Cardiac 2023 PDF

The Cardiovascular System PROBLEMS WITH THE PUMP, PIPES, AND ELECTRICAL SYSTEM By Steve Casarez RN, Paramedic, MICN  Figure 04.F05: Blood flow through the heart Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning....

The Cardiovascular System PROBLEMS WITH THE PUMP, PIPES, AND ELECTRICAL SYSTEM By Steve Casarez RN, Paramedic, MICN  Figure 04.F05: Blood flow through the heart Chiras, D. (2011). Human biology (7th ed.). Sudbury, MA: Jones & Bartlett Learning.  Figure 04.F03: A normal heart © SIU/Visuals Unlimted, Inc. Structures  Figure 04.F04: Heart valves © Phil Degginger/Alamy Cardiac Pathophysiology  Heart Valves and Heart Tones A Physician Takes Money! Aortic S2 Pulmonic S2 Tricuspid S1 Mitral S1  Heart Tones  S1  Closed Mitral Valve  Closed Tricuspid Valve  S2  Closed Aortic Valve  Closed Pulmonary Valve  Heart tones  S1 “LUB” comes after Atrial Contraction  S2 “DUB” comes after Ventricle Contraction  S3 “WOOSH” comes after S2 and it sounds like fluid. S3 represents too much fluid, Heart Failure, CHF  S4 “Stiff Wall” comes before S1 and it sounds like a stiffening sound. This is an indication of an MI S4 S1 S2 S3  Cardiac Medical Disorders  Cardiac Arrhythmias  Valvular Heart Disease  Heart Failure (CHF)  Mitral Valve Prolapse  Hypertension (HTN)  Cardiomyopathy  MI  Deep Vein Thrombosis  Coronary Artery (DVT) Disease  Raynaud’s Disease  Endocarditis  Varicose Veins  Myocarditis  Pericarditis  Rheaumatic Heart Disease Figure 04.F07: Electrical conduction through the heart  Cardiac Arrhythmias  Problems with the electrical system  Creating a misconnection in the main circuit  Can involve any portion the of the heart  Atria  Ventricles  Cardiac Arrhythmias  They vary in severity  These conditions lead to a cascade of issues  Depending on the location of the arrhythmias, it may influence cardiac output and stroke volume  Causes of Arrhythmias  Congenital defects (something you are born with)  MI  CHF  Drug use  Electrolyte imbalances  Acid-base imbalances  Hypertrophy (LVH)  Stress  Pathophysiology 1. Cardiac cells (increase or decrease) sensitivity  Automaticity  Creates a change in conduction rate and location of conduction  Either too slow or to fast  Long term effects changes the electrical make of the heart leading to pump failure 2. SA-AV nodes become overwhelmed  Creating a huge demand on the electrical system  Usually leads to a decrease in conduction  Leading to pump failure 3. Ischemia  Area of the heart muscle that lack oxygen  Cells in that area will die off  If these cells are in the path of the main electrical system conduit it will lead to immediate pump failure  S/S Common TX  ALOC  Cold, cool, clammy skin Find the Etiology. This will drive  Dyspnea your TX regimens.  Hypotension  Oxygen  Palpations  Cardiac monitor  Chest pain  12 lead EKG  Dizziness  IV  Syncope or near syncope  Cardiac markers and CBC  (90% of syncope are cardiac  Chest x-ray related)  Antiarrhythmic medications  Low urine output  Pain management  Cocaine use (will have problems  CPR with AV conductions)  Heart Failure  It’s a Volume and Perfusion issue  “A road to death”  Multiple syndromes that start the cascade to death  Leads to volume overloads  Poor tissue perfusion  Acidosis  Death  The key is management and education  Figure 04.F17: Course of heart failure Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA.  Causes  MI (number one cause for left-  Abnormal left ventricular sided failure) pressures  Cardiomyopathy  HTN  Abnormal left ventricular  Pulmonary HTN volumes  Valve problems  Hypovolemia  Abnormal left ventricular filling  MI  AFIB / AFLUTTER  Valve problems  Infections  Pathophysiology 1. Will have a decrease in Stroke Volume 2. Increase pressure on Kidney 3. Renin-Angiotensin System is activated, leading to vasoconstriction 4. Adrenal Cortex releases Aldosterone, causing retention and uptake of NA+, causing volume overload 5. Increases in Left Ventricular Volume leading to 1. Short term = Increase in cardiac fiber lengths creating a floppy muscle (Cardiomyopathy) 2. Long-term = LV hypotrophy leading to EKG changes 6. Key Countermeasures for Heart Failure: 1. Prostaglandins = regulates contraction/smooth muscle relaxant 2. Atrial Natriuretic Factors (ANP)= vasodilator released by the heart 3. Brain natriuretic peptide (BNP) = vasodilator released by the heart  Pathophysiology of CHF Left Side Right Side  Too much volume in LV  Too much volume in RV  May lead to LV Hypertrophy  Fluid backs up into the venous  Leads to EKG changes and axis return deviations  Creating changes in plasma  Fluid backs up into the lungs membranes creating a diffusion issue  Creating edema (C02/O2), hence CPAP use in EMS  Increase CVP  Compensatory mech. This leads to  Decrease in CO and Contraction systemic vasoconstriction leading  Ejection Fractions decreasing to HTN, hence tx with NTG use in  Leads to Left failure EMS  Ejection Fractions 30-50%  Figure 04.F18: Effects of left and right heart failure Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA. Table 04.T02: Comparison of Left- and Right-Sided Heart Failure Clinical Manifestations Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA.  