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Nursing 360 > CV I and II > Flashcards

CV I and II Flashcards

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1
Q

Cardiovascular Diseases (CVD)

A 
CAD/ CHD
Acute Coronary Syndrome
Metabolic Syndrome
Valvular Heart Disease 
Heart Failure
Cardiomyopathy 
Infective Endocarditis
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2
Q

Factors that lead into Cardiovascular Diseases

A

1) Smoking
2) Obesity
3) Pre-diabetes & Diabetes
4) Dyslipidemia
5) Hypertension
6) Genetics

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3
Q

Women and Heart Disease

A

Higher mortality after MI
Higher false positive stress tests
Higher mortality after CABG
Women diabetics have > risk for CAD

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4
Q

CAD Pathogenesis

A

CAD is a complex chronic inflammatory disease, characterized by remodeling and narrowing of the coronary arteries supplying oxygen to the heart
Two components:
Inflammation
Atherosclerosis

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5
Q

Inflammation in Heart

A

C-Reactive Protein (CRP) *Jan. 2003: All patients with moderate risks for heart disease should have CRP measured
Women with elevated CRP have twice the incidence of ischemic heart disease as women with normal levels.

CRP
0-1 low, 1-2 med, 2-3 high

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6
Q

Atherosclerosis:

A

Lipoprotein metabolism: transports fat into bloodstream; hastens buildup of cholesterol
Hemostasis: Fibrinogen
Endothelial dysfunction - Homocysteine: natural breakdown of methionine…leads to clots *decreased with folic acid, B6, B12

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7
Q

What does cholesterol do on the heart?

A

Cholesterol within cells lead to foam cells
Foam cells are earliest sign of endothelial dysfunction: core of lipid-engorged macrophages, extracellular lipids, cellular debris, fibrin and plasma proteins covered by a fibrous cap of SM cells and dense CT
Foam cells in intima create fatty streak

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8
Q

Target areas for Prevention of CAD

A

Cholesterol abnormalities
Tobacco use
HTN
DM

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9
Q

Normal Blood Lipid Profile

A

Total Cholesterol (TC): 200 or less (not > 4 x HDL)
HDL Cholesterol: Men 35-70; Women 35-85
TC/HDL Ratio: 4:1 or less
Triglycerides (TFG): 150 or less
LDL Cholesterol:

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10
Q

Other CAD risk factors

A

Sx of PCOS: male pattern acne, hirsutism, thinning hair, skin tags, central obesity, infertility/irregular cycles, ovarian cysts
Hyperuricemia (> 5.8 mg/dl in women; >7.4 mg/dl in men)
Acanthosis nigricans

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11
Q

Metabolic Syndrome: Cluster of risk factors for CAD

A 
Characterized by :
Insulin Resistance
High triglycerides, low HDL, possibly high LDL
Central obesity
Hypertension
Pro-inflammatory state 
Pro-thrombotic state
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12
Q

Hallmarks of Metabolic Syndrome

A 
BMI > 24.9
WHR > 0.8 in women and >0.95 in men
Waist >35” women, >40” men *12 x greater risk for diabetes
Triglyceride level > 150 mg/dl
HDL  130/85
FBG levels > 100 mg/dl or abnormal GTT
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13
Q

Treatment for Metabolic Syndrome

A 
Lifestyle modifications – FIRST LINE
Weight loss
Increased activity
Heart healthy dietary intake
Smoking cessation
If lifestyle changes do not achieve desired effects, medications are initiated
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14
Q

Medications for Metabolic Syndrome

A

Statins
ACEIs and ARBs preserve renal function
Beta-blockers prevent endothelial damage (but increase lipid levels and insulin resistance)
Thiazides are particularly effective in African Americans and elderly; prevent osteoporosis, but they increase LDL and triglycerides and increase uric acid
Calcium Channel blockers appropriate if patients don’t tolerate beta blockers
Oral anti-diabetics (metformin most commonly used)
Low-dose ASA
Folic acid and vitamin B6
Garlic
Omega-3 fatty acids/ Fish oil supplements

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15
Q

Stable angina

A

is substernal pain or discomfort that is provoked by exertion or emotional stress and is relieved by rest or nitroglycerin

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16
Q

Unstable angina

A

is ischemic chest pain that occurs at rest, in a crescendo pattern, or is severe and of recent onset; falls into category of ACS

