Disorders of cardiac Oxygenation and perfusion: Infective Endocarditis, AAA, Valvular disease, TAVR, Cardiac Arrest Flashcards

1
Q

Infective endocarditis

A
  • Microbial infection on the endothelial surface of the heart
  • Rare, high mortality (14-22% die in hospital, 40% die within one year)
  • Develops mainly in older pts or those with prosthetic heart valves or devices
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2
Q

Staphylococcal endocarditis

A
  • Infection of the valves in the right side of the heart (Tricuspid and pulmonic)
  • More common in IV drug users
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3
Q

Hospital acquired Infective endocarditis

A
  • Occurs mainly in debilitated pts
  • Long term indwelling cath
  • Pts receiving dialysis or prolonged IV antibiotics
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4
Q

Pericardium

A
  • Outermost layer of the heart
  • 2 thin fibrous layers that contain fluid to protect the heart from friction
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5
Q

Myocardium

A
  • Middle muscular layer of the heart
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6
Q

Endocardium

A

Innermost layer of the heart, comes into contact with the blood

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7
Q

Infective endocarditis (IE) Patho

A
  • Injury to the endocardium leads to the formation of a clot, Bacteria such as staph or strep invade the clot
  • Plt, fibrin, microorganisms cluster as vegetations on the endocardium
  • Vegetations may embolize to other vessels in the body
  • As the clot on the endocardium continues to expand the infecting organism is covered by a new clot, concealing it from the body’s defenses (Making a lot of chemotherapy kinda useless)
  • Infection may erode through the endocardium into underlying structures, causing tears, abscesses and deformities
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8
Q

Vegetations

A
  • Similar to biofilm, its an aggregation of bacteria or some other micro organism
  • Resistant to treatment due to how effectively it is anchored to the tissue
  • Able to break off from the main cluster to colonize somewhere else in the body
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9
Q

Manifestations of IE

A
  • S+S develop from toxic effects of the infection, destruction of heart valves and embolization of pieces of vegetation
  • Primary presenting S+S are Fever and heart murmur ~85% of patients, and if the murmur gets worse so is the pt
  • Clusters of petechiae may be seen as well
  • Small painful nodes (Osler nodes) may be seen in the pads of fingers and toes
  • Roth spots may be seen as well
  • Splinter hemorrhages
  • Embolization, leading to stroke
  • Heart failure due to valve deformity

With the presence of emboli, every area of the body has a presentation

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10
Q

Roth spots

A
  • Clinical manifestation of IE
  • Hemorrhages with pale centers caused by emboli
  • Can be seen in the Eye
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11
Q

Osler nodes

A

Small painful nodules seen in the pads of fingers and toes

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12
Q

Splinter hemorrhages

A

Clinical manifestation of IE
* Red-brown lines and streaks seen under the proximal half of nails

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13
Q

HF indications: IE

A
  • Indicates poor prognosis with meds alone and needs surgery
  • HF is the most frequent complication and may result from valve deformity from the vegetation
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14
Q

Embolic stroke

A
  • 22-50% of pt with IE have embolization
  • 65% if emboli target the CNS
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15
Q

Risk factors for IE

A
  • Prosthetic cardiac valves or prosthetic material
  • Implanted cardiac devices (Pacemaker, ICD)
  • History of bacterial endocarditis (Even without HD)
  • Congenital heart disease patients (Repaired or unrepaired)
  • IV drug abuse
  • Body piercing (Especially oral, nasal, nipple)
  • Hemodialysis pts

Essentially anything foreign to the body

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16
Q

Diagnositic testing IE

A
  • Microorganism found in two seperate blood cultures. And vegetation is found in imaging of heart (Echocardiogram and transesophageal echo)
  • 2 sets of blood cultures, from different venipuncture sites over 24 hours, must be drawn 2 hours apart before antibiotics can be started
  • Negative blood cultures don’t rule out IE (can embolize any time)
  • You may see elevated white blood cell counts, elevated ESR and C-reactive proteins
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17
Q

Med mgmt IE

A
  • Treatment is focused on eradication of invaded organisms through the use of appropriate antibiotics
  • Antibiotics are given for 2-6 weeks in high enough doses to ensure eradication of dormant bacteria with dense vegetations
  • Blood levels of antibiotics are drawn to ensure high enough levels, and repeat blood cultures are done
  • After antibiotics are given the patient should begin to feel better, less fatigued
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18
Q

