CH 14 and 15: Patients with Coronary Vascular Disorders Flashcards
1
Q
patho of coronary atherosclerosis
A
- Abnormal accumulation of lipid or fatty substances and fibrous tissue in arterial blood vessel walls
*** Create blockages and narrow coronary vessels reduced blood flow - Ruptured plaque can cause thrombus formation
- Can lead to ischemia (lack of oxygen) and infarction (tissue death)
2
Q
**uncontrollable (nonmodifiable) risk factors for coronary atherosclerosis
A
- Age (men >45, women >55)
- Gender (<55 men, >both, women <55 with early
menopause) - Race (Blacks, Mexican Americans, Native
Americans) - Family history of first degree relative
3
Q
**controllable (modifiable) risk factors for coronary atherosclerosis
A
- Diabetes and prediabetes
- HTN
- Smoking
- Obesity
- Physical inactivity
- High blood cholesterol
- Unhealthy diet
- Stress
4
Q
additional risk factors for coronary atherosclerosis
A
- Sleep apnea
- Increased BMI
- CKD
- Chronic infection
- Flu
- Nonalcoholic fatty liver
- Metabolic syndrome
- Cluster of metabolic abnormalities
5
Q
clinical manifestations and assessment of coronary atherosclerosis
A
- Progressive buildup
- Symptoms are based on location and degree of occlusion
- Can lead to ischemia
- Causing angina
- Significant damage can cause low cardiac output
6
Q
controlling cholesterol to prevent coronary atherosclerosis
A
*total cholesterol less than 200
* Have a fasting lipid profile every 5 years or more often if abnormal
* HDL >40 mg/dL (preferably more than 60) - take away LDL
* LDL - fat - less than 100
* triglycerides - less than 150
* Primary prevention with status reduces mortality
* Monitory for myopathy, liver disease; contraindication pregnancy
* Diet and physical activity
* Use meds in conjunction with diet and exercise
7
Q
ways to prevent coronary atherosclerosis
A
control cholesterol
treat hyperlipidemia
manage HTN
manage DM
8
Q
treating hyperlipidemia to prevent coronary atherosclerosis
A
Lipid-lowering meds
Lifestyle changes:
** Heart-healthy diet
** Increase physical activity 150 min of mod exercise or 75 min of vigorous activity
** Smoking cessation
** Stress management
** HTN and DM management
recheck labs 4-12 weeks
check liver enzymes
9
Q
managing HTN to prevent coronary atherosclerosis
A
- Elevated BP can increase
stiffness in vessel walls vessel injury - Therapeutic regimen
10
Q
managing DM to prevent atherosclerosis
A
- Hyperglycemia fosters
dyslipidemia and increased
platelet aggregation - Antihyperglycemic agents
and diet
A1C less than 7
11
Q
patho of angina pectoris
A
- Insufficient coronary blood flow decreased 02 supply with
increased 02 demand - Significant obstruction of amajor coronary artery
decreased blood flow ischemia - Similar risk factors as coronary atherosclerosis
12
Q
assessing angina
A
P - position - where does it hurt
Q - quality - type of pain
R - radiating
S - severity 1-10
T - timing - how long
13
Q
**characteristics of stable angina
A
- Chest pain/discomfort associated with physical activity
- Alleviated with rest and/or medications
- Associated with plaque build up
14
Q
**characteristics of variant/prinzmetals angina
A
- Form of chest pain
- Blockage of blood flow due to coronary artery spasm
- Occurs at rest
15
Q
**characteristics of unstable angina
A
- Chest pain that occurs at rest
- Considered initial phase of acute coronary syndrome
(ACS) - Precursor to MI
- Medical emergency
16
Q
clinical manifestations of angina pectoris
A
- Pain
- Feeling of impending death
- Pain/discomfort is poorly localized and can radiate to neck, jaw, shoulders, inner aspects of upper (left) arm
- Tightness
- Women have varying symptoms
- Unusual fatigue, weakness or numbness in arms, SOB, pallor, diaphoresis, anxiety, dizziness, headache, N/V
17
Q
assessment to diagnose angina pectoris
A
- Clinical manifestations of ischemia
- 12 lead ECG - ST elevation
- Echo - working valves? blood leaking
- Nuclear scan or invasive procedure
**stress test- medication to see how heart reacts to accelerated HR
18
Q
goal of angina pectoris
A
decreased 02 demand and increase 02 supply
19
Q
pharmacologic management of angina pectoris
A
Positive inotropes (increase contractility), negative inotrope,(decrease contractility)
