Cardio part 1 Flashcards
Pathophys of infective endocarditis
Bacteremia that delivers the organisms to the surface of the valve
Adherence of the organisms
Eventual invasion of the vavular leaflets
Etiology of endocarditis
Native valve: Rheumatic valvular disease- primarily involving the mitral valve Congenital heart disease Mitral valve prolapse Degenerative heart disease Prosthetic valve endocarditis: Local abscess and fistula formation, valvular dehiscence IVDA New therapeutic modalities
S/sx of infective endocarditis
Fever Chills Anorexia Wt loss Malaise HA Myalgias Night sweats SOB Cough Joint pains
What is the difference between acute and subacute endocarditis?
Subacute is characterized by a hx of an indolent process
Subacute process is caused by S. viridans
Interval between onset and dx averages about 6 wks
Acute is much more aggressive
PE of infective endocarditis
Fever Heart murmur Petechiae Subungual hemorrhages Osler nodes Janeway nodes Roth spots
Workup of infective endocarditis
CBC CMP Glucose Coag panel UA Three sets of blood cultures Echo- transthoracic U/s
Tx of infective endocarditis
Treat any congestive heart failure
Native valve- pen G and gentamicin
IVDU- vanc and gentamicin
Prosthetic valve- Vanc and gentamicin and rifampin
Consider linezolid sub for vanc with unstable renal function
Indications for surgery in infective endocarditis
CHF refractory to standard medical therapy
Fungal infective endocarditis (except H. capsulatum)
Persistent sepsis after 72 hrs of appropriate antibiotic tx
Recurrent septic emboli
Rupture of an aneurysm of the sinus of Valsalva
Conduction disturbances caused by a septal abscess
Kissing infection of the anterior mitral leaflet in pts with IE of the aortic valve
Pathophysiology of angina pectoris
Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand
Angina pectoris is the MC clinical manifestation of myocardial ischemia
Caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium
Precipitating factors of angina pectoris
Severe anemia Fever Tachyarrhythmias Catecholamines Emotional stress Hyperthyroidism
S/sx of angina pectoris
Retrosternal chest discomfort: -Pressure -Heaviness -Squeezing -Burning -Choking sensation Locations: -Epigastrium -Back -Neck -Jaw -Shoulders Radiation: -Arms -Shoulders -Neck Precipitated by exertion, eating, exposure to cold, or emotional stress Stable: Lasts 1-5 mins and relieved by rest of nitroglycerin Intensity does not change with respiration, cough, or change in position
PE of angina pectoris
Positive Levine sign
Workup of angina pectoris
CXR
Exercise stress test
Stress echo
Nuclear imaging for those with baseline EKG abnormalities
EKG
Procedures for those with inconclusive noninvasive study results or unstable angina despite maximal medical tx
Tx of angina pectoris
Treat RFs -Statins Daily aspirin Nitro Beta blockers Lifestyle modifications Consider revascularization with left main artery stenosis >50%, 2- or 3-vessel dz and LV dysfunction, poor prognostic signs during noninvasive studies, or severe sx despite maximum medical therapy
Pathophys of atrial fibrillation
Electrical remodeling
Contractile remodeling
Structural remodeling
RFs of AFib
Hemodynamic stress Atrial ischemia Inflammation Noncardiovascular respiratory causes EtOH and drug use Endocrine d/os Neurologic d/os Genetic factors Advancing age
S/sx of AFib
Wide variety Palpitations Dyspnea Fatigue Dizziness Angina Decompensated heart failure Poor exercise tolerance Presyncope or syncope Generalized weakness
PE of AFib
Irregularly irregular pulse
Tachycardia
May have exophthalmos, thyromegaly, elevated JVP, or cyanosis
May have heart failure, wheezes, or diminished breath sounds
May have displaced PMI or S3
Prominent P2 with pulmonary HTN
May have ascites, hepatomegaly, or hepatic capsular tenderness
Cyanosis, clubbing, or edema of lower extremities
Workup for AFib
EKG CBC Serum electrolytes and BUN/creatinine CK and/or troponin BNP D-dimer Thyroid function studies Digoxin level Toxicology testing or ethanol level Echo CTA if D-dimer pos CT or MRI if ablation is planned
RFs of stroke in pts with AFib
Advancing age Female HTN DM Heart failure Hx of stroke/TIA/thromboembolism CAD PAD Valvular heart disease
Management of new-onset AFib
BBs and CCBs are 1st line for rate control
Amiodarone for those intolerant or unresponsive to other agents
Anticoagulation
Cardioversion may be necessary
When should cardioversion be done on an AFib pt?
