cardiac

heart sounds

1. aortic area: second intercostal space, right sternal border 2. pulmonic area: second intercostal space: left sternal border 3. Tricuspid area: fourth( or fifth) intercostal space, left sternal border 4. mitral area: fifth intercostal space, left midclavicular line

Commotio Cordis

AKA cardiac concussion most common in male adolescents (~14 years old) with compliant chest walls.10 Usually from a baseball, softball, hockey puck, etc. 20% occur from contact with another person Survival depends on time to defibrillation and swift recognition of the condition

myocarditis

Abnormal heart Acute inflammation of the myocardium leads to an arrhythmogenic focus and sudden death. Coxsackie B virus is implicated in more than 50% of cases, but other viruses have also been associated. Acutely, presents with flulike symptoms, progressing to symptoms of congested heart failure. Symptoms include: prodromal viral illness, progressive exercise intolerance, congestive symptoms. Echocardiography confirms diagnosis.pero

Hypertrophic Cardiomyopathy (continue)

An electrocardiogram (ECG) will be abnormal in up to 95% of patients with HCM. Echocardiography remains standard to confirm diagnosis (LV wall thickness >16mm, nondilated LV with impaired diastolic function) MRI or repeat echocardiography after 4-6 weeks of deconditioning may help in distinguishing HCM from athletic heart syndrome.

PPE helps reduce SCD

Approximately 1:200,000/year in high school athletes Males at greater risk than females - 9:1 ratio 95% of these sudden deaths are due to structural cardiac problems

Marfan Syndrome (continue)

Autosomal dominant connective tissue disorder Physical Exam Signs Arm span-height ration > 1.05 Thumb sign Hyperextendible Ligamentous laxity Chest wall deformity (pectus excavatum) Cardiovascular signs Dilated aortic root (systolic murmur) Mitral Valve Prolapse (mid systolic click) Risk of SCD stems from rupture of aortic root dilatation Participation Restriction: typically low intensity Class IA sports, no body collision sports

Aortic Rupture in Marfan Syndrome

Causes progressive dilatation and weakness of the proximal aorta that can lead to rupture and sudden death. Risk of aortic rupture increases during adolescence and 50% of undiagnosed patients die by age 40. Symptoms of aortic dissection include excruciating chest pain, often described as tearing or ripping.

AHA recommendations

Check Heart murmur radial pulses Physical signs of Marfan syndrome What are some signs of this condition?? Brachial artery Blood pressure (sitting)

treatment and action SCA

Early recognition and activation of the local emergency response system (911) Early cardiopulmonary resuscitation (CPR) Early defibrillation (AED) Early advanced life support and cardiovascular care (hospital)

personal history (AHA recomm)

Exertional chest pain /discomfort Syncope/near syncope Excessive exertional/unexplained dyspnea or fatigue Heart murmur Elevated Blood pressure

treatment and action SCA (continue)

High flow oxygen 15L/min with BVM OPA Medications 2 Non-coated, chewable, low dose aspirin (total 160mg) Assist with nitroglycerin Sublingual or aerosol Do not administer if hypotensive or extreme bradychardia <50bpm

Long QT syndrome

Inherited or acquired Delayed repolarization of the heart following a heartbeat Increased risk of irregular heartbeat originating from the ventricles Named for ECG presentation--prolongation of the QT interval Acquired sources: Medications, malnutrition leading to low blood potassium or low blood magnesium (anorexia nervosa)

mitral valve prolapse

MV does not close properly Symptoms: Chest pain, heart palpitations, SOB, syncope Physical Exam Mid systolic click (valve leaflet flapping up) Mid systolic murmur (mitral regurgitation)

key population SCD

More common in males. Male-to-female gender differences range from 5:1 to 9:1 Most common in basketball and football (>40%) occurs in African American athletes

arrhythmic death syndrome

Normal heart AKA sudden unexplained death syndrome (SUDS cause in youth long-QT syndrome brugada syndrome catecholaminergic polymorphic ventricular tachycardia (CPVT) wolff-parkinson white (WPW) syndrome

pericarditis (continue)

Physical Exam Pericardial Friction Rub Heard best when effusion is minimal Increased intensity when leaning forward Harsh, machine like murmur typically heard throughout majority of cardiac cycle Signs of Congestive Heart Failure (results from cardiac tamponade) Participation Restriction: No competition during acute phase May return to participation with complete resolution of effusion and clinical symptoms resolved

Family history (AHA recomm)

Premature sudden death (<50 yrs age) Disability from Cardiovascular disease (<50 yrs age) Hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy, long QT, Marfan syndrome, clinically significant arrhythmias

