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117 Cards in this Set
- Front
- Back
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Describe the anatomy of a blood vessel and relevant areas of pathology?
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Intima (inner layer), media (middle layer), adventitia (outer layer.
In AD there is degeneration of the media (elastic tissue and smooth muscle fibers) In AAA there is localized dilatation of the aorta involving all 3 layers of the blood vessel |
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Would you describe the endothelium as an endocrine or paracrine organ?
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It is both - it produces angiotensin converting enzyme (ACE) which is an endocrine function and it produces nitric oxide which is a paracrine function
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Define Hypertension?
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SBP >140mmHg
DBP > 90mmHg |
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A patient started on a new antihypertensive still is not responding, his workup shows an increasing creatinine level. What is the likely medication? What is the problem?
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It is likely an ACE inhibitor and the problem is likely bilateral renal artery stenosis. The ACE results in efferent arteriole dilation resulting in the patient being unable to maintain a adequate GFR
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Which antihypertensive cannot be abruptly stopped?
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Clonidine
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Define hypertensive crisis?
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Increased BP and evidence of acute dysfunction in the CVS, neuro or renal system.
HTN encephalopathy Microvascular angiopathic hemolytic anemia (MAHA) ARF AD Eclampsia/Preeclampsia MI LV failure uncontrolled hemorrhage post reperfusion therapy post operative |
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Describe the indications and mechanisms of action of the following: nitroprusside, labetolol, nitroglycerin, phentolamine
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Nitroprusside - vasodilator of resistance and capacitance vessels
uses: accelerated (malignant) hypertension and hypertensive encephalopathy Labetolol - selective alpha and non selective beta blocker uses: aortic dissection or cardiac schema with intact LV function, in those where constant BP monitoring is not feasible Phentolamine: alpha blocker used in catecholamine induced HTN crisis (pheochromocytoma, MAOI, cocaine) Nitroglycerin: vasodilator (decreases pre-load and CO) used in cardiac ischemia or pulmonary edema |
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What are 5 differential diagnoses for ruptured AAA?
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-renal colic
-acute abdomen (pancreatitis, diverticulitis, cholecystitis, appendicitis) -AMI -musculoskeletal back pain |
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What is the critical diameter of a AAA requiring urgent referral?
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5cm
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Describe your management of AAA while waiting for OR?
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IV, O2, monitor, crossmatch
Permissive hypotension - keep BP at level to maintain cerebral and myocardial perfusion SBP 80-100mmHg |
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Describe the presentation of an aorto-enteric fistula?
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GI bleeding(melena/hematochezia) with aortic graft or known AAA
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Describe changes seen in arterial vs venous insufficiency?
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Arterial - muscular atrophy, decreased hair growth on the dorsal aspect of the foot, thickened nails with slow growth.
Venous insufficiency: swelling in the lower legs and ankles, varicose veins, leathery looking skin on the legs, stasis ulcers |
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What is normal blood pressure in adults?
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SBP <120mmHg
DBP <80mmHg |
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What is prehypertension in adults?
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SBP 120-139
DBP 80-89 |
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What is Stage I hypertension in adults?
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SBP 140-159
DBP 90-99 |
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What is Stage 2 hypertension in adults?
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SBP >/=160
DBP >/=100 |
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What is the significance of prehypertension?
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twice the risk of progressing to actual hypertension
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In younger patients, which is more important DBP or SBP?
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DBP (isolated SBP hypertension is more important in elderly patients
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What is the minimum that should be done in the ED for an isolated reading of a high blood pressure?
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After a reclining position for 10 minutes the BP should be repeated in both arms
If still elevated the patient should be referred for follow-up |
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What is the most important thing to do for patients with hypertensive urgencies (severely elevated BP in the ED without evidence of end organ damage)?
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Confirm a follow-up visit
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Define essential HTN?
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HTN for which no specific cause can be identified
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What are factors associated with essential hypertension?
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heredity
age race obesity dietary sodium |
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Describe the renin-angiotensin-aldosterone axis
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Renin - produced by the kidneys, converts angiotensinogen to angiotensin I.
Angiotensin I is converted to angiotensin II by an enzyme in the lungs (ACE) Angiotensin II is a vasoconstrictor and stimulates aldosterone which increases sodium and water retention |
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List causes of hyperaldosteronism?
