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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

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
Q

Beta Blockers

A 
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
Q

Nitrates

A 
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
Q

Chronotherapeutic Considerations

A

Chronotherapy: tailoring of drug delivery to the timing of circadian events (statins at HS)
Controlled-release, sustained-release, extended-release

28
Q

Nursing goals for angina

A 
Treatment when sx start
Prevention 
Reduction of anxiety/stress
Understanding of disease and tx
Absence of complications
Adherence to self-care plan
29
Q

Care and Teaching Post Cardiac Catheterization

A

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
Q

Exercise Testing (ETT)

A

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
Q

Pharmaceutical Stress Tests

A 
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
Q

Cardiac CT Angiography(64-slice CT)

A

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
Q

Echocardiography

A

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
Q

Cardiac Enzymes

A

Troponin T and I:

normal troponin T

35
Q

Invasive Cardiac Procedures

A

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
Q

Nursing Care with the Postoperative Cardiac Surgery Patient

A 
Maintain hemodynamic stability
Assist recovery from anesthesia
Pain management
Wound care
Progressive activity
Nutrition
Education about medication and activity
Psychosocial support
37
Q

Differentiation of Chest Pain

A

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
Q

Causes of Pericarditis

A 
Idiopathic
Infectious
MI
Neoplasm
CT disorders (lupus, RA)
39
Q

Acute Coronary Syndromes

A

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
Q

Immediate Goals with Acute MI

A

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
Q

Diagnosis of ACS and MI

A 
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
Q

Enzyme trends post damage

A

LOOK ON SLIDE

43
Q

Medications used with MI

A 
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
Q

Goals for MI

A 
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
Q

Suspected Acute MI in the Community

A

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
Q

Suspected Acute MI in Hospitalized Patients

A

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
Q

Major Focus of Nursing Care

A

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
Q

Potential Problems / Nursing Action

A 
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
Q

MI Patient Ed. & D/C Teaching

A

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
Q

Major Complications of MIs

A 
Dysrhythmias
Cardiogenic shock
Cardiac Tamponade
Ventricular Aneurysm
Left Ventricular Heart Failure
Pulmonary Edema
Papillary Muscle Dysfunction
Cardiac Arrest
51
Q

Cardiogenic Shock

A

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
Q

Cardiac Tamponade

A 
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
Q

Pulsus Paradoxus

A

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
Q

Pulsus Paradoxus

A

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
Q

Assessment of Pulsus Paradoxus

A
  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
Q

Nursing Care for Cardiac Tamponade

A

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
Q

Ventricular Aneurysm

A

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
Q

Papillary Muscle Dysfunction

A

Causes mitral valve regurgitation

Systolic murmur at apex

Dyspnea, pulmonary edema, decreased CO

Nursing 360 (1 decks)

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