Cardiovascular Complications Flashcards
Ineffective Endocarditis (IE)
Infection of heart valves or the endocardial surface, typically both become infected
Pathphys IE
infection leads to fibrin, leukocytes, platelets and microbes on the surface
then causes local heart tissue damage
can also cause embolisms to break off and affect other areas of the body
Etiology of IE
Community or healthcare
intracardiac and/or IV devices
Staphyloccus pneumonia, aureus or enteroccoci
gram +ve, fungi or virus
blood flow turbulence within the heart allows the organism to infect previously damaged valves
Risk Factors of IE
previous history prosthetic valves rheumatic heart disease IV drug use scarlet fever long hospital stays recent dental, urological, surgical or gynecological procedures poor dental health
CM of IE
fever murmurs in the mitral mid to late systolic weakness headaches night sweats weight loss fatigue coughing arialgias
Sub Acute CM of IE
joint aches and pains for muscle and back
finger clubbing
splinter hemorrhage
blood in urine
Petechiae - pinpoint round red spots from bleeding in lips, buccal mucosa, palate ankle, feet and antecubital and popiteal areas
Osler’s Nodes/Janeway’s Lesions - tender purple pink nodules with pale center
Roth’s Spots - small blood shot eyes
Diagnostics of IE
blood culture of two sets taken more than 60 mins apart or three sets taken less than 60 mins apart to be cultured for three weeks to test for organisms CBC and electrolyte panel ESR and CRP Uranalysis ECHO, ECG and CXR
Tx of IE
Prophylatic therapy with antibiotics
antibiotics IV 4-6 weeks with regular bloodwork
anti-inflammatories
antifever
light bed rest or complete bed rest if severe
Complications of IE
right sided can lead to embolisms in the lungs, limbs and brain
left sided can lead to embolisms in the kidneys, liver, spleen, limbs and brain
Pericarditis
inflammation of the pericardial sac/pericardium that’s typically a symptoms or complication of the disease, not a disease itself
Pericardium
inner serous layer of heart wall tissues that is closest to the epicardium
Pathophys of Pericarditis
inflammation of neutrophils, monocytes, and macrophages for to the hyperemic pericardium with an increased blood flow and fibrin deposits on the visceral pericardium
Etiology of Pericarditis
80-85% virus
within 48-72h post MI
Dressler’s syndrome
4-6 weeks post MI
CM of Pericarditis
sharp and pleuritic chest pain that gets worse with breathing in or lying down
radiate to traps and arms
pericardial friction rub that can be heard with stethoscope that can cause further damage
pulses paradoxes with inhalation
SOB
hyperventilation
Pericardium Friction Rub
complication of pericarditis that can be heard best in the left sternal boarder in time with the heart beat with scratching and grating noises
degenerate heart walls
Pericardial Effusion
complication of pericarditis
excess fluid in the pericardium related to inflammation response
Cardiac Tamponade
complication of pericarditis that is an increase in fluids in pericardial sac that can increase pressure in on the heart and vessels
Diagnostics for Pericarditis
ECG with widened ST segment and elevation CXR ECHO Pericardiocentesis pericardial biposy identify the cause
Tx of Pericarditis
antibiotics to treat the bacteria treat the cause Colline and asteroids as a last resort pain meds pericardiocentesis to remove the excess fluids elevate head of the bed anti-inflammatories monitor for complications
Myocarditis
focal or diffuse inflammation of the myocardium caused by virus, bacteria, fungi, radiation and/or pharmacological factors
causes cardiac dysfunction and has been linked to dilated cardiomyopathy
CM Early for Myocarditis
fever myalgia SOB vomiting and nausea lymphadenopathy
Post-Infection CM of Myocarditis
appears within 7-10 days of onset with extra pleuretic chest pain and pericardial friction rub
Late CM of Myocarditis
CHF with S3 sound syncope episodes peripheral edema jugular vein distension angina
Diagnostic for Myocarditis
ECG and ECHO
endomyocardial biopsy for blood culture
Tx of Myocarditis
inotropic and or vasopressor therapy
mechanical circulation support for increasing cardiac output
BB
ACE inhibitors
diuretics
immunosuppressants potentially, depending on the cause and severity of inflammatory response
bed rest or restricted activity with maintenance of activity tolerance
P Wave
atrial depolarization/contraction with a typical +ve deflection above the isometric line with an average of 0.06-0.12 sec
QRS Complex
beginning to end of ventricle depolarization that is slower, 0.6-0.12sec
shorter complexes means slower depolarization
longer time means cardiac dysfunction
T Wave
ventricle repolarization
PR Segment
flat line between the P and Q sections that sets the isometric line and represents conduction through the AV node