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17
Q

Angina Pain Characteristics

A

Retrosternal pain
Poorly localized, may radiate
May feel a “fullness” or choking sensation
DM patients, elderly patients, and female patients may all have different sx
SOB, pallor, diaphoresis, dizziness, n/v, weakness

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18
Q

Diagnosis of Angina

A

Important to r/o acute coronary syndromes whenever a person presents with chest pain

Probability of CAD is suggested by the presence of risk factors

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19
Q

AHA Guidelines for treating chronic stable angina

A 
A.  ASA and Anti-platelets
B.  Beta blockers and B/P 
C.  Cholesterol and cigarettes
D.  Diet and Diabetes
E.  Education and Exercise
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20
Q

Management and Treatment of Angina – Non-pharmacologic: aggressive management of risk factors

A

Smoking cessation
Weight loss
Exercise

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21
Q

Pharmacologic Management of CVD

A

Statins, ACE Inhibitors, Antiplatelet Therapy, Beta Blockers, Nitrates

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22
Q

Statins

A
  1. Statins: lower LDL-C to
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23
Q

ACE Inhibitors

A 
ACE Inhibitors/ARBs:  recommended for all patients with angina and DM and/or LV dysfunction. 
Adverse effects/side effects: 
Cough
Hyperkalemia
Hypotension
ARF especially if given with diuretics
Potential for anaphylaxis 
Nursing Implications
Hold for SBP
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24
Q

Antiplatelet Therapy

Study These Flashcards
A

Antiplatelet Therapy:
ASA 81-325 mg/day is first-line therapy
Clopidogrel (Plavix) for patients who cannot tolerate ASA
Glycoprotein (GP) IIb/IIIa inhibitor class of platelet antagonists (Integrilin, ReoPro, Aggrastat)
Nursing implications:
IV forms are used in acute MI
Monitor platelet counts
At increased risk for bleeding
Safety precautions and assessment for bleeding

