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Cc 6 cardiac
Critical Care (408)
Loma Linda University
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Cardiovascular Disease Peripheral Arterial Disease PAD | Signs and Symptoms intermittent claudication ischemic pain – cramp/ache while walking superficial femoral & popliteal
most common distal aortic & iliac
more intense w/ activity & relieved with rest
PAD atherosclerosis progress
narrow or block arterial blood flow
ischemia pain
rest pain more severe than intermittent claudication continuous burning pain of lower leg/feet aggravated when leg/feet elevated or recline IMMEDIATE catheter or surgery to save limb s/s acute occlusion pain, pulse loss, pallor, coldness, motor/sensory changes atrophic tissue changes skin & nail change, muscle/soft tissue wasting, skin ulcers, gangrene
CV dz leading cause of death in US coronary artery dz (CAD) biggest contributor to cardiovascular dz morbidity & mortality CAD = atherosclerosis of coronary artery & heart
structures imbalance
between myocardial O2 supply & demand Atherosclerosis affects medium-sized arteries that perfuse heart & other major organs develops by accumulation of macrophages & T-cells in
arterial intima wall chronic
inflammation
high LDL triggers vascular
inflammation monocytes
stick to endothelial cells &
migrate to vessel wall foam
cells = marker of atherosclerosis
venous dz more chronic
does NOT require ICU arterial disease more
serious & acute require ICU
admission for acute thrombotic occlusion or after vascular surgery Risk Factors (same as CAD) diabetes mellitus smoking hypertension, hyperlipidemia male presence of kidney dz Pathophysiology atherosclerosis/arteriosclerosis spasm/inflammation trauma compression thrombus/embolus (clots)
Ankle Brachial Index DX test for PAD & intermittent claudication arm SBP ÷ ankle/leg SBP normal: 0 – 1. mild PAD: 0 – 0. moderate PAD: 0 – 0. severe PAD: 0 or less
PAD | Medical Management elimination of risk factors pharmacologic therapy anticoagulants, antiplatelet, vasodilator percutaneous transluminal angioplasty (PTA) percutaneous coronary intervention (PCI) stent placement (PTCA) bypass surgery
PAD | Nursing Management monitor peripheral arterial pulses maintain skin integrity & prevent skin breakdown pain control (give pain meds) Nursing management after angioplasty dysrhythmias (atrial fibrillation) renal failure (r/t dye in vessels leaving body)
hematoma (r/t puncture) hold pressure
for 15min Cardiovascular Exam C-reactive Protein (CRP) normal: 0 – 0 mg/dL low risk: <1. average risk: 1 – 3. highest risk: >3. unspecified inflammation w/ increased risk of developing other CV risk factors (DM, HTN, ↑ wt.) Lipid Panel LDL: normal ≤ 130mg/dL (bad cholesterol) HDL: normal ≥ 35mg/dL (good cholesterol) cholesterol: normal ≤ 200mg/dL triglycerides: normal ≤ 150 mg/dL Homocysteine normal: 5-15 mmol/L
Imaging Studies chest x-ray (CXR) evaluates volume status & possible causes of chest discomfort echocardiogram assess left ventricle function & regional wall motion abnormalities cardiac stress testing treadmill/imaging/ echocardiogram help dx and risk stratify these patients coronary angiogram/cardiac catheterization reveal coronary artery luminal irregularities or stenotic lesions
PCI – nursing management H&P & 12 Lead EKG (w/in 10min of onset & before O2 or pain meds) Cardiac Enzyme (CE) biomarkers troponin I – indicates cardiac damage <0: normal >0: significant indicator of MI within 12hrs of chest pain troponin T creatine kinase-MB (CK- MB) – cardiac damage *cardiac enzymes may NOT be elevated initially
may continue to rise
after reperfusion
monitor for recurrent angina vasospasm or reocclusion monitor for reperfusion arrhythmias (A-fib , AIVR ) prevent acute kidney injury contrast dye can dmg
kidneys renal failure
provide adequate hydration maintain skin integrity angioseal: gauze w/ occlusive dressing leave angioseal on until it falls risk for hematoma r/t puncture risk for bleeding lay flat for 4-6hrs assess for back/flank
pain retroperitoneal
bleed assess peripheral pulses
Cardiovascular Symptoms Cardiovascular History Risk factors
Non- modifiable age sex family history race
Modifiable Risk factors smoking
quitting ↓ risk CAD by a
lot
↓HDL, ↑LDL,
↑triglycerides
HTN
hyperlipidemia foam cells in arteries
↑ risk
atherosclerosis physical inactivity diabetes stress obesity BMI >
chest pain chest pressure and heaviness shortness of breath (dyspnea) caused by congestion from HF dyspnea on exertion (DOE) orthopnea (SOB when lying flat) wheezing dizziness/syncope palpitation fatigue edema (d/t fluid accumulation) intermittent claudication cyanosis
history of present illness: chest pain pertinent past medical/surgical history OLDCART O: onset of pain/discomfort L: location of pain/discomfort D: duration of pain/discomfort C: characteristics of pain A: aggravating/associated factors SOB, n/v, syncope R: radiating pain to another area T: treatment