represents times taken from impulse to spread through the atria, AV node, bundle of His or bundle branches
QT Interval
full period of time for heart to contract and relax ventricle with inverse relationship with HR
typically 0.34 to 0.43sec
disturbances are from drugs, electrolyte imbalances, and changes in HR
ST Segment
measured from S to T wave that represents the time in-between the ventricle depolarization and repolarization that should be flat
disturbances are typically ischemia, MI or stroke
T Wave
time for ventricle repolarization, upright
S1 Sound
beginning of R wave and systole, typically together but the valves closing can rarely be heard separately
S2 Sound
closing of semilunar valves, splitting is normal when you can hear arteriole or peripheral sphincters close to create the sound
Atuomacitity
ability to initiate an impulse spontaneously and continuously
Conductivity
Ability to transmit an impulse along a membrane in an orderly fashion
Excitability
ability to be electrically stimulated
ECG
graphic tracing of an electrical impulse produced by the heart through the movements of charged ions for K+ and low NaCl
Tele Monitoring
46 lead over prolonged period of time to diagnosed and monitor arrhythmias
Artifact
disortion of the baseline and waveforms on the ECG, can be form the machine dysfunction or the actual heart problems
Ventricular Contraction
count R wave for 6 sec x10 and compare for seeing if the rhythm is regular
typical is 60-100
Atrial Rate
counting P waves within a 6 sec period and x10
Etiology of Arrhythmias
electrolyte imbalance drugs MI HF Myocardial cell degeneration conduction defects hypertrophy of cardiac muscle acid-base imbalance alcohol caffeine emotional crisis connective tissue disorders electrical shock hypoxia shock metabolic conditions near drowning physical deficits and defects
CM of Arrhythmias
Chest, shoulder, neck and or arm pain cold clammy skin decreased BP tachy or brady low O2 sat syncope SOB extreme restlessness pallor weakness fatigue
Normal Atrioventricular Impulse Transmission
conduction is delayed in ventricle which is prolonged R wave
Pre-Excititation
the accessory pathway between atria and ventricles where it bypasses the AV node
ST Segment Elevation
commonly seen in pt with MI or ischemia
ST Segment Depression
pt with hypokalemia, cardiac ischemia, or and digitalis toxicity
Sinus Arrhythmias
rhythm varies with breathing that is typically found in children that drops with exhalation and increases with inhalation
Premature Beat
isolated and too early beat that can occur regularly or every 3-4 beats
Pulse Deficit
weak contraction of the ventricles, occurs at atrial fibrillation, premature beats and HF
Sinus Bradycardia
low HR but regular ECG with prolonged beats
can occur with carotid massage, hypothermia, increased ICP, increased vagal tone and parasympathomimetic drug
Sinus Tachycardia
normal sinus and ECG showing, just really fast
can come from increased vagal inhibition, physical or mental stress, or sympathetic stimulation
Premature Atrial Contraction
contraction form somewhere other than the atria or sinus node that travels across a broad pathway
ECG downward deflection, hidden in preceding T wave, and shorter PR interval
indicator of more serious arrhythmia
Paraoxysmal Supraventricular Tachy
dysrhythmia from ectopic focus above the bifurcation of the Bundle of His from re-entrant phenomenon
Atrial Flutter
SEE SAW between QRS complex from an ectopic focus that typically cannot originate from a healthy heart
250-350 atrial rate with a 2:1 conduction regularly with a ventricle rate of 150
PR interval is funky and AV delays signals
Atrial Fibrilation
total disorganization of atrial electricity from multiple ectopic foci which indicates a total loss of effective atrial conduction
atrial rate is fucked lol
ventricle rate is 50-180
erratic P waves
If Jackson Pollock had an ECG and someone said be free
Pulselessness Electrical Activity
electrical ECG but not mechanical activity of the ventricles with no pulse
oh no, out pt…. it’s broken
Sudden Cardiac Death
heart really said well fuck me up the ass and call me bob, I’m DONE
Heart Murmurs
blowing swooshing sounds that occurs with turbulent blood flow in the heart or great vessels that can be heard, posture can affect it where leaning over can accentuate it
defined by loudness, location, and how frequent
Grade 1 Murmur
barely audible where it can only be heard in a dead silent room and stethoscope
Grade 2 Murmur
audible in any room but is very faint
Grade 3 Murmur
moderately loud with the stethoscope and easy to hear
Grade 4 Murmur
loud and associated with thrill palpable in the chest wall
Grade 5 Murmur
very loud, heard with the stethoscope having one side off the chest wall that is associated with a thrill
Grade 6 Murmur