Surg mgmt of IE

A
  • May be needed if pt develops
    1. HF or an intracardiac abscess
    2. Recurrent systemic embolizations
    3. If antibiotics do not clear infection
  • Surgery includes, valve repair, debridement of abscess and fistula closure
  • Most pts with prosthetic valve IE require a new valve replacement
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19
Q

Nursing mgmt of IE

A
  • Vitals: Making note of fevers
  • Admin antibiotics and education of pt
  • Timing of antibiotics to ensure high enough levels
  • Good infection control practices for RN and pt (Handwashing and all that)
  • Monitor for S+S systemic embolization
  • Patient care is directed to mgmt of infection, monitor invasive lines and wounds for S+S infection
  • Education is provided regarding activity, meds and S+S infection
  • Pts with IE are at high risk for another episode of IE
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20
Q

S+S systemic embolization: IE

A
  • Neuro changes
  • CP
  • Dyspnea
  • Weakness
  • Pain
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21
Q

Aneurysm

A
  • Local sac or dilatation found in a weak point in the wall of an artery
  • Classified by shape or form
  • Most common or saccular and fusiform
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22
Q

Saccular aneurysm

A
  • Projects from one side of the vessel
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23
Q

Fusiform aneurysm

A

Dilatation of the entire artery

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24
Q

Abdominal aortic aneurysm (AAA)

A
  • Aneurysm of the descending aorta
  • Most common cause is atherosclerosis
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25
Q

Who is most affected by AAA

A
  • Men are 2-6 times more likely than women to be affected
  • White people more than black people
  • Most prevalent in people under 65
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26
Q

Most common location AAA

A

Infrarenal, below the renal arteries

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27
Q

Patho AAA

A
  • Dmg to the media layer of the vessel
  • May be caused by congenital weakness, trauma, or disease
  • Once it develops it tends to enlarge
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28
Q

Risk factors AAA

A
  • Genetic predisposition
  • Nicotine use
  • HTN (1/2 of pts have HTN)
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29
Q

Clinical manifestations: AAA

A
  • 40% of people have symptoms, can feel heartbeat in abdomen when lying
  • Most important indication of AAA is a pulsatile mass in the middle and upper abdomen
  • If Aaa is associated with thrombus, a major vessel may be occluded or smaller distal occlusions may result from emboli
  • Know signs of impending rupture
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30
Q

Signs of impending rupture AAA

A
  • Severe lower back pain
  • Abdominal pain (Middle or lower abdomen, left of midline)
  • Falling BP (BP going down= less blood in the system)
  • Decreased blood count (Bleeding internally means less blood flow to go around)
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31
Q

Rupture into peritoneal cavity AAA

A
  • Rapidly fatal
  • Contained peritoneal rupture leads to hematoma formation in
    1. Scrotum
    2. Perineum
    3. Flank
    4. Penis
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32
Q

AAA diagnostic testing

A
  • Ultrasound or CTA to determine size, length and location
  • If its small, ultrasounds are given Q 6 mo until the size increases to the point where surgery is warranted, some stay stable over years
  • Most AAA occur in 60-90, rupture is likely with HTN and aneurysms greater than 6 cm wide
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33
Q

AAA risk factors for rupture

A
  • > 6cm
  • HTN
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34
Q

When is a patient considered for surgery: AAA

A

If the older pt is a surgical risk, the aneurysm is not repaired until its 5.5 cm wide

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35
Q

Med mgmt: AAA

A
  • Antihypertensive agents
  • Diuretics
  • BB
  • Ace inhibitors
  • ARBS
  • Calcium channel blockers
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36
Q

Endovascular and Surg mgmt:AAA

A
  • > 5.5 or enlarging, treatment is open surgical repair by resecting the vessel and sewing a bypass graft in place
  • Endovascular aortic repair is mainstay of therapy by placement and attachment of aortic graft (stent) across the aorta
  • Can be performed with local or regional anesthesia (for pts that may not tolerate general anesthesia)
  • Endovascular repair can be performed if pts abdominal aorta and iliac arteries are not tortuous, calcified and full of thrombi
37
Q

Complications of AAA surgery

A
  • Bleeding
  • Hematoma
  • WOund infection
  • Ishemia or embolization
  • Graft thrombosis
  • Graft leaks
  • Delayed rupture
  • bowel ischemia