Hemodynamically unstable Severe dyspnea or CP Preexcited AFib Rate-control is not working Echo does not reveal any valvular or functional abnormality of the heart
Pathophys of atrial flutter
Single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus, with an area of slow conduction between tricuspid valve annulus and the coronary sinus ostium
Etiology of atrial flutter
Coronary artery disease Hypertensive heart disease Rheumatic heart disease Congenital heart disease Pericarditis Cardiomyopathy Hypoxia COPD PE Hyperthryoidism Pheochromocytoma DM Electrolyte imbalance EtOH consumption Obesity Digitalis toxicity Myotonic dystrophy in childhood
Typical sx of atrial flutter
Palpitations
Fatigue or poor exercise tolerance
Mild dyspnea
Presyncope
Less common sx of atrial flutter
Angina
Profound dyspnea
Syncope
Workup for atrial flutter
EKG Vagal maneuvers if flutter waves are not seen Adenosine Exercise testing TTE
Tx of atrial flutter
CCBs or BBs for rate control
May need cardioversion
Anticoagulation
Consider radiofrequency ablation
Etiology of SVT
Triggered by a reentry mechanism Premature atrial or ventricular ectopic beats Other triggers: -Hyperthyroidism -Stimulants -Alcohol
Hs and Ts of arrhythmias
Toxins Thromboses Temperature Tension pneumo Tamponade Trauma Hypoxia Hypovolemia Hypokalemia/hyperkalemia Hydrogen
Common sx of SVT
Palpitations Dizziness SOB Syncope CP Fatigue Diaphoresis Nausea
Workup of SVT
Cardiac enzymes Electrolyte levels CBC Thyroid studies Digoxin level Electrophysiologic studies EKG CXR TTE
Tx of SVT
Hypotensive or unstable: immediate cardioversion
Stable: try vagal maneuvers, then if unsuccessful, adenosine
Pathophys of VTach
Caused by electrical reentry or abnormal automaticity
Caused by electrical reentry or abnormal automaticity
Ischemic heart dz Structural heart dz with disruption of nl conduction patterns Congenital structural cardiac d/os Acquired channelopathies Inherited channelopathies Electrolyte imbalances Sympathomimetic agents Digitalis toxicity Systemic diseases causing infiltrative cardiomyopathy or scar
S/sx of VTach
Palpitation Lightheadedness Syncope CP Can also be asymptomatic
PE of VTach
Hypotension Tachypnea Diminished LOC Pallor Diaphoresis High JVP Mental status changes: Anxiety Agitation Lethargy Coma
Workup of VTach: labs
Electrolytes
Serum levels of therapeutic drugs
Toxicology
Serum cardiac markers
Workup of VTach: imaging, other
Echo
EKG
Holter monitoring with recurrent syncope or palpitations
Tx of VTach: stabilization
VT associated with loss of consciousness or hypotension needs immediate cardioversion with 100-200J biphasic
Address reversible RFs
Lidocaine if pts have ongoing myocardial ischemia
Pulseless VT- high-dose unsynchronized energy
Tx of VTach: postabilization management
Referral to a cardiologist
Admission to a monitored bed
Further studies, such as electrophysiologic study
Consideration for radiofrequency ablation
Consideration for ICD placement
Tx of VTach: long-term tx
Depends on cause:
Amiodarone in combo with BBs for pts with left ventricular dysunction d/t previous MI
Heart failure: BB, ACE, aldosterone antagonists
Stains for coronary heart disease
Pathophys of VFib
Most often associated with CAD
Can result from AMI or ischemia or from myocardial scarring from an old infarct
VTach can aslo degenerated into VFib
Reentrant patterns break up into multiple smaller wavelets and the level of disorganization increases, with reentrant circuits producing high-frequency activation of cardiac muscle fibers
Etiology of VFib
Acute and chronic ischemic heart disease Valvular disease Congenital structural heart disease Paroxysmal VFib or short-coupled torsades Idiopathic VFib and VTach PE Aortic dissection Electronic control devices Nonstructural abnormalities Catecholaminergic polymorphic VTach WPW syndrome Brugada syndrome
Presentation of VFib
Pts at risk may have prodromes of CP, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic
What is the single greatest RF for sudden death from VF?
Hx of left ventricular dysfunction
Considerations when thinking about VFib?
CAD Previous cardiac arrest Syncope or near-syncope Prior MI, esp within 6 mos LVEF <30-35% H/o frequent ventricular ectopy Drop in SBP or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia Dilated cardiomyopathy from any cause HCM Use of inotropic meds Valvular heart disease Myocarditis
Triggers of VFib
Antiarrhythmic drug administration
Hypoxia
Ischemia
Atrial fibrillation with very rapid ventricular rates in the presence of preexcitation
Electric shock administered during cardioversion
Electric shock caused by accidental contact with improperly ground equipment
Competitive ventricular pacing to terminate VTach
Workup for VFib
Confirm only with EKG Echo Nuclear imaging for assessment of pts at risk Labs: 'lytes, including calcium and magnesium Cardiac enzymes CBC ABG Quantitative drug levels Tox screens and levels TSH BNP
Tx of VFib
Defibrillation
Postresuscitation:
Admit to ICU with close monitoring
Assess for complications and establish the need for emergent interventions
Mild therapeutic hypothermia
BBs
Thorough diagnostic testing to establish underlying etiology
When is radiofrequency ablation indicated for the prevention of VFib?
AV bypass tracts
Bundle branch block ventricular tachycardia
Right ventricular outflow tract tachycardia
Idiopathic left ventricular tachycardia
Idiopathic VFib
Rare forms of automatic focal VTach
Scar-related VTach due to ischemic or nonischemic myopathy
