cardiovascular emergencies – part ii. uncommon but lethal! tear in the intimal layer of the aorta...

Cardiovascular Emergencies –

Part II

Uncommon but lethal!Tear in the intimal

layer of the aorta that results in a false lumen that is usually anterograde in nature.

Usual locations:Usual locations:ascending aorta superior to aortic valveascending aorta superior to aortic valvedescending aorta at the ligamentum arteriosmdescending aorta at the ligamentum arteriosm

Most common in men between the ages of 60 & 70

Factors:hypertensionhereditary defects of

connective tissue (Marfan’s)

pregnancyblunt traumaiatrogenic factors (intra-

arterial catheterization)

SUBJECTIVE DATAHistoryPain – sudden, sharp, tearing, excruciating,

medications may not relieve, substernal (ascending), back/flank (descending)

SyncopeAltered LOCParaplegia

OBJECTIVE DATAPhysical Exam - variable BPs on right vs left - decreased peripheral pulses/

peripheral cyanosis - murmur - pallor, oliguria, altered LOC, - BP: hyper with distal dissection,

hypo with proximal - extreme pain

OBJECTIVE DATADiagnostics - CBC (Hct tends to fall, WBC 12,000-20,000) T&C,BUN/Creatinine - EKG:

Normal in 1/3, LV hypertrophy if hx of HTN, signs of MI if proximal dissection

-

CXR: -widened aortic silhouette -widened mediastinum, -left-sided pleural effusion

Diagnostics cont. - CT Scan

INTERVENTIONS ABC Pain relief Large bore IVs

– minimum of two sites Monitoring Medications:

1) to lower arterial BP: nitroprusside, labetalol

Medications cont: 2) To decrease contraction force: beta blockers preferred, may give

calcium channel blockers if beta blockers contraindicated

3) To relieve pain: MorphinePosition of comfortIVF in hypotensive settingFoley

Anticipate: ED thoracotomy, immediate need for

OR, arterial & central venous cannulationTherapeutics: Explain all procedures to patient/family,

maintain calm, allow family at bedside if possible

Result of inflammation of the pericardium that may extend to adjacent structures and may produce exudate.

Factors: - infections: idiopathic, viral,

bacterial, fungal - connective tissue disease

(lupus, rheumatoid) - renal disease - neoplastic disorders - tissue injury

SUBJECTIVE DATA

General malaise, fever, chills, weight loss

Dyspnea, cough

Chest Pain – deep inspiration, Chest Pain – deep inspiration, recumbent, movement, recumbent, movement, severe, sharp or dull ache, severe, sharp or dull ache, retrosternal or epigastric retrosternal or epigastric radiating to back/neck/ side, radiating to back/neck/ side, sudden, persistentsudden, persistent

SUBJECTIVE DATA cont.Medical History may

include:TB, congenital anomalies,

immune disorders, MI, neoplastic disease, drug use, uremia, cardiac surgery, cardiac trauma, infections

OBJECTIVE DATAPhysical Exam - pericardial friction rub (hallmark) – heard

best at the left lower sternum during end

expiration with patient leaning forward - tachycardia, fever, tachypnea

INTERVENTIONSSupplemental O2, cardiac

monitoringPosition of comfortAnti-inflammatory medicationsPericardiocentesis if necessaryLabs as orderedAntibiotics as ordered

INTERVENTIONS contMonitor/reassessTherapeutics:

maintain calmexplain all proceduresallow family at bedside

if possiblereassurance

Infection of the endocardium and heart valvesSBE

subacute bacterial endocarditis usually occurs in patients with congenital or acquired valvular disease; patients are less toxic

ABE acute bacterial endocariditis usually affects normal

heart valves and has a greatly accelerated pace of development; patients are extremely toxic with metastatic infections.

Infective agents (most common): - ABE: staphylococcus aureus - SBE: streptcoccus viridansRisk factors: - Valvular disease, congenital heart

defects, rheumatic heart disease, prosthetic heart valves, IV drug abusers, LT vascular access catheters

General pathophysiology:platelets and fibrin deposit on abnormal endotheliumorganisms adhere and colonization beginsmicroorganisms or fragments shed into bloodinfarction or infection can occur at any distal siteinfection of cardiac tissue can lead to progressive

heart failure, conduction disturbances, and dysrhythmias.