S/S TX Left Side Failure Find the Etiology and treat S/S  Dyspnea  Elevate the head  Orthopnea  Oxygen if indicated  Hemoptysis  Cardiac Monitoring  Tachycardia  12 lead EKG  S3, S4 heart tones  IV with blood work (CBC, Cardiac  Cool, pale Right Side Failure markers)  JVD  Chest xray  RUQ pain  Blockers (ABCD)  N/V/D  Dilators ie: NTG drip/patch  Weight gain  CPAP / BiPAP  Edema, Ascites, Anasarca  Surgery  Sleep apnea  Hypertension (HTN) “The silent killer”  Elevation in systolic and diastolic pressures  Elevation is afterload and preload  Elevation is contraction (heart is working harder)  Elevation in cardiac output  HTN two types Primary Secondary  Family history  Excess Renin  Age  Electrolyte issues  Race  DM  Obesity  Heart problems  Smoking  Endocrine problems  High intake of NA+ (hormones)  High intake of saturated fats  Pregnancy  ETOH  Lazy lifestyles  Pathophysiology  Increase in central venous pressures  Increasing cardiac output  Decreasing lumen sizes  Systemic vasoconstriction  Increasing viscosity  Increase in fatty deposits forming a narrow pathway  HTN is not an EMS crisis  HTN by itself with no other symptoms is not an emergency  TX for this condition is slow and done outside of an acute care facility  TX with education  Risk Factors  Diet  Encourage to be evaluated by PCP  Progression of HTN must have 2 of these measurements within 2 months to be considered HTN Stage 1 Stage 2  Systolic 130-139 mmhg  Systolic >140 mmhg  Diastolic 80-89 mmhg  Diastolic > 90 mmhg Treatment Treatment  Outpatient  Encourage to see primary care  Education physician immediately  Diet  Education  PO (ABCD) blocker medication  IV medications  Medical workup by Dr.  PO medications UPDATED NEW NATIONAL STANDARDS OF 2019  HTN LV Hypertrophy  Complications with HTN  Stroke  MI  Heart Failure  Arrhythmias  Retinopathy  Encephalopathy  Renal Failure  Symptomatic S/S TX  HTN above the pt’s baseline  Comfort measures  Headache  Cardiac monitor  Dizzy  12 EKG  Blurred vision  PO or IV medications  Epistaxis  Blood work  Edema  Chest xray  12 lead shows Left Axis  Education Deviation  CVA  SZ  PEA  MI  Myocardial Infarction  Acute coronary syndrome (ACS)  The flow of blood perfusing the heart becomes impaired  Leading to ischemia  Leading to Coronary Artery Disease (CAD)  Classified as STEMI or NONSTEMI  NONSTEMI is an MI without ST changes but DX with laboratory findings (Troponin)  Troponin is a blood draw check done 3 times 6-8 hours apart  Table 04.T06: Cardiac Markers Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA.  Pathophysiology of an MI overview  Occlusion occurs somewhere around the hearts circulatory system  Circumflex branch of the left coronary artery  Left anterior descending artery  Right coronary artery  Ischemia starts  The longer the injury, more of the damage  Damage Location  Infarction will take place from hypoxia  Necrosis will be immediate to the location of injury  Distal to injury relies on collateral circulation  Necrosis  Damages surrounding muscle making scar tissue  Decrease the muscle to expand and contract  Lost of electrical kick in the damage area location  Remodeling occurs to chambers typical left ventricle  It changes CHAMP  Figure 04.F33: Myocardial infarction. (a) An overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. (b) A cross-section of the coronary artery with plaque buildup and a blood clot. National Heart, Lung and Blood Institute (www.nhlbi.nih.gov)  MI Causes  CAD  HTN  Coronary Spasms  Thrombosis  DM  Obesity  Poor Diet  Drugs, Smoking  Elevated triglyceride and cholesterol  MI Contributors Triglycerides Cholesterol  Stores unused calories  Used to build cells  Stored in fat  Production of hormones  Provides body with  Production of bile energy  Insulates nerve fibers  Lipid Panels  HDL = good lipids  LDL = bad lipids  Figure 04.F22: Transportation of lipids in the blood Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA.  Table 04.T03: ATP III Classification of LDL, Total, and HDL Cholesterol (mg/dL) Story, L. (2012). Pathophysiology: A practical appraoch. Jones & Bartlett Learning: Burlington, MA.  