Cardiovascular Em

Front 1

CARDIOVASCULAR EMERGENCIES: DYSRHYTHMIAS, HTN, AORTIC, VENOUS, ISCHEMIC

Back 1

CARDIOVASCULAR EMERGENCIES: DYSRHYTHMIAS, HTN, AORTIC, VENOUS, ISCHEMIC

Front 2

Define Dysrhythmia:

Back 2

an abnormal rhythm; especially a disordered rhythm exhibited in a record of electrical activity of the brain or heart

Front 3

Define Ectopic focus:

Back 3

originating in area of heart other than the sinoatrial node <ectopic beats> also initiating ectopic heartbeats <an ectopic pacemaker>

Front 4

Define Reentry:

Back 4

cardiac mech that explain's certain abn heart actions (eg tachycardia) & involves transmission of wave of depolarization along alternate pathway when original pathway is blocked with return of impulse along blocked pathway when alternate pathway is refractory & then transmission along open pathway resulting in abnormality

Front 5

Define Cardiac pacing:

Back 5

the act or process of regulating or changing the timing or intensity of cardiac contractions (as by an artificial pacemaker)

Front 6

Define Tachycardia:

Back 6

relatively rapid heart action whether physiological (as after exercise) or pathological

Front 7

Define Sinus nodal activity:

Back 7

Electrical activity in the heart originating at the sinus node--a small mass of tissue that is made up of Purkinje fibers, ganglion cells, and nerve fibers, that is embedded in the musculature of the right atrium of higher vertebrates, and that originates the impulses stimulating the heartbeat -- called also S-A node

Front 8

Define Atrioventricular block: (heart block):

Back 8

incoordination of the heartbeat in which the atria and ventricles beat independently due to defective transmission through the bundle of His and which is marked by decreased cardiac output often with cerebral ischemia

Front 9

Define Bradycardia:

Back 9

relatively slow heart action whether physiological or pathological

Front 10

Define Arrhythmia:

Back 10

irregularity or loss of rhythm (of heart)

Front 11

Define Cardiac arrhythmia :

Back 11

irregular heart action caused by physiological or pathological disturbances in the discharge of cardiac impulses from the SA node or their transmission through conductive tissues of the heart.

Front 12

Define Reperfusion arrhythmia:

Back 12

arrhythmia that occurs as the infracted heart is re-supplied with blood following angioplasty or thrombolysis

Front 13

Define Sinus arrhythmia:

Back 13

cardiac irregularity marked by variation in the interval between sinus beats and evident on EKG as alternately long and short intervals between P waves.

Front 14

Compare and contrast the mechanisms and treatment for tachydysrhythmias

Back 14

Moi: 1.increased automaticity in normal or ectopic site 2.reentry in normal or accessory pathway 3.after depolarizations causing triggered rhythms
Urgency of tx: depends on hypoperfusion evidence 2. potential of lethal rhythm
Tx: IV drugs if stable, cardioversion or defibrillation if unstable.

Front 15

Compare and contrast the mechanisms and treatment for bradydysrhythmias

Back 15

MOI: 1.depression of sinus nodal activity or 2.conduction system blocks subsidiary pacemakers take over & pace heart
Urgency of tx: depends on 1. hypoperfusion & 2.potential to degenerate into profound Bradycardia or asystole e.g. HR < 50 with hypoperfusion or Bradycardia 2nd to structural disease of conducting system with risk of complete AV block.
Tx: Atropine, isoproterinol, transcutaneous pacing

Front 16

Discuss the clinical significance for the following: Sinus Bradycardia

Back 16

Represents suppression of sinus node discharge rate. May be 1.physiologic: athletes, sleep, vagal stimulation 2.pharmacologic: digoxin, opioids, CCB or 3.pathologic: acute inferior MI, increased ICP, hypothyroidism

Front 17

Define Sinus Bradycardia

Back 17

when the sinus node rate falls below 60 – characterized by normal P wave and PR interval, 1:1 AV conduction; atrial rate < 60.

Front 18

Discuss the most common treatments for the following: Sinus Bradycardia

Back 18

only if HR <50 with hypoperfusion: 1.Atropine 2.isoproterinol if atropine not effective 3.External cardiac pacing if refractory to drugs 4.internal pacing if symptomatic and recurrent

Front 19

Define Sinus tachycardia

Back 19

results from acceleration of sinus node discharge rate. Characterized by normal P waves and PR intervals, 1:1 AV conduction and atrial rate of 100-160

Front 20

Discuss the clinical significance for the following: Sinus tachycardia

Back 20

acceleration of sinus node discharge rate, usually secondary to stimuli 1. physiologic: exertion, anxiety 2.pharmacologic: atropine, epi, ETOH, nicotine, caffeine 3. pathologic: fever, hypoxia, anemia, hypovolemia, PE. Usually represents effort to increase cardiac output

Front 21

Discuss the most common treatments for the following: Sinus tachycardia

Back 21

treatment of underlying condition. With acute MI, may decrease HR with beta-adrenergic antagonists

Front 22

Define premature atrial contractions: PAC

Back 22

premature cardiac beat arising from an ectopic atrial focus - just like it sounds!