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Primary hyperaldosteronism
Isolated adrenal aldosteronoma Bilateral microscopic adrenal hyperplasia Macroscopic adrenal hyperplasia Glucocorticoid remedial hyperaldosteronims adrenal carcinoma |
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What are causes of secondary hypertension?
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Renovascular hypertension (renal artery stenosis, fibromuscular dysplasia)
primary renal disease (chronic pyelonephritis, nonspecific glomerulonephritis) Arterial disease (coarctation of the aorta, renal artery stenosis, arterosclerosis, decreased vascular compliance) Glucocorticoids Thyroid storm hypothyroid hyperparathyroidism sleep apnea pheochromocytoma sympathomimetic drugs MAOI reaction |
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What patients have an increased risk of pheochromocytoma?
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neurofibromatosis
multiple endocrine neoplasia type 2 |
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WHat is the typical clinical presentation of pheochromocytoma?
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paroxysms of hypertension, malaise, apprehension and sweating
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What test can be done to help diagnose pheochromocytoma?
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urine catecholamines, metanephrines, vannillymandelic acid
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What is the treatment for patients with pheochromocytoma?
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Alpha blockade
Later beta blockade Surgical removal |
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What foods can cause a hypertensive crisis in patients taking MAOI?
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Natural or aged cheeses
Pickled herring Chicken liver Coffee in large amounts Chocolate Beer, wine Snails Yeast |
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What drugs can cause hypertensive crisis in patients taking MAOIs?
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Sympathomimetic amines
Methyldopa Dopamine Tryptophan TCA |
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What are 4 general ED presentations of hypertension in the ED?
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Hypertensive emergency
Hypertensive urgency Mild hypertension without end organ schema Transient hypertension related to anxiety or the primary complaint |
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What is the time goal for BP reduction for a true hypertensive crisis?
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<1 hour
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What conditions define a hypertensive crisis?
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Hypertensive encephalopathy
Microangiopathic hemolytic anemia Acute renal failure aortic dissection Eclampsia/pre-eclampsia Myocardial ischemia Left ventricular failure Uncontrolled hemorrhage systemic reperfusion therapy for stroke or mi |
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Define cerebral autoregulation?
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Ability of the brain to modulate vascular tone to maintain cerebral blood flow throughout the normal range of BP
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What is the approximate upper limit of cerebral auto regulation?
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MAP>160
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What happens at BP above level that can be accommodated by cerebral auto-regulation?
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Vasospasm
ischemia Increased vascular permeability Punctate hemorrhages Brain edema |
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List components of the clinical picture of hypertensive encephalopathy?
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Severe headache
Vomiting Drowsiness Confusion Seizures blindness Focal neurological deficits Coma Papilledema |
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What is the definition of hypertensive emergency?
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Acute end-organ schema requiring control of BP within 1 hour
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What is the definition of hypertensive urgency?
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A historical term of no clinical value, related to arbitrarily elevated BP with nonspecific symptoms. These patients probably are best referred to as having poorly controlled or inadequately controlled HTN.
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What is malignant hypertension?
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Severe hypertension associated with evidence of acute and progressive damage to end organs (heart, kidney, brain) The diastolic pressure is usually >130mmHg
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What is the treatment of malignant hypertension?
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Decrease the MAP by 25% over 1 hour
Then try to achieve a target of 160/100 over 2-6 hours using nitroprusside, labetalol or fenoldopam |
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What are 2 mechanisms of HTN in the context of ongoing pulmonary edema?
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1) increased PVR caused by increased catecholamines associated with the stress of pulmonary edema
2) Pulmonary edema results from an abrupt severe elevation of BP that precipitates acute left ventricular failure -> BP must be lowered with nitroglycerin or nitroprusside |
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What is a true hypertensive emergency in a pregnant patient?
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Any acute elevation of the DBP >100mmHg
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What is the treatment of choice for accelerated hypertension and hypertensive encephalopathy?
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Nitroprusside
Second choice - labetalol or nicardipine |
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What is the treatment of hypertension in intracranial hemorrhage?
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Labetalol
Alternative: Nitroprusside, nicardipine |
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What is the treatment of hypertension in acute pulmonary edema?
