Cardiac Module 9 2024 PDF

STRUCTURE AND FUNCTION OF THE CARDIOVASCULA R SYSTEM Dr. Norris & Dr. Williams Copyright © 2015 Wolters Kluwer Health | Lippincott Williams & Wilkins  Main function is transport....

STRUCTURE AND FUNCTION OF THE CARDIOVASCULA R SYSTEM Dr. Norris & Dr. Williams Copyright © 2015 Wolters Kluwer Health | Lippincott Williams & Wilkins  Main function is transport. Delivers oxygen and nutrients to the tissues Carries waste products FUNCTI from cellular metabolism ONS OF to the kidneys and other THE excretory organs Circulates electrolytes and CIRCUL hormones ATORY Transports various SYSTEM immune substances that contribute to the body’s defense mechanisms Helps to regulate temperature Copyright © 2020 Wolters Kluwer All Rights Reserved  Moves blood through the lungs and Pulmon creates a link TWO ary circulati with the gas exchange PARTS on function of the respiratory OF THE system CIRCUL ATORY Systemi Supplies all the c SYSTEM circulati on other tissues of the body TYPES OF CIRCULATION Central circulation Blood that is in the heart and pulmonary circulation Peripheral circulation Blood that is outside the central circulation  COMPONENT S OF THE CIRCULATOR Y SYSTEMS Pulmonary circulation  Right heart  Pulmonary artery, capillaries, and veins Systemic circulation  Left heart  Aorta and its branches  Capillaries supplying the brain and peripheral tissues  Systemic venous system and the vena  The circulatory system is a closed system in which the heart consists of two pumps in series. CIRCUL Blood pressure  Arterial ATORY  Higher pressure, 90–100 mm SYSTEM Hg  Propel blood to all other tissues PRESSU of the body (i.e., systemic circulation) RE  Venous  Lower pressure, 12 mm Hg  Propel blood through the lungs (i.e., pulmonary circulation) Copyright © 2020 Wolters Kluwer All Rights Reserved Laminar blood flow  Layering of blood components in the center of the bloodstream  Reduces frictional forces and prevents clotting factors from coming in contact with BLOOD the vessel wall FLOW Turbulent flow Disordered flow The blood moves crosswise and is disordered isle What might cause turbulent flow?ngthwise Copyright © 2020 Wolters Kluwer All Rights Reserved LAPLACE LAW Describes the relation between wall tension, transmural pressure, and radius States that wall tension becomes greater as the radius increases Wall tension is also affected by wall thickness; it increases as the wall becomes thinner and decreases as the wall becomes  C = V/P  Compliance (C) COMPLIANC E  A change in volume (V) causes less of an increase in transmural pressure (P) in a more compliant vessel.  A vein is 24 times more compliant than its corresponding artery.  FUNCTIONAL ANATOMY OF THE HEART Pericardium  Forms a fibrous covering around the heart holding it in a fixed position and providing physical protection and a barrier to infection Layers of the Heart Wall: Epicardium  Outermost layer of heart wall (innermost layer of pericardium); made of connective tissue and fat Myocardium  Muscular portion; forms the wall of the atria and ventricles Layers of the heart video Endocardium  Thin, three-layered membrane lining the heart FUNCTIONAL One-way valves  Atrioventricular ANATOMY OF valves and THE HEART semilunar valves are pressure valves that ensure one-way flow. Fibrous skeleton  Provides structural support and isolating force for electrical impulse  FACTORS DETERMINI NG THE WORKLOA D OF THE HEART  CARDIA C OUTPUT Amount of blood the heart pumps each minute Determined by  CO = SV x HR  Stroke volume: the amount of blood pumped with each beat  Heart rate: the number of times the heart beats each  Frank-Starling FRANK- Mechanism: the greater the volume of STARLI blood in the heart NG before contraction, the greater the AND volume of blood ejected from the heart CARDI Cardiac reserve: maximum percentage AC of increase in cardiac RESER output achieved above normal resting VE level  Tunica externa or COMPOSITION tunica adventitia (outermost covering) OF BLOOD  Composed of fibrous and connective tissues VESSELS that support the vessel Tunica media (middle layer)  Largely a smooth muscle layer that constricts to regulate and control the diameter of the vessel Tunica intima (inner layer)  An elastic layer that joins