Front 23

Discuss the clinical significance for the following: premature atrial contractions

Back 23

Originate from ectopic pacemakers. Common all ages often without heart disease. causes: stress, fatigue, ETOH, tobacco, coffee. Frequent PAC’s seen with chronic lung disease, ischemic heart disease, digoxin toxicity. May precipitate atrial tachycardia, flutter or fibrillation

Front 24

Discuss the most common treatments for the following: premature atrial contractions

Back 24

discontinue precipitating drugs or toxins, treat underlying disorders

Front 25

Define Atrial flutter

Back 25

rapid regular atrial contractions occurring usually at rates 250-350 min. and often producing saw-tooth waves in ECG leads II, III & aVF

Front 26

Discuss the clinical significance for the following: Atrial flutter

Back 26

originates from a localized area in the atria. MOI unknown. associated with heart disease, ischemic heart disease or acute MI, congestive cardiomyopathy, PE, myocarditis, blunt chest trauma, digoxin toxicity. May be transitional between sinus rhythm and atrial fibrillation

Front 27

Discuss the most common treatments for the following: Atrial flutter

Back 27

1.low energy cardioversion 2.if cardioversion contraindicated: digoxin, verapamil, diltiazem, esmolol or propranolol 3. quinidine or procainamide after ventricular rate control 4.IV esmolol for new onset A flutter 5.IV verapamil or diltiazem 6. newer antiarrhythmics e.g. ibutilide

Front 28

Define Atrial fibrillation

Back 28

fibrillation wherein normal rhythmic contractions of cardiac atria are replaced by rapid irregular twitchings of muscular wall. the ventricles respond irregularly to dysrhythmic bombardment from atria

Front 29

Discuss the clinical significance for the following: Atrial fibrillation

Back 29

multiple areas of atrial myocardium continuously discharging and contracting. No uniform depolarization, only quivering of atrial wall. increased atrial size/mass; increased vagal tone; found in 1.rheumatic heart disease 2. HTN 3.ischemic heart disease 4.thyrotoxicosis.

Front 30

Discuss the most common treatments for the following: Atrial fibrilliation with rapid ventricular response and acute hemodynamic deterioration

Back 30

synchronized cardioversion If not successful then procainamide IV and continue with cardioversion

Front 31

Discuss the most common treatments for the following: Stable Atrial fibrilliation

Back 31

diltiazem, verapamil, beta-adrenergic blockers, digoxin for pt with ventricular failure. After ventricular rate control: chemical conversion with procainamide, quinidine or verapamil, ibutilide, amiodarone.

Front 32

Define Supraventricular tachycardia

Back 32

a regular, rapid rhythm arising from reentry or ectopic pacemaker in areas above bifurcation of bundle of His.

Front 33

Discuss the clinical significance for the following: Supraventricular tachycardia

Back 33

pt's with acute MI, chronic lung disease, pneumonia, ETOH & digoxin toxicity. Reentrant can occur in normal heart or rheumatic heart disease, acute pericarditis, MI, mitral valve prolapse. may cause palpitations, lightheaded, anginal CP & dyspnea, CHF, pulmonary edema

Front 34

Discuss the most common treatments for the following: Supraventricular tachycardia

Back 34

maneuvers increase vagal tone (carotid sinus massage, cold water facial immersion, valsalva maneuver 2.adenosine 3.verapamil 4. 5.increasing BP with meds and carotid sinus massage 6. esmolol, propranolol or digoxin, external pacing

Front 35

Discus Junctional premature contractions

Back 35

ectopic pacemaker within AV node or AV bundle. QRS is premature; P wave may occur before or after QRS; PR interval shorter; occur in CHF, digoxin toxicity, ischemic heart disease, acute MI

Front 36

Discuss treatment for junctional premature contractions

Back 36

Tx: tx underlying disorder. If frequent or symptomatic may use antiarrhythmics

Front 37

Discuss Junctional rhythms

Back 37

a long pause in impulses reaching AV junction: sinus brady, AV block or during pause after premature beats. sustained with CHF, myocarditis, hypokalemia or digoxin toxicity. Myocardial or cerebral ischemia may develop. Accelerated junctional rhythm & tachy may occur from dig toxicity, acute rheumatic fever or inferior MI.

Front 38

Discuss treatment for Junctional rhythms

Back 38

Tx: Do not require treatment if isolated, infrequent beats. If sustained, tx underlying cause.

