitations
signs of HF
dyspnea
peripheral edema
weight gain
ascites
JVD
Restrictive cardiomyopathy Nursing management
- Treatment aims to improve diastolic filling and treating underlying disease process
- similar treatments as HF and dysrhythmias
- teach to avoid situations that impair ventricular filling and increase systemic vascular resistance such as strenuous activity and dehydration
- Patient specific teaching, symptom management
- can be at risk for IE from any procedure that may cause bacteremia
□ will need prophylactic abx
Hypertrophic cardiomyopathy Pathophysiology
Genetic disorder
young adults; active, athletic persons
M > W
early identification is key
ventricular hypertrophy is associated with thickened septum and ventricular wall → poor filling, obstruction to outflow → decreasing CO
4-main characteristics of Hypertrophic cardiomyopathy
massive ventricular hypertrophy
rapid, forceful contraction of the L ventricle
impaired relaxation (diastole)
obstruction to aortic outflow
Hypertrophic cardiomyopathy Clinical manifestations
- can be asymptomatic
- DOE, dyspnea
- fatigue
- angina
- syncope
Hypertrophic cardiomyopathy Dx
exaggerated and displaced apical pulse
S4 and systolic murmur
EKG abnormalities
Echo with wall motion abnormalities
Hypertrophic cardiomyopathy nursing management
- improve ventricular filling by reducing ventricular contractility and relieve LV outflow obstruction
- beta blockers, calcium channel blockers, antidysrhythmics
- may need an ICD if at risk for SCD
- AV pacing
- surgical intervention for those that are unresponsive to medication therapy
- relieving symptoms, observing for and preventing complications, emotional support
- teach to avoid strenuous exercise and dehydration
- rest and elevation of feet can improve venous return
- Low sodium diet and fluids
Cardiogenic shock Pathophysiology
● Occurs when either systolic or diastolic dysfunction of the heart’s pumping action results in reduced CO, SV and BP → compromising myocardial perfusion and depressing myocardial function and decrease CO and perfusion
● multiple causes
● leading cause of death from an acute MI
● systolic dysfunction primarily affects the LV
● when systolic dysfunction effects the R side of the heart, blood flow through the pulmonary circulation is reduced
● ⬇️ filling of the heart → ⬇️ SV
Cardiogenic shock Clinical manifestations
tachycardia
hypotension
narrow pulse pressure
⬆️ SVR → ⬆️ myocardial O2 consumption
Cardiogenic shock goals/Nursing management
- Keep them alive
- ABCs
- Restore cardiac function
- Balance oxygen supply/demand, Trach?
- Cardiac cath
□ Angioplasty
□ Stenting
□ Valve replacement - Support heart to optimize perfusion/ stroke volume
-⬇️workload of heart with medications & mechanical interventions:
□ VAD
-⬇️ systemic vascular resistance and left ventricular work load
Cardiomyopathy: causes high diastolic filling pressure
Restrictive
Cardiomyopathy: changes structure and function of the heart
Cardiomyopathy
Cardiomyopathy: a type of murmur with this disease
Systolic
Cardiomyopathy: this form of the disease leads to impaired diastole
Hypertrophic
Cardiomyopathy: this happens to the L ventricle
Dilation
Cardiomyopathy: we need to control this chronic disease that develops
Heart failure
Cardiomyopathy: teach to avoid ______ activity
Strenuous
Cardiomyopathy: common clinical manifestation of this form of disease
Dyspnea
Cardiomyopathy: this can occur due to ⬇️ in CO, SV, AND BP
Shock!
