Cardio part 2 Flashcards
Pathophys of premature ventricular contractions
Suggested mechanisms are reentry, triggered activity, and enhanced automaticity
Etiology of premature ventricular contractions
Cardiac: Acute MI or myocardial ischemia Myocarditis Cardiomyopathy Myocardial contusion Mitral valve prolapse Other causes: Hypoxia and/or hypercapnia Medications Illicit substances Hypomagnesemia, hypokalemia, hypercalcemia
Hx of PVCs
Pts are usually asymptomatic
Paplpitations and neck and/or chest discomfort
Pt may report feeling that his or her heart stops after a PVC
Pts with frequent PVS or bigeminy may report syncope
Long runs of PVCs can result in hypotension
Exercise can increase or decrease the PVC rate
PE of PVCs
BP- frequent PVCs may result in hemodynamic compromise
Pulse- ectopic beat may produced a diminished or absent pulse
Hypoxia may precipitate PVCs- check pulse oximetry
Cardiac findings- Cannon A waves may be observed in the jugular venous pulse
Cardiopulmonary- Elevated BP and S4 or S3 and rales are important clues to the cause and clinical significance of PVCs
Neuro- Agitation and findings of sympathetic activation suggest that catecholamines may be the cause of the ectopy
PVCs workup
In young, healthy pts without concerning concomitant sx, labs are not typically necessary Otherwise: Serum electrolyte levels Drug screen Drug levels Echo EKG Holter monitor Exercise stress testing used complementary to Holter monitoring
Tx of PVCs
In absence of cardiac disease, no tx needed
Otherwise:
Establish telemetry and IV access, initiate oxygen, and obtain 12-lead
Treat the underlying cause of hypoxia
Treat any drug toxicity
Correct electrolyte imbalances
BBs with those who have sustained an MI
Amiodarone
In PVCs from the right or left ventricular outflow tract that occur in structurally nl hearts, catheter ablation
Hx of congestive heart failure- what to ask
Ask about the following: Myopathy Previous MI Valvular heart dz, familial heart dz Alcohol use HTN DM Dyslipidemia Coronary/peripheral vascular dz Sleep-disordered breathing Collagen vascular dz, rheumatic fever Pheochromocytoma Thyroid dz Substance abuse Hx of chemo/radiation to the chest
Hx of left-sided heart failure
Exertional dyspnea Orthopnea PND Dyspnea at rest Acute pulmonary edema CP/pressure Palpitations Anorexia Nausea Wt loss Bloating Fatigue Weakness Oliguria Nocturia Cerebral sx of varying severity
Cerebral sx of congestive heart failure
Confusion Memory impairment Anxiety HAs Insomnia Bad dreams or nightmares Rarely, psychosis with disorientation, delirium, or hallucinations
PE of congestive heart failure
Obvious dyspnea during and immediately after moderate activity
Dyspneic when lying flat without elevation of the head for more than a few minutes
Chronic severe heart failure- malnourished and sometimes even cachectic
Exophthalmos
Severe tricuspid regurgitation
Visible pulsation of the eyes and of the neck veins
Severe- central cyanosis, icterus, and malar flush
Stroke volume reduced
Pulse may be weak, rapid, and thready
Ascites
Tachycardia
Diaphoresis
Pallor
Peripheral cyanosis with pallor and coldness of the extremities
Obvious distention of the peripheral veins
Rales
JVD
Kussmal’s sign
Hepatojugular reflux
Hepatomegaly- right sided
S3 gallop
Stage A heart failure
At high risk for heart failure but do not have structural heart disease or sx of heart failure
Treat HTN
Encourage smoking cessation
Treat lipid d/os
Encourage regular exercise
Discourage alcohol intake and illicit drug use
Stage B heart failure
Asymptomatic, with LV dysfunction from peveious MI, LV remodeling form LV hypertrophy, and asymptomatic valvular dysfunction
Treat with Stage A tx
ACE/ARB and/or BB
Stage C heart failure
Structural heart disease and current or previous sx of heart failure Treat like stage A ACEI/ARBs BBs ARNIs Ivabradine
Stage D heart failure
Pts have refractory heart failure that requires specialized interventions
Tx for stage A, B, C
Heart transplantation or placement of an LV assist device in eligible pts
Pulmonary catheterization
Options for end of life care
Workup of congestive heart failure
CBC Serum electrolyte levels Renal and liver function studies Assessment for iron deficiency BNP or NT-proBNP ABG EKG CXR Echo MUGA CT or MRI
Tx of congestive heart failure
Encourage physical activity Sodium restriction Fluid restriction Diuretics for symptomatic relief ACE ARBs Hydralazine and nitrates to improve sx or for those who can't tolerate ACE/ARB or as add-on Beta-adrenergic blockers Aldosterone antagonists as adjunct Digoxin Anticoagulants Inotropic agents Pacemakers Cardiac resynchronization therapy ICDs
RFs for CAD
Age >45 years in men Age >55 years in women FHx of early heart disease Lipoprotein a levels Low HDL HLD HTN Cigarette smoking DM Obesity Lack of physical activity Metabolic syndrome Mental stress Depression
Primary prevention of CAD- statin therapy
Statin therapy is appropriate for
- Those with clinical ASCVD
- Those with primary elevations of LDL of 190 or greater
- Those aged 40-75 yrs old with DM and LDL levels of 70-89 without clinical ASCVD
- Those without clinical ASCVD or DM aged 40-75 years who have LDL level of 70-189 as well as an estimated 10-year ASCVD risk of 7.5% or higher
Primary prevention of CAD- other measures
BP control Antioxidants ASA Smoking cessation Dietary modifications Physical activity Wt management
Pathophys of HTN
Multifactorial
Multiple factors modulate the BP, including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation
Etiology of HTN
Primary- from environmental or genetic causes
Secondary
Etiology of HTN, secondary causes: kidney
Polycystic kidney disease CKD Urinary tract obstruction Renin-producing tumor Liddle syndrome
Etiology of HTN, secondary causes: vascular
Coarctation of aorta
Vasculitis
Collagen vascular dz
Etiology of HTN, secondary causes: endocrine
Exogenous: steroids, oral contraceptive use, NSAIDs Endogenous: Primary hyperaldosteronism Cushing syndrome Pheochromocytoma Congenital adrenal hyperplasia