Front 39

Discuss PVC's

Back 39

originate from single or multiple areas in ventricles. common. Occur in pts with ischemic heart disease, acute MI. Other causes: digoxin toxicity, CHF, hypokalemia, alkalosis, hypoxia, sympathomimetic drugs

Front 40

Discuss treatment for PVC's

Back 40

Tx: IV lidocaine, procainamide

Front 41

Discuss ventricular tachycardia

Back 41

occurrence of 3+ depolarizations from ventricular ectopic pacemaker at rate 100+/min. Rare in pts without underlying heart disease. causes, hypertrophic cardiomyopathy, mitral valve prolapse, drug toxicity. exacerbated by hypoxia, alkalosis, & electrolyte abnormalities. Unstable pts should be cardioverted.

Front 42

Discuss treatment for ventricular tachycardia

Back 42

Unstable or cardiac arrest—with synchronized cardioversion. Symptomatic v-tack with pulse—synchronized cardioversion. Pulseless v-tach—unsynchronized Stable: IV antiarrhythmics, amiodarone, procainamide

Front 43

Discuss ventricular fibrillation

Back 43

totally disorganized depolarization & contraction of ventricular myocardium – no effective ventricular pumping activity. EKG shows fine to coarse zigzag pattern without discernible P waves or QRS. Never accompanies pulse, BP or awake, responsive pt. Pts with ischemic heart disease, with or without acute MI. suddenly or after prolonged left ventricular failure and/or circulatory shock, digoxin quinidine toxicity, hypothermia, blunt chest trauma or severe electrolyte abnormality

Front 44

Discuss treatment for ventricular fibrillation

Back 44

Immediate electrical defibrillation. Initiate CPR and administer other IV drugs according to current ACLS guidelines

Front 45

Define 1st degree AV block

Back 45

delay in AV conduction manifest by prolonged PR interval. Each atrial impulse conducted in ventricles but slower than normal. Causes: increased vagal tone, digoxin toxicity, acute inferior MI, myocarditis. No tx usually required

Front 46

Discuss 2nd degree AV block: Mobitz I - Wenckebach

Back 46

progressive prolongation of AV conduction & PR interval til artrial impulse completely blocked. Associated: acute inferior MI, digoxin toxicity, myocarditis, post cardiac surgery.

Front 47

Discuss treatment for 2nd degree AV block: Mobitz I - Wenckebach

Back 47

no tx necessary unless slow ventricular rate produces signs of hypoperfusion.

Front 48

Discuss 3rd degree AV block

Back 48

No AV conduction. Ventricles paced by escape pacemaker at rate slower than atrial rate. Indicate structural damage to infranodal conducting system. Usually inadequate to maintain cardiac output, unstable, periods of ventricular asystole

Front 49

Discuss treatment for 3rd degree AV block

Back 49

Nodal 3rd* tx like Mobitz I with atropine or ventricular demand pacemaker. Infranodal 3rd* block: ventricular demand pacemaker. Isoproterenol used temporarily. External cardiac pacing done before transvenous pacer placement

Front 50

Discuss PEA: pulseless electrical activity

Back 50

Presence o electrical complexeswithout accompanying mechanical contraction of hear. Cardiac arrest due to metabolic abn of myocardium.

Front 51

Discuss treatment for PEA

Back 51

continue CPR and alpha adrenergic drugs. May be associated with severe hypovolemia, cardiac tamponade, tension pneumo, massive PE, ruptured ventricular wall

Front 52

Discuss Agonal rhythm

Back 52

occurance of very broad and irregular ventricular complexes at slow rate usually without associated ventricular contractions

Front 53

Discuss Cardiac Asystole

Back 53

complete absence of cardiac electrical activity. Tx is to stimulate electrical activity and mechanical contractions with CPR and alpha-adrenergics.

Front 54

Know predisposing factors for atrial fibrillation

Back 54

increased atrial size, mass, vagal tone, varying refractory periods, rheumatic heart disease, HTN, ischemic heart disease, thyrotixicosis

Front 55

Disuss relationship of atrial fibrillation to heart failure

Back 55

L. ventricular failure, L. atrial contraction contributes significantly to cardiac output; loss of effective atrial contraction as in A-fib may produce heart failure

Front 56

Know predisposing factors for emboli in pts with A-fib

Back 56

up to 15% of pts in chronic A-fib have at least one embolic episode each yr. (conversion to sinus rhythm from A-fib carries risk of arterial embolism. They are frequently anticoagulated

Front 57

Discuss treatment of A-fib in the unstable patient

Back 57

synchronized cardioversion, if not successful, procainamide IV and continue with cardioversion

Front 58

Discuss treatment of A-fib in unstable pts

Back 58

diltiazem, verapamil, IV beta-adrenergic blockers, IV digoxin

Front 59

Discuss the causes and treatment of Ventricular Tachycardia in regard to: unstable patients

Back 59

Unstable or those in cardiac arrest—treat with synchronized cardioversion. Symptomatic v-tack with a pulse—synchronized cardioversion at 100J. Pulseless v-tach—unsynchronized at 200J.