25
Beta Blockers
``` Beta Blockers and Calcium Channel Blockers: Beta Blockers are first-line therapy; calcium blockers are used when beta blockers are contraindicated or not effective; they may be used in combination Nursing implications I&Os and daily weights Assess for s/sx of HF If HR ```
26
Nitrates
``` Prevent angina in stable angina Nitroglycerin ointment (Nitro-Bid) and extended release capsules SE & Nursing measures Treat Angina IV – ACS SL for “chest pain” SE & Nursing measures ```
27
Chronotherapeutic Considerations
Chronotherapy: tailoring of drug delivery to the timing of circadian events (statins at HS) Controlled-release, sustained-release, extended-release
28
Nursing goals for angina
``` Treatment when sx start Prevention Reduction of anxiety/stress Understanding of disease and tx Absence of complications Adherence to self-care plan ```
29
Care and Teaching Post Cardiac Catheterization
Changes can occur very fast Frequent assessments (VS, ECG, pulse ox, urine output, lung sounds, peripheral vascular assessment, LOC) Bedrest with HOB 30 degrees Firm pressure / pressure dressing – prevention of bleeding Monitor for signs of hemorrhage or hypovolemia Affected extremity straight Monitor for infection during recovery period
30
Exercise Testing (ETT)
Exercise ECG should be performed in most patients with suspected or known CAD Monitoring of heart during exercise on a treadmill or stationary bike
31
Pharmaceutical Stress Tests
``` Lasts 1-3 hours, lots of nursing monitoring Done on those unable to exercise Reveals area of heart muscle not getting adequate perfusion To dilate vessels: Adenosine (Adenocard) Dipyridamole (Persantine) Thallium (nucleotide) Dobutamine used if the others cannot be ```
32
Cardiac CT Angiography(64-slice CT)
Use of CT imaging to get 3D picture of heart and coronary arteries made visible by contrast dye Detects Ca++, fatty deposits and narrowed arteries Non-invasive Used for high risk, unusual Sx and inconclusive stress tests Less expensive and less recovery than cardiac catheterization
33
Echocardiography
Echocardiography Ejection Fraction (EF) Normal - A normal heart's ejection fraction is between 55% and 70%.Example: An EF of 60 % means that 60% of the total amount of blood in the left ventricle is pushed out with each heartbeat.*You can have a normal ejection fraction reading and still have heart failure. Abnormal - 75% or greater - may indicate a heart condition like hypertrophic cardiomyopathy 36-49% = pumping ability below normal indicates damage, perhaps from a previous heart attack, but it may not indicate heart failure. 35% and below = pumping ability is low A low EF is a sign of heart failure.
34
Cardiac Enzymes
Troponin T and I: | normal troponin T
35
Invasive Cardiac Procedures
PCI (percutaneous coronary intervention): 1. PTCA (percutaneous transluminal coronary angioplasty) Intracoronary stent implantation (DES: Drug-eluting stents) Atherectomy: extraction 2. Brachytherapy: radiation (per catheter or implanted with stent) 3. Laser revascularization 4. EPS: radiofrequency catheter ablation for recurrent SVT 5. Transmyocardial laser revascularization: forms new vessels following laser burns 6. MAZE procedure for atrial fibrillation 7. Pulmonary Vein Isolation/Ablation CABG (coronary artery bypass grafting) **Big ones to know are PTCA, stent implantation EPS for arrhythmias You may get to see these MAZE is open heart
36
Nursing Care with the Postoperative Cardiac Surgery Patient
``` Maintain hemodynamic stability Assist recovery from anesthesia Pain management Wound care Progressive activity Nutrition Education about medication and activity Psychosocial support ```
37
Differentiation of Chest Pain
Angina: 5-15 minutes Usually r/t exertion, emotion, eating, cold MI: > 15 minutes Spontaneous onset Often unrelated to activity Esophageal Pain: 5-60 minutes Pain increased with lying, cold liquids Treated with antacids, PPI, H2 Agonists, NTG ``` Anxiety: 2-3 minutes no radiation may have numbness and tingling Treated with relaxation ``` Pericarditis - Sharp, severe pain - May radiate, sudden onset, intermittent, increases with DB, swallowing, coughing - Treat with analgesia, anti- inflammatory meds, upright position
38
Causes of Pericarditis
``` Idiopathic Infectious MI Neoplasm CT disorders (lupus, RA) ```
39
Acute Coronary Syndromes
A spectrum of clinical disorders caused by ischemic heart disease including: STEMI (ST segment elevation acute MI)* most vulnerable NSTEMI: non-ST elevation acute MI) UA: Unstable Angina Syndromes that may present when MI occurs, ranging from unstable angina to acute MI; common ER admission
40
Immediate Goals with Acute MI
Restore Perfusion and decrease mycardial necrosis (prevention of heart failure) Reduce pain and dyspnea Prevent and Treat Complications – V fib, pulseless VT, Symptomatic bradycardiac, unstable tachycardia
41
Diagnosis of ACS and MI
``` History of symptoms and PE Serum Biomarkers EKG Elevated ST segment (STEMI vs NSTEMI) Inverted T wave Pathologic (deep) Q wave (QwMI vs NQMI) ```
42
Enzyme trends post damage
LOOK ON SLIDE
43
Medications used with MI
