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CARDIOVASCULAR EMERGENCIES: DYSRHYTHMIAS, HTN, AORTIC, VENOUS, ISCHEMIC
CARDIOVASCULAR EMERGENCIES: DYSRHYTHMIAS, HTN, AORTIC, VENOUS, ISCHEMIC
Define Dysrhythmia:
an abnormal rhythm; especially a disordered rhythm exhibited in a record of electrical activity of the brain or heart
Define Ectopic focus:
originating in area of heart other than the sinoatrial node <ectopic beats> also initiating ectopic heartbeats <an ectopic pacemaker>
Define Reentry:
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
Define Cardiac pacing:
the act or process of regulating or changing the timing or intensity of cardiac contractions (as by an artificial pacemaker)
Define Tachycardia:
relatively rapid heart action whether physiological (as after exercise) or pathological
Define Sinus nodal activity:
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
Define Atrioventricular block: (heart block):
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
Define Bradycardia:
relatively slow heart action whether physiological or pathological
Define Arrhythmia:
irregularity or loss of rhythm (of heart)
Define Cardiac arrhythmia :
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.
Define Reperfusion arrhythmia:
arrhythmia that occurs as the infracted heart is re-supplied with blood following angioplasty or thrombolysis
Define Sinus arrhythmia:
cardiac irregularity marked by variation in the interval between sinus beats and evident on EKG as alternately long and short intervals between P waves.
Compare and contrast the mechanisms and treatment for tachydysrhythmias
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.
Compare and contrast the mechanisms and treatment for bradydysrhythmias
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
Discuss the clinical significance for the following: Sinus Bradycardia
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
Define Sinus Bradycardia
when the sinus node rate falls below 60 – characterized by normal P wave and PR interval, 1:1 AV conduction; atrial rate < 60.
Discuss the most common treatments for the following: Sinus Bradycardia
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
Define Sinus tachycardia
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
Discuss the clinical significance for the following: Sinus tachycardia
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
Discuss the most common treatments for the following: Sinus tachycardia
treatment of underlying condition. With acute MI, may decrease HR with beta-adrenergic antagonists
Define premature atrial contractions: PAC
premature cardiac beat arising from an ectopic atrial focus - just like it sounds!
Discuss the clinical significance for the following: premature atrial contractions
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
Discuss the most common treatments for the following: premature atrial contractions
discontinue precipitating drugs or toxins, treat underlying disorders
Define Atrial flutter
rapid regular atrial contractions occurring usually at rates 250-350 min. and often producing saw-tooth waves in ECG leads II, III & aVF
Discuss the clinical significance for the following: Atrial flutter
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
Discuss the most common treatments for the following: Atrial flutter
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
Define Atrial fibrillation
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
Discuss the clinical significance for the following: Atrial fibrillation
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.
Discuss the most common treatments for the following: Atrial fibrilliation with rapid ventricular response and acute hemodynamic deterioration
synchronized cardioversion If not successful then procainamide IV and continue with cardioversion
Discuss the most common treatments for the following: Stable Atrial fibrilliation
diltiazem, verapamil, beta-adrenergic blockers, digoxin for pt with ventricular failure. After ventricular rate control: chemical conversion with procainamide, quinidine or verapamil, ibutilide, amiodarone.
Define Supraventricular tachycardia
a regular, rapid rhythm arising from reentry or ectopic pacemaker in areas above bifurcation of bundle of His.
Discuss the clinical significance for the following: Supraventricular tachycardia
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
Discuss the most common treatments for the following: Supraventricular tachycardia
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
Discus Junctional premature contractions
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
Discuss treatment for junctional premature contractions
Tx: tx underlying disorder. If frequent or symptomatic may use antiarrhythmics
Discuss Junctional rhythms
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.
Discuss treatment for Junctional rhythms
Tx: Do not require treatment if isolated, infrequent beats. If sustained, tx underlying cause.
Discuss PVC's
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
Discuss treatment for PVC's
Tx: IV lidocaine, procainamide
Discuss ventricular tachycardia
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.
