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Leading cause of death in the US
- Coronary Artery Disease
- (over 60 million people have CAD)
- (kills 10x more women than breast cancer)
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Cause of Coronary Artery Disease
Atherosclerosis ("hard fatty streaks")
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Pt Hx when presenting with cardiac issues consists of:
- History of Present Illness
- (analysis of chest discomfort or presenting symptoms, also recent symptoms...PQRST method!)
Past history of cardiac problems & evaluations
- Risk Factors
- (cultural/ethnic factors, Family Hx)
- Medications they are on
- Allergies
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Analysis of Chest Pain using this method:
PQRST
- P- precipitating events
- Q- quality of pain (tightness, dull, sharp?)
- R- radiation of pain? (neck, jaw, arms)
- S- severity of pain (rate on pain scale, but MI doesn't always present as a "10")
- T- timing (how long does it last, start?)
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Risk factors for CAD
- Nonmodifiable:
- Age
- Gender
- Ethnicity
- Family Hx
- Modifiable:
- Abnormal serum lipid levels
- Hypertension
- Tobacco use
- Inactivity
- Obesity
- Diabetes
- Metabolic Syndrome
- High Homocysteine
- Psycological states
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Cultural/Ethnic Factors affecting CAD:
Caucasian- men have highest incidence of CAD
African American- earlier onset, women have higher incidence, mortality, and severity of CAD
Native American- <35 yrs old has double mortality of other Americans (Obesity and DM are major risk factors)
Hispanic- lower mortality rates
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3 ways that CAD may present:
Angina Pectoris
- Acute Coronary Syndrome
- -unstable angina
- -non-STEMI
- -STEMI
Sudden Cardiac Death
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All symptoms of CAD are the result of:
ishchemia
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When lack of oxygen is temporary and reversible, but causes pain:
STABLE angina
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When lack of oxygen is prolonged ____ results which presents in what 3 ways?
Acute Coronary Syndrome
- 1- Unstable Angina
- 2- Non-ST elevation myocardial infarction
- 3- ST-elevation myocardial infarction
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Ischemia may result when the heart muscle:
Has an increased demand/need for oxygen
OR
Has a decreased supply of oxygen
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Factor that could increase the heart's demand for oxygen
Exercise
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Factors that could cause a decreased supply of oxygen to the heart:
Stimulants/Drugs, Impairments of airway exchange, Hypovolemia
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The myocardium becomes cyanotic within ____
the 1st 10 seconds of coronary occlusion.....
Anaerobic metabolism begins > the byproduct of anaerobic metabolism is lactic acid > this acid irritates nerve fibers in the myocardium > pain occurs
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Angina is a syndrome due to _____ , but damage to cells is _____
Ischemia, Reversible
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Myocardial Infarction means that there has been _______ which has caused cell _____
sustained ischemia, dead (forever and ever)
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Chest discomfort which occurs intermittently over a long period of time with the same pattern of onset, duration and intensity of symptoms
Stable Angina
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Stable angina lasts for how long?
5-15 minutes, but stops when the precipitating factor is relieved
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EKG changes indicating Stable Angina
ST depression
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What are the "4 E's" that precipitate angina?
- Exercise
- Emotion
- Eating a large meal
- Extreme Temperatures
(also strong stimulants like cocaine, amphetamines, tobacco, sex, circadian rhythm)
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Why do many people have early morning angina?
Most of the cortisol in the body is released in the morning
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Angina due to spasm of a major coronary artery
Prinzmetal's Angina (variant angina)
Occurs at REST
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Prinzmetal's Angina is usually seen in people with:
Raynaud's disease
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EKG change related to Prinzmetal's Angina
ST elevation (disappears spontaneously)
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When there is a change in the established pattern of angina or a new onset of symptoms occurs, it is considered:
UNSTABLE angina
*Emergency! (often means the atherosclerotic plaque has been deteriorated or changed)
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Treat a Non-STEMI like ____ because occlusion to the coronary artery is incomplete
Unstable Angina
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Non-Stemi has a ____ plaque
Stable
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A STEMI has an _____ plaque
Unstable Plaque
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S/S of MI
Sustained pain not relieved by anything
Can occur at rest/active
Statistically more common in early morning
Possible radiation to the jaw, neck, arm, back but primarily substernal
N/V
Cool, clammy skin with ashen color
Feeling of impending doom
Denial that anything bad will happen
BP initially goes by but may crash once damage is done to the heart
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How do women present differently than men with s/s of MI?
SOB/crippling fatigue may be first symptom
Pain may not be as distinct as it is for men (may be described as dull or more like GI pain)
Frequent radiation into jaw and shoulder
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How do diabetics/elderly commonly present MI s/s?