MI Complications  Arrhythmias  Cardiogenic shock  Heart failure  Valve problems  Stroke  S/S TX  Chest pain  Oxygen  Radiation of pain to jaw, arm,  Close cardiac monitoring back, shoulders  12 lead EKG  Moist skins  Pain management  SOB  Nitro  Weakness  IV  12 lead changes  Cardiac panel workup  N/V  Chest X-ray  JVD (rare)  Echocardiogram 3D Women have Atypical S/S  Troponin trending  Abdominal pain  May say “I just don’t feel right” with no other complaint  Coronary Artery Disease  “Occlusion prevents perfusion”  Takes many years to damage  Narrowing of the Coronary Arteries  It diminishes oxygen supply and nutrients to the heart muscle Causes  Atherosclerosis  Dissecting aneurysm  Congenital abnormalities  Figure 04.F23: Possible complications of atherosclerosis Story, L. (2012). Pathophysiology: A practical approach. Jones & Bartlett Learning: Burlington, MA.  Figure 04.F24: Development of atherosclerosis Story, L. (2012). Pathophysiology: A practical approach. Jones & Bartlett Learning: Burlington, MA.  Pathophysiology of CAD 1. Fatty plaques stick to the walls of the coronary artery (atherosclerosis) 2. Reduced blood flow distal to the build-up occurs 3. Creates turbulence in the build-up area 4. Major occlusion leads to myocardial ischemia 5. Tissue and cell death occur 6. Creating an anaerobic state 7. Creating lactic acid 8. Leading to tissue necrosis and death 9. Result is Myocardial Infarction and death  Table 04.T04: Risk Factors for Coronary Artery Disease Madara, M., & Pomarico-Denino, V. (2008). Quick look nursing: Pathophysiology (2nd ed.). Sudbury, MA: Jones & Bartlett Learning.  Treatment  Cath. Lab  ABCD blockers  Coronary artery bypass graft  CABG  Angioplasty  Stent placement  Education  Lifestyle changes  Figure 04.F25: Principles of Angioplasty Crowley. (2012). An Introduction to Human Disease, 9th edition. Jones & Bartlett Learning: Burlington, MA.  Figure 04.F30: Pulmonary embolism © Jones & Bartlett Learning  Figure 04.F29: Deep vein thrombosis © Jones & Bartlett Learning  Cardiomyopathy Three Types Pathophysiology 1. Dilated  Damage to cardiac muscle 2. Hypertrophic fibers that reduces contractility 3. Restrictive (strength of the muscle)  Decrease in CO Common Causes  Pulmonary HTN 1. HTN  Pulmonary Congestion 2. MI 3. DM Cardiomyopathy  Endocarditis  Infection of the endocardium, heart valves, or cardiac prosthesis  Bacterial or viral Common Causes  Dental Infections  Prosthetic heart valves  Rheumatic heart disease  Syphilis  Staphylocci  streptococci  Figure 04.F14: Ineffective endocarditis © Dr. E. Walker/Science Source  Pathophysiology  Pathogen enters the blood stream  Causes fibrin platelets to aggregate  On a heart valve, endocardial lining, epithelium  Creating inflammation  Creating higher demand on the heart  S/S TX  Malaise, weakness  PCN  Intermittent fever  Gentamicin  Night sweats, chills  Cardiac murmurs  Infarction anywhere in body  Myocarditis  Focal or diffuse inflammation of myocardium  My not have any EKG changes  Complete recovery without residual defects Causes  Infections  Rheumatic fever  Radiation tx  Chronic ETOH  Autoimmune disorders  systemic Lupus  Pathophysiology  Infectious organism triggers an autoimmune response  Inflammation causes hypertrophy, fibrosis  May change conduction system  Heart muscles weakens  Decrease in CO  Heart muscle becomes dilated and flabby  S/S TX  Chest pain  ABX  Fever  Antipyretics  S3 and S4  Oxygen  JVD  ABCD blockers  Fluid volume overloaded  Pericarditis  Inflammation of the Paricardium  Very common  It initiates a cascade of events  Inflammatory process  Heart failure  Pathophysiology  Infection (bacteria) is introduced to the pericardium  Inflammation response is activated  Inflammatory process is started in the affected tissue  Edema occurs in the pericardium layers that creates friction and pain  Histamine is release that dilates vessels  This creates fluid shifts into the pericardium  It decreases CO and SV  It affects the electrical system giving you global ST elevation in all leads  S/S TX  Flu like symptoms  ABX  Fever  Lasix  Fluid retention  Dialysis  JVD  Steroids  Dyspnea  Paracardiocentesis  Chest pain  S3  Body edema  12 lead global changes  Cardiogenic Shock  Heart inability to supply blood TX to the heart  Correcting the underlying  Dropping CO and SV Etiology Is the number one TX  It is a pump problem goal with Cardiogenic shock  The compensatory mechanism  Supportive care worsens the problem  CPR Most Common Causes  Pacemakers  Trauma  MI  CHF