Cardiovascular.docx

Cardiovascular Leading cause of death is HEART DISEASE for BOTH MEN AND WOMEN! Happens more often in men but more likely to KILL women, less likely to get a full work-up in hospital Cardiovascular 1- RoadMap Problems with Cardiac Output to cardiovascular system (Focused on CO) Pericarditis Endocardi...

Cardiovascular Leading cause of death is HEART DISEASE for BOTH MEN AND WOMEN! Happens more often in men but more likely to KILL women, less likely to get a full work-up in hospital Cardiovascular 1- RoadMap Problems with Cardiac Output to cardiovascular system (Focused on CO) Pericarditis Endocarditis Myocarditis Valvular diseases Cardiomyopathies Electrical alterations Heart Failure Congenital Heart Defects Anatomy and Physiology Review The heart must overcome the pressure of pulmonary and systemic circulations Heart Anatomy The Cardiovascular System Anatomy and Physiology Review (Con’t) Blood vessels Arteries and veins Three layers of tissue for vessel walls Blood pressure and cardiac output Variables and factors affecting blood pressure Lymphatic system Returns excess fluid to circulatory system Electrical Conduction Cardiac Output The amount of blood the hear pump each minute Cardiac output = heart rate x stroke volume Heart rate: how often the heart beats each minute Regulated by a balance between the activity of the sympathetic nervous system (increases heart rate), and the parasympathetic nervous system (slows heart rate) Stroke volume: how much blood the heart pumps with each beat A function of preload, afterload, and cardiac contractility (myocytes drive this) Ejection fraction will be affected by preload and afterload! 50-75% is NORMAL. Concern comes when it’s under 30% Preload and Afterload Preload Volume at the end of diastole Volume of blood stretching the heart muscle at the end of diastole Determine by the venous return to the heart Afterload Force that the heart must generate to eject blood from the ventricles Affected by systemic (peripheral) vascular resistance and ventricular wall tension Myocardial Contractility Shortening or stretching of the muscle Contractile elements (actin and myosin elements) of the heart muscle to interact and shorten against a load Contractility increases cardiac output independent of preload and afterload Disorders of the Pericardium Acute Pericarditis Pericardial effusion and Cardiac Tamponade (not all patients who have acute pericarditis will develop a tamponade) Constrictive Pericarditis Pericardium (has about 30-50 mL of fluid) A double-layered serous membrane Isolates the hear from other thoracic structures Maintains its position in the thorax Prevents it from overfilling Contributes to coupling the distensibility between the two ventricles during diastole; they both fill equally Fluid decreases friction and protects the heart Acute Pericarditis Inflammation of the pericardium Causes Viral (most common)-coxsackieviruses, echoviruses Bacterial-staphylococcus, streptococcus Fungal Parasitic-usually patients with myocarditis Uremia-not clearly understood Post-cardiac surgery Acute Pericarditis Inflammatory process Serous pericardium become permeable Plasma proteins, including fibrinogen, enter the pericardial space Clinical Manifestations Chest pain (worse when breathing, especially when laying down) SOB Pericardial friction rub EKG changes Diagnosis Clinical Manifestations EKG ST segment elevations PR segment depression CXR (enlarged silhouette) CXRs can’t tell differentiate between the heart and pericardium bc it only picks up water densities. SO it just looks like cardiomegaly Echocardiogram Golden standard for diagnosis! Leukocytosis (lymphopenia b/c of viral illnesses) Increased ESR Increased CRP Treatment NSAIDS Idiopathic pericarditis Colchicine (gout can cause pericarditis) Antibiotics Bacterial pericarditis Corticosteroids (those on Anticoags) Pericardial Effusion Accumulation of fluid in the pericardial cavity most common because of an inflammatory or infectious process (example Pericarditis) Inflammation can cause vaso-dilation and therefore fluid accumulation! The pericardial friction rub can lead to bleeding! It may also develop because of: Neoplasms Cardiac surgery Trauma Dissecting aortic aneurysm Cardiac Tamponade Pericardial effusion can lead to a condition called cardiac tamponade, in which there is