Acute Coronary Syndrome (CAD sx: unstable acute MI)
Acute Coronary Syndrome - Management (MONA/s) M – morphine IV per protocol decreases cardiac preload &
afterload lower O2 demand
relieve ischemic pain O – O nasal cannula
start low & go slow maintain
SpO2 >92% N – nitroglycerin (NTG) sublingual, paste, IV stable angina 0 SL q5min up to 3 doses when stable, use prophylactic patch on chest wall q4-6hr prn NSTEMI
multiple SL doses IV if no
response to SL titrate to relieve chest pain & prevent HypoTN anticoagulation (heparin) also started interacts w/ sildenafil (Viagra) NTG used w/ caution in any patient w/ presumptive evidence of right ventricular infarction because of profound effect on preload A – aspirin 81-650mg chewable non-enteric coated S – surveillance for complications
Myocardial Infarction (MI)
Stable Angina predictable relieved by rest and nitroglycerin blockage from stable plaque or
spasm decreased blood flow
myocardial ischemia Unstable Angina/ACS unpredictable may awaken from sleep and need something in addition to nitrate to relieve pain
plaque ruptured thrombus
formation can lead to MI unstable angina w/o ST elevation requires immediate medical attention Variant/Prinzmetal’s Angina caused by vasospasm involves ST elevation CYCLICAL, at rest same time of day treated w/ nitrates & CCB Silent Ischemia objective evidence on EKG but pt doesn’t have chest pain
STEMI – ST Elevation Myocardial Infarction ST segment changes ST elevation > 1mm (1 small box)
total occlusion of coronary artery
transmural ischemia of the
myocardial tissue myocardial
necrosis persistent ST elevation
on EKG NSTEMI – Non-ST Elevation Myocardial Infarction no ST segment changes absent ST segment elevation on 12lead EKG cardiac enzymes (CE) elevated MI pathophysiology initially: myocardial ischemia (T wave inversion) due to atherosclerosis or spasm
cells still viable priority to
save muscle repolarization is temporarily impaired but will eventually restore to normal
myocardial injury (ST elevation)
infarcted zone surrounded by
injured zone still potentially
viable
myocardial infarction (long Q
wave)
necrosis in myocardium
irreversible pathologic Q wave d/t lack of depolarization from cardiac surface involved in MI cells in necrotic area replaced w/ scar tissue
locatio n
vessel ek g lea
s/s MI – Management
TIME IS TISSUE cardiac tissue
12 lead EKG within 10min of contact w/ healthcare system MONA (morphine, o2, nitrate,
dyspnea) crackles edema manifestations of inadequate tissue perfusion fatigue or poor activity tolerance ↑SVR, ↓BP, ↓CO, ↑HR, ↑preload Diagnostics
ANP/BNP – ↑in heart failure
ANP – atria BNP - ventricle EKG – arrhythmias, axis deviation left ventricular hypertrophy: R wave in aVL >11mm CXR – cardiomegaly echocardiograph: ventricular dysfunction and/or valve abnormalities stress/exercise test: ventricular dysfunction PCI: CAD, ventricular dysfunction
beta blockers used in systolic HF to improve EF/prevent cardiac remodeling increase contractility (need help w/ pump blood out) Management - pharmacological Impaired Contractility inotropic agents (digoxin, dopamine, dobutamine)
both ↑ CO
dopamine: for cardiac contractility initial: 5mcg/kg/min increase by 5mcg/kg/min (q10-30min) max rate: 50mcg/kg/min dopamine doses < 5mcg/kg/ min are for renal perfusion pacemaker
Nursing Actions monitor BNP oxygenation hemodynamic monitoring rest & pain control emotional support nutrition & education
Prevention/Monitoring exacerbation prevention symptom medication adherence diet exercise symptom monitoring daily weight ankle assessment symptom management diet changes extra dose of Lasix (if there’s more edema than expected |
s/s of worsening HF give
more Lasix)
Fluid overload diuretics (loop/K- sparing) fluid & sodium restriction Increased overload beta blocker vasodilator (hydralazine)
Increase preload vasodilator ACE inhibitor ARB Hypokalemia potassium Dysrhythmias antiarrhythmic agents Other drugs anticoagulant Cardiomyopathy – disease of heart muscle
Cardiomyopathy Management Impaired Contractility inotropic agent (digoxin, dopamine, dobutamine) pacemaker Left Ventricle Dysfunction beta blocker (carvedilol, atenolol) Dysrhythmias anti-arrhythmic agent (amiodarone) Dilated Cardiomyopathy (DCM) ACE inhibitor (lisinopril) first line of treatment regardless if asymptomatic or symptomatic
Cardiomyopathy education catered to type of CM and HF fluid balance low Na, reduce fluid, I/O, s/s edema daily weights breathlessness (SOB, wheezing) sleep upright w/ pillows activity conserve energy w/ rest medications follow-up & symptoms to report
Primary unknown cause viral (chagus) autoimmune hypertrophic- narrowing of ventricular space, impaired systole 20-50% Dilated
Secondary result of systemic disease valvular dz CAD HTN alcohol abuse autoimmune
Mechanical Circulatory Assist Device
