Critical Care > CAD > Flashcards

CAD Flashcards

(57 cards)

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1
Q

What is CAD?

A

gradual buildup of plaques in arteries, as plaques grow they can rupture or disrupt blood flow. If plaques form in vessels that feed into heart muscle, rupture or disruption of flow can cause MI. MI = lack of O2 to tissue of heart muscle.

Platelets will try to repair artery where plaque has ruptured, but that clotting can also block blood flow and cause MI.

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2
Q

CAD: RFs

A

Nonmodifiable:

  • age
  • gender (high in males initially although equalizes after age 75)
  • ethnicity (more common in Caucasian background)
  • family history
  • genetics

Modifiable:

  • elevated serum lipids
  • elevated BP
  • tobacco use
  • physical inactivity
  • obesity
  • diabetes
  • metabolic syndrome
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3
Q

Nursing Care of Pt with CAD

A

Decrease modifiable risk factors. Educate on diet, exercise, quitting smoking, blood sugar control.

Meds:

  • statins: lower cholesterol
  • fibric acid derivatives (gemfibrozil): give if statins cannot be tolerated b/c statins can cause rhabdomyolysis and liver injuries in which case you need to take them off statins and give gemfibrozil
  • antiplatelet (baby aspirin, Plavix, Xeralto): to prevent clot from forming (move away from warfarin b/c you need to have regular labs done w/ it)
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4
Q

Angina: Types

A
  • chronic stable angina
  • silent ischemia
  • unstable angina
  • microvascular angina
  • prinzmetal’s angina

*Can have chronic stable and develop unstable

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5
Q

Chronic Stable Angina

A

Intermittent
Predictable
Discerned pattern
Managed w/ rest and meds

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6
Q

Silent Ischemia

A
  • No subjective symptoms
  • Area of heart is not getting O2, but person doesn’t’ know d/t no symptoms
  • often seen in pt w/ DM b/c ability to feel s/sx of chest pain are decreased
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7
Q

Unstable Angina

A 
new
occurs at rest
increasing frequency and duration
need prompt care
may present differently in men than women

dangerous b/c women can have vague symptoms like fatigue, indigestion, SOB, and anxiety

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8
Q

ACS

A

Acute Coronary Syndrome

sudden onset of chest pressure/pain and sometimes include sudden stop of the heart.

symptoms likely with angina (mostly unstable)

caused by plaque blockage or rupture in heart

doesn’t always indicate MI happening, person can have ACS, need to do all testing and find out if they have MI or not (troponins)

Tx: thrombolytics (stop clotting from happening), beta blockers

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9
Q

Microvascular Angina

A
  • spasm of the small distal vessels of coronary circulation
  • prolonged, brought on by exertion
  • inconsistent response to nitrates (d/t how distal and far away from main vessels that feed the heart)

Sx = chest pain brought on by exertion, not very responsive to nitrates so they get angioplasty to increase blood flow

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10
Q

Prinzmetal’s Angina

A
  • Rare
  • coronary artery spasm
  • transient ST elevation seen
  • result of increased O2 demand

Tx:

  • determine that it’s Prinzmetal’s b/c it presents as MI
  • meds: vasodilator usually but depends on what is causing and how severe it is for the pt
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11
Q

What happens during an MI?

A

Most commonly as a result of CAD, a fatty plaque causes a blockage in the heart vasculature that feeds the heart muscle.

Can present as ACS (crushing chest pain, not feeling well, unstable)

Ischemia = lack of O2 to heart tissue > tissue damage which can be permanent

In MI there is SNS stimulation – adrenal response (sweating, anxious, they don’t feel right, irritable, know something is wrong but may not be able to pinpoint it)

Other sx: Nausea/Vomiting/low grade fever

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12
Q

What distinguishes MI from Angina?

A

Need cardiac biomarkers (troponins)

Need EKG that shows ST elevation or depression (indicating vessel in heart is not getting enough blood flow)

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13
Q

MI: Pain

A

NOT consistent between male and female:

  • Females may have jaw pain, indigestion, heart burn, GI upset
  • Men tend to present w/ more predictable symptoms (chest pain, left arm pain, neck pain)
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14
Q

What diagnostic tests are run when MI is suspected?

A

cardiac biomarker (Troponin)

  • cardiac specific enzyme released during cardiac muscle injury (normal = 0.0-0.04 ng/mL)
  • Hospitals now look at higher sensitivity troponin (even more cardiac specific, can pick up lower levels earlier on). Normal = less than or equal to 14.

EKG

Coronary Angiography: looking at heart vessels and possibly performing some sort of intervention to open up those vessels if they aren’t intact or open enough. Gold standard for MI to get them from door entering ED into cath lab to do angiography is less than 90min. Over 90min will lead to tissue damage.

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15
Q

What medications would anticipate giving in MI?