``` MSO4 5 mg IV Oxygen 2 liters/cannula NTG (sl) X 3 Q 5 minutes ASA 1 tablet, chewed (or Plavix) Metroprolol (Lopressor) 5 mg IV Q 5” X3 Fibrinolytic agent within 30-60 minutes or PCI within 60-90 minutes IV Heparin 45 min after fibrinolytic (TPA) Anti-platelet agents (Integrilin) Magnesium Sulfate 1 mg slow IV, then 15 mg over 24h Lidocaine should be avoided ACE inhibitors 24 h after MI Statins at discharge ```
44
Goals for MI
``` Onset of Sx: call within 5 minutes EMS: arrive within 8 minutes Pre-hospital: EKG, fibrinolytics within 30” ER: PCI within 90 minutes GOLDEN HOUR: first 60 minutes TOTAL ISCHEMIC TIME: within 120” ```
45
Suspected Acute MI in the Community
Recognize Symptoms Activate EMS Confirm with EKG and Early Defibrillation ASA (325 mg PO) and NTG (SL) Transport to hospital for PCI (within 90 minutes) or pharmacologic (fibrinolytics) management (within 30 minutes of arrival) 1:300 transported cardiac patients go into cardiac arrest; only 23% of patients with MI use EMS
46
Suspected Acute MI in Hospitalized Patients
Diagnosis with EKG and enzymes (see Enzymes slide) ASA (325 mg po) and NTG (usually SL) O2 via n.c. Ensure IV access Bedrest Prepare for PCI Relief of sx, especially CP & dyspnea Decrease amount of myocardial necrosis to preserve LV function and prevent HF Prevent major adverse cardiac events (MACE): death, nonfatal MI Treat acute life threatening complications: V Fib, pulseless VT, symptomatic bradycardia, unstable tachycardia
47
Major Focus of Nursing Care
Assess heart (rhythm and for S3 or S4 gallop), lungs, and for edema/urine output (hourly) Monitor cardiac rhythm (continuous) Assess and monitor pain and response to meds Monitor labs (particularly troponin) closely Maintain BR and O2 Assess and treat anxiety Monitor environmental stimulation Implement crisis intervention & patient education Medication management: SL or IV NTG, IV morphine, ACE I to decrease BP and increase fluid/Na+ excretion, beta blockers, ASA, IV heparin (monitor aPTT), clopidogrel (Plavix ®), glycoprotein IIb/IIIa inihibitor IV (Aggrastat ®)
48
Potential Problems / Nursing Action
``` Alt in comfort: pain Impaired gas exchange: dyspnea Anxiety/fear of death Activity intolerance Alt in elimination Decreased CO; potential arrhythmias Rest, narcotics, O2, NTG, calm & quiet Positioning; O2 Pt. ed, reassurance Space activities Stool softeners, I&O Monitor EKG, VS assess for major complications ```
49
MI Patient Ed. & D/C Teaching
Smoking cessation: The 5 A’s: ask, advise, assess, assist, arrange follow up Ensure they go home with Beta Blocker; ACE I; ASA and Plavix; Statins; NTG NSAIDS are absolutely contraindicated Mediterranean Diet, Low Na+ diet, and weight reduction Cardiac Rehab S/Sx of stable angina versus ACS S/Sx of depression Beta-blocker related erectile dysfunction
50
Major Complications of MIs
``` Dysrhythmias Cardiogenic shock Cardiac Tamponade Ventricular Aneurysm Left Ventricular Heart Failure Pulmonary Edema Papillary Muscle Dysfunction Cardiac Arrest ```
51
Cardiogenic Shock
Failure of the heart to pump adequately to meet perfusion needs of the body *ineffective pumping (decrease in CO leads to hypoperfusion {shock}) >40% damage to myocardium 85% mortality Tachycardia, hypotension, decreased urine output, cold, clammy skin, mental changes, s/sx of HF, CP, tachypnea
52
Cardiac Tamponade
``` Fluid accumulates rapidly in the pericardium  decrease in cardiac output Can be caused by myocardial rupture following an MI or during cardiac surgery Symptoms (Beck’s Triad): JVD Muffled heart sounds Hypotension / tachycardia (Decreased CO) **Pulsus Paradoxus Also: narrowed pulse pressure ( ```
53
Pulsus Paradoxus
Drop in systolic B/P of 10 mmHg or more on inspiration (r/t decreased CO) An accentuation of the normal decrease in systolic B/P with inspiration Caused by decrease LV stroke volume
54
Pulsus Paradoxus
Drop in systolic B/P of 10 mmHg or more on inspiration (r/t decreased CO) An accentuation of the normal decrease in systolic B/P with inspiration Caused by decrease LV stroke volume
55
Assessment of Pulsus Paradoxus
1. Establish systolic B/P 2. Inflate cuff slowly until no sounds are heard 3. Deflate slowly till systolic sounds are first heard and note pressure 4. Deflate till systolic sounds are heard throughout respiratory cycle and note pressure 5. Note difference between 3 and 4 * Normal difference is 10: P.Paradoxus
56
Nursing Care for Cardiac Tamponade
Continuously monitor ECG for dysrhythmia formation, which may result of myocardial ischemia secondary to epicardial coronary artery compression. Monitor the BP every 5 to 15 minutes during the acute phase. Monitor for pulsus paradoxus via arterial tracing or manually Monitor urine output hourly; a drop in urine output may indicate decreased renal perfusion as a result of decreased stroke volume secondary to cardiac compression. Contact cardiology – will need to have surgically relieved (pericardial window/pericardiocentesis) at the bedside in ICU or in the OR
57
Ventricular Aneurysm
Infarcted myocardium is thinned and bulges out during contraction (ischemic bulge in acute stage of MI) Dx with Xray, ECHO, long-term ST elevation; angiography is definitive
58
Papillary Muscle Dysfunction
Causes mitral valve regurgitation Systolic murmur at apex Dyspnea, pulmonary edema, decreased CO

Nursing 360 (1 decks)

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