compression of the heart due to the accumulation of fluid, pus, or blood in the pericardial sac. Decreasing preload and therefore decreasing afterload affecting the cardiac output into the systemic circulation Diagnosis Pulsus Paradoxus A drop in systolic blood pressure exceeding 10mm Hg during inspiration Echocardiogram Rapid, very accurate Anechoic collection, collapse of right ventricle. Anechoic anything black which what fluid comes up as EKG Nonspecific T wave changes Beck’s Triad – for tamponade JVD Hypotension Muffled heart sounds Treatment Pericardiocentesis Pericardiectomy (Window) Constrictive Pericarditis (chronic pericarditis!) Calcified scar tissue develops between the visceral and parietal layers of the serous pericardium. Decreased preload and affects the cardiac output! Causes Mediastinal radiation Cardiac Surgery Infection Manifestations Ascites, pedal edema, dyspnea on exertion, fatigue Kussmal sign (a sucking effect on venous return when it should be plump!) Inspiratory distention of the jugular veins Infective Endocarditis Microthrombi tend to from and valvopathies! Invasion of the heart valves (aortic & mitral) and endocardium by a microbial agent Formation of bulky, friable vegetations and destruction of underlying cardiac tissues Staphylococcus Streptococci Enterococci Haemophilus sp. Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae Gram-negative bacilli Fungi Clinical Manifestations of IE Acute Symptoms Initial infection S/S Malaise, weakness, night sweats, joint pain Microthrombi FEVER and NEW ONSET MURMURS/CV FAILURE Osler nodes (fingers) Janeway Leison (palm) ROTH SPOTS (fundoscopic exam) SPLINTER HEMORRHAGE( nails) @ greater risk: those who use IV drugs, hemodialysis patients patients with mechanical valves Invasive hospital surgeries Myocarditis Inflammation of the myocardium Clinical Manifestations Fever, dyspnea, chest pain Causes Virus - coxsackievirus B Bacterial, fungus, autoimmune disease Diagnostic Endomyocardial biopsy—gold standard Echo, Cardiac Markers Treatment Oxygen, bed rest, steroids, Antibiotics if bacterial ICD in severe cases Valvular Heart Disease (Particularly assessing the mitral and aortic valves L. side of heart) Stenosis Narrowing of the valve opening, so it does not open properly Incompetent or regurgitant valve: Distortion of the valve, so it does not close properly Permits backward flow to occur when the valve should be closed Valve Disorders Mitral Valve Disorders Mitral valve stenosis Mitral valve regurgitation Mitral valve prolapse Listen for a mid-systolic CLICK Systolic murmur Aortic Valve Disorders Aortic valve stenosis Aortic valve regurgitation Cardiomyopathy (this is an umbrella term) Diseases of the heart muscle Can lead to structural and functional changes Three Main Groups Dilated Dilation of ventricle Hypertrophic Muscle overgrowth Restrictive Heart muscle doesn’t have compliance Influence of genetic abnormalities (about 50% of occurrence is due to a genetic mutation) Linked with over 100 genes Identifying benign or pathologic genomic variations Cardiomyopathy Dilated cardiomyopathy (DCM) Develops when ventricles become enlarged Systolic dysfunction Noncardiac causes due to genetic and systemic abnormalities Increased age Familial Hx Cocaine & amphetamine use Other causative factors HIV Obesity Intense emotions or stress Peripartum Cardiomyopathy Occurs during the last trimester of pregnancy or the first 5 to 6 months after delivery Presents with LV dysfunction such as dyspnea, palpitations, edema Criteria for Diagnosis Heart Failure in the last month of pregnancy or within 5 months after delivery No identifiable cause of heart failure No identifiable cause of heart failure before the last month of pregnancy Evidence of systolic dysfunction Stress Cardiomyopathy (Looks like a STEMI heart attack) Neuro- Reversible left ventricular dysfunction in response to profound psychological or emotional stress Women (Takotsubo cardiomyopathy)– most affected who presents with angina and no evidence of CAD in Cath Impaired myocardial contractility Etiology is unclear- neurohormonal theory due to extreme emotional or physical stress Hypertrophic (HCM) (athletes and young kids-teens) Mainly affects diastolic function Hypertrophied ventricular wall Sudden cardiac death in young people Droping dead- especially in teens or younger adults