Front 60

Discuss the causes and treatment of Ventricular Tachycardia in regard to: stable patients

Back 60

IV antiarrhythmics 1) lidocaine followed by infusion 2)amiodarone 3) procainamide

Front 61

Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Where the rhythm arises from

Back 61

arises from reentry or an ectopic pacemaker in areas above the bifurcation of the bundle of His.

Front 62

Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: What it is associated with

Back 62

Ectopic seen in patients with acute MI, chronic lung disease, pneumonia, ETOH intoxication and digoxin toxicity. Reentrant can occur in a normal heart or in association with rheumatic heart disease, acute pericarditis, MI, or mitral valve prolapse.

Front 63

Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Associated signs and symptoms

Back 63

SVT may cause palpitations and lightheadedness, anginal chest pain and dyspnea (in CAD) and heart failure and pulmonary edema (in those with left ventricular dysfunction).

Front 64

Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Treatment maneuvers

Back 64

1) maneuvers that increase vagal tone (carotid sinus massage, facial immersion in cold water, valsalva maneuver)

Front 65

Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Pharmacologic treatment

Back 65

1) adenosine—6 mg rapid IV push followed by rapid saline flush in lg vein. 2nd dose 12 mg after 2 min if not effective; no proven benefit to doses of >20 mg; 2) verapamil 0.075-0.15 mg/kg (3-10 mg) IV over 15-60 sec, may repeat in 30 min; 3) diltiazem 20 mg IV over 2 min; 4) increase vagal tone by increasing BP with meds & carotid sinus massage 5) esmolol, propranolol or digoxin, external pacing are other alternatives

Front 66

Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Non-pharmacologic treatment:

Back 66

Syncronized cardioversion for unstable patient with hypotension, pulmonary edema or severe chest pain. Usually < 50J.

Front 67

Understand Sick Sinus Syndrome (Tachycardia-Bradycardia Syndrome) in regards to: clinical significance
a. Clinical significance:

Back 67

symptoms are due to effects of fast or slow heart rate. Symptoms include syncope or near syncope, palpitations, dyspnea, chest pain and CVA. Dysrhythmia produced by wide variety of cardiac disease; ischemic and rheumatic disease, myocarditis, pericarditis, rheumatologic disease, metastatic tumors, surgical damage or cardiomyopathies.

Front 68

Understand Sick Sinus Syndrome (Tachycardia-Bradycardia Syndrome) in regards to: How it is diagnosed

Back 68

routing EKG will not normally demonstrate the intermittent dysrhythmia—requires ambulatory EKG monitoring or EP studies.

Front 69

Understand Sick Sinus Syndrome (Tachycardia-Bradycardia Syndrome) in regards to: Treatment

Back 69

Permanent pacemaker

Front 70

Have an understanding of Wolff-Parkinson-White in terms of: Appearance on EKG

Back 70

Shortened PR interval with initial distortion of ventricular activation (delta wave). Sometimes QRS is normal. 3 types: A: + initial deflection with dominant R wave seen in V1, Q waves in leads II, III & AVF. B: neg initial deflection & RS or QS pattern in lead V1. C: + delta wave in lead V1 with negative or esoelectric delta wave in leads V5 & V6. Repolarization often abn with change in ST segments & T waves. EKG changes of WPW mimic changes with MI or ventricular hypertrophy

Front 71

Have an understanding of Wolff-Parkinson-White in terms of: Mechanism

Back 71

Anatomic basis is that Kent bundles are composed of myogenic tissue and directly link the atria to the ventricles, completely bypassing the AV node and infranodal system (pre-excitation syndrome)

Front 72

Have an understanding of Wolff-Parkinson-White in terms of: Potential complications:

Back 72

high incidence of tachyarrhythmia – A flutter in 5 percent, A-fib in 10-20 percent, SVT in 40-80 percent. May precipitate V-fib.

Front 73

Have an understanding of Wolff-Parkinson-White in terms of: Treatment

Back 73

1) Reentrant SVT in WPW can be treated like other cases of reentrant SVT (verapamil or adenosine). 2) antidromic tachycardia

Front 74

Have an understanding of Wolff-Parkinson-White in terms of: Treatment

Back 74

1) Reentrant SVT in WPW can be treated like other cases of reentrant SVT (verapamil or adenosine) 2) antidromic tachycardia presents risk for degeneration into V-fib—stable patients tx with IV procainamide, unstable should be cardioverted 3) a-flutter or fib with rapid ventricular response should be cardioverted

Front 75

Define Malignant hypertension

Back 75

essential hypertension characterized by acute onset, severe symptoms, rapidly progressive course, and poor prognosis

Front 76

Define Hypertensive encephalopathy

Back 76

when elevated blood pressure exceeds the limits of cerebral autoregulation of the low-resistance arteries, resulting in cerebral hyperperfusion with loss of integrity of the blood-brain barrier—usually associated with MAP of 150-160 or greater—usually acute and reversible, with severe H/A and N/V.

