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56 Cards in this Set
- Front
- Back
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What do you expect to see clinically with a patient who has hyperaldosteronism? |
New onset HTN and low potassium. (Postassium stays low despite replacement and HTN is resistant to treatment).
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What initial lab work would you obtain to diagnose hyperaldosteronism?
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Aldosterone level and renin level (specifically the plasma renin activity). The aldosterone/renin ratio confirms diagnosis. Aldosterone is usually greater than 16, renin is suppressed, usually unmeasurable.
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Once lab work has confirmed hyperaldosteronism, what study should be ordered?
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CT scan of the abdomen and pelvis to look at the adrenal glands.
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What is the most common cause of hyperaldosteronism?
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adrenal adenoma (treatment - surgery)
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What is the second most common cause of hyperaldosteronism?
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bilateral adrenal hyperplasia (treatment - bock aldosterone secretion with aldosterone blocker like spironolactone (aldactone).
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What is the major side effect of spironolactone
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Hyperkalemia
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What is pheochromocytoma?
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An adrenal-producing tumor which can cause refractory labile hypertension.
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What initial screening should I obtain if I suspect pheochromocytoma?
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Plasma metanephrines and/or 24-hour urinary collection for vanillylmandelic acid (VMA) and urinary metanephrines. The metanephrines tst is the more sensitive.
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With pheochromocytoma evaluation and elevated metanephrines, what study should I order?
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CT scan to look at the adrenal glands for an adrenal adenoma.
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What is the 10% rule in pheochromocytoma?
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The pheochromocytoma is familial 10% of the time, extra-adrenal 10% of the time, malignant 10% of the time and present in both adrenal glands 10% of the time.
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Coarctation of the aorta is common in what population?
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Common congenital pediatric cause of hypertension
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What causes Ductus arteriosus in coarctation of the aorta?
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Narrowing of the aorta causes a difference in the blood pressure between the upper and lower extremities.
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In a patient with coarctation of the aorta, what is a classic physical exam finding?
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Radial - femoral delay.
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Coarctation of the aorta can cause this observation on initial presentation.
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Caludication - type symptoms
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What are typcal exam findings with coarctation of the aorta?
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Upper extremitiy HTN and lower extremity hypotension with decrease palpable pulses.
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What is the treatment of coarctation of the aorta?
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Dependent on the clinical presentation, however consider conservative treatment or surgery of the senosed area.
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Name several other illnesses that may cause resistant HTN.
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Cushing's syndrome, carcinoid syndrome, obesity and obstructive sleep apnea.
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Define Hypertensive Urgency
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Blood pressure ≥ 180 mmHg or a diastolic blood pressure ≥ 110 mmHg. Relatively asymptomatic and no signs of end organ damage.
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How do you treat Hypertensive Urgency?
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Aggressive blood pressure management and follow-up.
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Define Hypertensive Emergency
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Blood pressure ≥ 180 mmHg systolic or ≥ 120 mm Hg diastolic WITH signs and symptoms of end-organ damage.
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How do you treat Hypertensive Emergency?
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Hospitalized, usually in the ICU with gradual blood pressure reduction over 24-48 hours.
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What is the general rule in Hypertensive Emergency blood pressure reduction?
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Lower the blood pressure by no more than 20% of the mean arterial pressure daily for the first couple of days.
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What are the commonly used medications to treat hypertensive emergency?
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1.)Nitroprusside - potent vasodilator. SE include cyanide toxicity. Careful in kidney disease or dialysis patients.
2.)Labetalol - alpha and beta blocker. 3.) Nicardipine - IV CCB |
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What can cause hypotension?
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Infection, volume depletion, adrenal insufficiency, anemia, blood pressure medications, cardiac tamponade.
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What medical emergency can cause hypotension?
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Cardiac tamponade
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In a patient with cardiogenic shock, what exam findings do you expect to see?
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Significant JVD, rales, hypoxemia, +/- edema
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What hemodynamic pattern do you expect in cardiogenic shock?
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Elevated systemic vascular resistance, low cardiac output, elevated pulmonary capillary wedge pressure, elevated central venous pressure and elevated pulmonary artery diastolic pressure
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What is the mainstay treatment of cardiogenic shock?
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Ionotropes and/or diuretics (as BP allows).
Ionotropes - dopamine, dobutamine, milrinone |
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In the patient that has cardiogenic shock and poor systolic function, what procedure may be beneficial?
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Intra-aortic balloon pump (IABP) insertion
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A myocardial infarction (MI) is considered positive when this happens.
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Positive enzyme leak in the blood and accompanying ECG changes
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What labs are use to evaluate and MI?
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1.)Troponin I rises within the first few hours and can stay elevated for at least a week, in some cases longer.