A-fib Clinical characteristics
- PR interval is not measurable, “no discernable P wave”
- atrial rate can be 350-600 beats/min
- ventricular rates vary
- QRS is normal shape and duration
- can co-exist with A-flutter
A-fib goal
⬇️ ventricular response**to <100 bpm
prevent stroke, convert to NSR if possible
A-fib medications that might be used
■ calcium channel blockers
■ beta blockers
■ amiodarone
■ digoxin
A-fib nurse management
● electrical conversion
● anticoagulation therapy to prevent stroke
○ warfarin
■ frequent INR monitoring
■ pt education
○ other anticoagulants
■ dabigatran
■ apixaban
■ rivaroxab
Symptomatic A-fib not responsive to
medications or electrical conversion → ____________
ablation
○ destruction of the AV node
○ insertion of a permanent ventricular pacemaker
A flutter Clinical characteristics
Atrial rate 200-350 beats/min
• Ventricular rate varies, typically 2:1
○ 2 atria to 1 ventricular beat
○ typically around 150 beats/min
• PR variable and not measurable
• QRS normal
A flutter goal
slow ventricular response and restore normal sinus rhythm
A flutter meds
Calcium channel blockers
beta blockers
antidysrhythmics
cardioversion in emergent situation
ablation
SVT clinical characteristics
*P wave may have abnormal shape or be hidden in preceding T wave
○ HR 151-220
○ regular or slightly irregular rhythm
○ PR interval may be shortened or normal
○ QRS complex is usually normal
SVT meds
-IV beta blockers
-IV calcium channel blockers
-IV adenosine if unstable or has not responded to treatment
SVT nurse management
• Vagal stimulation
○ valsalva
○ coughing
• Synchronized cardioversion
○ used if patient becomes
hemodynamically unstable,
medication before synchronized
shock
V-tach clinical characteristics
*QRS complex is wide and distorted, greater than 0.12 seconds
*P wave is typically “buried” in the QRS
complex
*T wave is in the opposite direction of the QRS complex
*PR interval is not measurable
Ventricular rate is about 150-250 bpm
rhythm may appear regular or irregular
V-tach nurse management for Stable patient with a pulse and decent left ventricular function
Identify the precipitating/underlying causes
○ IV medications
■ procainamide
■ lidocaine
■ amiodarone
○ electrolyte replacement (Mag)
○ stop meds that increase QT interval
○ cardioversion if medication therapy is ineffective
V-tach nurse management for pulseless patient
LETHAL
● Treatm the same as V-fib
● No pulse = CPR with rapid defibrillation
● This may be followed by
○ vasopressors (epi)
○ antidysrhythmics
V-fib clinical characteristics
*the ventricle is “quivering” with no effective contraction
irregular waveforms, varying shapes and
amplitude
V-fib nurse management
LETHAL
● Immediate initiation of CPR and defibrillation
● may use medication as well
○ epinephrine
○ amiodaron
Asystole clinical characteristics
*total absence of ventricular electrical activity
● no ventricular contraction
● patient will be unresponsive, pulseless and
apenic
Asystole nurse management
LETHAL…immediate treatment…CPR
■ ABCs!
🚫cannot defib
○ medications you may use
■ epinephrine
PVC Clinical characteristics
HR varies according to intrinsic rate and
number of PVCs
● Rhythm is irregular
● P is rarely visible
○ can be lost in the QRS complex
● PR interval not measurable
● QRS is wide and distorted, >0.12 sec
● T wave is generally large and opposite in
direction to the major direction of the QRS
complex
PVC nurse management
Goal = relates to the cause of the PVCs (treating the underlying cause)
○ O2 for hypoxia
○ electrolyte replacement
○ hemodynamic stability
○ medications may be used
■ beta blockers
■ lidocaine
■ amiodaron
Antidysrhythmic med nurse management
thorough assessments
baseline EKG
VS
s/s of decreased CO
baseline HR and rhythm
lung and heart sounds
review lab work
ongoing telemetry
frequent assessments
medication education
ABCs!
Common dysthymic meds
Diltiazam
Digoxin
Beta blockers
Amioderone
Acls meds
Epinephrine
AdioderonE
Bicarbonate
Atropine
Lidocaine
Adenosine
D-fib is tx for…..?
V-fib
Pulseless V-tach
Synchronized cardio version can treat…..?
V-tach with a pulse
SVT
A-flutter with rapid ventricular rate