Front 77

Define Pheochromocytoma

Back 77

a tumor that is derived from chromaffin cells and is usually associated with paroxysmal or sustained hypertension

Front 78

Define Hypertensive retinopathy

Back 78

directly observable example of the vascular changes due to hypertension. Grades I – IV, from focal narrowing of arterioles to cotton-wool spots and disc edema.

Front 79

Define Transient hypertension

Back 79

occurs in association with other conditions such as anxiety, alcohol-withdrawal syndromes, sudden cessation of medications and some toxic substances (e.g. “white-coat hypertension”

Front 80

Define Hypertensive emergency (malignant hypertension)

Back 80

not defined by absolute blood pressure values, but contingent on presence of relative blood pressure increases combined with evidence of injury to any of the target organs.

Front 81

Define Hypertensive urgency

Back 81

Relative increase in blood pressure values which represents a risk for imminent target-organ damage (but in which the damage has not yet occurred); influenced by presence of risk factors (renal insuff, CHF, CAD, CNS disorders)

Front 82

Define Acute Hypertensive Episode

Back 82

When a patient is found to have stage 3 HTN (>180/>110) with no signs or symptoms of evolving or impending target-organ damage.

Front 83

Understand the pathophysiology of HTN in terms of How hypertension develops

Back 83

1) result of alterations in contractile properties of smooth muscle in arterial walls 2) failure of normal autoregulatory mechanisms. Most have elevated peripheral vascular resistance with normal cardiac output (some have elevated CO as result of increased alpha- and beta-adrenergic tone

Front 84

Understand the pathophysiology of HTN in terms of Target-organ damage

Back 84

when poorly controlled blood pressure is allowed to persist over time, it can cause damage to specific organs and vascular beds – involves fibrinoid necrosis of small arterioles

Front 85

Understand the pathophysiology of HTN in terms of Vascular changes

Back 85

vessels in capillary beds dilate in response to elevated blood pressure that overwhelms autoregulatory mechanism – causes injury to endothelium, increased vascular permeablility & vascular wall injury—leads to deposition of fibrin within vessel walls & causes activation of mediators of coagulation, etc

Front 86

Understand the pathophysiology of HTN in terms of Decreased renal perfusion

Back 86

Impaired autoregulation due to elevated blood pressure results in decreased renal perfusion which stimulates the renin-angiotensin I and II cascade, leading to increased vasoconstriction

Front 87

Understand the pathophysiology of HTN in terms of Pheochromocytomas

Back 87

tumors arising from the cells of the sympathetic nervous system which produce catecholamines—cause paroxysms of HTN with palpitations, tachycardia, malaise, apprehension and sweating

Front 88

Describe how hypertensive encephalopathy presents

Back 88

acute and reversible. severe HA, NV, Confusion, drowsiness, seizures, decreased visual acuity, focal deficits, coma. Can progress over hours and lead to coma and death.

Front 89

Describe how hypertensive encephalopathy is treated

Back 89

Close cardiac monitoring, supplemental oxygen, IV access, arterial monitoring. Immediate reduction of BP by 20-25%--with sodium nitroprusside at initial dose of 0.3 micrograms/kg per min and titrated up to max of 10 micrograms per kg/min. IV nitroglycerin and labetolol can also be effective but nitroprusside is first-line tx

Front 90

Discuss the indications for Nitroprusside in the treatment of hypertension

Back 90

excellent agent for all hypertensive emergencies except eclampsia prior to delivery (crosses placenta) Only used for postpartum eclampsia or eclampsia resistant to other interventions

Front 91

Discuss the adverse effects for Nitroprusside in the treatment of hypertension

Back 91

hypotension. Rare cyanide toxicity in hepatic dysfunction and thiocyanate toxicity with renal failure. May worsen myocardial ischemia and may cause increased ICP

Front 92

Discuss the contraindications for Nitroprusside in the treatment of hypertension

Back 92

pregnancy, hepatic and renal dysfunction, elevated ICP, myocardial ischemia

Front 93

Discuss the indications for Labetalol in the treatment of hypertension

Back 93

May be used IV for hypertensive emergencies and is easily converted to oral dose for hypertensive urgencies. Safe in cerebral vascular disease and CAD. Class C for use in pregnancy induced HTN

Front 94

Discuss the Adverse effects for Labetalol in the treatment of hypertension

Back 94

orthostatic hypotension; long half-life. May exacerbate heart failure and induce bronchospasm. Paradoxical hypertensive effect in certain cases. Exacerbation of angina; MI after abrupt d/c.

