Cardiac Perfusion SG PDF

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Review of the Cardiac Anatomy and Physiology, Risk Factors, and Diagnostic Procedures    

Heart is a pump that is responsible to circulate blood throughout the entire body as well to its self Heart is comprised of a structural component as well as the electrical component. Both work together but the electrical refers to the heart beat itself Main purpose of the cardiovascular system is to deliver O2 and nutrients to the body

The structural component:  

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Location is chest with 2/3 of heart l of the midline 4 chamber pump with the upper 2 chambers working together and the lower chambers working together At the base of the heart is located the right and left atria, thin walled upper chambers of the heart. The ventricles are located at the apex (pointed end), thick walled lower chambers. Two sets of valves, atrioventricular (tricuspid and mitral) which separate the upper heart chambers from the lower chambers and the semilunar valves (pulmonic and aortic) which separate the ventricles from rest of the body. Flow of blood through the heart right atrium-tricuspid-right ventricle-pulmonic-lungs-left atrium-mitral-left ventricle-aorticperipheral system/organs of the body. Unlike other organs which are perfused during systole (contraction), the heart is perfused during relaxation or diastole. (This is Cardiac Perfusion) The LAD supplies the anterior wall of the heart and the ventricular septum. The Circumflex supplies oxygen to the left atrium, posterior and inferior wall of the left ventricle.

Physiology: Structural Component 

Heart is a pump and this pump has 2 basic phases diastole (Relaxation) and systole (Contraction)

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Cardiac cycle is one complete rotation through relaxation and contraction Diastole-This is the filling or passive stage of the cardiac cycle (relaxation) (think of filling a balloon with water. Systole-This is the active or contracting phase of the cardiac cycle, blood is pumped to the lungs from the right ventricle and pumped from the left ventricle to the systemic circulation.

Blood pumped out of the heart is the cardiac output Cardiac Output   

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Cardiac output is defined as the amount of blood ejected per minute. The resting is 6 L/min and the exercise is 20 L/min Cardiac Output= heart rate x stroke volume (need to know cardiac output) Along with CO need to know about the Ejection fraction which is the % of the total volume of blood that was ejected from the ventricle with each beat (normal is 65% which means 35% of the total volume of blood in the ventricle remains- this is reserve for increase activity, etc) Any changes in the anatomy either structural or electrical will impact the cardiac output During pregnancy increase in blood volume leads to increase in cardiac output this peaks around 20-24 weeks gestation (30-50% above pre-pregnancy level) Ejection fraction can be determined by dividing the stroke volume by the end diastolic volume

Cardiac Health Promotion and Risk Factors        

Smoking Hypertension Control DM Sedentary Lifestyle Obesity Menopause Diet High cholesterol

Diagnostic Tests 

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ECG/EKG (12 Leads)-non invasive what are we looking for with perfusion issues- St segment or T-wave changes (indicate cardiac ischemia) Echocardiogram (also stress echo using Dobutamine) basic echo is noninvasive and assesses the structure and function of the heart using sound waves- becomes invasive with the use of meds as stressors Stress test: exercise electrocardiogram Nuclear perfusion studies: an example is the Exercise Thallium Scan – radioisotope- uses treadmill and meds to stress the heart and its response to the stress- a damaged cardiac cell does not take the radioactive isotope-small amount of the isotope injected thru the antecubital vein Doppler MRI-non invasive-images the heart and great vessels Coronary (Angiogram / Arteriography) Heart Catheterization – Diagnostic but also can be an intervention-will discuss it more

Acute, Complex and Life-threatening Cardiac Perfusion Issues    

The impact of cardiac perfusion on the performance of the heart and other body systems Specific Assessment/Diagnostic tests for acute, complex and lifethreatening cardiac perfusion issues The Role of the Nurse in caring for clients with acute, complex and life-threatening cardiac perfusion issues Management of acute, complex and life-threatening cardiac perfusion issues

Cardiac Perfusion and Impact on Performance of the Heart    1. 2.