They many not have pain due to neuropathy.... "silent ischemia"
SOB, decreased LOC, etc
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Any unexpected death from cardiac source:
- Sudden cardiac death
- (accounts for 50% of all deaths from CV sources)
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Sudden Cardiac Death is usually caused by
Acute Ventricular Arrhythmia
***If people survive give anti-arrhythmic meds and implantable ICD needed long term
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The _______ is divided into 2 branches and perfuses the ANTERIAL WALL
Left Coronary Artery
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The artery between the left atrium and ventricle that Perfuses the Lateral Wall of the heart
Circumflex Artery
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Artery that Perfuses the INFERIOR WALL of the heart
Right Coronary artery
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Stage of circulation when blood is filling into the coronary arteries:
- Ventricular Diastole
- (anything that increases HR puts at risk for angina because the heart doesn't have time to rest and fill completely)
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Complications of MI
Arrhythmias are #1 (80% of people have them, number 1 cause of death)
Heart Failure
Cardiogenic Shock
Papillary muscle dysfunction --> mitral regurgitation
Pericarditis--> infarcted area inflamed
Dressler's Syndrome--> antigen/antibody reaction
Ventricular Septal Defect
Ventricular Aneurysm
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Priority of MI patient
PUT ON MONITOR! (monitor rhythm and HR)
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Sx of Heart Failure:
- Respiratory symptoms
- SOB, sitting up to breath, crackles
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S/s of cardiogenic shock:
- low BP
- low MAP (norm = 70-92)
- cold, clammy, diaphoretic
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If you hear a new murmur on a pt, they likely have:
papillary muscle dysfunction (mitral regurgitation)....they may be going into cardiogenic shock
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S/s of Pericarditis
- Friction Rub
- (due to cytokines being released)
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Syndrome when the body is trying to get rid of the infarcted heart tissue (antigen/antibody reaction)
Dressler's Syndrome
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Hole in the ventricular septum causing a very loud murmur and palpable THRILL
Ventricular Septal Defect (VSD)
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When the ventricle that is affected is dead and won't contract (balloons out)...sometimes gets clots in it and puts pt at risk for emboli
Ventricular Aneurysm
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Patient assessment of a pt presenting with MI
- Pain
- Color/Temp = low grade fever, cool, ashen color
- BP/HR= will tell us how hard heart is working
- Lung Sounds- listen for crackles
- Heart Sounds- Gallops, Murmurs, Thrills
- N/V
- Cardiac Rhythm
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When heat is having difficulty/abnormal ventricular filling, a ____ will be heard
S3 gallop -- "A-slosh-ny"
*Turn pt on lateral recumbant position
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Sound heard due to the thickened heart muscle...atrium is trying to pump against resistant ventricle (caused by prolonged blood pressure)
S4 gallop -- "A-Stiff-Heart"
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Physician Orders for a pt presenting with MI s/s
Vital Signs STAT, then HR/BP every 15 min
Continuous pulse ox
ECG STAT and every 8 hours x2
Cardiac Isoenzymes STAT & every 8 hrs x2
CBC and CMP STAT
Portable CXR now
NPO except meds
IV access (INT) x2
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How often are EKG's required for MI patient?
Every 8 hours to fully see changes
(may take several hours before MI s/s are seen)
Don't be fooled if EKG looks ok in ER!!!
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T-wave inversion represents:
Ischemia
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ST segment Elevation (>1mm) represents:
Severe Injury
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An elevation of _____ on 2 consecutive leads is diagnostic indicator of MI
ST segment
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To measure ST elevation, start at this point:
- J-point
- (.06-.08 after end of QRS segment)
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Significant Q wave changes on ECG represents:
Necrosis of heart
(if Q wave shows up .04 seconds or 25% of R wave depth WITHOUT STsegment or Twave changes...indicates Old MI)
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Abnormal Q wave measurements:
.04 seconds or 25% of R-wave depth
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Serum Cardiac Markers (Enzymes)
- Troponin (norm = <.4)
- CK-MB (norm= 0-5)
- Myoglobin
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Most sensitive muscle protein...Blood levels rise in few hours and stay up for weeks
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Cardio-sepcific isoenzyme that goes up in a few hours after MI, peaks in 24 hours, and returns in 2-3 days
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Least specific cardiac enzyme that increases in 1-3 hours, peaks within 12 hours
Myoglobin
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Diagnostic Tests for MI
- EKG
- Enzymes
- Stress Test
- Cardiac Cath (coronary angiography)
- Echocardiogram (tells us ejection fraction, ishemia, infarct)
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Normal Ejection Fraction:
>60%
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Everyone presenting with chest discomfort or s/s of MI will get:
ASPIRIN! (acts as anti-platelet until MI discovered)
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Treatment of Angina:
"ABCDE" (ASA, ACE inhib, Anti-anginal meds; Beta blockers, BP control; Cholesterol management, Cigarette Cessation; Diabetes control, Diet management; Exercise and Education)
OR
Nitrates, Beta Blockers, Calcium Channel Blockers, Anti-platelet/Anticoagulation therapy, Ranexa (anti-anginal), Oxygen
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Types of Anti-platelet and Anticoagulation Therapy:
- Aspirin
- Thienopyridines (Plavix, Effient)
- IV Heparin or SQ LMWH
- Lovenox
- Fragmin
- Glycoprotein llb/llla agents
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Treatments of Severe CAD and history of MI
Percutaneous Coronary Intervention (angioplasty) -- STENTS
Myocardial Revascularization (Coronary Artery Bypass Surgery...CABG) -- new vessels around blockages to promote bloodflow
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Total Treatment of MI
- Rapid Diagnosis and Treatment to save muscle
- Chew ASA or give heparin
- Establish IV access
- IV morphine 2-4 mg every 3-5 min for pain
- Oxygen (2-4 L/min)
- Cardiac Monitor
- IV nitro
- IV amiodarone drip (if arrhythmias)
- Frequent VS
- Complete Bed Rest!!!