positive chronotrope (increase HR) , negative chronotrope (decrease HR)
Beta-Adrenergic Blockers (lol) (negative chronotrope and inotrope)
** Reduce myocardial 02 consumption by blocking sympathetic stimulation
** Don’t stop taking abruptly; cautious of admin with low heart rate, monitor resp. rate - rebound hypertension
Calcium channel blockers (amlodipine (Norvasc) and diltiazem (Cardizem))
** Decrease HR, decrease workload of the heart (LV), vasodilate (negative chronotrope and inotrope)
**check BP and HR before administration
Oxygen therapy - start on 2L
20
Q
nitrates in management of angina**
A
- Reduce myocardial 02 consumption to relieve pain, VASODILATES
- SL (tablet or spray) administration under tongue
- Always carry med in original container
- Renew supply every 6 months
- Taken in anticipation of any activity that can cause pain; take BEFORE pain develops for stable
- If pain persists after 5 minutes of first administration, call EMS. Two more doses in 5 min intervals
(PUT PT IN TRENDELENBUG IF BP DROPS - LESS THAN 90) - Side effects: flushing, throbbing, headache, hypotension, and tachycardia
- Precautions for side effects
**Do not give if patient is on ED drugs
21
Q
antiplatelets (aspirin, clopidogrel (Plavix), glycoprotein IIb/IIIa inhibitors) management of angina
A
- Prevent platelet aggregation
- Monitor for bleeding
- Takes a few days for clopidogrel to start working
- Monitor for s/s of aspirin toxicity (abd pain, seizures, SOB, stroke signs)
- Prevention for GI upset
22
Q
Anticoagulant (heparin, enoxaparin) management of angina
A
- Prevent thrombosis
- Monitor for s/s of bleeding; monitor coag studies
- Place on bleeding precautions
23
Q
patho of MI
A
- Area of myocardium is permanently destroyed due to reduced blood flow from ruptured
plaque and occlusion of an artery by a thrombus - Profound imbalance b/w 02 supply and demand
- As cells are deprived of 02 ischemia cellular injury infarction (death of cells)
- Acute coronary syndrome = continuum from unstable angina to acute MI
- Classified by type (NSTEMI or STEMI), location of injury (anterior, inferior, posterior,
lateral wall), point of time (acute, old) and extent of damage (partial or full) - Risk factors similar as atherosclerosis and angina
24
Q
clinical manifestations of MI
A
- Cardiac: Chest pain continues despite rest and meds, increased BP, JVD
- Resp: SOB, Dyspnea, tachypnea, crackles
- Neuro: Fatigue, syncope, lightheadedness, restlessness, anxiety; fear of impending doom
- GI: N/V
- GU: decreased U/O
- Skin: cool, clammy, diaphoresis
- Women have atypical symptoms = fatigue, shoulder blade discomfort, indigestion, and/or
SOB
25
assessment of MI
* Patient history
* ECG
*** Obtained within 10 minutes!! of report of
pain or arrival to ED
*** Assess for ST elevation
*** STEMI: ECG evidence of acute MI;
significant damage to myocardium
*** NSTEMI: Elevated biomarkers but not
definite ECG evidence of acute MI
*** Echocardiogram
*** Labs
26
Creatinine kinase- myocardial band (CK-MB)
purpose:
normal value:
significance:
peak, return, normal:
Determine damage to cardiac cells
0-3 ng/mL or 1-3 μg/L
increases with damage to cells
peaks around 24 hours, no longer evident after 3 days
27
Myoglobin serum test
purpose:
normal value:
significance:
peak, return to normal
Helps transport 02 found in cardiac and skeletal muscle
5-70 ng/mL or 5-70 μg/L
Increases, but not specific to cardiac event
Peaks in 12 hours, no longer evident after 24 hours
28
Troponin I and Troponin T
purpose
normal value
significance
peak, return to normal
Regulates myocardial contraction;
Determines damage to cardiac cells, most sensitive for MI
< 0.5 ng/mL
Increases indicate MI; levels >1.5
ng/mL are critical
Increases within a few hours of MI; no longer evident after 1-3 weeks
29
medical treatment guidelines for acute MI
Rapid transit to hospital 12 lead ECG read within 10
minutes of arrival Labs for cardiac biomarkers Other diagnostics
Medical interventions
* Supplemental 02
* Nitro
* Morphine
* Aspirin 162-325 mg
* Beta blocker
* ACE or ARB within 24 hours
Evaluate for reperfusion therapy (percutaneous
coronary intervention or thrombolytic therapy)
Continue therapy as indicated
* IV hep or enoxaparin
* Clopidogrel or antiplatelet
* Glycoprotein
How would YOU prioritize???