VF

Probability of successful defibrillation for VF diminishes rapidly, with survival rates declining 7-10%/minute for every minute that defibrillation is delayed. VF deteriorates to asytole survival is unlikely. CPR is important before and after defibrillation (via AED) to provide a small but critical amount of blood flow to the heart and brain and increases the likelihood that defibrillation will restore a normal rhythm.

mitral valvue prolapse (continue)

Progression of mitral regurgitation may create need for valve replacement Higher risk of infectious endocarditis (antibiotics with dental work) Asymptomatic patients without other anomalies or cardiac issues may participate in all sports without restriction Athletes with syncope, sustained or repetitive arryhthmia, severe mitral regurgitation, systolic dysfunction, history of cardiac embolus, or family history of SCD with MVP are restricted to Class IA

recognition of SCA (continue)

Prompt recognition and a high index of suspicion for SCA must be maintained in any collapsed and unresponsive athlete. SCA is commonly mistaken for a seizure and brief seizure-like activity or myoclonic jerks have been reported in ~50% of SCA.25 Agonal/occasional gasping can occur and should not be misinterpreted as normal breathing. A collapsed and unresponsive athlete should be treated as a SCA until a noncardiac cause of collapse can be clearly determined.

delay use of an AED

Rainy or icy environment A patient lying on a wet surface or in a puddle should be moved to a dry location Metal conducting surface (e.g., stadium bleacher) Patient should be moved to a nonmetal surface Lightning Ensure everyone's safety by moving the patient indoors if possible

coronary artery anomalies

Second leading cause of SCD in athletes (17% of all cases). If suspected, transthoracic echocardiography can identify the coronary artery origins in 80-97% of patients. Some cases may require advanced cardiac imaging.

recognition of SCA

Sudden cardiac arrest Immediately Precollapse Most are asymptomatic, and SCD is often the first clinical event. Collapse is rapid, and no significant period of prodromal symptoms such as chest pain/light-headedness occur.

s/s Acute myocardial infarction

Sudden onset of weakness, nausea, and sweating without an obvious cause Chest pain, discomfort, or pressure that is described as crushing or squeezing and that does not change with each breath Pain, discomfort, or pressure in the lower jaw, arms, back, abdomen, or neck (referred pain) Irregular heartbeat and/or syncope (fainting) Shortness of breath or dyspnea Pink, frothy sputum (indicating possible pulmonary edema) Sudden death

Catecholamingeric Polymorphic Ventricular Tachycardia

VT induced by intense emotional stress or exercise 15% of all unexplained SCDs in young people Syncope during exercise or during sympathetic activation is the key to identifying the disease

Pathophysiology SCD

Vigorous exercise appears to be the trigger for lethal arrhythmias with underlying heart disease. Precise mechanism depends upon the underlying heart condition ventricular fibrillation (VF) the heart loses its ability to pump blood effectively

pericarditis

abnormal heart Inflammatory cardiac process resulting excess fluid contained within the pericardial sac (known as pericardial effusion Many etiologies including infectious, thyroid, auto-immune disease, malignancy, and idiopathic Symptoms: Similar to myocarditis Chest Discomfort (rest or exertional)

ventricular fibrillation(VF)

characterized by chaotic, rapid ventricular depolarization that leads to disorganized and asynchronous contraction of ventricular muscle.

Emergent cardiac condition

field assessment Sudden cardiac arrest (SCA) should be suspected for any athlete who has collapsed, is unresponsive, and pulseless CPR should be provided while waiting for an AED to arrive Barriers to appropriately recognizing SCA: Inaccurate assessment of pulse or respirations Occasional or agonal gasping Myoclonic jerking or seizure-like activity Pre-hospital ECG may enable abnormal heart function to be recognized earlier

immediate management of SCA

immediate activation of EMS Early CPR AED application

Marfan Syndrome

is the most common inherited disorder of connective tissue that affects multiple organ systems

Sudden cardiac death

result of undiagnosed structural or electrical cardiovascular disease. Leading cause of death in young athletes. SCD is defined as the sudden death of an individual during or within 1 hour after exercise due to a cardiovascular disorder.

Brugada syndrome

syncope genetic atrial arrhythmias ventricular arrhythmias SCD in absence of myocardial ischemia or over heart diseas

Arrhythmogenic Right Ventricular Cardiomypathy (ARVC)

what heart condition is a progressive fibro-fatty replacement of the right ventricular myocardium, resulting in right ventricular dilatation. diagnostic cardiac MRI or by histologic analysis in selected cases.

hypertrophic cardiomyopathy deg

what heart condition is asymmetric left ventricular (LV) hypertrophy. and develops in early adolescence to young adulthood

mitral valve prolapse heart

what heart condition is known as a heart murmer