Discuss treatment for ventricular tachycardia
Unstable or cardiac arrest—with synchronized cardioversion. Symptomatic v-tack with pulse—synchronized cardioversion. Pulseless v-tach—unsynchronized Stable: IV antiarrhythmics, amiodarone, procainamide
Discuss ventricular fibrillation
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
Discuss treatment for ventricular fibrillation
Immediate electrical defibrillation. Initiate CPR and administer other IV drugs according to current ACLS guidelines
Define 1st degree AV block
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
Discuss 2nd degree AV block: Mobitz I - Wenckebach
progressive prolongation of AV conduction & PR interval til artrial impulse completely blocked. Associated: acute inferior MI, digoxin toxicity, myocarditis, post cardiac surgery.
Discuss treatment for 2nd degree AV block: Mobitz I - Wenckebach
no tx necessary unless slow ventricular rate produces signs of hypoperfusion.
Discuss 3rd degree AV block
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
Discuss treatment for 3rd degree AV block
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
Discuss PEA: pulseless electrical activity
Presence o electrical complexeswithout accompanying mechanical contraction of hear. Cardiac arrest due to metabolic abn of myocardium.
Discuss treatment for PEA
continue CPR and alpha adrenergic drugs. May be associated with severe hypovolemia, cardiac tamponade, tension pneumo, massive PE, ruptured ventricular wall
Discuss Agonal rhythm
occurance of very broad and irregular ventricular complexes at slow rate usually without associated ventricular contractions
Discuss Cardiac Asystole
complete absence of cardiac electrical activity. Tx is to stimulate electrical activity and mechanical contractions with CPR and alpha-adrenergics.
Know predisposing factors for atrial fibrillation
increased atrial size, mass, vagal tone, varying refractory periods, rheumatic heart disease, HTN, ischemic heart disease, thyrotixicosis
Disuss relationship of atrial fibrillation to heart failure
L. ventricular failure, L. atrial contraction contributes significantly to cardiac output; loss of effective atrial contraction as in A-fib may produce heart failure
Know predisposing factors for emboli in pts with A-fib
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
Discuss treatment of A-fib in the unstable patient
synchronized cardioversion, if not successful, procainamide IV and continue with cardioversion
Discuss treatment of A-fib in unstable pts
diltiazem, verapamil, IV beta-adrenergic blockers, IV digoxin
Discuss the causes and treatment of Ventricular Tachycardia in regard to: unstable patients
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.
Discuss the causes and treatment of Ventricular Tachycardia in regard to: stable patients
IV antiarrhythmics 1) lidocaine followed by infusion 2)amiodarone 3) procainamide
Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Where the rhythm arises from
arises from reentry or an ectopic pacemaker in areas above the bifurcation of the bundle of His.
Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: What it is associated with
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.
Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Associated signs and symptoms
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).
Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Treatment maneuvers
1) maneuvers that increase vagal tone (carotid sinus massage, facial immersion in cold water, valsalva maneuver)
Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Pharmacologic treatment
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
Be familiar with Paroxysmal Supraventricular Tachycardia in regards to: Non-pharmacologic treatment:
Syncronized cardioversion for unstable patient with hypotension, pulmonary edema or severe chest pain. Usually < 50J.
Understand Sick Sinus Syndrome (Tachycardia-Bradycardia Syndrome) in regards to: clinical significance
a. Clinical significance:
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.
Understand Sick Sinus Syndrome (Tachycardia-Bradycardia Syndrome) in regards to: How it is diagnosed
routing EKG will not normally demonstrate the intermittent dysrhythmia—requires ambulatory EKG monitoring or EP studies.
Understand Sick Sinus Syndrome (Tachycardia-Bradycardia Syndrome) in regards to: Treatment
Permanent pacemaker
Have an understanding of Wolff-Parkinson-White in terms of: Appearance on EKG
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
Have an understanding of Wolff-Parkinson-White in terms of: Mechanism
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)
Have an understanding of Wolff-Parkinson-White in terms of: Potential complications:
high incidence of tachyarrhythmia – A flutter in 5 percent, A-fib in 10-20 percent, SVT in 40-80 percent. May precipitate V-fib.