30
pharmacological treatment for MI
MONA
(start on statin, ACE or ARB, BB, aspirin)
* Aspirin
** Give prior to arrival to ED unless absolute contraindication
** Che the tablet to increase absorption faster
* Nitro
* Morphine
** Reduces preload and afterload; promotes vasodilation, decreases workload of
heart
** Monitor BP and resp rate
* Beta blocker
* Documentation of ARB or ACE AND aspirin upon D/C
(SAAB)
31
thrombolytic therapy for MI
* Used when there is no PCI capable center within 120 minutes; with < 6 hours of chest pain; ST-elevation; chest pain >20 min with no relief
* Used to dissolve clots and lyse thrombus in coronary artery increased blood flow
* Must administer with 30 minutes of arrival to ED!
32
nursing considerations for thrombolytic therapy
* Avoid punctures to skin and continuous BP measurement
* Start access before therapy
* Monitor for bleeding, arrythmias, and hypotension
* Treat major bleeding with D/C and applying pressure; immediately call provider!
* Be aware of absolute contraindications
33
patho of percutaneous coronary intervention (PCI) or stent
* The occluded artery is opened and reperfusion to the area is re-established to improve blood flow
* Used for angina and acute MI
* PCI should be performed with !!60 minutes!! of arrival to ED
* Includes balloon angioplasty with intracoronary stent placement
* Can be done in combination with a cardiac catheterization
** Procedure where a vascular catheter is inserted, and dye is injected for visualization
** Used for diagnosis
34
complication of percutaneous coronary intervention
-Bleeding or hematoma
**Suture line leak, increased intraabdominal pressure
**Apply manual pressure, outline hematoma, monitor H/H, blood transfusion, keep bedrest or site immobile
-Lost/weakened pulse on extremity
**Arterial thrombus/embolus
**Asses perfusion and circulation, notify provider; anticipate surgery or thrombolytic therapy
-Retroperitoneal bleeding
**Blood accumulates in retroperitoneal space; tearing in flank from femoral access
**Notify provider, anticipate surgery or ultrasound guided compression, keep leg straight
-Acute kidney failure
**Nephrotoxic dye
**Monitor U/O, BUN, creatinine; ensure adequate hydration (IV/PO)
-Allergic reaction
**Reaction to dye
**Prepare for epi, prednisone, antihistamines, H2 blockers depending on severity
-Cardiac tamponade
**Bleeding into pericardial space from mediastinal tubes; reduces CO
**Monitor for JVD, pulsus paradoxus, cessation of previous heavy drainage, cardiovascular collapse, muffled heart sounds; emergency sternotomy with
drainage and volume expansion
-Chest pain/acute event/spasm
**Vasospasms, acute stent thrombosis, occlusion, abrupt vessel closure
**Notify provider of chest pain; monitor VS, 02 sat, perfusion, ECG, serial markers; prepare for cardiac cath
35
acute post-pocedure care of percutaneous coronary intervention
* Monitor for bleeding, changes in sensation, hematoma, absence of pulse, variance in VS
* Hemostasis achieved after sheath removal with direct manual pressure, mechanical compression device, or pneumatic compression device
** Sheaths removed when heparin is not active and clotting times are normal
** Removal can cause bradycardia have atropine ready; have patient in sitting/lying position
** Place occlusive dressing (keep for 24 hours)
* Remain in bed and avoid bending affected limb
** Remain in bed for 3-6 hours
* VS and Neurovascular checks Q15 min x4, Q30 min x4, Q1hr x4, then Q4hrs****
36
discharge teaching after percutaneous coronary intervention
*Report any abnormalities or complications
*For 24 hours, minimalize movement of extremity (no weight bearing)
*Do not drive for 24 hours or operate heavy machinery
*No heavy lifting (over 5 lbs.)