A

MONA:

  • morphine: vasodilation effects and reduces chest pain
  • O2: help bring O2 to areas not getting any
  • nitro: vasodilator (SE = hypotension)
  • aspirin: decrease platelets and hopefully prevent clot

Beta blockers and ACE-I
-long term meds to prevent remodeling of heart and help increase cardiac function

Anticoagulation and thrombolytics (agrostat for stent then switched to long term med like aspirin, eloquist, xerolto, Plavix)

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16
Q

PCI

A

Percutaneous Coronary Intervention

catheter is inserted and you treat vessel that is blocked or narrowed (opening it back up w/ balloon or stent)

in cath lab

want this done w/in 90 min of their arrival to ED

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17
Q

MI: Tx

A

depends on what happened during MI

  • CABG (in severe cases)
  • Rehab. (aerobic programs to slowly increase activity for heart muscle)
  • Manage risk factors.(educating about modifiable RF and eliminate them if possible)
  • Lifestyle education.
  • Gradual return to physical activity.
  • Resuming sexual activity. (decision is left up to doctor if there is concern about this and doc will speak to pt , nurse needs to be prepared to talk about this though and answer questions)
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18
Q

MI: What meds is pt on at discharge?

A

Beta blockers
ACE-I
Anti-Platelet

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19
Q

Post-MI Nursing Considerations

A
  • Anxiety. (normal for a pt who went through this)
  • Rest.
  • Continuous monitoring. (in hospital and at home)
  • Pain. (not uncommon, but should improve slowly)
  • Psychological response. (may have PTSD situation, anxiety/fear)
  • Still an MI risk – short term and long term.
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20
Q

Cardiac Cath

A
  • Usually done via radial artery or femoral artery.
  • Outpatient procedure in most cases.
  • Diagnostic tool in non-emergency (in emergency it’s PCI)
  • Differences between right heart and left heart cath has to do with what they are doing:
  • Left heart cath: looking at vessels feeding heart
  • Right heart cath: looking at hemodynamic numbers for someone who doesn’t have Swan-Ganz catheter
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21
Q

Cardiac Cath: Nursing Care

A
  • Manage anxiety (normal)
  • Check renal status (dye used during cardiac cath can be nephrotoxic, check UO, bolus w/ fluids after if needed)
  • Monitor puncture site. (accessing major arteries directly, monitor by checking site, make sure it’s not actively bleeding or has hemotoma)
  • Retroperitoneal bleed risk (if procedure is done femorally, pressure and bleeding can surround kidney area which is very dangerous)
  • If femoral, pt remains on bedrest and flat for 2-6 hrs post procedure (not discharged right away)
  • Monitor UO (need 0.5ml/kg/hr)
  • Pulse checks in affected limb
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22
Q

Targeted Temperature Management

A

If patient has cardiac arrest as a result of MI, then ROSC, but does not wake up.

Cooled (to 33 degrees C) for 24 hours.

Allows for decreased O2 demand and rest for heart and organs (since they depend on heart)

After cooling, rewarming process takes about 8 hours and then we wait and see if they wake up.

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23
Q

Targeted Temperature Management: Nursing Management

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A

Electrolytes are a concern b/c of:

  • Process of how they go and out of cell is altered when cooled
  • May need to replete them
  • When the pt is warmed up the electrolytes may spike up (especially potassium)
  • Need to monitor closely

Update family (this is traumatic and scary)

Meds: sedation and paralytic (stop shivering, and never give paralytic w/o sedative)

24
Q

Rheumatic Fever

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A

Delayed result of strep A – get antibiotics early!
Scarring/deformity of the heart valves.

Why is scarring bad?
-alters heart valve function, if it’s not opening or closing fully there is a disruption in blood flow to pulmonary or cardiac circuit therefore not providing adequate blood flow