Have an understanding of Wolff-Parkinson-White in terms of: Treatment
1) Reentrant SVT in WPW can be treated like other cases of reentrant SVT (verapamil or adenosine). 2) antidromic tachycardia
Have an understanding of Wolff-Parkinson-White in terms of: Treatment
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
Define Malignant hypertension
essential hypertension characterized by acute onset, severe symptoms, rapidly progressive course, and poor prognosis
Define Hypertensive encephalopathy
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.
Define Pheochromocytoma
a tumor that is derived from chromaffin cells and is usually associated with paroxysmal or sustained hypertension
Define Hypertensive retinopathy
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.
Define Transient hypertension
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”
Define Hypertensive emergency (malignant hypertension)
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.
Define Hypertensive urgency
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)
Define Acute Hypertensive Episode
When a patient is found to have stage 3 HTN (>180/>110) with no signs or symptoms of evolving or impending target-organ damage.
Understand the pathophysiology of HTN in terms of How hypertension develops
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
Understand the pathophysiology of HTN in terms of Target-organ damage
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
Understand the pathophysiology of HTN in terms of Vascular changes
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
Understand the pathophysiology of HTN in terms of Decreased renal perfusion
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
Understand the pathophysiology of HTN in terms of Pheochromocytomas
tumors arising from the cells of the sympathetic nervous system which produce catecholamines—cause paroxysms of HTN with palpitations, tachycardia, malaise, apprehension and sweating
Describe how hypertensive encephalopathy presents
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.
Describe how hypertensive encephalopathy is treated
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
Discuss the indications for Nitroprusside in the treatment of hypertension
excellent agent for all hypertensive emergencies except eclampsia prior to delivery (crosses placenta) Only used for postpartum eclampsia or eclampsia resistant to other interventions
Discuss the adverse effects for Nitroprusside in the treatment of hypertension
hypotension. Rare cyanide toxicity in hepatic dysfunction and thiocyanate toxicity with renal failure. May worsen myocardial ischemia and may cause increased ICP
Discuss the contraindications for Nitroprusside in the treatment of hypertension
pregnancy, hepatic and renal dysfunction, elevated ICP, myocardial ischemia
Discuss the indications for Labetalol in the treatment of hypertension
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
Discuss the Adverse effects for Labetalol in the treatment of hypertension
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.
Discuss the Contraindications for Labetalol in the treatment of hypertension
heart failure, ischemic heart disease
Define Aneurysm
an abnormal blood-filled dilatation of a blood vessel and especially an artery resulting from disease of the vessel wall
Define Pseudoaneurysm
a vascular abnormality (as an elongation or buckling of the aorta) that resembles an aneurysm in radiography
Define Dissection
a pathological splitting or separation of tissue
Compare and contrast risk factors common to all aortic dissection and aneurysms
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)
Compare and contrast presenting s/sx for abdominal aortic aneurysms
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
Compare and contrast findings on PE for abdominal aortic aneurysms
tenderness to palpation, evidence of retroperitoneal hematoma (periumbilical ecchymosis or flank ecchymosis, scrotal hematoma or inguinal mass, iliopsoas sign, femoral neuropathy
Compare and contrast diagnostic imaging for abdominal aortic aneurysms
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
Compare and contrast treatment for abdominal aortic aneurysms
all symptomatic aneurysms require urgent surgical consultation. Ruptured should have immediate surgery or pine box...
Compare and contrast presenting s/sx for thoracic aortic aneurysms
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
Compare and contrast findings for thoracic aortic aneurysms
mostly deadness
Compare and contrast diagnostic imaging for thoracic aortic aneurysms
usually not necessary due to deadness of patient but would otherwise be the same as for AAA
Compare and contrast diagnostic treatment for thoracic aortic aneurysms
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
Compare and contrast presenting s/sx of dissecting aortic aneurysms
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
Compare and contrast PE findings for dissecting aortic aneurysms
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
Compare and contrast diagnostic imaging for dissecting aortic aneurysms
plain films (widened mediastinum, abnormal aortic contour, pleural effusion, deviation of trachea, mainstem bronchi or esophagus); CT scanning, angiography (gold standard)
Compare and contrast treatment for dissecting aortic aneurysms
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
Define LMWH
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)
Define DVT (deep vein thrombosis)
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
Define Doppler ultrasound
non-invasive, accurately evaluates proximal DVT; however is technician-dependent and has poor sensitivity for distal DVT
Define Thrombophlebitis
inflammation of a vein with formation of a thrombus
Define Virchow’s triad
venous stasis, endothelial damage, and a hypercoagulable state (emedicine.com)
Define D-dimer
fibrin degradation products measured when evaluating patients for DVT or PE (elevated in any condition where clots form)
Define Impedance plethysmography
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.