- Emotional Support
" MONA"-- morphine, oxygen, nitro, aspirin
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MONA stands for:
Morphine, oxygen, nitro, aspirin
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Medications used for MI
- Nitrates (IV while in ER/ICU)
- Antiarrhythmic Drugs
- Morphine
- Beta Blockers
- ACE inhib (captopril, ramipril, enalapril)
- Anti-dyslipidemic meds (statins)
- Stool Softeners
- Anti-anxiety meds
- Anti-platelet agents (includes IV Glycoprotein IIb/IIIa inhibitors (to inhibit and block the final pathway for platelet aggregation)
- IV Access
- Oxygen
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Nursing Care for pt with recent MI
- -Med Admin
- -Monitoring for complications
- -Monitoring/Titration for desirable drug effect and adverse reactions
- -Prioritization of care delivery
- -Pt/Family education and emotional support
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Goal of Emergent Percutaneous Coronary Intervention (PCI)
Door to Balloon within 90 minutes!
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Advantages to PCI for MI pt
Early ambulation, discharge, and return to work
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Complications of PCI
- Coronary dissection (causes acute closure)
- Plaque dislodgement
- Coronary Spasm
- Restenosis (insetnt--closes off inside stent)
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Clot Busters (Fibrinolytic Therapy)
Tissue Plasminogen activator or STREPTOKINASE
(if done in first hour or two, can stop infarction and save muscle...dissolves clot and re-establishes blood through coronary artery...pt selection is critical! Follow clot busters with PCI)
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Goal of Clot Busters
Give within 30 min arrival!
(make sure you have all IV access ready in case of complications)
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Complications from Clot Buster
BLEEDING!
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Hospital Discharge process for post-MI pt
- Education!
- -patho
- -recovery procedure
- -low fat, low salt diet
- -proper use of nitro (sitting down)
- -how to check pulse
- -important of exercise routine
- -resuming ADL
- -resuming sexual activity
- Follow-up appointments with Doctors
- List of Medications and reasons for taking them
- Other written instructions
- Cardiac Rehab Phase II
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Core Measures for a patient that has had an acute myocardial infarction:
- ACEI on discharge for LVEF <40%
- Beta Blockers
- Statin prescribed if LDL >100 (lipid profile done within 24hrs admission)
- Aspirin given on arrival/prescribed at discharge
- Smoking Cessation Info
- Thrombolytics received within 30 min OR PCI received within 90 min of hospital arrival
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Procedure that redirects blood through a graft from aorta to coronary artery just beyond the obstruction
CABG (bypass)
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Vein used from lower leg that is grafted on heart and attached proximally to aorta and distally to the coronary artery below the obstruction
Saphenous Vein
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Graft of choice used in a CABG and attached to the coronary artery below the area of obstruction...has a superior patency rate (longer than saphenous vein)
Internal Mammary Artery
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Pt undergoing CABG are put in cardioplegia (heart stopped) by using ____
Hyperkalmic Solution
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Functions of Cardiopulmonary Bypass Machine
Extracorpeal Circulation (blood bypasses the heart so that it can be still during surgery)
Maintains adequate hemodynamics and metabolic conditions during surgery
Allows surgeons to work on bloodless field
Hypothermia used to reduce oxygen requirements
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Complications during CABG
Ischemic Myocardial injury
Heart Failure
Arrhythmias
Limb Ischemia
Excessive Bleeding (over 200cc/hr...ANYTHING OVER 100 IS TOO MUCH)
Hyper/Hypovolemia
Respiratory Complications/Infections
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Nursing Care following CABG
People usually in ICU for 24-48 hours...can go home in 5-7 days
Assess S/S of angina (indication of grafts closing)
Deep Breathing, ROM, Dressing changes, support hose to decrease swelling at site of vein removal, should be no more than 100cc blood/ hour from chest tube!!!