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Nitroglycerin
Alternative: ACE inhibitor |
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What is is the treatment of hypertension in cardiac ischemia?
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Nitroglycerin
Alternative: nitroprusside |
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What is the treatment of hypertension in aortic dissection?
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nitroprusside
Alternative: Labetalol |
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What is the treatment of hypertension in adrenergic crisis?
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Phentolamine
Alternative: Labetalol |
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What is the treatment of hypertension in eclampsia and pre-eclampsia?
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Labetalol
Alternative: nicarpine |
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Under what conditions should nitroprusside not be used?
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Increase ICP in stroke
Renal failure (prolonged treatment may lead to thiocyanate toxicity) Hypothyroidism Methemoglobinemia |
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In which patients should you be cautious with nitroglycerin?
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Those with RV dysfunction as it may lead to hypotension
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In what patients should you avoid labetalol?
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Heart failure
AV block Asthma Cocaine intox Pheochromocytoma |
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What is the pathophysiology of nitroprusside toxicity?
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Nitroprusside is metabolised to thiocyanate of whihc cyanide is an intermediate metabolite.
this toxicity presents as weakness, hypoxia, nausea, tinnitus, muscle spasm and disorientation |
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What are the two strongest indications for antihypertensive therapy in stroke syndromes?
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Strokes due to aortic dissection
Stroke patients who have received fibrinolytic therapy and are hypertensive |
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If hypertension in stroke syndromes is to be treated, what is the most rational agent to choose?
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Labetalol - shifts the autoregulation curve and preserves the reactivity to PCO2
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What is the goal of treating BP in aortic dissection?
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SBP <100-120mmHg
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What is the dose of nitroprusside?
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0.25mcg/kg/min - 5.o mcg/kg/min (or higher, though greater risk of toxicity)
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What is the ratio of alpha to beta receptor blockade of labetalol?
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1:3 for PO
1:7 for IV |
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How is labetalol dosed?
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20mg over 2 min
Then repeat every 10 minutes by doubling the dose |
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What are the RF associated with aortic dissection?
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Epidemiologic
-Male sex -Increasing age Chronic conditions -Hypertension -Bicuspid aortic valve -Marfan's syndrome -Ehlers-Danlos syndrome -Giant cell arteritis -Prior cardiac surgery -Family history of aortic dissection Trauma -Exertion -Trauma -During Cardiac Surgery -During IABP insertion Medications -Stimulant use |
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What are the 3 layers of the aortic wall and where does dissection occur?
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Intima
Media Adventitia Dissection occurs in the media |
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What is the pathophysiology of aortic dissection?
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Medial degeneration
-loss of smooth muscle cells and elastic tissue -scarring, fibrosis and hyaline-like changes -stress tears the aortic intima and blood gains access to the media -the hematoma forms a false lumen which can propagate and rupture back into the true lumen |
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What is the most important clinical factor favoring continued dissection?
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BP elevation
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How are aortic dissections classified?
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Stanford and De Bakey
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What is the Debakey classification of AD?
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Type I - Ascneding aorta + arch + descending
Type II - ascending aorta Type III - descending (distal to takeoff of the left subclavian) A - above the diaphragm B - below the diaphragm |
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What is the Stanford classification of AD?
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Type A - all dissections involving the ascending aorta regardless of the site of origin
Type B - all dissections not involving the ascending aorta |
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Name 2 aortic conditions closely related to aortic dissection that are managed similarly?
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Intramural hemorrhage = contained hematoma within the aortic wall
Penetrating atherosclerotic aortic ulcers = occurs in older hypertensive patients with CAD |
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Define acute and chronic aortic dissection?
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Acute <2 weeks
Chronic >2 weeks |
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What are the symptoms of aortic dissection?
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1. Pain - excruciating, occurs abruptly, most severe at onset
2. Neuro symptoms - focal weakness or change in mental status 3. Syncope - often occurs early and is the result of dissection into the pericardium or from transient interruption of blood flow to the cerebral vasculature |
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What are the physical findings of aortic dissection?
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Hypertension
Hypotension Pseudohypotension (BP in arms is low or unobtainable but central arterial pressure is normal or high) Pulse deficits and BP differences AMI Aortic regurgitation Signs of tamponade Neuro deficits Signs of distal extension |
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What is the role of CXR in the diagnosis of AD?