SUBJECTIVE DATAFever: SBE – low grade, ABE – 102

degrees FAnorexia, weight loss, night sweatsArthralgia, myalgia, fatigue, malaiseDyspnea, cough, pleuritic chest pain,

hemoptysisHA, signs of stroke, confusionAbdominal and back pain

Cardiac surgeryCongenital or

aquired heart valve disease

IV drug useRheumatic heart

disease

Cardiac pacemakerRecent GI or GU

disorder with valve disease

Prosthetic valves with recent dental procedures without prophylactic ATX

Subjective Data Suspect if history of:

OBJECTIVE DATAFever – may be absent in elderly, chronic

renalMurmur“Janeway lesions” - petechial lesions on

hands, feet; “Roth’s Spots” on ophthalmic exam; splinter hemorrhages on nails; “Osler’s nodes” – painful lesions of fingertips; petechiae

Splenomegaly, hematuria, proteinuria, clubbing with LT SBE, neurological changes

DIAGNOSTICSBlood cultures – most important in

decision making process!CBC (anemia common with SBE), BUN/Cr,

Electrolytes, Glucose, Sed rate (elevated in both types), UA

EKG – conduction abnormalities may be present with septal abscess

Echocardiogram – can view vegetation and amount of dysfunction

Head CT

INTERVENTIONSABC/monitoring/reassessmentsIV and NS at TKOLabs as ordered – especially MULTIPLE

blood cultures!Medications: Anti-pyretics, antibioticsTherapeutics – family at bedside, calm,

etc.

Caused by acute disruption of blood flow from an embolism (most common), thrombosis, or trauma.

Majority of emboli lodge in femoral artery.

Leads to ischemia in areas/tissues supplies by the affected artery

Immediate recognition and treatment required to maintain limb or organ viability.

SUBJECTIVE DATAPain

with movement or rest, burning, throbbing, radiates distal to occlusion, excruciating, relentless

Coldness, numbnessParalysisPast Medical HX:

MI, Rheumatic heart disease, a-fib, cardiac surgery, LV aneurysm, chronic CHF, extremity trauma, recent placement of intra-atrial catheters.

OBJECTIVE DATAPallor, cyanosis, mottled, coldnessPulseless (distally), paresthesia,

paralysisTenderness on palpation, muscle

rigor with prolonged ischemiaPetechiae

DIAGNOSTICSPT, PTT, CBCEKG

INTERVENTIONSElevate HOB (allow for

increased flow to ischemic extremity

Anticoagulants as ordered

INTERVENTIONS contMonitor and reassess (especially the 5 Ps)Position of comfortWarm environment (DO NOT apply heat to

area!)Maintain extremity at level position (DO

NOT elevate)Explain procedures and allow family as

able

An occlusion of a vein by a blood clot, commonly of the lower extremities, often involves inflammation.

Etiology – “Virchow’s Triad” - integrity of veins, stasis of blood flow, &

hypercoagulability statesFactors: age > 40, cardiac disease,

malignancy, hx of hypercoag., and use of estrogens and BCPs

The major complication

associated with venous

thrombosis is ? emboli.

SUBJECTIVE DATAPain – aching, localized at point of occlusion,

constant, worse with walking

Swelling, deep muscle tenderness, fever

Medical Hx Recent surgery or anesthesia, recent

traumatic event, postpartum, prolonged bedrest, heart failure, malignancy, obesity, BCPs, recent MI, thrombotic disease, hematological disorders

OBJECTIVE DATAErythema, swelling, indurations, warmthDeep muscle tendernessAsymmetry between extremitiesFeverPositive Homan’s sign

DIAGNOSTICSCBC, Sed rate, PT/PTTDoppler US flow study

INTERVENTIONSPosition of comfort, elevate effected

extremity, bed restAnalgesia, anticoagulants, and

thrombolytics as ordered Warm, moist compresses to areaElastic stockings or ACE wraps as orderedI&O, reassessments

Major cause is arteriosclerosis, or hardening of the large and medium-sized arteries.

Symptoms related to the decrease in blood flow to the specific areas; Worsen as disease worsens.

Factors: Heredity, male sex, increasing age, cigarette smoking, HTN, & hyperlipidemia.

Other types: Raynaud’s Disease & Buerger’s Disease

RAYNAUD’SEpisodic intense vasospasms of

the digits in response to cold or stress.

Affects women more than men.Vasospasm produces ischemia,

which produces pallor followed by cyanosis, coldness, and numbness of the affected digit.

As spasm resolves, there is an intense rubor and throbbing pain prior to digit returning to normal.

BUERGER’S DISEASEInflammatory disorder characterized by

thrombous formation in usually medium sized arteries of the lower leg and foot.

Men affected more than women.Results in ischemia, pain, intermittent

claudication, decreased or absent pulses, and changes in skin color.

Skin becomes thin and shiny, hair growth retarded, nails thicken, and gangrene/ulcerations may develop.

SUBJECTIVE DATAPain – cold environment, stress, exercise,

relieved by removal of agonist, severe, throbbing

Numbness, tinglingOBJECTIVE DATACold to touch, decreased/absent pulses, pallor,

cyanosis, ruborThin, shiny skin; thickened nails; ulcerations/

necrosis

DIAGNOSTICSCBCDoppler studies

INTERVENTIONSStop precipitating factorsVasodilators (calcium channel blockers or

adrenergic blockers) and analgesics as ordered

Reassess 5 P’sPosition of comfort, DO NOT elevate affected

extremityWarm environmentGeneral therapeutics

Usually a result of blunt traumaInjuries may range from petechiae to full-thickness

contusions to rupture of the heartLesions caused are similar to that of acute MI from

occlusions; major difference is amount of hemorrhage!RARELY FATAL!At risk for sudden dysrhythmias