Risks are small in comparison to the complications of rupture

38
Q

Endovascular repair of AAA

A
  • Can be done locally or regionally
  • Placement of a stent graft over the aneurysm, forcing blood to flow through it instead of blood exerting pressure on the vessel walls, reducing the ability for the aneurysm to grow
  • Cannot be performed if the pts abdominal aorta and iliac arteries are tortuous, small, calcified and full of thombi

Risks are small in comparison to the complications of rupture

39
Q

Nursing mgmt: AAA

A
  • Guided by anticipating the pt might have CV, cerebral, pulmonary, and renal impairment from atherosclerosis
  • after endovascular repair, pt MUST lie flat for 6 hrs hob may be elevated to 45 degrees after 2 hours
  • Monitor VS and pulses (Doppler) every 15 min then advanced (Pulses may feel weak and need doppler)
  • Access site, usually femoral needs close assessment, skin changes, signs of embolization need prompt notification
  • Huge bleeding risk, monitor
40
Q

Mgmt of post AAA repair: Temp and postimplantation syndrome

A
  • Begins within 24 hours of placement of stent
  • Fever leukocytosis and occasionally thrombocytopenia occur
  • Attributed to complex immunologic changes due to the manipulation of aortic lumen
  • mgmt is with mild analgesic or nsaids, subside within week
41
Q

Nursing mgmt of AAA: Hemodynamics

A
  • Notify provider of persistent coughing, sneezing, vomiting or >SBP 180 due to increased risk of bleeding
  • Fluids are needed to both maintain blood flow to arterial repair site and excretion of IV contrast agents
  • 6hrs after procedure, pt can ambulate (prevent blood clots)
42
Q

Post op complications: AAA repair

A
  • Arterial occlusion
  • Hemorrhage
  • infection
  • Ischemic bowel
  • Kidney injury
43
Q

Valvular heart disease

A
  • Heart valve does not open or close properly affecting blood flow
  • Decreases CO of the heart, which can lead to cardiac remodeling and HF
  • Both regurgitation and stenosis fall in this umbrella
  • Regurg and stenosis can both affect the same valve or different valves
  • Can affect any valve
44
Q

How do the valves of the heart function

A

Blood pressure changes

45
Q

How many leaflets does the tricuspid valve have

A

3

46
Q

Regurgitation

A
  • Also called insufficiency
  • Heart valves do not close completely, blood flows back through a valve
47
Q

Stenosis

A
  • Valve does not open completely, blood flow through valve is reduced
48
Q

Tricuspid valve disease

A
  • Rare, occurring secondary to endocarditis or IV drug use
49
Q

Age on valve function

A
  • As you increase in age, fibrotic thickening occurs in the mitral and aortic valves
  • With age, the aorta becomes stiffer, increasing SBP and stress on the MV
50
Q

Causes of valvular disease: Congenital

A
  • Can affect all 4 valves and cause either stenosis or insufficiency
51
Q

Causes of valvular disease: Degenerative disease

A
  • Acquired valvular disease
  • Due to dmg over time, from mechanical stress, atherosclerosis and htn
52
Q

Causes of valvular disease: Rheumatic disease

A
  • Acquired valvular disease
  • Gradual fibrotic changes
  • Calcification of valve cusps
  • Most common in developing countries
53
Q

Causes of valvular disease: Infective endocarditis

A
  • Acquired valvular disease
  • Infectious organism destroys the valve
  • Strep infections are common cause
54
Q

Risk factors for valvular disease

A
  • Htn
  • Rheumatic fever (Mitral stenosis and insufficiency)
  • Infective endocarditis
  • Congenital malformations
  • Marfan syndrome (Lincoln)
  • In older adults the main cause are degenerative calcification and atherosclerosis, papillary muscle dysfunction and IE
55
Q

Marfan syndrome

A
  • Connective tissue disorder which affects the heart and other areas
  • Big tall people skinny limbs
  • Causes big heart. not good
  • Lincoln
56
Q

Manifestations of valvular heart disease

A
  • Depends which valve and what type of dysfunction
  • Many don’t have symptoms until late into the disease progression
  • A murmur is heard in turbulent blood flow, location and timing of murmurs are used to determine the valve involved
  • Murmurs are graded 1-6 with 6 being the loudest
  • LV dmg increases, pulmonary artery pressure, LV hypertrophy, decreased CO resulting in dyspnea and fatigue
57
Q