Front 95

Discuss the Contraindications for Labetalol in the treatment of hypertension

Back 95

heart failure, ischemic heart disease

Front 96

Define Aneurysm

Back 96

an abnormal blood-filled dilatation of a blood vessel and especially an artery resulting from disease of the vessel wall

Front 97

Define Pseudoaneurysm

Back 97

a vascular abnormality (as an elongation or buckling of the aorta) that resembles an aneurysm in radiography

Front 98

Define Dissection

Back 98

a pathological splitting or separation of tissue

Front 99

Compare and contrast risk factors common to all aortic dissection and aneurysms

Back 99

AAA has clear familial trend. Marfan syndrome, Increasing age, male, hx of other aneurysms & peripheral arterial disease, connective tissue disorders, atherosclerotic risk factors (age, smoking, HTN, hyperlipidemia, DM)

Front 100

Compare and contrast presenting s/sx for abdominal aortic aneurysms

Back 100

syncope, back or abdominal pain, shock, sudden death. Pain is severe and abrupt, ripping or tearing. May present in flank, groin, hip, etc. may have tenesmus, NV

Front 101

Compare and contrast findings on PE for abdominal aortic aneurysms

Back 101

tenderness to palpation, evidence of retroperitoneal hematoma (periumbilical ecchymosis or flank ecchymosis, scrotal hematoma or inguinal mass, iliopsoas sign, femoral neuropathy

Front 102

Compare and contrast diagnostic imaging for abdominal aortic aneurysms

Back 102

plain radiography (may show calcified and bulging aortic contour; ultrasound (ideal for unstable patients who cannot undergo CT scanning); CT scan (with IV contrast to show detail and any retroperitoneal hemorrhage); or MRI

Front 103

Compare and contrast treatment for abdominal aortic aneurysms

Back 103

all symptomatic aneurysms require urgent surgical consultation. Ruptured should have immediate surgery or pine box...

Front 104

Compare and contrast presenting s/sx for thoracic aortic aneurysms

Back 104

become symptomatic by compressing or eroding into adjacent structures. esophageal, tracheal, bronchial or even neuro disorders. Generally immediately fatal, rare patients survive with assistance of hemodynamic resuscitation

Front 105

Compare and contrast findings for thoracic aortic aneurysms

Back 105

mostly deadness

Front 106

Compare and contrast diagnostic imaging for thoracic aortic aneurysms

Back 106

usually not necessary due to deadness of patient but would otherwise be the same as for AAA

Front 107

Compare and contrast diagnostic treatment for thoracic aortic aneurysms

Back 107

usually not necessary given the fact that the patient has already cashed in the chips, but if not then hemodynamic resuscitation and/or surgery may be in order

Front 108

Compare and contrast presenting s/sx of dissecting aortic aneurysms

Back 108

abrupt, chest px or between scapulae, described as ripping or tearing. Px in anterior chest may involve ascending aorta; back pain may involve descending aorta. Other sxs depend on anatomic course of lesion: carotid – CVA presentation

Front 109

Compare and contrast PE findings for dissecting aortic aneurysms

Back 109

normal heart & lung exam. Decreased pulses in radial, femoral carotid arteries. HTN or hypotension; tachycardia; muffled heart tones; elevated jugular venous pressure, pulsus paradoxus; compression of laryngeal nerve or cervical sympathetic ganglion may cause hoarseness or Horner’s syndrome

Front 110

Compare and contrast diagnostic imaging for dissecting aortic aneurysms

Back 110

plain films (widened mediastinum, abnormal aortic contour, pleural effusion, deviation of trachea, mainstem bronchi or esophagus); CT scanning, angiography (gold standard)

Front 111

Compare and contrast treatment for dissecting aortic aneurysms

Back 111

antihypertensive treatment (meds with negative inotropic effects—beta blockers) plus vasodilators e.g. nitroprusside. Rapid referral to surgeon—if involves ascending aorta, will require prompt surgical repair

Front 112

Define LMWH

Back 112

low molecular weight heparin—dosage is weight adjusted—provides more predictable anticoagulant effect, ease of administration, longer half-life, no need to monitor anticoagulant effect, lower incidence of major bleeding (e.g. Lovenox)

Front 113

Define DVT (deep vein thrombosis)

Back 113

formation of thrombus in a deep vein (as of the leg or pelvis) that may be asymptomatic or be accompanied by sxs and potentially life threatening if dislodgment of thrombus results in PE