the media and a thin layer of endothelial cells that lie adjacent to the blood EFFECTS Blood pressure = OF cardiac output × PERIPHER peripheral vascular AL resistance CO is variable. RESISTAN BP is variable but to a CE AND much lesser degree. PVR is regulated by the THE baroreceptor reflex in REGULATI order to maintain pressure and perfusion. ON OF Factors affecting hemodynamic function BLOOD FLOW – Volume REVIEW Pressure Resistance SLIDE LOCAL CONTROL OF BLOOD FLOW Autoregulation of blood flow is mediated by changes in blood vessel tone due to changes in flow through the vessel or by local tissue factors. Vasodilator and vasoconstrictor substances in the blood (ex)  Norepinephrine  Epinephrine  Angiotensin II  Histamine  Serotonin  Bradykinin  Prostaglandins HUMORAL CONTROL OF VASCULAR FUNCTION - REVIEW SLIDE  Nutrient flow versus non- FUNCTION nutrient flow Capillary— OF THE interstitial fluid MICROCIRC exchange Controlled by the ULATION hydrostatic and osmotic pressures  Vessels commonly travel along with an arteriole or venule or with its THE companion artery and vein. LYMPH Lymph is derived from ATIC interstitial fluids. SYSTE  Plasma proteins and other osmotically active particles M  Filters the fluid at the lymph nodes and removes foreign particles such as bacteria  EDEMA – REVIEW SLIDE Definition  Excess interstitial fluid in the tissues Causes  Imbalance of any of the factors that control the movement of water between the vascular compartment and the tissue spaces  The disproportionate increase in capillary fluid pressure or permeability, decreased capillary colloidal osmotic pressure or impaired lymph flow  DISORDERS OF CARDIAC CONDUCTIO N AND RHYTHM Copyright © 2015 Wolters Kluwer Health | Lippincott Williams & Wilkins  Controls the rate and direction of electrical impulse conduction in the heart Impulses are generated in the SA node, which has the fastest rate of firing, and Cardiac travel to the Purkinje Conducti system in the ventricles. on In certain areas of the heart, System the myocardial cells have been modified to form the specialized cells of the conduction system. The conduction system maintains the pumping efficiency of the heart. Copyright © 2020 Wolters Kluwer All Rights Reserved Cardiac Conduction System Copyright © 2020 Wolters Kluwer All Rights Reserved Phases of Cardiac Potentials Phase Phase Phase Phase Phase 0 1 2 3 4 rapid early plateau final diastolic upstroke of repolarizati repolarizati repolarizati the action on on period on period potential Copyright © 2020 Wolters Kluwer All Rights Reserved Phases of Cardiac Potentials Copyright © 2020 Wolters Kluwer All Rights Reserved  Refractory Periods Effective (Absolute) Relative Refractory Period Refractory Period No stimuli can generate Greater than normal stimulus another action potential. response Includes phases 0, 1, 2, and Repolarization returns the part of phase 3. membrane potential to below The cell cannot depolarize the threshold, although not again. yet at the resting membrane potential. Begins when the transmembrane potential in phase 3 reaches the threshold potential level Ends just before the terminal portion of phase 3 Copyright © 2020 Wolters Kluwer All Rights Reserved Refractory Periods Copyright © 2020 Wolters Kluwer All Rights Reserved  Electrocardiography Provides a graphic representation of cardiac electrical activity Major components of an ECG P wave Depolarization in the atria QRS complex Depolarization of the ventricles T wave Repolarization of the ventricles Three other components PR interval QT interval ST segment Copyright © 2020 Wolters Kluwer All Rights Reserved  Electrocardiography Twelve leads Each provides a unique view of the electrical forces of the heart Diagnostic criteria are lead-specific. Improper lead placement can significantly change the QRS morphology. Misdiagnosis of cardiac arrhythmias or the presence of conduction defects can be missed. Copyright © 2020 Wolters Kluwer All Rights Reserved  Shifted from simple heart rate and arrhythmia Goals of monitoring to Continuou Identification of ST s Bedside segment changes Advanced arrhythmia Cardiac identification Monitoring Diagnose Provide treatment Copyright © 2020 Wolters Kluwer All Rights Reserved Types Types Disorders of