SUBJECTIVE DATARecent blunt trauma to chest, chest pain similar to

MI but does not respond to vasodilatory drugsPain with inspiration usually secondary to fractured

sternumMedical HX – angina, previous MI, HTN, CHF, ETOH

or drug use, previous CV surgery

OBJECTIVE DATAExam may be normal without signs of trauma

or may be associated with severe traumaContusion to chest wall, tachycardia,

tachypnea, hypo- or hypertensionSigns of LV failure

crackles

DIAGNOSTICSEKG: Premature atrial or ventricular

contractions, A-Fib, SA block, nodal rhythm, AV block, nonspecific ST & T wave abnormalities, BBB (usually right), and infarct pattern.

Cardiac serum markersEchocardiographyCXR

INTERVENTIONSABCSupplemental O2, monitoringLarge bore IV (minimum of 2) & IVF as

neededMedicate with antidysrhymics and analgesics

as ordered/neededPosition of comfortGeneral therapeutics

Fluid accumulation in the pericardial sac, which elevates intracardiac pressure, progressive decrease in diastolic pressure, and ultimately decrease in stroke volume and cardiac output. Prognosis dependent on etiology & timelines of intervention.

Causes: - malignancies, pericarditis, uremia, &

traumaTypes: - acute: patient is in extremis; may be less

than 100c - chronic: patient not in extremis; may be 1-

2L

SUBJECTIVE DATAPenetrating or blunt injury, recent

repair of cardiac lesionsDyspnea, anxious, chest pain,

fatigue, malaiseMedical Hx: Cardiac disease, infectious or

neoplastic disease, renal failure

SUBJECTIVE DATA cont.Cold, moist skin; cyanotic

lips and digitsDecreased UODecreased LOC, comaHepatomegaly

OBJECTIVE DATAVisual woundTachypnea, rales,

Kussmal’s sign (rise in venous pressure with inspiration)

JVD,tachycardia

OBJECTIVE DATABeck’s Triad:

Venous pressure elevationArterial pressure declineMuffled heart tones

DIAGNOSTICSCXRPericardiocentesis (Hct will be lower in

pericardial blood than venous sample & generally pericardial blood will not clot)

EchocardiogramT&C, CBCEKG

ANALYSISCardiac output

decreased related to impaired cardiac filling and contractility and decreased venous return secondary to increased intrathoracic pressure

INTERVENTIONSABCLarge bore IVs (minimum of 2),

IVF as neededMonitoring, reassessmentPrepare: pericardiocentesis,

thoracotomy, internal cardiac massage

Foley & NGPrepare for immediate surgical

intervention

Result from blunt or penetrating trauma - MVCs are the most common cause

90% result in complete rupture and sudden death at “the scene”

Tearing may occur at points of attachment or may be pinched between the spinal column and manubrium.

Tears not involving the adventital layer (outer) may result in patient survival.

SUBJECTIVE DATADeceleration mechansim, blunt force to chest

or abdomenPain: severe, unrelenting pain in chest,

midscapular, or back regionMedical Hx: atherosclerotic heart disease,

prior thoracic injuries or surgeries

OBJECTIVE DATAOBJECTIVE DATADyspnea, tachypneaDyspnea, tachypneaTachycardia, discrepancy between BPs in Tachycardia, discrepancy between BPs in

right and left arms, harsh systolic murmur, right and left arms, harsh systolic murmur, varying degrees of shock, decreased quality varying degrees of shock, decreased quality of femoral vs radial pulsesof femoral vs radial pulses

Chest wall ecchymosis, paraplegiaChest wall ecchymosis, paraplegia

DIAGNOSTICSCXR: widened mediastinum,

obliteration of aortic knob, tracheal deviation to the right, presence of pleural cap, fx of 1st & 2nd ribs, depression of left main stem bronchus, deviation of esophagus to right, shift of right main stem bronchus up and to right

DIAGNOSTICS contCT scanEKGT&CCBC

INTERVENTIONSABC, monitoring, reassessmentLarge bore IVs (minimum of 2), IVF as neededPrepare for blood transfusion & autotransfusion as

neededFoley & NGMonitor arterial pHPrepare for immediate surgical interventionAdminister antihypertensives & beta blockers as

ordered if surgical repair delayed

Result from blunt (MVC & crush injuries) or penetrating (GSW & stab wounds) trauma

Vessels injuries include lacerations, hematomas, and pseudoaneurysms

Neurological signs usual present due to close proximity of nerves

Major consequence is ischemia distal to injury; immediate surgery required is damage is severe

SUBJECTIVE DATANumbness, tingling, pain, paralysisMechanism Medical Hx: diabetes, PVD

OBJECTIVE DATAHemorrhage from wound, varying stages of shock

related to volume of blood loss, pulsatile or expanding hematoma

Difference in BPs in different extremities, prolonged cap refill, diminished or absent distal pulses

Pallor, paresthesia, coolness, paralysis

DIAGNOSTICDoppler study