A fib and CO

A

Kills CO by only ejecting a little bit of blood into the ventricle

58
Q

Mitral stenosis

A
  • Apical diastolic murmur
  • Dyspnea on exertion (DOE), Paroxysmal nocturnal dyspnea (PND)
  • Afib, palpitations
  • JVD, pitting edema hepatomegaly
  • Hemoptysis

Symptoms are similar to HF

59
Q

Mitral insufficiency

A
  • Systolic murmur of the apex
  • DOE, PND
  • AFib, palpitations, Fatigue
  • JVD, pitting edema, hepatomegaly
  • Atypical CP

Similar to HF

60
Q

Aortic stenosis

A
  • Systolic murmur
  • DOE, PND
  • Angina, fatigue
  • Syncope
  • Narrowed pulse pressure
61
Q

Aortic insufficiency

A
  • Diastolic murmur
  • DOE, PND
  • Palpitations, fatigue
  • Widened pulse pressure
  • Sinus tachycardia
62
Q

Diagnostic procedures: Valvular disease

A
  • Chest x-ray, show chamber enlargement, pulmonary congestion
  • 12 lead EKG shows chamber enlargement
  • Echo: shows chamber size, hypertrophy, specific valve dysfunction, EF
  • Transesophageal echo (TEE) Same as echo but provides visualization of the mitral and aortic valves
  • Angiography: Evaluates the coronary arteries, right heart cath measures pressure in atrium RV and pul artery (Swan)
63
Q

Valvular disease mgmt: Meds

A
  • Diuretics: Remove excess fluids
  • Afterload reducing agents help the heart pump against less resistance (BB, ace/ARBS, CCB, vasodilators
  • Inotropic agents such as digoxin are used to increase contractility and improve CO
  • Anticoagulants for pts with AFIB and severe LV dysfunction
64
Q

Valvular disease mgmt: Percutaneous balloon valvuloplasty

A
  • Balloon is inserted into either the mitral or the aortic valves affected by STENOSIS. This is done by insertion of a cath into the femoral and threaded to the heart, breaking up Ca ‘
  • Risk of emboli or stroke
65
Q

Valvular disease mgmt: Valve replacement

A
  • Replacement of damaged valve with mechanical or tissue valves, usually done open heart
66
Q

Valve replacement: Mechanical valves

A
  • Requires lifelong Coumadin therapy
67
Q

Valve replacement: Tissue valves

A
  • Only last 7-10 yrs
68
Q

Patient education: Valve replacement

A
  • Prophylactic antibiotics before dental or other invasive procedures
  • Weight daily (3lbs in a day 5 lbs in a week notify provider)
  • Adhere to dietary restrictions , avoid sodium and alc
  • Energy conservation
  • Wound care, if post op surgery
  • Read labels of OTC meds, avoid ones that include alc, ephedrine or epinephrine, these can cause arrythmias
  • Report s+S HF, fever, petechial rash to provider
  • those who underwent open heart surgery need the same care as CABG
69
Q

Valvular disease mgmt: Transcatheter Aortic valve replacement (TAVR)

A
  • Used in treatment of severe, symptomatic aortic stenosis, starting to be done for those who are lower risk
  • minimally invasive AV (aortic valve) replacement done in cath lab
  • Does not involve CPB or a sternotomy
  • Still general anesthesia, a balloon is inserted with an artificial valve that sits directly over the faulty one
  • Functions without needing an external power source, but on pt blood flow
70
Q

Aortic stenosis (AS)

A
  • Narrowing between the valve between the LV and aorta
  • Gradually occurs over several years or decades
  • As the valve orifice narrows, cardiac remodeling occurs and the LV hypertrophies
  • After a while these compensatory mechanisms fail and don’t allow normal heart function, HF will develop
71
Q

Aortic stenosis: Calcification

A
  • Can be caused by changes occurring from normal mechanical stress. Either from congenital differences or rheumatic endocarditis can cause adhesions or fusions of the commissures and valve ring, stiffening the cusps
72
Q

Clinical manifestations of Aortic stenosis

A
  • Most pts are asymptomatic
  • First symptoms for most is dyspnea on exertion (DOE), caused by increased pulmonary pressure, due to a dilating LV. this will over time lead to LV failure causing PND and Pulmonary edema
  • Reduced blood flow can cause dizziness or syncope
  • Pts can report angina from increased cardiac demand and decreased blood flow
  • BP may be normal or low
  • Low pulse pressure (20mmHg or less)
73
Q