Perfusing heart itself – from aorta Provides heart with most nutritious blood Cardiac perfusion - 2 systems for perfusion pump electricity to make pump work

Ultimate goal: REPERFUSION OF THE HEART: anytime pump or electrical system fails – heart is not being perfusing Coronary arteries    

L descending perfuses left side – if not perfused Causes fatal heart attacks/MI – “widow maker” (left ventricle pumps out to body) If blockage – L or R ascending – create large problems

Cardiac Perfusion: Impact on Performance of the Entire Body If there is a cardiac issue – Examples:       

low UOP because kidneys are not perfused LOC – brain isn’t perfusing GI Muscle fatigue/weakness Peripheral pulses weak Extremities – cool to touch Impacts everything in the body bc it controls where the blood goes

RN Process / Role as RN:    

Assessment from fam hx Teaching/education Interventions Change across life span

Peds:  

SS of heart defects – know normal VS – NB, infant, toddler, etc Normal BP

Elderly:  

Baseline – LOC, ask about meds, HR, BP Looking at pain – subjective

Assessment: What defines acute, complex or life-threatening

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Decreased CO= decreased UOP, cap refill > 2 sec Smoking Activity level – define it – what is normal Sedentary lifestyle Current chest pain

4 things for assessment  

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Inspection Auscultation - s1, s2, listening for different sounds – abnormalities – s3, s4, mitral valve regurg, murmur – if so, what does it sound like, lungs as well (crackles, etc) Palpitation Percussion

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Palpitations of heart Orthopnea Dyspnea Nocturia Clubbed fingernails – very late sign – chronic HD Peripheral edema JVD Heart sounds or friction rubs VS that deviate from patients normal Infants – specifically - pallor, cyanosis, watching 02 sat’s - < 94% Gen peds – tachy, coolness/mottling of extremities, delayed cap refill, decreased UOP, hypotension Metabolic acidosis – happens fast

Pregnancy  

Increased palps and fatigue Baby puts strain on heart

Elderly 

Same for adult

Looking for the difference in signs in VS re: aging

#1 SS of assessment  

CHEST PAIN – remember – can be from several things Must define/describe pain

Chest Pain Assessment: What defines acute, complex or life-threatening Chest Pain: PPQQRRSST, pg 849, table 29-3   

General decreased CO SS           

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Placement – where is it? Show exact location. Provocation – Is there anything that brought the chest pain on? Were you being active? Were you laying down? Quality – Describe pain “it’s the worst pain I’ve ever had.”, “Heaviness”, etc Quantity – “how long? – constant, intermittent, one-time episode? Radiation – typical – left shoulder – women – jaw or shoulder, back = where is it radiating? Relief – is there anything you do to relieve the pain? Take antacid? Might be reflux. Severity – How bad is it? 0-10 pain scale. Tell me about the pain. Have you experienced this before? Had pain similar to this in the past? Symptoms – SOB, difficult with LOC, nauseated, diaphoretic, etc Timing – when did pain start? Ex: typically – when the person starts moving out of bed in the morning

Where is it located?       

Use chart above to see the different locations and different indicators Biggest indication of chest pain/MI: Shoulder pain Need to be able to dx chest pain to determine cardiac or another issue Tell me about chest pain When did it happen? Big meal? Activity? How did it happen?

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Physical exam: Show me where the pain is Previous hx of chest pain and what was the dx SOB, heaviness from chest pain, weakness DM? HTN? Smoke? Sedentary lifestyle? Illicit drugs? Fam hx? What meds are you taking? Taken anything that wasn’t yours?

Need to determine what meds they are taking Narrow down what the chest pain is and what it pertains to in the body Cardiac Output Assessment:     

Decreased UOP Decreased VS (LOC, BP, Pulses) Cool, clammy skin EJ Telemonitor

Pregnancy:      

SS – life threatening Irregular or dec. Heartbeat Dyspnea Edema in hands and face O2 sat: less than 95% -- o2 fast Postpartum – developing chest pain – possible hemorrhage

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Echocardiogram TEE PET Holter Monitor Scans Cardiac Catheterization

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Cardiac Markers – *very important to know* - labs – markers looking for: muscle tissue death – pg 889 – CPK, CK-MB, **Know: Troponin I and T = specially related to cardiac muscle damage - KNOW Troponin I - Chronic Angina -> Acute / Unstable coronary syndrome -> MI SS increase with intensity start with CAD  

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CHD/CAD – usually rel’d to coronary arteries – b/u of plaque in vessels – occurs naturally w/ age Angina – chest pain – o 15-20 mins pain o 3 types: stable vs unstable Ischemia; deficient blood flow to tissue may be caused by partial obstruction of coronary artery, CA spasm, or thrombus Acute coronary syndrome/unstable coronary syndrome – increasing frequency, severity, and duration. Pain is unpredictable, occurs w/ decreasing levels of activity or stress, may occur at rest o Sudden, onset or slowly over few weeks o Non-stemi, partially occluded o NOT DX, it is a syndrome (collection of symptoms) o Cool, clamy skin, fatigue, chest pain longer than 10 mins, each episode pain and time will inc, SOB, N/V, would not be relieved by Nitro o RF: 50 yrs or older, smoking o Tx: dec. workload of heart MI – myocardial infarction – necrosis of myocardial tissue, results from complete blockage of coronary artery o Goal: restoration of bld vessels ASAP