rhythm and Disorders of impulse Causes conduction of Causes Disorders Congenital defects or degenerative changes in of the the conduction system Cardiac Myocardial ischemia and infarction Conducti Fluid and electrolyte on imbalances Effects of drug ingestion System Copyright © 2020 Wolters Kluwer All Rights Reserved  Arrhythmia An abnormality in the rhythm of the heartbeat (also known as dysrhythmia) Arrhythmia (Dysrhythmi Caused by a problem with a) the electrical conduction system Virtually all drugs that treat dysrhythmias can also cause dysrhythmias Copyright © 2020 Wolters Kluwer All Rights Reserved  Types of Arrhythmias Sinus Node Arrhythmias Sinus bradycardia Sinus tachycardia Arrhythmias of Atrial Origin Paroxysmal supraventricular tachycardia Atrial flutter Atrial fibrillation Ventricular Arrhythmias Premature ventricular contractions Ventricular tachycardia Ventricular flutter and fibrillation Copyright © 2020 Wolters Kluwer All Rights Reserved Types of Arrhythmias Copyright © 2020 Wolters Kluwer All Rights Reserved  Types of Arrhythmias: Heart Blocks Disorders of Atrioventricular Conduction First-degree AV block Second-degree AV block Third-degree AV Copyright © 2020 Wolters Kluwer All Rights Reserved Types of Arrhythmias: Heart Blocks Copyright © 2020 Wolters Kluwer All Rights Reserved Types of Arrhythmias: Heart Blocks Copyright © 2020 Wolters Kluwer All Rights Reserved Cardiac Rhythms (you need to know) Copyright © 2020 Wolters Kluwer All Rights Reserved  Correction of Conduction Defects, Bradycardias and Tachycardias Pharmacological Treatments Electronic pacemaker Temporary Permanent Cardioversion Defibrillation Synchronized Ablation Surgical interventions Copyright © 2020 Wolters Kluwer All Rights Reserved  Pharmacologic Treatment of Arrhythmias Class I drugs: act by blocking the fast sodium channels Class II agents: β-adrenergic–blocking drugs that act by blunting the effect of sympathetic nervous system stimulation on the heart Class III drugs: act by extending the action potential and refractoriness Class IV drugs: act by blocking the slow calcium channels, thereby depressing phase 4 and lengthening phases 1 and 2 Copyright © 2020 Wolters Kluwer All Rights Reserved  Balancing risks and benefits Consider properties of Principles of dysrhythmias Antidysrhyth Sustained versus mic non-sustained Asymptomatic versus Drug Therapy symptomatic Acute and long-term treatment phases Copyright © 2020 Wolters Kluwer All Rights Reserved  EKG Cheat Sheet Nurse Labs Study Tools Copyright © 2020 Wolters Kluwer All Rights Reserved Pharmacology 46 Classification of Antidysrhythmic Drugs Vaughan Williams classification Class I: Sodium channel blockers Class 1A: Quinidine and Procainamide Class 1B: Lidocaine and Mexilitine Class 1C: Flecainide and Propafenone Class II: Beta blockers Class III: Potassium channel blockers Amiodarone, sotalol, dofetilide 47 CLASS IA Agent: Quinidine Quinidine Adverse drug effects Mechanism: Effects on Diarrhea-can be intense the heart Cinchonism-tinnitus, Blocks sodium reversible hearing loss, channels headache, vertigo, visual Slows impulse disturbance conduction Cardiotoxicity- high doses Delays repolarization may cause widening of Blocks vagal input to QRS complex and QT the heart prolongation Effects on the ECG Arterial embolism Widens the QRS Alpha-adrenergic blockade, complex resulting in hypotension Prolongs the QT Hypersensitivity reactions- interval rare Therapeutic uses For supraventricular 48 Class 1A: Quinidine Drug interactions Digoxin- quinidine displaces digoxin binding to albumin and decreases its metabolism. The result is digoxin toxicity. Nursing Evaluation and Intervention: Advise clients to take quinidine with food to assist with diarrhea. Educate clients on symptoms of cinchonism and to report it. Report changes in EKG such as QT prolongation and QRS simplex widening, especially if greater than 50% Monitor digoxin levels, if client is taking this drug. 49 Other Class IA Agents: Procainamide Procainamide [Procanbid]: IV and PO Mechanism: Similar to quinidine Actions: Similar to quinidine Only weakly anticholinergic Adverse effects: Symptoms of systemic lupus erythematosus (SLE) Blood dyscrasias- Black Box warning for BMS, agranulocytosis, neutropenia, thrombocytopenia