Define Inferior vena cava filter
used to prevent PE when oral anticoagulation is contraindicated.
Define Thrombectomy:
surgical excision of a thrombus
Define Warfarin (brand name Coumadin)
anticoagulant or ibuprofen in war or the name of some star treck character
Be familiar with signs and symptoms, site of most common occurrence of thrombophlebitis
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.
Be familiar with risk factors of thrombophlebitis
“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
How are DVT's diagnosed
duplex ultrasonography. Also helpful to differentiate venous thrombosis from hematoma, Kaker cyst, abscess and other causes of leg px and edema
Discuss usefulness of D-dimer in the evaluation and management of a patient with DVT
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.
Discuss the primary objective in treating DVT's
To prevent PE
Discuss how a proven proximal DVT is treated
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
Discuss criteria for hospital admission and treatment for DVT
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
Discuss outpatient management and the use of low molecular weight heparin and warfarin for DVT
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
Discuss the indications for inferior vena cava filter placement for DVT
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
Know common signs and symptoms for superficial thrombophlebitis
local pain, redness, and tenderness of a cord along the course of the involved vein; bruising or bleeding also
Know how to diagnose superficial thrombophlebitis
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
Know treatment options for mild, sever and refractory cases for thrombophlebitis
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
Define Limb ischemia
true emergency requiring immediate therapy to salvage the limb. Mortality >25%; amputation ~ 20%
Define thrombosis
the formation or presence of a blood clot within a blood vessel
Define Embolism
the sudden obstruction of a blood vessel by an embolus
Define Claudication
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
Define Raynaud’s disease
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
Define Limb salvage
preserving/reperfusing circulation to the limb via use of thrombolytics, anticoagulants, sometimes surgery
Define Chronic peripheral arterial insufficiency
chronic insufficiency of blood supply to peripheral arteries. Characterized by intermittent claudication which may progress to ischemic pain at rest
Define Doppler flow
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
Define ABI: (ankle-brachial index)
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.
Define Thrombolytics
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)
In regards to oclusive arterial disease, have an understanding of the epidemiology: age, gender, medical hx, frequently diseased arteries:
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
In regards to oclusive arterial disease, have an understanding of the pathophysiology of limb ischemia
results from blood supply inadequate to meet tissue oxygen and nutrient requirements, leading to cell death and irreversible tissue damage
In regards to oclusive arterial disease, have an understanding of the pathophysiology of reperfusion
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
In regards to oclusive arterial disease, have an understanding of the pathophysiology of atherosclerosis
is the cause of nonembolic limb ischemia in vast majority of patients
In regards to oclusive arterial disease, have an understanding of the etiology and the most common cause
thrombotic occlusion
In regards to oclusive arterial disease, have an understanding of the etiology thrombotic vs. embolic
thrombotic occlusion more common cause of acute limb ischemia than is embolism
In regards to oclusive arterial disease, have an understanding of the etiology and vasospastic / inflammatory
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.
In regards to occlusive arterial disease, have an understanding of the signs and symptoms: 6 "P's"
Pain, pallor, polar (cold), pulselessness, paresthesias, and paralysis
In regards to occlusive arterial disease, have an understanding of the diagnosis: bedside exams:
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
In regards to occlusive arterial disease, have an understanding of treatment options
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
Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of commonality
less common in upper extremities
Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of ischemic rest pain
rare in upper limb in the absence of distal embolization
Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of etiology
vasospasm, arteritis, trauma, atherosclerotic plaque rupture, embolism, iatrogenic injury, thoracic outlet syndromes, aneurysms and hypercoagulable states
Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of diagnostic evaluation
segmental blood pressure measurements above and below the elbow, Doppler evaluation, duplex ultrasonography and arteriography
Compare and contrast acute acute arterial occlusion in the upper extremities with the lower extremities in terms of treatment
Heparinization and emergent surgical thromboembolectomy