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-cannot exclude dissection
-normal in 12% of patients |
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What are CXR findings suggestive of AD?
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-Wide mediastinum
-Calcium sign - calcium deposit separated from the outermost portion of the aorta by >5mm -double density appearance of the aorta -localized bulge along a normally smooth aortic contour -disparity in the caliber of the ascending and descending aorta -obliteration of the aortic knob -displacement of the trachea or NGT to the right |
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What is the role of ECG in the diagnosis of AD?
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It can exclude STEMI, inferior MI
It can show ischemic changes, LVH or it can be normal |
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What is the role of TTE in the diagnosis of AD?
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Insensitive and may be suboptimal depending on body habitus
It does not visualize the aortic arch or much of the descending aorta Can exclude pericardial tamponade Can identify aortic regurgitation |
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What is the role of TEE in the diagnosis of AD?
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It can be done at the bedside
Highly sensitive Can visualize the entire aorta It is the procedure of choice in unstable patients |
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What is the role of CT in the diagnosis of AD?
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Cannot be done at the bedside
Findings suggestive of aortic dissection include: dilatation of the aorta, intimal flap, identification of true and false lumens IV contrast improves the accuracy |
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What is the role of MRI in the diagnosis of AD?
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Useful to evaluate chronic dissection, to f/u post-op patients, to monitor non-operative patients
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What is the sensitivity and specificity of TEE for the diagnosis of AD?
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Sensitivity 98%
Specificity 95% |
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What is the sensitivity and specificity of Helical CT for the diagnosis of AD?
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Sensitivity 100%
Specificity 98% |
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What is the sensitivity and specificity of MRI for the diagnosis of AS?
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Sensitivity and specificity 98%
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What is the mortality rate after onset of aortic dissection?
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1% per hour
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What is the management of Aortic dissection?
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-opioids for analgesia and to decrease sympathetic tone
-Target SBP 100-120 -Target HR <60 (to decrease the shear stress on the aorta - which is a function of sBP and HR) -Avoid vasodilators in isolation because they cause tachycardia Best choice Labetalol and esmolol Can use nitroprusside in addition to BB (0.3-5mcg/kg/min) Type A - Surgery Type B - BP control for uncomplicated cases |
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What are the indications for surgery in Type B ADs?
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uncontrolled HTN
persistent pain occlusion of a major arterial trunk aortic leakage or rupture development of a localized aneurysm |
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What is a true aortic aneurysm?
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Localized dilation of the aorta cause by weakening of its wall
-it involves all 3 layers (intima, media and adventitia) |
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What is a false aneurysm (pseudo aneurysm)?
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Collection of flowing blood that communicates with the arterial lumen but is contained only by the adventitia or surrounding soft tissue. Can arise from a defect in the arterial wall or a leaking anastomosis after AAA repair.
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What is the normal diameter of the aorta what what diameter defines AAA?
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Diameter of the normal adult infrarenal aorta: ~2cm
Diameter >/=3cm -> AAA |
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What is the epidemiology of AAA?
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Age >50
Men >>>women atherosclerosis (coronaries, peripheral vessels, carotids) Family history of AAA |
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What is the diameter above which the risk of rupture increases?
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Rupture is rare if diameter <4cm
Most ruptured AAA have a diameter >5cm |
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What are complications associated with an unruptured AAA?
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Blue toe syndrome (distal embolization)
Embolization and acute arterial occlusion Aortic thrombosis Compression of adjacent structures (ex duodenum, ureters) Abdo pain, back pain, flank pain |
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What is the classic triad of ruptured AAA?
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Pain
Hypotension Pulsatile abdominal mass |
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What are the different types of fistula that a rupturing AAA can create?
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1. Primary aortoenteric fistula (unoperated AAA ruptures in to the GI tract)
2. Secondary aortoenteric fistula (site of previous aortic surgery communicates with the GI tract) 3. Aortocaval fistula (IVC) results in shunting of blood from the arterial to the venous system resulting in increased venous return and high output CHF |
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What are the xray findings of AAA?
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Curvilinear calcification of the aortic wall
Paravertebral soft tissue mass |
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What is the sensitivity of US for detecting AAAs?
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100% provided that a technically adequate study can be obtained
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What is the sensitivity and specificity of CT for detecting AAAs?