this heart is a death metal concert, don’t even need the stethoscope close to the wall of the chest
Innocent Murmur
no valvular or probable cause, that’s typically only a grade 2 no thrill soft sounds mid-systolic, short, crescendo-decrescendo
typically goes away with posture correction
Functional Murmur
due to the increase of blood flow in the heart with multiple presentations
Defibrilation
terminating ventricular and pulseless VT by giving a jumper start t the heart with a DC shock throughout the heart that allows it to depolarize and have CPR to get mechanical flow to instigate the repolarization process
Synchronized Cardioversion
therapy for hemodynamically unstable ventricular and supraventricular tachydysrhythmias, counter shock placed on the R wave while being sedated
Implantable Cardioverter Defrubillator
sustained SCD, spontaneous sustained VT, syncope with includible VT or fibrillation during EPS and a high risk for future life threatening dysrhythmias
lead system SUBQ that shocks the heart back into normal rhythm
Pacemaker
set to change the heart rhythm by placing leads on the myocardium for stimulating regular contractions with an internal power conductor
Radiofrequency Ablation Therapy
low voltage high frequency shock to the heart to stim contractions
The nurse has identified a nursing diagnosis of acute pain related to inflammatory process for a client with acute pericarditis. Which of the following actions is best for the nurse to implement?
- Force fluids to 3 000 mL/day to decrease fever and inflammation.
- Teach about deep, slow respirations to control the pain.
- Remind the client to ask for the opioid pain medication every 4 hours.
- Position the client in Fowler’s position, leaning forward on the overbed table.
- Position the client in Fowler’s position, leaning forward on the overbed table.
Cardiac tamponade is suspected in a client who has acute pericarditis. Which of the following actions should the nurse implement to assess for the presence of pulsus paradoxus?
- Check the electrocardiogram (ECG) for variations in rate in relation to inspiration and expiration.
- Note when Korotkoff sounds are audible during both inspiration and expiration.
- Auscultate for a pericardial friction rub that increases in volume during inspiration.
- Subtract the diastolic blood pressure (DBP) from the systolic blood pressure (SBP)
2.Note when Korotkoff sounds are audible during both inspiration and expiration.
Which of the following techniques should the nurse use to assess the client with pericarditis for the presence of a pericardial friction rub?
- Auscultate with the stethoscope diaphragm at the lower left sternal border.
- Listen for a rumbling, low-pitched, systolic sound over the left anterior chest.
- Feel the precordial area with the palm of the hand to detect vibration with cardiac contraction.
- Ask the client to stop breathing during auscultation to distinguish the sound from a pleural friction rub.
- Auscultate with the stethoscope diaphragm at the lower left sternal border.
The nurse is admitting a client with possible acute pericarditis. Which of the following diagnostic assessments should the nurse plan to teach the client about?
- Electrolyte levels
- Echocardiography
- Daily blood cultures
- Cardiac catheterization
- Echocardiography
The nurse is planning care for a client hospitalized with streptococcal infective endocarditis (IE). Which of the following interventions should the nurse include?
- Monitor laboratories for streptococcal antibodies.
- Arrange for insertion of a long-term IV catheter.
- Encourage the client to get regular aerobic exercise.
- Teach the importance of completing all oral antibiotics.
- Arrange for insertion of a long-term IV catheter.
The nurse identifies the nursing diagnosis of decreased cardiac output related to valvular insufficiency for the client with infective endocarditis (IE). Which of the following findings support this diagnosis?
- Fever, chills, and diaphoresis
- Urine output less than 30 mL/hour
- Petechiae of the buccal mucosa and conjunctiva
- Increase in pulse rate of 15 beats/minute with activity
- Urine output less than 30 mL/hour
The nurse is assessing a client with infective endocarditis (IE). Which of the following findings should the nurse expect to assess?
- A new regurgitant murmur
- A pruritic rash on the trunk
- Involuntary muscle movement
- Substernal chest pain and pressure
- A new regurgitant murmur
The nurse is obtaining a health history from a client with a prosthetic mitral valve who has symptoms of infective endocarditis (IE). Which of the following questions by the nurse is best?
“Have you been to the dentist lately?”
“Do you have a history of a heart attack?”
“Is there a family history of endocarditis?”
“Have you had any recent immunizations?”
“Have you been to the dentist lately?”