Jaw, neck, shoulder, lightheadedness (women), back pain, feeling of impending doom, vomiting Dx: tropin (elevated), ST segment (elevated or depressed), ABG, EKG Tx: cath: repair, stents Pharm: morphine, Nitro, aces/arbs/ beta blockers, stool softeners Interventions: VS, O2 sats, pain relief, bed rest, calm environment Acute pain, ineff tissue perfusion, RF: Obesity, males over 45, women 55, alc/drug use, Complication: Vtach/Vfib, structural defects, pericarditis, DEATH

Coronary Heart Disease (CHD) 

Impaired blood flow to the myocardium

Cause  

Leading cause of death with all Americans, except Asian American women Higher incidence – white males, women after menopause

Precipitating Factors or Risk Factors   

Fatty diets (fast food), smoking, genetics, sedentary lifestyle, HRT Soft plaque – more pliable, less of a concern Hard plaque – obstructive, cause more angina

Signs/Symptoms  

Some level of chest pain (mild), weakness, diaphoresis Or no SS at all

Diagnosis 

Cardiac cath to find plaque

Complications 

Will lead to angina, then MI, dysrhythmia, sudden death

Treatment  

Goal: Reperfusion of the heart Lipids, cholesterol meds, reduce risk factors, start exercising, maybe reperfusion procedures

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Definition: unstable coronary ischemia – condition of unstable ischemia – unstable angina or acute myocardial ischemia w or w/o significant injury of myocardial tissue Non stemi – non stable MI (bc it wasn’t completely occluded)

Cause:

Angina 

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Definition – transient chest pain resulting from reduced coronary blood flow, which causes a temp imb b/w myocardial blood flow Cause - activity, smoke inhalation, atherosclerosis, heart disease, vessel constriction that impairs blood supply to myocardial Precipitating Factors- extreme exercise, sedentary to active, emotional stress, consumption of heavy meal, extreme temps, stimulant abuse (cocaine), other heart probs, ventricular hypertrophy Sudden onset of chest pain – described sometimes as vice-like gripping pain

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Diagnostics: o

full cardiac work up - changes on EKG, changes in lab work, stress test, can be intermittent (ex: on and off for 2 weeks)

SS: chest pain, usually substernal or epigastric – often radiates to neck, L shoulder and or arm, typically lasts longer than 10-20 minutes, diaphoresis, SOB, n/v, pallor, cool skin (not enough CO), increasing intensity ST elevation during chest pain but goes away after pain has resolved o

Types (3) 1. Stable – insufficient and temporary – usually dt PF’s. Predictable 2. Prinzmetal’s (vasospastic) – not predictable, results from coronary arteries spasming. Once spasm has subsided, angina dissolves 3. Silent- angina that does not have normal SS – chest pain. More heart burn, or related to DM

Thrombus, not total occlusion, progression of plaque, inflammation of artery, smaller passageway for artery but req’g more o2 for heart

 Tx:

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decrease workload of heart – lie down/bed rest – some meds – antiplatelet – if clot was thrown – might be doing thrombolytics – must be given w/in 6-8 hrs

KEY: any pain with rest or meds that resolves within 15-20 minutes = angina Pharm   

Signs/Symptoms Complications – MI in future – warning sign Treatment –nitrates – nitroglycerin, calcium channel blockers, beta blockers – anything that will decrease CO of heart – rest/lie down

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If clots are present–

Key to angina – let heart rest / Goal – reperfusion Acute Coronary Syndrome

aspirin/day (to thin blood, prevent clot), Plavix, Calcium channel blockers, Beta blockers

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anticoags

***Start MONA possibly  

Morphine O2

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Nitrates Aspirin

Myocardial Infarction (STEMI/NON-STEMI)  

Persistent ischemia or lack of blood supply > 30 minutes Death/necrosis of myocardial cells

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Non STEMI – not a complete blockage STEMI - complete blockage Ischemia – starts in endocardium (inner aspect) and then travels to myocardium causing death of heart tissue (necrosis)

Based on o2 level

SS: Pain lasting >20-30 mins w/ or w/o chest pain, substernal or precordial, usu radiate to neck, down to arm, n/v, anxious, syncope, diaphoresis 