Watch urine output carefully (renal perfusion) -- we want over 30ml/hr...give lasix if not!!!
Foley cath, hemodynamic monitoring, arterial line
Assess neuro status, strict I/O, give narcotics for pain
Watch for shivering, warming blanket prn
Teach family how loved ones will look/feel after surgery
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Amount of blood in ventricles at the end of diastole, affected by venous return to the heart
Preload
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Resistance against which the left ventricle must pump; affected by BP, Systematic Vascular Resistance, and Aortic Valve
Afterload
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Force opposing movement of blood created mostly in small arteries and arterioles
SVR (Systemic Vascular Resistance)
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What does vasoconstriction do to the SVR?
Increase SVR
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Volume of blood ejected from heart with each contraction
Stroke Volume
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Volume of blood ejected from heart per minute (SV*HR)
Cardiac Output
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Normal cardiac output
4-8 Liters/min in resting adults
Affected by HR, Contractility, Pre/afterload
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Normal Cardiac Index (CI)
2.2-4 Liters/min
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What is involved/ What is the purpose of Hemodynamic Monitoring?
Done to monitor cardiovascular function and blood volume
-place catheters in vascular system and hook them up to transducer and monitor! (invasive)
-we can measure wave forms to see how the heart is functioning
-Done for critically ill patients with heart or fluid volume problems
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Indicates the driving or perfusion pressure to the organs
Mean Arterial Pressure
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Formula for MAP
[SBP +2 (DBP)]/3
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Normal MAP
- 70-92 mm Hg
- (when you get below 60 your organs are at RISK!!!)
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A low MAP indicates
low perfusion which leads to ischemia
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Pressure in the right atrium and in the great veins as they enter the right atrium...indicator of circulating blood volume and right-heart pumping strength
Central Venous Pressure
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The CVP reading is dependent on:
The volume of blood entering the great veins, pumping of Right Ventricle, and the degree of Vasoconstriction in the vascular system
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A high CVP indicates
Hypervolemia or poor RV contraction
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A low CVP indicates
Hypovolemia
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Nursing intervention related to high CVP
slowing down rate of IV fluids OR give diuretic
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Nursing intervention related to low CVP
increase the rate of fluid (pt probably dehydrated)
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Pressure that reflects left ventricular function
Pulmonary Artery Pressure
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Normal PAP
15-30 / 4-12 mm Hg
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A high PAP indicates:
LV is failing as a pump and blood is backing up into pulmonary bed (or hypervolemic state)
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A low PAP indicates:
hypovolemia
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Normal PAWP (Pulmonary Artery Wedge Pressure)
6-12 mm Hg
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Why is PAWP a great indicator of Left Ventricular function?
Because during diastole the mitral valve is open, and the pressure in the pulmonary capillaries is the same as the pressure in the left ventricle
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Cardiac Output can be determined at bedside using:
- swan-ganz catheter
- (normal cardiac output = 4-8 L)
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If the left ventricle is failing, the ___ will be low
Cardiac Output
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Cardiac output adjusted for the patient's size
Cardiac Index (must determine pt surface area)
***no matter how large/small, CI should be 2.2-4L
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Catheter used to do all hemodynamic monitoring except arterial BP
Swan-Ganz Catheter
(CVP, PAP, PAWP, CO)
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Normal Strove Volume
60-100
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Systemic Vascular Resistance formula:
(MAP-CVP/CO) * 80
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PAWP and CO are _____ related
- Inversely
- (PAWP will go UP if heart cannot pump blood, CO will go DOWN)
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Maintenance of Hemodynamic Catheters:
-attached to bag of saline which is under pressure...serves as flush
-when attached to transducer, only 3cc of saline per hour (prevention of clots in cath)
-change every 7 days!
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Referencing for Transducer and Flush Set Up
Position stopcock nearest transducer at phlebostatic axis (midaxillary line and 4th ICS)
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Complications of PA Catheters
- Infection/Sepsis
- Air Embolus
- Pulmonary Infarction
- PA rupture
- Ventricular Arrhythmias
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Perform _____ before insertion of catheter to monitor Arterial Blood Pressure
Allen's Test
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Key Nursing role when monitoring Arterial Blood Pressure:
- Monitor for hemorrhage, infection, thrombus, neurovascular changes, loss of limb
- HOURLY!!!!
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