Diagnostic testing Aortic stenosis

A
  • Cardiac imaging is used to diagnose and monitor the progression of AS
  • May be echo, cardiac MRI, or CT
  • Surgery may have to be considered once AS progresses, cardiac cath is needed to measure the severity of the valve abnormality and eval the coronary arteries
  • Pressure measurements are taken from the LV and base of aorta
74
Q

Med mgmt of aortic stenosis

A
  • Meds to treat arrhythmias or HF
  • Meds only treat symptoms does not improve valve function
75
Q

Diagnostic work up for TAVR

A
  • Echo or TEE to diagnose valve stenosis
  • Coronary angio to rule out CAD (IV Dye, nephrotoxic)
  • CTA of chest, abdomen, pelvis, to measure valve size and assess vasculature for access site (More iv dye)
  • Lab work, EKG, CXR
  • Pts must meet criteria for severe AS based on echo
  • pts must be seen by cardiology and cardiac surgeon
76
Q

T/F you can deploy a TAVR on a mechanical valve that has failed

A

False, but you can do it on a tissue valve

77
Q

TAVR: improvement in a patient with regurgitant valve

A

May take months for the chamber affected to achieve its optimal functioning

78
Q

TAVR: improvement in a patient with a stenotic valve

A

Blood flow improves, and S+S of HF improve in days

79
Q

Complications of TAVR

A
  • Bleeding from the insertion site, artery, retroperitoneal bleeding
  • Thromboembolism: Piece of Ca breaks off and embolize, causing a stroke
  • Arrhythmias can occur
  • Renal issues: From all the contrast dye
80
Q

Complications of TAVR: arrhythmias

A
  • When the valve is deployed, rapid pacing is done so the heart is unable to push the valve out of place
  • Bradycardia or heart blocks may occur with TAVR due to AV node dysfunction
  • May be transient or need a pacemaker
81
Q

Nursing mgmt: TAVR

A
  • Frequent checks for bleeding, check all access sites, retroperitoneal bleeding, lab work
  • Frequent neuro checks, Calcium can embolize causing stroke. Check pulses, extremities and any change in neuro status must be reported to provider
  • Monitor closely for arrhythmias especially bradycardia and heart block
  • Monitor renal functions: I/O lab work
82
Q

Cardiac arrest (CA)

A
  • Sudden cardiac arrest or SCA is the sudden loss of all heart activity due to an irregular heart rhythm
  • Breathing stops, person becomes unconscious, without treatment this is death
  • Treatment for CA is CPR and Defibrillation
  • Not the same as MI, not due to a blockage however an MI can lead to a change in the hearts electrical activity which can lead to CA

Usually V fib

83
Q

Cardiac arrest (CA)

A
  • Sudden cardiac arrest or SCA is the sudden loss of all heart activity due to an irregular heart rhythm
  • Breathing stops, person becomes unconscious, without treatment this is death
  • Treatment for CA is CPR and Defibrillation
  • Not the same as MI, not due to a blockage however an MI can lead to a change in the hearts electrical activity which can lead to CA

Usually V fib

84
Q

Causes of CA

A
  • Caused by basically any heart condition
  • Usually due to electrical component of the heart causing rhythms such as V-Tach or V-fib. but some can be caused by bradycardia
  • Can also occur due to scarring of the heart tissue from a prior MI or another cause, leading to a ventricular arrhythmias
  • Thickened heart muscle: From Htn, valvular heart disease or other causes
  • Heart meds: Some can cause arrhythmias or CA
  • Significant changes in Potassium or mg
  • Electrical abnormalities
  • Drugs use
85
Q

When are you at greatest risk of CA after MI

A

The 6 months after inpatients with atherosclerotic heart disease

86
Q

What illicit drugs cause CA

A

Coke and meth

87
Q

Electrical abnormalities leading to CA

A
  • Wolff-Parkinson-white syndrome
  • Long QT syndrome

Causes A fib

88
Q

Proarrhythmic effect

A
  • antiarrhythmic drugs that are used to treat arrhythmias produce ventricular arrhythmias at normal doses
89
Q

4 Rhythms seen in CA

A
  • V fib (VF) Jiberish
  • Pulseless V-Tach (VT). waves, no pulse
  • Pulseless electrical activity: appears as any rhythm other than VF, VT and asystole even sinus rhythm, no pulse tho
  • Asystole: Nada