How IABP Works – inflates on onset of diastole
↑ perfusion to coronary arteries
↑ perfusion to kidneys
displaces blood ↓afterload
↑CO
improves O2 supply/demand balance inflation occurs prior to dicrotic notch (AV closure) = pressure rise/AUGMENTATION. AUG > systole IABP Contraindications aortic aneurysm, severe aortic regurg, severe coag
IABP Nursing Actions maintain perfusion pulse, color, temp, cap refill, calf circumference anticoagulation balloon rupture* blood in tubing balloon migration* upwards: assess radial pulse (tachy), LOC (ALOC) down: assess urine output, GI s/ s timing of IABP 1:2, 2:
intraabdominal balloon pump (IABP) ventricular assist device (VAD) used to treat HF when pharmacological therapy has failed goal
↓ myocardial workload
maintain adequate perfusion to vital organs allow myocardium time to recover
aortic valve insufficiency severe peripheral vascular disease Effects of IABP Increased coronary blood flow CO UOP improved mentation Decreased s/s myocardial ischemia angina, ST changes, ventricular arrhythmias myocardial oxygen demand heart rate
4:1, 8:1 – weaning only for a short time prevent complications log roll q2h maintain skin integrity incentive spirometer; prevent atelectasis monitor platelet count risk for thrombocytopenia d/t mechanical destruction of plts by balloon pumping psychosocial needs sleep deprivation anxiety education explain device, activity restriction report pain in back, legs, chest
IABP Indications failure to wean to bypass recurrent angina after acute MI hemodynamic support for high-risk PCI and CABG complications of acute MI cardiogenic shock papillary muscle dysfunction or rupture w/ mitral regurgitation ventricular septal rupture bridge to definitive therapy (LVAD, cardiac transplant) AUG PEAK (diastole) > dicrotic notch = (GOOD) Dicrotic notch = aortic valve closure. Inflate before!! VAD partially or completely replace heart function continuous flow rotary pump produces nonpulsative flow used for failing right ventricle, left ventricle, or both flow rate 1-10L/min
↓ ventricular workload
maintain adequate CO
VAD Indications bridge to recovery persistent HF despite aggressive medical tx & potential to regain normal function if heart given time to rest acute post-surgical myocardial dysfunction refractory cardiogenic shock after acute MI or acute viral myocarditis bridge to transplantation decompensated chronic HF needing circulatory support until heart transplant destination therapy therapy for severe HF pts who are not candidates for heart transplant & all other medical options have been exhausted
LVAD Nursing Actions continuous-flow hemodynamics pulseless machine-like heart tones use MAP for BP (not systole/diastole) pulse ox may/may not work PUMP IS VOLUME DEPENDENT (PRELOAD) basic assessment circulation mentation urine output prevent line infection
Heart Failure & Pacers 1/3 of HF pts have conduction delays hemodynamic consequences of dyssynchrony impaired ventricular filling w/
↓EF, CO, MAP
cardiac resynchronization therapy (CRT) atrial pacing plus stimulation of both LV and RT (bivent pacing)
3 pacing leads one each in
RA and RV inserted thru
coronary sinus to pace the LV
Implantable Cardioverter Defribillator (ICD) identify & terminate life threatening V-dysrhythmias qualified: survivors of cardiac arrest d/t VF or VT current HF guidelines to recommend ICD EF <35% even w/o incidence of VT/VF Endocarditis Aortic Aneurysm Assessment Findings not always symptomatic detected on palpation of umbilical area midline or left hypertension fleeting peripheral pulses (comes and goes) aortic regurgitation murmur bruit acute neurological changes severe, intense, tearing PAIN (dissected AAA) chest, abdomen, back, lower
bacteremia thrombotic
vegetation colonization
encasement in fibrin shell protecting from phagocyte
destruction localized
agranulocytosis lesions may invade adjacent tissues aortic or mitral valves Predisposing Factor IV drug abuse: 60x or higher 75% pre-existing structure abnormality
abdominal aortic aneurysm (AAA) most common
localized dilation of arterial wall
alteration in vessel shape and BF pulsatile mass in umbilical region (can palpate it) etiology atherosclerosis/arteriosclerosis hypertension (90%) blunt trauma tear or shearing of the aorta marfan syndrome pregnancy
Bradycardia, AV block, N/V INFERIOR - RCA
Bradycardia, AV block, N/V INFERIOR - RCA
Sick, left ventricular failure, cardiogenic shock ANTERIOSEPTAL
- LAD
arrhythmias (v-fib, v-tach, PVCs) LATERAL - CIRCUMFLEX
DVT predisposition: Need two of three: (Virchow’s triad) need US -stasis of blood -endothelial injury -hypercoagulability Also assess for HOMAN’S sign. (pain in calf on dorsiflexion) Mgmt: confirmed? IV HEP, ORAL ANTI-PLT, ANTICOAGS Monitor for s/s PE: chest pain, dyspnea, hemoptysis, tachypnea, ALOC (need CT) Mgmt: thrombolytics, airway/intubation
Cc 6 cardiac
Course: Critical Care (408)
University: Loma Linda University