Women – jaw pain, chest pain ebb and flow, neck, shoulder, back, SOB, h/a, n/v

Diagnosis: depression T-wave inversion or elevated ST elevation, Q wave formation, EKG’s, cardiac markers, by hours, - STEMI – stays KEY: Difference between CS and MI MI – ST elevation does not resolve; CS the ST elevation resolves 

Damage depends on: Size and depth of MI, limited time frame or prolonged time (minutes to days), artery involved, comorbidities (COPD, emphysema, renal disease)

Typical tx of reperfusion of heart - MONA

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Morphine –morphine - used strictly for pain (nitro – used for angina) Oxygen Nitroglycerin - used to dilate vessels Aspirin – platelet inhibitor

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Bedrest – reduce workload Light diet – reduce workload Calm environment

Or

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Cardiac cath for treatment CABG Pharma: pain meds, thrombolytics, stool softeners, anti-emetics, lipid meds, dopamine to increase BP or BP med to lower BP, antiplatelet, anticoag Post MI: cardiac rehab Complications of MI: extension of MI – cardiac tamponade (compression of the heart DT fluid B/U in sac surrounding heart), cardiac rupture, dysrhythmias

Major Complications Post MI  

Dysrhythmias (V-Tach/V-fib)- most common - R side – right sided dysrhythmia; L side - ventricular v-fib, v-tach Pericarditis (2-3 days)

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Infarct Extension (10-14 days) Congestive Heart Failure Structural Defects (area of infarct thinner) – (septal defects) Cardiogenic Shock –shock related to pump failure – when the pump fails (occurs when the heart has been damaged so much that it is unable to supply enough blood to the vital organs of the body) o SS: tachypnea, hypotension, Confusion or lack of alertness, loss of consciousness, tachycardia, diaphoresis, pale skin, weak pulse, decreased or no urine output, cool hands and feet Cardiac Rupture dt thinning of the walls from MI o Immediate surgery Decreased Ejection Fraction – from 65% to 45% - fatigued Cardiac tamponade – fluid build up in pericardial sac: dec expansion, pressure on heart, not allowing to pump efficiently o SS: confusion, hypotension, SOB, lightheadedness, syncope, sharp chest pain, swelling of extrem, wheezing o Pulse pressure: narrowing of pulse pressure: difference bt systolic and diastolic Occlusion within 24 hrs

Management: Reperfusion Procedures and Pharmacological Agents

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Transmyocardial laser revascularization – break up plaque by laser

PTCA  

Cardiac cath – procedure to fix blockage by balloon – inflating balloon; intent to crack off plaque with suction Complication – emboli, hemorrhage, hematoma, damage to vessels – pseudoaneurysm, vasospasm, dysrhythmia

Stent 

tube-shaped device placed in the coronary arteries that supply blood to the heart, to keep the arteries open in tx of coronary heart disease

Atherectomy 

Knife blade: shaving off the walls to rid of plaque

Transmyocardial laser revascularization 

Laser – breaks up plaque

CABG – Coronary Artery Bypass Graft Take another vessel from part of body, bypass coronary artery, use the other vessel to re-perfuse heart

Examining heart vessels to correct issues: – CABG, PCA, PTCA   

Percutaneous Coronary Intervention Coronary Artery Bypass Graft (CABG) Heart Transplant

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Ultimate: Reperfusion of the heart Percutaneous Coronary Revascularization (Intervention) PTCA-Percutaneous Transluminal Angioplasty (repair): 

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cardiac cath – radial/femoral – instead of just looking, will use instrument to rid the plaque causing block – balloon, shave, cut, or stent Stent- keeps the vessel open Atherectomy – rem’l of plaque

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Indictors to do CABG o 3 vessels - 70-75% occluded o L main is 50-60% occluded o other previous approaches (PTCA, Transmyocardial Laser Revascularization, Atherectomy, Stent)– cardiac cath w/ tx, meds did not work o a lot of unstable angina death rates are higher when o more vessels are occluded o L main is occluded o Older age

Prep - Surgery

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First need to harvest vessel (mammary, thigh) Bypass machine Stop the heart, crack open chest, bypass flow, bypass heart

During – Surgery: avg. 7-8 hrs      

Average vessel Restart heart – paddles to shock the heart Chest tubes Vent placed 2 incisions Pacer wires as b/u if heart does not beat

Post - Surgery       

Straight to ICU A line Cath Vent Ches...