*Plan for follow up appointment
*Remove dressing after 24 hours and leave OTA; avoid submersion in water
*If bleeding occurs hold pressure; if >10 minutes call 911
37
Coronary Artery Revascularization: Coronary Artery Bypass Graft (CABG)
* Blood vessel is grafted to bypass occlusion for 70% occlusion
* Indications: alleviation of angina
uncontrolled by meds, treatment of CAD, prevention/treatment of MI or HF, treatment of complications from unsuccessful PCI
* Can be elective or emergent
* D/C within 3-5 days without complications
38
pre-op care for Coronary Artery Bypass Graft (CABG)
Informed consent
CXR, ECG, labs, baseline assessment
* Preop antibiotic prophylaxis
* Anticholinergics to decrease secretions
* Anxiolytics
Administer meds
Continuous monitoring
Post-op education and expectations
Verbalize fears and feelings with client and family
D/C meds that cause bleeding
39
intraop care of Coronary Artery Bypass Graft (CABG)
* Padding bony prominences
* Communicate surgical progress to family/loved ones
* Continuous monitoring
* Arrange ICU placement after surgery
40
postop care assessment of CABG
*neuro assessement
*NG tube to decompress stomach
*ETT provide vent support, suction, end-tidal CO2
*central venous or Swan-Ganz catheter for monitoring central venous pressure, etc.
* ECG monitoring
* SpO2 monitoring
* assess skin color and temp
* epicardial pacing electrodes
* mediastinal and pleural chest tubes
* radial arterial line - blood pressure
* indwelling catheter
* assess pulses
41
postop cardiac care - restoring cardiac output
* Evaluate cardiac status and kidney
function
* Monitor for Afib, decreased cardiac output
* Stabilize rhythm as necessary
* Check patency of mediastinal tube
* Diuretics, dig, and IV inotropics
for cardiac failure
* Treatment for tachycardia and/or bradycardia
* Monitor for cardiac tamponade
42
postop cardiac care - maintaining adequate perfusion
Report s/s of emboli/thrombus
Prevent venous stasis
* Compression wraps, elastic
stocking, discourage
crossing legs, early
frequent ambulation
Report U/O < 30 ml/hr Monitor kidney function
Fluids replacement with colloids, PRBCs, or crystalloids
Change dosage of vasopressors (reduce blood flow to kidneys) CRRT or dialysis if necessary
43
Postop cardiac Care ~ Maintaining Normal Body Temperature
* Warm to temperature gradually (98.6)
** Warm ventilator air
** Warming system, blankets, heated lamps
* Prevent hypothermia
** Makes clotting less efficient, prone to arrhythmias, oxygen doesn’t readily transfer from hemoglobin to tissues, and causes vasoconstriction
44
Postop cardiac Care ~ Monitoring and Managing Potential Complications (infection control and F&E balance)
Infection Control
* Hand hygiene
* Antibiotics
* Remove all invasive equipment ASAP
* Aseptic technique with wound care and dressing changes
F&E imbalance
* Nursing assessment of I&O, weight, hemodynamics, hematocrit, neck veins,
edema, breath sounds, electrolytes, glucose
* Administer insulin if necessary
(regardless of dx of DM)
* Potassium, mag, sodium, and calcium treatment (high or low)
45
Postop cardiac Care ~ Monitoring and Managing Potential Complications (impaired gas exchange)
* Impaired gas exchange
** ETT with ventilator assistance initially
** Maintain patency of ETT
*** Suction
*** Secure the tube
*** Extubated as soon as possible
* Pulmonary interventions
*** Turning
*** Coughing and deep breathing
*** IS
46
Postop Cardiac Care ~ Monitoring and Managing Potential Complications
* Impaired Cerebral Circulation
* Observe for s/s of hypoxia
* Assess neuro status
* Note any immediate change to the provider
* Monitor for s/s of stroke
47
Postop Cardiac Care ~ Minimizing Sensory-Perception Imbalance
Prevention and treatment of delirium
* Treat cause
Be aware of sleep deprivation in ICU
Careful explanation of procedures
Continuity of care Welcome family at bedside
