Week 7-Cardiac I - PDF

Circulatory and Tissue Perfusion Part I Intro to the Heart N3910a  TABLE OF CONTENTS 01 A/P REVIEW CARDIAC 02 CARDIAC 04 DISORDERS ASSESSEMENT CARDIAC 03 PHARMACOLOGY  01 A/P REVIEW ...

Circulatory and Tissue Perfusion Part I Intro to the Heart N3910a  TABLE OF CONTENTS 01 A/P REVIEW CARDIAC 02 CARDIAC 04 DISORDERS ASSESSEMENT CARDIAC 03 PHARMACOLOGY  01 A/P REVIEW  The Heart In periphery, RBCs drop off oxygen and pick up CO2 Venous system brings deoxygenated blood back to the heart Drops deoxygenated into the R atria, then moves to R ventricle From R ventricle through pulmonary vessels to lungs to re-oxygenate Reoxygenated blood back to L atria, then L ventricle From L ventricle, out to periphery  The Heart Relies on 3 interconnected systems: 1. Structures 2. Electrophysiology 3. Vasculature  Perfusion Heart is central in perfusion Perfusion=flow of blood through circulatory system to oxygenate cells and remove waste ○ Poor perfusion=cell death over time Perfusion depends on: 1. Sufficient cardiac output & 2. Sufficient blood pressure to move blood to periphery & complementary action of adequate coagulation to prevent hemorrhagic blood loss  Perfusion Cardiac Output Cardiac Output relies on=Heart Rate & Stroke Volume ○ Heart Rate: electrical activity that pumps heart ○ Stroke volume: volume of blood in the heart when it pumps Cardiac Output = Heart Rate X Stroke Volume (beats/min) (ml/beat) NORMAL CO = 75 x 70 = 5250ml/min  Perfusion Cardiac Output Cardiac Output Heart Rate X Stroke Volume Nervous system: chronotropes Preload: End diastolic volume Sympathetic ↑ Influenced by: venous return, fluid Parasympathetic ↓ volume, atrial contraction Drugs Afterload: pressure in aorta that LV must overcome to eject Influenced by: hypertension, CO=Heart Rate * Stroke Volume vasoconstriction, artherosclerosis Key factors that influence: nervous Contractility: inotropes systems, fluid volume, heart Sympathetic ↑ muscle contraction, resistance in Parasympathetic ↓ vessels  Perfusion Blood Pressure Blood Pressure relies on=Cardiac Output and Peripheral Resistance ○ Cardiac output: amount of blood heart is pumping ○ Peripheral resistance: resistance of the arteries to blood flow Blood = Cardiac X Peripheral Pressure Output Resistance  Perfusion Blood Pressure Blood Pressure Cardiac Output X Peripheral Resistance Heart Rate Blood Viscosity -contractility Stroke Volume Radius of Vessel -many factors: fluid, contraction, -constriction return, constriction -artherosclerosis -blood volume Heart Rhythm  Primary Causes of Problems with Perfusion 1. Vascular volume disorders ○ FVO ○ FVD 2. Electrical disorders ○ Dysrhythmias (ex. atrial fibrillation) 3. Mechanical disorders ○ Cardiac Myopathy ○ CHF 4. Coagulation disorders ○ Blood clots (ie. Lead to MI)  02 Cardiac Assessment Assessment Health history Physical Exam ○ Vital signs ○ Cardiac assessment ○ Respiratory assessment ○ Other systems assessment Labs & Investigations  Health History: Risk Factors for Cardiovascular Disease HYPERTENSION OBESITY FAMILY HISTORY Damage to vessels over Increase demand on all Increase risk for diagnosis in time body systems immediate family DYSLIPIDEMIA SLEEP APNEA GENETICS Hypoxia = compensation May modify cholesterol Buildup blocks vessels = damage dev, heart structure, etc and impacts flow DIABETES SMOKING GENDER Damage to vessels over Increase plaque Men=CVD, time formation Women=Stroke LIFESTYLE Diet, Exercise, Smoking, alcohol  Health History: Risk Factors for Cardiovascular Disease HYPERTENSION OBESITY FAMILY HISTORY Damage to vessels over Increase demand on all Increase risk for diagnosis in time body systems immediate family DSYLIPIDEMIA SLEEP APNEA GENETICS May modify cholesterol Buildup blocks vessels Hypoxia = compensation dev, heart structure, etc and impacts flow = damage DIABETES SMOKING GENDER Damage to vessels over Increase plaque Men=CVD, time formation Women=Stroke Identify risk factors through health history & assessment LIFESTYLE Diet, Exercise, Smoking, Consider modifiable vs non-modifiable alcohol RACE does NOT equal RISK  Physical Assessment: Vital signs Cardiac assessment Respiratory assessment Pain assessment * chest pain  Physical Assessment Red Flags! Something might be wrong with our cardiac system & our perfusion if… Changes in VS Compensation Altered breath sounds Impaired movement through pulmonary vessels *CHF Restlessness, changing LOC Brain hypoxia Changes in cardiac assessment Structures, electrophysiology, vasculature Fatigue Body systems not functioning SOB Compensation for decreased oxygenation to body Pain Tissue hypoxia Associated symptoms… Cardiac: squeezing, racing, palpitations Pulmonary: SOB GI: nausea MSK: shoulder pain, jaw pain (L commonly) Neuro: anxiety, impending doom, fatigue, dizziness  Labs and Investigations ELECTROcardiogram: electrical system ECHOcardiogram: mechanical system Lab Values: ○ Cardiac: K, platelets, troponin, BNP, PT/INR, aPTT ○ Risk Factors: BUN/Cr, BG, HbA1C, Lipid Panel  03 Cardiac Pharmacology Pharmacology Goal of medication therapy with any cardiac patient is to DECREASE cardiac workload through manipulating SV, HR, preload, afterload, and contractility. Classes: ACE inhibitors ARBs Beta blockers Calcium channel blockers Nitrates Diuretics  ACE Inhibitors ARBs Angiotensin I ACE Angiotensin II Vasoconstriction INCREASE BP Beta Blockers Epi Beta receptor Increase contraction, Increase HR Ca Ca Channel Blockers  Pharmacological Treatments PRILs: Rami-, Perindo-, Lisino- Therapeutic Class: Antihypertensives Pharmacologic Class: ACE inhibitors Action: vasodilate, lower BP Side Effects: Drowsiness, Dizziness, Headache, Persistent Dry Cough Caution: risk of angioedema (fluid below skin could block airway-emergency!) Nursing Considerations:Monitor for hypotension (hold SBP >90), change position slow, fall risk, advocate for change in medication if client is having trouble coping with dry cough SE, metabolized by liver, excreted by kidney  Pharmacological Treatments SARTANs: Cande-, Lo-, Val- Therapeutic Class: Antihypertensives Pharmacologic Class: Angiotensin II Receptor Blockers Action: treat hypertension, lower BP Side Effects: Dizziness, Headache, N/V/D Caution: Nursing Considerations:Monitor for hypotension, may be appropriate for clients who cannot tolerate ACE inhibitors “-PRILs”  Pharmacological Treatments OLOLs: Metor-, Carvedi Therapeutic Class: Antihypertensives & Anti Dysrhythmics Pharmacologic Class: Beta Blockers Action: decreases HR/cardiac contractility, lowers BP, treats dysrhythmias, HF, HTN, acute MI, CAD Side Effects: Dizziness, lightheadedness, hypotension/ortho hypo, bradycardia, dry mouth Caution: may worsen CHF over time, therefore contraindicated in late stage Nursing Considerations:Assess VS prior to admin (hold in HR 180/120 Hypertensive Crisis Notify provider Assessment: ○ VS monitoring: Q 5 minutes ○ Systems Assessment: S&S of organ damage (remember findings associated with lack of perfusion!) ○ Bloodwork: Urinalysis Electrolytes (K, Mg, Cl, Na) Kidney markers Lipids Blood sugars ○ 12 lead ECG ○ I/O Pt education: bedrest, notify of change in symptoms  Hypertensive Crisis: Nurse Management Administer O2 Monitor BP FREQUENTLY  E.g. q 5 min x 3 Monitor Cardiac, Resp and Neuro frequently Initiate IV Access Administer medications – IV antihypertensive Assess cardiac monitor Encourage rest & quiet room 55  5 ATRIAL FIBRILLATION  ATRIAL FIBRILLATION Definition Arrhythmia Irregular and often rapid heart rhythm caused by uncoordinated contraction of atrial muscles. Normal: atria fire synchronously to pump blood into ventricles A Fib: rapid, chaotic, and irregular contraction pattern of the atria; caused by electrophysiological or structural changes of the atria tissues Significant increase in mortality! A Fib Rhythm Explained  A Fib Rhythm Explained Rate: Usually over 100 Rhythm: Irregular P wave: non-existent PR interval: Impossible to compute QRS complex: Normal Controlled: rate normalized Uncontrolled: over 100 ○ Some patients live with uncontrolled and cannot be converted  ATRIAL FIBRILLATION Causes Hypertension: chronic activation of compensation mechanisms cause structural and electrophysiological changes Diabetes: vascular changes Smoking: nicotine causes inflammation and oxidative stress Obesity: weight-related changes to structure Alcohol: triggers arrhythmias  ATRIAL FIBRILLATION Outcomes Rapid firing of atria = blood pooling = clot formation ○ TIAs ○ Ischemic stroke ○ MI ○ Pulmonary embolism ○ Heart Failure Rapid firing of atria = poor pumping = lower CO = poor perfusion  Assessment Health history/ Family History Physical Exam ○ Cardiac exam ○ Systems assessment Labs & Investigations  Health History Non-Modifiable Risk Factors Family history Other Relevant Data Age Comorbidities: HTN, Gender hyperthyroidism (increased Genetics palpitations/irregular heart rates), SDOH hypokalemia, hypomagnesmia S&S Modifiable Risk Factors Lifestyle: activity & diet Physical activity level *sedentary Diet: sodium consumption Alcohol consumption Smoking Weight  Physical Assessment Respiratory Cardiac Shortness of breath Irregular increased HR, weak pulses Exertion fatigue Palpations Hypotension (light headed/dizziness) Abnormal heart sounds Chest pain Labs and Investigations ELECTROcardiogram Identify rhythm  Nursing Priorities Decrease Risk Rhythm Health of Emboli Control Teaching Treatment/lifestyle modifications Manage arrythmia Anticoagulation therapy Health literacy through medication Readiness for change Support system  Pharmacological Intervention 1. Calcium Channel Blockers Medications for a fib target: 2. Beta Blockers 3. Cardiac Glycoside (Digoxin) Heart Rate 4. Oral Anticoagulants * monitoring Heart Rhythm Coagulation (clot prevention) Acute Intervention: Transesophageal Echocardiogram (TEE) and Synchronized Cardioversion Acute Intervention: Catheter Ablation See you next week!!