Cardiac arrhythmias Muscle is so enlarged the ventricle is not able to hold enough blood to pump out OR the septum muscle gets so big that it blocks the outflow into the aorta Restrictive Cardiomyopathy (rare in the U.S. seem a lot more in Asians, LATAM, African countries too!) Excessive rigidity of the ventricular walls Restricted ventricular filling Cardiomyopathy Clinical manifestations Type of dysfunction Stage of disease presentation Diagnosis and treatment Detailed family history Treatment dependent on type and cause Surgical removal or ablation may be needed Genetic testing may be warranted Treatment of Cardiomyopathy Treatment depends on the type of Medication Implanted pacemakers Defibrillators Ventricular assist devices Ablation The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant. Electrical Alterations Due to impulse formation and/or conduction problems Bradyarrhythmia or tachyarrhythmias Clinical manifestations Vary according to dysrhythmia Diagnosis and treatment History, physical exam, and EKG Pharmacology as mainstay of treatment Impulse Conduction & the ECG Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers Action Potential Sequential change in electrical potential that occurs across a cell membrane when excitation occurs and cause the heart to conduct the atrium and ventricle. Majors charge carries in cardiac muscle cells—Na, K, Ca Phases of Action Potentials Resting or Unexcited State Depolarization Repolarization Phases of Action Potential Resting State (refractory state) Membrane is permeable to K and nearly impermeable to Na Depolarization (shifting of ions moving in(K) and out(Na)) Cell membrane becomes permeable to a current-carrying ion like Na Repolarization Reestablishment of the resting membrane Membrane is permeable to K Adenosine phosphatase (ATPase)-dependent sodium-potassium pump assist in repolarization (this pump resets the electrolytes!) Pumping Na out and K in Action Potentials in Cardiac Muscles Cardiac muscle has three types of membrane ion channels—fast Na channels, slow Ca channels, and K channels Phases Phase 0—upstroke or rapid depolarization Phase 1—early repolarization period Phase 2—plateau Phase 3—final, rapid repolarization period Phase 4—diastolic depolarization Phase 0—upstroke or rapid depolarization(NA influx)→ Phase 1—early repolarization period (K efflux) Phase 2—plateau (Can influx-SLOW) Phase 3—final, rapid repolarization period (repolarization of ventricle) Phase 4—diastolic depolarization (electrolytes going back to normal) Phase 0 In atrial and ventricular muscle and in the Purkinje system, the fast Na channels in the cell membrane open (depolarization threshold), resulting in the rapid influx of Na Responsible for the QRS complex on the ECG Phase 1 Peak of the action potential Inactivation of the fast Na+ channels with an abrupt decrease in sodium permeability. The slight downward slope is thought to be caused by the influx of a small amount of negatively charged chloride ions and efflux of potassium. Phase 2 The plateau of the action potential. If K+ permeability increased to its resting level at this time, as it does in nerve fibers or skeletal muscle, the cell would repolarize rapidly. Instead, K+ permeability is low, allowing the membrane to remain depolarized throughout the phase 2 plateau. A concomitant influx of Ca++ into the cell through the slow Ca++ channels contributes to the phase 2 plateau. Calcium ions entering the muscle during this phase also play a key role in the contractile process. **The phase 2 plateau coincides with the ST segment of the ECG.** Phase 3 Rapid repolarization and begins with the downslope of the action potential. The slow Ca++ channels close and the influx of Ca++ and Na+ ceases. There is a sharp rise in K+ permeability, contributing to the rapid outward movement of K+ and reestablishment of the resting membrane potential (-90 mV). At the conclusion of phase 3, the distribution of K+ and Na+ returns the membrane to the normal resting state. The T wave on the ECG corresponds with phase 3 of the action potential. Phase 4 Represents the resting membrane potential. The activity of the NA+/K+-ATPase pump contributes to maintaining the resting membrane potential by transporting Na+ out of the cell and moving K+ back in. Phase 4 corresponds to diastole. Heart Rhythms, Let’s Keep It Simple! Steps