25
Rheumatic Fever: S/Sx
- joint pain/tenderness (moving is uncomfortable) - fatigue - fever - activity intolerance - murmurs - palpitations - rash - sore throat (sx are result of disease process)
26
Rheumatic Fever: Tx
Penicillins NSAIDs may need heart valve replacement d/t scarring
27
Endocarditis
Infection of heart valves Effects valves and endocardium Causes: - IV drug use w/ dirty needles (bacteria introduced into blood and builds plaque on heart valve) - Presence of artificial valve - Prior endocarditis - Pacemakers - Marfan’s syndrome - Cardiomyopathy
28
Endocarditis: Sx
- Dysrhythmias - valve dysfunction - HF - sepsis (from infection, d/t growth/vegetation on valve) - Splinter hemorrhage - Petechiae - new or worse murmurs - embolization (clot could move from infected valve to pulmonary circuit)
29
Endocarditis: Diagnostic Tests
- Positive cultures (need to actively have infection) - Elevated ESR (sedimentation rate), CRP – indicate inflammatory processes in body which indicates infection - Echocardiogram: U/S of heart, shows if valves aren’t working as they should - ECG – heart block - May need a cardiac cath. - Decreased CO, activity intolerance (valve has growth on it that’s blocking blood flow so this is common)
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Endocarditis: Tx
- Long term, IV antibiotics. (4-12 weeks) | - Valve replacement.
31
Pericarditis
- inflammation of the sac that surrounds the heart - acute or chronic - diffuse ST changes - differs from MI, b/c MI is only in one area and pericarditis is across all leads
32
Pericarditis: Dx
Echo – best tool to dx b/c it allows us to visualize sac around heart and see if it’s filled w/ fluid Will hear pericardial friction rub (like plastic grinding on plastic sound) Will see cardiac tamponade signs (decreased CO, narrowing pulse pressure, feelings of doom, anxiousness)
33
Pericarditis: S/Sx
- severe, sharp chest pain - diffuse ST changes - decreased CO
34
Pericarditis: Tx
NSAIDs Corticosteroids Pericardiocentesis (fluid drawn out should not be blood b/c that would be a cardiac tamponade)
35
Myocarditis
- Inflammation of the myocardium - viral causes - symptoms will be present 7-10 days post infection - best outcome for pt is quick diagnosis and time of rest - heart muscle may not fully recover and pt may need LVAD, IABP, or transplant
36
Myocarditis: S/Sx
- HF symptoms - chest pain - pericarditis (as result of myocardial tissue being infected and inflamed)
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Myocarditis: Dx
Biopsy for infection in tissue
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Myocarditis: Tx
- manage symptoms (most often all that is needed is time) - ECMO (allows for time and heart and lungs to rest) - antivirals
39
Dilated Cardiomyopathy
- Left ventricle is larger and wall is thinner (floppy ventricle) - pumping action is significantly decreased d/t how weak and floppy the ventricle is
40
Dilated Cardiomyopathy: Causes
- cardiotoxic agents (like chemotherapy) - cardiac-effecting diseases (HTN, heart has to work harder against more resistance and it gets tired) - pregnancy (blood volume increases during pregnancy, thinning of wall and fatigue of heart occur d/t having to pump all that blood) - genetics
41
Dilated Cardiomyopathy: Sx
- HF symptoms (gradual or rapid) - fatigue - activity intolerance - swelling of extremities - slow HR
42
Dilated Cardiomyopathy: Dx
Cardiac cath to r/o ischemic causes | So we know HF isn’t because of lack of O2 but a weak left ventricle
43
Dilated Cardiomyopathy: Tx
- focuses on enhancing contractility and deceasing workload for the heart - decrease BP w/ beta blockers - increase contractility w/ inotropes - control HTN -no cure w/ this disease so need to address quality of life and may need LVAD or transplant
44
Hypertrophic Cardiomyopathy
Too much muscle (very thick wall) > no room for blood b/c muscle has taken over space. Concern is how much volume is getting out to body. Seen in men and athletes SCD may occur d/t this
45
Hypertrophic Cardiomyopathy: Causes
- idiopathic | - genetics
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Hypertrophic Cardiomyopathy: S/Sx
- dyspnea - fatigue - angina - syncope
47
Hypertrophic Cardiomyopathy: Dx
- Echo - LVH on ECG - dysrhythmias - pronounced apical pulse (very loud)
48
Hypertrophic Cardiomyopathy: Tx
- slow HR (reduce contractility) - AICD/pacemaker - cut down some of thickened wall - septal wall ablation -educate pt to avoid strenuous activity and drink lots of fluids! (dehydration is dangerous)
49
Mitral Regurgitation
- acute: presents with loud holosystolic murmur and pulmonary edema > cardiogenic shock - chronic: weakness, fatigue, exertional dyspnea, S3 gallop - prolapse: palpitations, chest pain, dyspnea (typically not emergency)
50
Aortic Regurgitation
Acute: abrupt onset of dyspnea, chest pain, LV failure, and shock Chronic: PND, fatigue, dyspnea, orthopnea, Austin Flint murmur
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Tricuspid Regurgitation
Sx of right heart failure
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Pulmonic Regurgitation
Fatigue | Loud mid-systolic murmur
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Regurgitation
Valve doesn’t fully close so blood goes backwards
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Stenosis
Hardening of valve so valve doesn’t fully open Affects HF b/c now heart has to work harder to push blood out b/c valve is fighting against it the whole time
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Mitral Stenosis
Blood is getting backed up into the pulmonary circuit as the mitral valve is only opening a little ``` Sx: Dyspnea on exertion Hemoptysis Fatigue AF Diastolic murmur ```
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Aortic Stenosis
Blood is staying in the LV and backing up to the pulmonary circuit since the valve is not fully opening Risk for MI! ``` Sx: Angina Syncope HF Systolic murmur S4 ```
57
ECMO
Mechanical pump that works outside the body to oxygenate blood when the heart and/or lungs cannot Two kinds: - VA: venous-arterial – provides support for both heart and lungs - VV: veno-veno – lung support only Pt cannot get out of bed depending on cannulation site Risk of bleeding from large cannulation Anxiety provoking Meds: anticoagulation Used for: Severe MI, myocarditis, cardiogenic shock, VV seen in flu season when lungs are diseased and can’t treat safely with just vent
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