Front 114

Define Doppler ultrasound

Back 114

non-invasive, accurately evaluates proximal DVT; however is technician-dependent and has poor sensitivity for distal DVT

Front 115

Define Thrombophlebitis

Back 115

inflammation of a vein with formation of a thrombus

Front 116

Define Virchow’s triad

Back 116

venous stasis, endothelial damage, and a hypercoagulable state (emedicine.com)

Front 117

Define D-dimer

Back 117

fibrin degradation products measured when evaluating patients for DVT or PE (elevated in any condition where clots form)

Front 118

Define Impedance plethysmography

Back 118

recording changes in blood volume of an extremity, directly related to venous outflow. different techniques can be used to measure changes, including electrical impedance. In proximal vein thrombosis, venous outflow from lower extremity is slowed and blood volume or venous capacitance is increased.

Front 119

Define Inferior vena cava filter

Back 119

used to prevent PE when oral anticoagulation is contraindicated.

Front 120

Define Thrombectomy:

Back 120

surgical excision of a thrombus

Front 121

Define Warfarin (brand name Coumadin)

Back 121

anticoagulant or ibuprofen in war or the name of some star treck character

Front 122

Be familiar with signs and symptoms, site of most common occurrence of thrombophlebitis

Back 122

Pain, redness, swelling, warmth, tenderness present in less than ½. Homan’s sign not reliable. Physical findings depend on location and degree of venous obstruction, inflammation and collateral blood flow.

Front 123

Be familiar with risk factors of thrombophlebitis

Back 123

“THROMBOSIS” T: trauma, travel H: hypercoagulable, hormone replacement R: recreational drugs (IV) O: old >60 M: malignancy; B: birth control pill, blood group A O: obesity, obstetrics S: surgery, smoking I: immobilization; S: sickness

Front 124

How are DVT's diagnosed

Back 124

duplex ultrasonography. Also helpful to differentiate venous thrombosis from hematoma, Kaker cyst, abscess and other causes of leg px and edema

Front 125

Discuss usefulness of D-dimer in the evaluation and management of a patient with DVT

Back 125

D-dimer fibrin fragments present in fresh fibrin clot & degradation. low specificity for DVT and should only be used to rule out not confirm dx, remains elevated in DVT for 7 days.

Front 126

Discuss the primary objective in treating DVT's

Back 126

To prevent PE

Front 127

Discuss how a proven proximal DVT is treated

Back 127

aggressive anticoagulation prevents extension of the clot and allows for its lysis by the intrinsic fibrinolytic pathways. Treat post-phlebitic syndrome with leg elevation, compression stockings and pain meds prn

Front 128

Discuss criteria for hospital admission and treatment for DVT

Back 128

instability to ambulate, poor social support, unreliable follow-up, difficulty with education for drug administration, need for lytic or invasive therapy, and other serious diagnosis requiring treatment

Front 129

Discuss outpatient management and the use of low molecular weight heparin and warfarin for DVT

Back 129

LMWH daily or bid (adjusted for weight), discharge home from ED with next-day follow-up, institute warfarin at the same time as LMWH. Heparin is used if LMWH is not available or is contraindicated

Front 130

Discuss the indications for inferior vena cava filter placement for DVT

Back 130

when oral anticoagulation is contraindicated a major complication of anticoagulation occurs (e.g. bleeding, HIT) a DVT persists or propagates despite adequate medical treatment, or embolization occurs after 1-2 weeks of therapeutic anticoagulation

Front 131

Know common signs and symptoms for superficial thrombophlebitis

Back 131

local pain, redness, and tenderness of a cord along the course of the involved vein; bruising or bleeding also

Front 132

Know how to diagnose superficial thrombophlebitis

Back 132

Doppler ultrasound may be used to confirm the diagnosis if there is any ambiguity or if an alternative dx such as DVT, cellulitis or lymphangitis is possible

Front 133

Know treatment options for mild, sever and refractory cases for thrombophlebitis

Back 133

Mild: warm compresses, analgesia and elastic supports for involved extremities, ADL’s as tolerated. Severe: bed rest, elevation of extremity, support stockings, analgesia. Anti-inflammatory meds

Front 134

Define Limb ischemia

Back 134

true emergency requiring immediate therapy to salvage the limb. Mortality >25%; amputation ~ 20%

Front 135

Define thrombosis

Back 135

the formation or presence of a blood clot within a blood vessel

Front 136

Define Embolism

Back 136

the sudden obstruction of a blood vessel by an embolus

Front 137

Define Claudication

Back 137

cramping pain and weakness in the legs and especially the calves on walking that disappears after rest and is usually associated with inadequate blood supply to the muscles

Front 138

Define Raynaud’s disease

Back 138

vascular disorder marked by recurrent spasm of capillaries and especially those of the fingers and toes upon exposure to cold, characterized by pallor, cyanosis, and redness in succession usually accompanied by pain, and that in severe cases progresses to local gangrene