Other effects similar to quinidine such as widening QRS and QT prolongation, cardiotoxicity, hypotension etc. Nursing Evaluation and Intervention Advise clients to report fever, joint and muscle pain, butterfly rash related to SLE Monitor CBC and report symptoms of infection, bleeding Monitor BP, ECG/QT prolongation, procainamide 50 level  Lidocaine [Xylocaine]- used for ventricular dysrhythmias Mechanism: Blocks cardiac sodium channels Slows conduction in the atria, ventricles and His-Purkinje system Reduces automaticity in the ventricles and Class IB His- Purkinje system Accelerates repolarization Adverse effects Agents CNS effects (altered mental status), confusion, drowsiness, paresthesias. (Lidocaine) Seizures and respiratory arrest may occur at high doses. Nursing Evaluation and Interventions: Monitor adverse effects above; be prepared to treat seizures and for resuscitation Other class IB agents Mexiletine Oral analog of lidocaine Used for symptomatic ventricular dysrhythmias 51  Flecainide (Tambocor)- oral Actions: Blocks cardiac sodium channels Delays ventricular repolorization Adverse effects: Widening of QRS complex and Class IC PR prolongation; new and Agents worsened arrythmias Black Box warning for increased (Flecainide mortality and proarrythmic effects May worsen heart failure due to ) negative ionotrope effects Nursing Evaluation and Intervention: Monitor adverse events, especially for new arrythmias Other agents Propafenone (Rythmol) 52  Beta-adrenergic blocking agents Only four approved for treating dysrhythmias 1. Propranolol 2. Acebutolol 3. Esmolol 4. Sotalol Propranolol [Inderal]: Nonselective Class II: beta-adrenergic antagonist- refer to hypertension notes for more Beta information on propranolol Effects on the heart and ECG Decreased automaticity of the SA Blockers node Decreased velocity of conduction through the AV node Decreased myocardial contractility Therapeutic use Dysrhythmias caused by excessive sympathetic 53 stimulation Class II: Beta Blockers (Cont.) Propranolol [Inderal] Adverse efects- see hypertension notes Cardiac effects – due to blocking beta 1 receptors Heart block Heart failure AV block Sinus arrest Hypotension Other adverse effects: Bronchospasm (in asthma patients)- due to blocking beta receptors in the lungs Other class II: Beta blockers Acebutolol [Sectral] Esmolol [Brevibloc] Sotalol is a beta blocker but it is classified as a class III agent 54  Amiodarone [Cordarone, Class III: Pacerone] Therapeutic use For life-threatening ventricular Potassium dysrhythmias only Recurrent ventricular Channel fibrillation Recurrent hemodynamically unstable ventricular Blockers tachycardia Amiodarone Mechanism: Blocks Adverse effects potassium, sodium and Protracted half-life calcium channels as well Pulmonary toxicity- as alpha and beta pulmonary fibrosis blocking properties Cardiotoxicity- may Effects on the heart and cause dysrhythmia ; ECG heart failure Reduced automaticity Hypo and in the SA node hyperthyroidism Reduced contractility Toxicity in pregnancy and Reduced conduction breast-feeding- avoid velocity Optic neuropathy- stop QRS widening drug 55  (amiodarone increases levels of these drugs) Class III: Quinidine Diltiazem Potassium Cyclosporine Channel Digoxin Procainamide Blockers (Cont.) Diltiazem/ (Amiodarone) verapamil Phenytoin Warfarin Lovastatin, simvastatin, atorvastatin Amiodarone levels can be increased by grapefruit juice and by inhibitors of CYP3A4. Toxicity can result. Amiodarone levels can be reduced by cholestyramine (which decreases amiodarone absorption) and by agents that induce CYP3A4 (eg, St. John’s wort, rifampin). Combining amiodarone with a beta blocker, verapamil, or diltiazem can lead to excessive slow of the heart. Diuretics decrease Mag and K+ that increase risk of torsades de pointes 56 Amiodarone Nursing Evaluation and Intervention: Monitor PFT, X-rays and observe for pulmonary symptoms such as cough, chest pain, difficulty breathing. Also advise client to report any symptoms. Monitor EKG and blood pressure and observe for symptoms of heart failure Advise client to report any changes in vision Clients should use birth control and report pregnancy Monitor magnesium, potassium, liver function test, thyroid test Observe and advise client to report photosensitivity reactions/blue-gray skin as well as protection from sun, including sunscreen and protective clothing. 