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100% and contrast is not necessary
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What is the management of a ruptured AAA?
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2 large bore IV accesses
Blood type and cross match 6U on hold (notify the bloodbank that much more will potentially be needed) EDE US CT only for stable patients once Vascular surgery is involved Raise BP only to a level that maintains adequate cerebral and myocardial perfusion (Reasonable target 80-100mmHg) No evidence that lowering the BP is beneficial in the patient with a ruptured AAA Emergency surgery (laparotomy vs endovascular repair) |
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What is the surgical mortality in patients with ruptured AAA?
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50%
Preoperative hypotension is the most important factor predicting mortality (overall mortality including the patients that do not reach the OR is 80-90%) |
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What is the mortality associated with elective AAA repair?
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5%
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What are common misdiagnoses in patients with ruptured AAA?
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Renal colic
Acute abdomen pancreatitis intestinal ischemia diverticulitis appendicitis perforated viscus bowel obstruction MSK back pain acute myocardial infarction |
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What is Leriche's syndrome?
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Sexual impotence in men caused by aortoiliac obstruction
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What is the history obtained from patients with acute arterial occlusion vs chronic arterial insufficiency?
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acute arterial occlusion:
some variant of the 5 Ps: pain, pulselessness, paresthesias, paralysis chronic arterial insufficiency: intermittent claudication or ischemic pain at rest |
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What are signs of chronic arterial insufficiency?
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Muscular atrophy
Loss of hair growth over the dorsum of the toes and feet thickening of the toenails resulting from slow nail growth Shiny, scaly, skeletonized skin localized pallor or cyanosis blanching with finger pressure with delay in return of normal color Buerger's sign: redness or rubor when the extremity is dangling and then pale when elevated |
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What is Buerger's disease?
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Idiopathic inflammatory occlusive disease primarily involving the medium-sized and small arteries of the hands and feet, usually seen in men between 20-40 years who use tobacco
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Describe the ulcers of arterial insufficiency
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5% of LE ulcers
Distal aspects of digits Painful Signs of chronic arterial insufficiency Gray, yellow or black Small, shallow, dry Sharp rim No granulation tissue |
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Describe ulcers of venous insufficiency
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90% of LE ulcers
Proximal to or in the region of the ankle (especially near the medial malleolus) Mildly painful Signs of chronic venous insufficiency (edema, prominent superficial veins, stasis dermatitis) Weeping base Extensive granulation tissue Develop rapidly |
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Describe ulcers of diabetic neuropathy
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5% LE ulcers
Location reflects site of repeated trauma Painless Deep Suppurative drainage Surrounded by a rim of thick callus |
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Describe hypertensive ulcers
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rare
near the lateral malleolus severely painful reddish blue areas of infarcted skin with hemorrhagic blebs and superficial ulcers minimal drainange little granulation tissue |
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What is Virchow's triad?
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Endothelial injury
Stasis Hypercoagulability |
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What conditions may cause an elevated D-dimer?
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Malignancy
Pregnancy Advanced Age Prolonged bedrest Recent surgery infection inflammation new indwelling catheter Stroke MI |
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What is the PERC rule?
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Age <50
HR <100 O2sat >94 no hemoptysis no unilateral leg swelling No recent major surgery or trauma No prior PE/DVT No hormone use (age, HR, O2, HUMPH) |
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What are the CXR findings in PE?
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Normal CXR
Pleural effusion Unilateral basilar atelectasis Hampton's hump - pulmonary infarction, pleural-based, wedge-shaped Westermark's sign - unilateral lung oligemia |
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What did PIOPED show regarding the results for VQ scans for PE diagnosis
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High probability VQ => diagnostic of PE
normal VQ - excludes PE moderate probability requires additional formal pulmonary angiography or CTPA |
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What is the definition of massive PE?
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-sustained hypotension SBP<90mmHg at least 15 minutes
-pulselessness -persistent profound bradycardia |
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What is the definition of submassive PE
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-RV dysfunction or myocardial necrosis
-no systemic hypotension |
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What is the definition of non-massive PE
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Normotensive
normal biomarker levels and no RV dysfunction on imaging |
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What is the risk of ICH post-fibrinolysis in the context of PE?
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2%
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