to Rhythm Interpretation: Is it regular or irregular? (12 lead view 2) What is the rate (too slow or too fast)? Is there a P for every QRS? (SA “normal” rhythm) Is there a QRS for every P? What is the P-R interval? What is the QRS duration (QRS wide or narrow)? ECG Rate Calculation: Rule of 300 A normal rhythm will having 3-5 big boxes between each R-R interval Less than 3 boxes it will be tachycardia Take the number of “big boxes” between neighboring QRS complexes and divide this into 300. The result will be approximately equal to the rate Although fast, this method only works for regular rhythms. What is the heart rate? OK, you have analyzed your strip when assessing your patient, what do you look for? Is your patient? : Alert and oriented Skin warm and dry Short of breath (at rest or post activity, remember to ask) Experiencing palpitations (is the pulse slow/fast, regular/irregular). Complaining of lightheadedness or dizziness Be sure to obtain a set of vital signs NORMAL SINUS RHYTHM Sinus Bradycardia Greater than 5 big boxes then it is considered brady! Criteria: Rate : < 60bpm Rhythm: regular sinus PR: regular-0.12- 0.20 sec, P wave for every QRS QRS: ≤ 0.12 seconds Sinus Tachycardia There is always a P before a QRS here differs from SVT where there isn’t a p-wave seen. Criteria: Rate : > 100bpm Rhythm: Regular sinus PR: regular-0.12- 0.20 sec, P wave for every QRS QRS: ≤ 0.12 seconds Atrial Fibrillation A-fib for less than 7 days – paroxysmal afib Longer than 7 days- persistent afib affect Longer than 1 year- permanent afib One of most common supraventricular tachyarrhythmia in adults Possible structural changes Increases risk of stroke, heart failure, dementia, and mortality Chronic Heart failure can lead to heart remolding because of increase SVR In atrial fibrillation you are LOSING the atrial kick which squeezes the last little bit of blood from the atrial when the blood is being transferred from atria to ventricles Rapid, chaotic, ectopic atrial impulse formation Classified by duration Asymptomatic or variable symptoms Diagnosis and treatment History, physical, and EKG 12 lead, Holter monitor, TEE or Echo TSH/T4, hypo or hyperthyroidism, Anemias? Not every pulse is going to be felt if you’re assessing pulse Management involving rate and/or rhythm control Anticoagulation for stroke prevention (biggest risk of Afib because of blood that backs up and causes venostasis) DO NOT use the 300-method on an irregular rhythm like Afib- use a 6 second strip Junctional Rhythm An escape rhythm serves as a protective mechanism when higher centers in the conduction system fail to fire. Occurs with hypoxemia, and digitalis toxicity Criteria: Rhythm: Regular Rate: 40 – 60 bpm P wave: Before QRS, inverted (retrograde conduction) (P-waves too close to QRS) Absent QRS: <.12 seconds, unless prolonged by aberrant conduction 1st degree the PR is greater than 5 small boxes Measure P-Q time (the same 0.32 seconds) in that picture 2nd degree-longer, longer, longer drip then you have a Wenckebach ^^^^ More Ps than Qs then you have a Mobitz II 2nd degree type II and 3rd degree are high degree blocks and will cause the BP to DROP 3rd degrees are non-perfusing rhythm. Atropine is sometimes given but won’t work because these patients need PACING (transcutaneous or transvenous) ***Remember** symptomatic bradycardias that is perfusion will most likely be treated with ATROPINE But with unstable (low BP) we pace! Heart Failure Decreased cardiac output and inadequate perfusion Problem with ventricular filling or ejection fraction Structural or functional impairment Two categorizations Heart failure with reduced EF (HFrEF) Heart failure with preserved EF (HFpEF) Heart Failure Most common causes Coronary artery disease Hypertension Cardiac and noncardiac causes Compensatory mechanisms SNS and RAAS stimulation Systemic system alpha & beta activation. It increases SVR & Beta increases HR & Contractility End product of RAAS is very potent vasoconstriction (increase in Na&H2O and this increases BP) Can cause heart remolding when these mechanisms are used for extended periods Lead to excessive preload and afterload HFrEF vs HFpEF (Systolic and Diastolic) HFrEF: Impaired ejection of blood during systole (EF<40%) Ejection fraction (EF): percentage of blood pumped out the ventricles with each contraction (Normal would be 