57 Additional Class III: Potassium Channel Blockers (Cont.) Dronedarone [Multaq] Sotalol [Betapace] Combined class II and class Derivative of amiodarone III properties Effects on the heart Beta blocker that also delays and ECG repolarization Pharmacokinetics Dofetilide [Tikosyn] Adverse effects Oral class III antidysrhythmic Cardiac effects in Predisposes patient to torsades de pointes severe heart failure Ibutilide [Covert] Liver toxicity Class III agent Toxicity in pregnancy IV agent used to terminate and breast-feeding atrial flutter/fibrillation Drug interactions Multiple; many involve Note: For all Class III CYP3A4 agents, monitor magnesium and K+ Note: For all Class III 58  Verapamil [Calan, Covera, Verelan] and Diltiazem [Cardizem]- see hypertension handout for more information Both can be give oral and IV (but IV Mechanism: Class IV: Calcium Reduce SA nodal Channel Blockers automaticity Verapamil and Delay AV nodal conduction Diltiazem Reduce myocardial contractility Therapeutic uses Slow ventricular rate (atrial fibrillation or atrial flutter) Terminate SVT caused by an AV nodal reentrant circuit 59  Verapamil [Calan, Verelan] and diltiazem [Cardizem] Adverse effects Bradycardia Hypotension AV block Heart failure Peripheral edema Class IV: Constipation Interactions Calcium Can elevate digoxin levels Channel Cardiac effects increased risk when combined with a beta Blockers blocker (Cont.) Nursing Evaluation and Intervention Monitor cardiac adverse effects, including ECG, heart rate for bradycardia and report if below 50, blood pressure for hypotension. Educate client to increase water and fiber for constipation. 60 Other Antidysrhythmic Drugs- Adenosine Adenosine (Adenocard)- short half life < 10 sec Effects on the heart and ECG Decreases automaticity in the SA node Slows conduction through the AV node Prolongs PR interval Therapeutic use: Termination of paroxysmal SVT Adverse effects Cardiac: Sinus bradycardia, hypotension, chest discomfort Dyspnea Facial flushing Drug interactions Methylxanthines (theophylline and caffeine) block adenosine receptors making the latter ineffective; larger adenosine doses are needed Dipyridamole blocks adenosine cellular uptake intensifying its effects Nursing Evaluation and Intervention Give bolus dose via line close to the heart followed by flushing with 61 saline Other Antidysrhythmic Drugs (Cont.) Magnesium Use: Magnesium has been used to prevent and treat arrhythmias- atrial fibrillation, supraventricular tachycardia, ventricular fibrillation and drug induced torsade de pointes. It impacts the movement of sodium, potassium and calcium through the channels. Low levels of magnesium has been linked to several cardiac conditions including atrial fibrillation, hypertension and cardiovascular death. Digoxin [Lanoxin] Primary indication is heart failure (discussed in more details in heart failure) Also used to treat supraventricular dysrhythmias (inactive against ventricular dysrhythmias) Suppresses dysrhythmias by decreasing conduction through AV node and automaticity in the SA node QT interval may be shortened Adverse Effect: Cardiotoxicity Risk increased by hypokalemia Nursing evaluation and Intervention Monitor digoxin levels, and symptoms of digoxin toxicity , K+ levels 62 Other Antidysrhythmic Drugs- Atropine Atropine: IV adminstration Use: Mainly for bradycardia, brady-asystole cardiac arrest Mechanism: blocks muscarinic receptors in the heart resulting in increased heart rate and atrioventricular block Adverse effects: Dry mouth, constipation, urinary retention, blurred vision, photophobia, tachycardia, glaucoma, confusion, hyperthermia due to decreased sweating Overdose may cause palpitation, dilated pupils, tremor, excitation, delirium, coma, respiratory collapse, death Interactions:Drugs with anticholinergic effects (antihistaminesmay increase these effects Nursing Evaluation and Intervention Monitor vital signs for tachycardia Monitor adverse events and educate clients such as sipping water or hard candy for dry mouth; avoiding bright lights or use sunglasses for photophobia; 63