Won’t get back to baseline for 3-12 months
48
Postop Cardiac Care ~ Relieving
Pain
NO IV and oral NSAIDs
* To decrease opioid use
Administer analgesics as
necessary
Splinting with increased intra-
abdominal pressure
Improvement in pain after removal of mediastinal tubes
49
what is the purpose of cardiac rehab
* Active rehab program to reduce cardiac risk through education, individual and group support,
and physical activity
* Assist patient with cardiac disease to achieving a productive life while remaining within the limits of their heart’s ability to respond to increases in activity and stress
50
3 phases of cardiac rehab
Phase 1
* Starts with acute illness
* Consist of low-level activities and initial education
Phase 2
* After discharge into a cardiac rehab program at home
* Supervised exercise training
Phase 3
* Long-term conditioning and maintaining cardiovascular stability
51
nursing management during cardiac rehab
Implement orders to relief pain and other s/s of ischemia
Assess VS frequently
Physical rest with semi-Fowler’s position to decrease 02 demand
*If hypotensive, place in supine position with legs elevated
Health promotion activities after an MI/ACS
Alleviate fears and anxiety
Closely report and monitor changes
52
patho of acute HF
*Inability of the heart to pump sufficient blood to meet the needs of the tissues for 02 and nutrients
*Issue with contraction of the heart (systolic dysfunction) or filling of heart (diastolic dysfunction)
53
medical management of Chronic HF
* Lifestyle changes - decrease weight, exercise, decrease sodium, decrease fluid, no alcohol or smoking,
--report fluid weight gain
* Pharm (diuretics, inotropes, ACE inhibitors, ARBs, beta blockers, nesiritide, digoxin, vasodilators)
54
nursing management of chronic HF
medication effects
assess emotional response
resources
assess health history
assess ADLS
daily weights
making urine?
pitting edema
55
digitalis toxicity
56
Risk factors for chronic HF
HTN
dm
abd obesity
high cholesterol
CAD
previous stroke
PVD
increased fasting glucose
atherosclerosis
57
Right sided heart failure
ventricle pump fails leading to cengestion in peripheral tissues
enlarge liver
JVD
edema in LE
ascites
anorexia
N
fluid retetnion
weight gain
decrease in perfusion to systemic organs
fatigue from decreased CO
58
Left sided HF
left ventricle can no longer pump blood into the aorta and systemic circulation
leads to pulmonary congestion
dyspnea
orthopnea - lying down - pt has to sit up when sleeping (how many pillows?)
crackles
decreased O2 sats
S3
cough
tachypnea
weak thready pulse
fatigue a
activity intolorence
59
NSTEMI vs STEMI
NSTEMI - ST not elevated or depressure - partial occlusion of vessel
STEMI - ST elevated
get
60
abnormal accumulation of fluid in lungs
* Increased resistance to left ventricular filling blood to backup
fluid accumulates in alveoli
pulmonary edema
61
cause of acute HF/pulmonary edema
* Cardiogenic or noncardiogenic (AKI, liver failure, rapid admin of IVF, oncologic disorders)
* Leads to impaired gas exchange and hypoxemia (HA, confusion, SOB, restlessness)
62
clinical manifestations of pulmonary edema
* Restless, anxious
* Sudden onset of breathlessness, sense of suffocation, persistent cough with pink-tinged frothy
sputum, pulmonary crackles, expiratory wheezing, tachypnea, orthopnea
* Cold moist skin, cyanotic nail beds
* Weak and rapid pulse, JVD
* Reduced U/O
63
medical and nursing management of pulmonary edema
* Oxygen
* Diuretics
* Hemodynamic monitoring - decrease pre and after load
* Noninvasive mask ventilation
* Bronchodilator therapy with albuterol
* High fowlers position with dependent position (decrease preload)
* Morphine
* Inotropes (dig, dobutamine)
* Check ABGs, CXR, Sa02, electrolytes
* Restrict fluid intake
64
treatment for pulmonary edema (MAD DOG)
Morphine
Airway
Digitalis
Diuretics
Oxygen
Blood gases