55%-70%) HFpEF: EF greater than 50% Diastolic dysfunction Impaired filling of ventricles during diastole Most heart failure is a combined systolic and diastolic failure Depending on the severity of EJ that is going to dictate the treatment for the patient Right-Side vs Left-Side Failure RIGHT SIDE (SECOND most common which comes from L. sided heart failure) Inability to move deoxygenated blood from the systemic circulation into the pulmonary circulation Common Causes Left Heart Failure Pulmonary Hypertension Tricuspid Valve Stenosis or Regurgitation Pulmonic Valve Stenosis or Regurgitation Cardiomyopathy LEFT SIDE (Most common coronary heart disease & uncontrolled HTN) because it’s the higher pressured chamber Inability to move oxygenated blood from the left-side of the heart to the systemic circulation Common Causes Hypertension Myocardial Infarction Mitral Valve Stenosis or Regurgitation Aortic Valve Stenosis or Regurgitation Rales, crackles, dyspnea on exercsion and paroxysmal exertion dyspnea Cyanosis, hypoxemia Stage A- AT risk for getting HF= HTN, Diabetes, Smoking (In the ER, Heart Failure doesn’t get diagnosed because of reimbursement) Stage B= physiological change assoc. from the risk factors. L. vent hypertrophy Axis on EKG is deviated PMI is displaced to the axila (or in a large area) Stage C= physiological symptoms and signs of HF (R v L symptoms) Stage D- marked symptoms of HF. They require IV inotropes and keep bouncing back to the hospital THE AHA IS NEVER GOING TO PUSH YOU BACK ONCE YOU GET TO THE NEXT STAGE. EVEN IF YOU GET BETTER THE STAGE YOU STOP GETTING WORSE AT IS THE STAGE YOU STAY IN. So, you wanna address these issues as soon as possible! NYHA Functional Classification This one has to do with activities or ADLs Diagnosis of CHF EKG: Ventricular hypertrophy Cardiac conduction abnormalities & arrhythmia Echocardiography: gold standard to diagnose Heart Failure Hypertrophy Abnormal contraction & relaxation CBC, Thyroid function panels, proBNP(a natural diuretic in our bodies, with atrial stretching it is high and it’s an indirect measurement of heart failure-trend it) Chest x-ray-enlarged cardiac silhouette HF Treatment Prevention Chronic disease management (DM, HTN, CKD, Tobacco use) Medications (ACEi, BB, ARBs, ARNIS, Diuretics, Aldosterone antagonist, cardiac glycosides, Phosphodiesterase, SGLT2 inhibitors) Cardiac Resynchronization therapy (Biventricular ICDs) Dyssynchronous issues of the ventricles can lead to a cardiac output drop and can lead to vtach and sudden cardiac death. So these devices will 1. Resync 2 Shock any arrhythmias sensed (Vtach or Vfib- D-Fib!) Mechanical assist devices (LVADs) Transplant Alterations in Cardiovascular Function in Pediatrics Congenital heart disease is present in approximately 1% of live births. Leading cause of death in the first year of life (70% die within the first 28 days). Children survival rates have improved because of diagnostic advances, surgical interventions, and ICU care. Alterations in Cardiovascular Function in Pediatrics Congenital defect, acquired infection, injury all lead to ALTERATIONS in CV fxn Cardiovascular Disorders Congenital Heart Defects Are anatomic abnormalities present at birth that result in abnormal cardiac function. Consequences: Congestive Heart Failure Hypoxemia Acquired Cardiac Disorders Disease processes or abnormalities that occur after birth and can be seen in the normal heart or in the presence of congenital heart defects. Endocarditis Kwasaki’s disease Fetal Circulation Fetal brain —needs the highest oxygen concentration Lungs —are essentially nonfunctional Liver —is only partially functional Fetal Circulation The ducts enable most of the blood to bypass the lungs because fetal blood is oxygenated via the placenta. Once the baby is born and takes a breath, the ducts should close spontaneously. In some instances, however, the foramen ovale or the ductus arteriosus remains open. Postnatal Circulation As soon as baby takes its first breathe Right side: Receives blood from superior and inferior venae cavae. Pumps blood through pulmonary arteries to pulmonary circulation. Left side: Receives blood from pulmonary veins. Pumps blood through aorta into systemic circulation Shunts A shunt is an opening or connection that lets blood move from one side of the circulation to the other Most shunts occur in