2.) Creatine phosphokinase (CKB) and the CK-MB fraction start elevating during first few hours, peak around 24 hours and return to baseline in 2-3 days. |
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What is the Thrombolysis in Myocardial Infarction (TIMI) mnemonic?
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AMERICA
A - age; M - markers; E - ECG; R - risk factors (+3); I - ischemia; C - CAD; A - ASA |
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What are the two types of myocardial infarctions?
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non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI)
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How is a NSTEMI diagnosed?
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positive cardiac enzyme changes and likely ST depression or T-wave inversion.
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What is the classic ECG pattern for a STEMI?
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Hyperacute ST segment elevation with eventual formation of Q waves post infarct.
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What ECG changes are seen with an anterior wall MI and which vessel is affected?
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ST elevation in leads V1 - V3 (and sometimes V4)
LAD |
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What ECG changes are seen with an inferior wall MI and which vessel is affected?
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ST elevation in leads II, III and aVF
Right coronary artery (MCA) |
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What ECG changes are seen with a lateral wall MI and which vessel is affected?
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High lateral wall involvement - ST segment elevation in leads I and aVL. Affects the circumflex artery.
Low lateral wall involvement - ST elevations in leads V5 and V6. Affects the circumflex artery |
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What ECG changes are seen with a posterior wall MI and which vessel is affected?
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See ST depression in the anterior leads (V1 & V2). Affects posterior descending artery
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Standard of care treatment for a STEMI is what?
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Emergent cardiac cath with angioplasty and possible stent deployment
*if cath lab NOT available, second-line tx is thrombolysis with TPA. |
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Mnemonic for treating unstable angina and NSTEMI
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OH BATMAN
O - Oxygen; H - Heparin; B - Beta blocker; A - ASA; T - thrombolysis; M - Morphine; A - ACE inhibitor; N - Nitroglycerin |
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Describe Variant Angina or Prinzmetal's Angina
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Crushing chest pressure, ECG changes indicate acute coronary syndrome, + enzyme leak (+trops & CK-MB)
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How is Variant angina diagnosed?
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Ergonovine challenge test
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How is variant angina treated?
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Vasodilators (nitro) & CCB (Nifedipine)
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What are some of the common clinical presentations of congestive heart failure (CHF)?
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Shortness of breath (SOB) at rest, orthopnea, paroxysmal nocturnal dyspnea, edema and weight gain.
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What common clinical findings would you expect in CHF?
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Hypoxemia, JVD, S3 gallop in systolic heart failure, S4 in dystolic dysfunction or heart failure, possibly heaptojugular reflux (HJR) and possibly increased abdominal girth
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Why does a person have CHF?
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- Systolic heart failure
- Diastolic heart failure - Valvular dysfunction |
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What do I expect an echocardiogram to show in a patient with systolic heart failure?
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Reduced ejection fraction (anything less than 50% represents some degree of a pump problem)
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What are common causes of systolic heart failure?
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ischemic cardiomyopathy, HTN and other causes of cardiomyopathy, esp dilated cardiomyopathy
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What drugs are commonly used to treat systolic heart failure?
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Furosemide, ACE Inhibitors, ARBs, Digoxin, Beta blockers, Spironolactone.
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Discuss Furosemide in it's treatment for systolic heart failure & key SE.
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Treats volume overload and pulmonary edema. Given orally or by IV. It facilitates diuresis and works in the pulmonary circulation to decrease preload. SE include hypokalemia, hypomagnesemia and metabolic alkalosis.
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Discuss ACE Inhibitors and ARBS for systolic heart failure & key SE.
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ACE/ARBs prolong morbidity and mortality in systolic CHF. Cause remodeling of cells of left ventricle and decrease left ventricular hypertophy. SE include cough (ACE), angioedema (ACE) & hyperkalemia (both).
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Discuss Digoxin for systolic heart failure & key SE..
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Improves systolic heart failure symptoms and morbidity, does not improve mortality, reduces sympathetic tone, used for rate control in A-fib. Digoxin is renally excreted, use w/caution in renal disease. Watch for dig toxicity (N/V/dizzy/palpitations).
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What is the most common arrythmia seen with digoxin toxicity?
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Paroxysmal atrial tachycardia with block.
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Discuss Beta blockers for systolic heart failure.
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Improve morbidity, mortality, reduce sympathetic tone, mortality benefit in treating the post MI patient.
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Other than medications, what else should a heart failure patient attempt to do?
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Daily exercise, low sodium diet (1,000 - 2,000 mg/day), increase fruits/veggies, possibly restrict fluids & avoid NSAIDs (can cause HTN, salt/H20 retention and blunt the effect of loop diuretics, promote hyperkalemia and AKF)
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