Front 139

Define Limb salvage

Back 139

preserving/reperfusing circulation to the limb via use of thrombolytics, anticoagulants, sometimes surgery

Front 140

Define Chronic peripheral arterial insufficiency

Back 140

chronic insufficiency of blood supply to peripheral arteries. Characterized by intermittent claudication which may progress to ischemic pain at rest

Front 141

Define Doppler flow

Back 141

a hand-held Doppler can document amplitude of flow or absence when held over dorsalis pedis, posterior tibial, popliteal or femoral arteries in lower limbs and over the radial, ulnar, brachial or axillary arteries in arm

Front 142

Define ABI: (ankle-brachial index)

Back 142

ratio of the systolic blood pressure with cuff just above the malleoli (with Doppler probe over posterior tibial or dorsalis pedis artery) to brachial pressure in arm. difference of 30 mm Hg or more between any adjacent levels accurately localizes the site of obstruction.

Front 143

Define Thrombolytics

Back 143

use of thrombolytics as the sole or part of combination therapy for acute limb ischemia is controversial—catheter-directed, intraarterial thrombolysis has better reperfusion rates than systemic thrombolysis for arterial clots. Not standard for routine use but attractive for selected pts(e.g. poor surgical risks)

Front 144

In regards to oclusive arterial disease, have an understanding of the epidemiology: age, gender, medical hx, frequently diseased arteries:

Back 144

peripheral arterial disease in 11-27% elderly men & women equally, though sxs more in men; hx of smoking, DM, hyperlipidemia, HTN are risk factors. Coronary or cerebrovascular disease present in ½. Severity linked to MI, stroke. Affects femoropopliteal, tibial, aortoiliac, brachiocephalic vessels

Front 145

In regards to oclusive arterial disease, have an understanding of the pathophysiology of limb ischemia

Back 145

results from blood supply inadequate to meet tissue oxygen and nutrient requirements, leading to cell death and irreversible tissue damage

Front 146

In regards to oclusive arterial disease, have an understanding of the pathophysiology of reperfusion

Back 146

may not be fully attainable with prolonged arterial obstruction due to distal edema and thrombi forming in the microcirculation; reperfusion injury can occur as oxygen radicals form and cause further cell injury

Front 147

In regards to oclusive arterial disease, have an understanding of the pathophysiology of atherosclerosis

Back 147

is the cause of nonembolic limb ischemia in vast majority of patients

Front 148

In regards to oclusive arterial disease, have an understanding of the etiology and the most common cause

Back 148

thrombotic occlusion

Front 149

In regards to oclusive arterial disease, have an understanding of the etiology thrombotic vs. embolic

Back 149

thrombotic occlusion more common cause of acute limb ischemia than is embolism

Front 150

In regards to oclusive arterial disease, have an understanding of the etiology and vasospastic / inflammatory

Back 150

peripheral arterial supply also can be obstructed by vasospastic or inflammatory conditions, e.g. Reynaud’s involves vasospasm, and inflammatory conditions such as RA and lupus can impede arterial supply also.

Front 151

In regards to occlusive arterial disease, have an understanding of the signs and symptoms: 6 "P's"

Back 151

Pain, pallor, polar (cold), pulselessness, paresthesias, and paralysis

Front 152

In regards to occlusive arterial disease, have an understanding of the diagnosis: bedside exams:

Back 152

visible skin changes, with initial pallor that may be followed by blotchy, mottled areas of cyanosis and associated petechiae and blisters. Hypoesthesia or hyperesthesia due to ischemic neuropathy, muscle weakness. Anesthesia and paralysis foreshadow impending gangrene

Front 153

In regards to occlusive arterial disease, have an understanding of treatment options

Back 153

goals are restoration of blood flow, preservation of limb and life, & prevention of recurrent throbosis or embolism. Tx is immediate administration of IV UFH (heparin) Fluid resuscitation & tx of heart failure & dysrhythmias sometimes needed to improve perfusion. Tx obstructive clot (e.g. surgery) Thrombolysis controversial

Front 154

Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of commonality

Back 154

less common in upper extremities

Front 155

Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of ischemic rest pain

Back 155

rare in upper limb in the absence of distal embolization

Front 156

Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of etiology

Back 156

vasospasm, arteritis, trauma, atherosclerotic plaque rupture, embolism, iatrogenic injury, thoracic outlet syndromes, aneurysms and hypercoagulable states

Front 157

Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of diagnostic evaluation

Back 157

segmental blood pressure measurements above and below the elbow, Doppler evaluation, duplex ultrasonography and arteriography

Front 158

Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of treatment

Back 158

Heparinization and emergent surgical thromboembolectomy