the heart and move blood either from the left to the right or from the right to the left Because the left side is stronger, blood is usually pushed from the left to the right side Shunts are normal before birth Foramen ovale (PFO) Lets blood go from the right atrium to the left atrium to bypass the lungs Ductus arteriosus (PDA) Lets blood go from the pulmonary trunk to the aorta to bypass the lungs Ductus venosus Lets blood go from the visceral veins to the vena cava, bypassing the liver CONGENITALHEART DEFECTS Usually a genetic problem in utero or passed down General Clinical Findings Dyspnea, especially on exertion. Feeding difficulty and failure to thrive, often first sign noted by parent. Stridor or chocking spells. HR over 200, RR about 60 in the infant. Recurrent respiratory tract infections. Cyanosis and clubbing of fingers and toes. Squatting or knee-chest position is assumed because it decreases venous return by constricting the femoral veins. Heart murmurs Excessive perspiration Signs of Heart Failure Tachycardia and hypotension progressing to extreme pallor. Tachypnea, dyspnea, and costal retractions progressing to grunting respirations. Weight gain, ascites, and pleural effusions progressing to peripheral edema. Congenital Heart Disease Acyanotic ASD-atrial septal defect. PDA-patent ductus arteriosus. VSD-ventricular septal defect. AS-aortic stenosis PS-Pulmonic stenosis Coarctation of the aorta Cyanotic (Shunted away from the lungs) TOF-Tetralogy of Fallot Tricuspid atresia Transposition of great vessels Increased Pulmonary Blood Flow Common Clinical Manifestations: Tachypnea Tachycardia Congestive heart failure Fatigue/SOB Poor appetite/poor growth/↓weight gain Eating consumes a lot of energy/calories Sweating with minimal activity Respiratory infections/retractions Atrial Septal Defect (ASD) Base murmurs Ventricular Septal Defect (VSD) LR Increased blood flow into pulmonary artery Systolic murmur at the apex Patent Ductus Arteriosus (PDA) LR Continuous murmur like machinery Indomethacin closes the PDA Decreased Pulmonary Blood Flow Common Clinical Manifestations RL shunting Cyanosis, clubbing of digits Hypercyanotic spells “Tet” Spells - squat Poor feeding/ ↓weight gain Tube feedings to conserve energy Polycythemia (excessive amount of RBC’s) Fatigue, activity intolerance Frequent respiratory infections Pulmonic Stenosis (PS) severe pulmonic stenosis can causes cyanosis!! Systolic EJ murmur 1 R. vent hypertrophy 2 pulmonary stenosis 3 VSD 4 overriding aorta Tetralogy of Fallot (TOF) Signs and Symptoms (TOF) Pressure will be higher in the right side of the heart. Period of cyanosis- “blue spells or TET” In a child (1-2yo) symptoms occur when they are walking or playing. Squatting-compensatory mechanism Playing sitting Remember runners Tricuspid or Pulmonary Atresia PDA needs to stay open! Allows for some of the blood to make it into the system circulation Patients need surgery and prostaglandins to keep PDA open! A Child with Unrepaired Defect of Decreased Pulmonary Blood Flow Mixed Defects Defects which fall into the category of increased or decreased pulmonary blood flow, but in these defects survival of the infant is dependent on mixing of the pulmonary and systemic circulations. Transposition of the great Arteries (TGA) Truncus Arteriosus Mixed Defects Care Life threatening shock in newborns Need PDA open Treatment with Prostaglandin E (PGE) Transposition of the Great Arteries WITH ANY CYANOTIC DEFECT WE NEED TO HAVE A PDA OPEN Mixed Defects Care Cyanosis O2 sats often < than 85% Surgery Aggressively treat CHF (Digoxin and Diuretics) Obstructed Systemic Blood Flow Common Clinical Manifestations Diminished pulses Pale color Delayed capillary refill Decreased urinary output S/S of congestive heart failure Pulmonary edema Feet cooler than hands Stronger upper body pulses than lower body Aortic Stenosis Cardiac output is severely decreased depending on the severity of the defect Coarctation of the Aorta Depending on the coarctation happens the upper extremities and upper extremities can have different BPs Prostaglandin E to keep PDA open Balloon angioplasty main surgical intervention Meat and potatoes L r shunt acyanotic Patient with problems getting blood into the pulmonary system are CYANOTIC Ventricular prob apex murmurs Atrial problem base murmurs Machinery-like murmur PDA