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
Etiology of HTN, secondary causes: neurogenic
Brain tumor
Autonomic dysfunction
Sleep apnea
Intracranial HTN
Etiology of HTN, secondary causes: drugs and toxins
Alcohol Cocaine Cyclosporin, tacrolimus NSAIDs Erythropoietin Adrenergic meds Decongestants containing ephedrine Herbal remedies containing licorice or ephedrine Nicotine
Etiology of HTN, secondary causes: other causes
Hyperthyroidism and hypothyroidism Hypercalcemia Hyperparathyroidism Acromegaly OSA Pregnancy-induced
Pathophys of heart failure
Adaptations:
-Frank-Starling mechanism, where an increased preload helps to sustain cardiac performance
-Alterations in myocyte regeneration and death
-Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented
-Activation of neurohumoral systems, such as RAAS, sympathetic nervous system
Angiotensin II
Myocytes and myocardial remodeling
Activation of atrial natriuretic peptide and B-type natriuretic peptide
LV chamber stiffness
Etiology of heart failure: underlying causes of systolic heart failure
CAD DM HTN Valvular heart disease Arrhythmia Infections and inflammation Peripartum cardiomyopathy Congenital heart disease Drugs Idiopathic cardiomyopathy Rare conditions
Etiology of heart failure: underlying causes of diastolic heart failure
CAD DM HTN Valvular heart disease HCM Restrictive cardiomyopathy Constrictive pericarditis
How should BP be checked on the first visit?
Check in both arms and in one leg to avoid missing the dx of coarctation of aorta or subclavian artery stenosis
PE of hypertension- what to check?
Do a fundoscopic exam
Palpate all peripheral pulses
Absent, weak, or delayed femoral pulses suggests coarctation of the aorta or severe peripheral vascular dz
Examine the neck for carotid bruits, distended veins, or enlarged thyroid gland
Careful cardiac examination
Workup of HTN
UA Fasting BG or A1c Hct Serum sodium Potassium Creatinine Calcium Lipid profile
Workup of HTN based on suspected secondary causes: chronic kidney dz
Estimated GFR
Workup of HTN based on suspected secondary causes: coarctation of the aorta
CTA
Workup of HTN based on suspected secondary causes: Cushing syndrome; other states of glucocorticoid excess
Dexamethasone suppression test
Workup of HTN based on suspected secondary causes: drug-induced/drug-related HTN
Drug screening
Workup of HTN based on suspected secondary causes: pheochromocytoma
24-hr urinary metanephrine and normetanephrine
Workup of HTN based on suspected secondary causes: primary aldosteronism, other states of mineralcorticoid excess
Plasma aldosterone to renin activity ratio
If abnl, refer for further eval such as saline infusion to determine if aldosterone levels can be suppressed, 24-hr urinary aldosterone level, and specific mineralocorticoid tests
Workup of HTN based on suspected secondary causes: renovascular HTN
Doppler flow u/s
MRA
CTA
Workup of HTN based on suspected secondary causes: sleep apnea
Sleep study with oxygen saturation
Workup of HTN based on suspected secondary causes: thyroid/parathyroid dz
TSH
Serum parathyroid hormone level
What is the criterion standard for the evaluation of renal and pulmonary causes of HTN?
Digital subtraction angiography with arterial injection of radiocontrast dye
What is the main indication for echo in HTN?
Eval for end-organ damage in a pt with borderline-high BP
Presence of left ventricular hypertrophy despite nl or borderline-high BP measurements
Nonpharm tx of HTN
Moderate reduction in salt
DASH diet
Reduce alcohol consumption
Wt loss and exercise
Pharmacologic tx of HTN
Initiate ACE/ARB, BB or CCB, thiazide diuretic
If not working, titrate up to max dose
Still not working, add another agent
Meds used to treat dyslipidemia
HMG-CoA reductase inhibitors (statins) Cholesterol absorption inhibits Bile acid resins Niacin Fibrates Long-chained omega 3 fatty acids PCSK-9 inhibitors Lomitapide Mipomersen
What is usually first-line pharmacotherapy for dyslipidemia?
Statins
MOA of statins
Inhibit HMG-CoA reductase, which is the rate-limiting step in cholesterol biosynthesis
Long-term effects of statins
Reduce ASCVD, mortality
Effect seen across age, genders, disease states
Most common SEs of statins
Constipation Abdominal pain Diarrhea Dyspepsia Nausea
Who is more likely to have myopathy with statins?
Small body frame
Multisystem dz
Perioperative periods
Taking interacting meds/substances
Other AEs of statins
Elevation in LFTs
Increased BG/A1c
Cognitive impairment
Pregnancy category X
Monitoring of statins
LFT
CK
Which statins are preferred in renal impairment?
Atorvastatin
Fluvastatin
What is contraindicated with statins?
Gemfibrozil
Grapefruit juice and statins
Only drink <8 oz grapefruit juice daily or 1/2 grapefruit
Which statins are better at preventing myalgia?
Pravastatin and pitavastatin
Rosuvastatin
Use of ezetimibe
Mostly used in combo with a statin
Shown a reduction in ASCVD events s/p MI when combined with moderate intensity statin
CIs of ezetimibe
Acute liver dz or persistent elevations in LFTs
