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37 Cards in this Set

  • Front
  • Back
Arteriosclerosis
 Abnormal thickening and hardening of arterial walls
 Narrowed lumen
 Atherosclerosis
 Most common form of arteriosclerosis
 Fat & fibrin on vessel walls
 → CAD, cerebrovascular disease
 Causes: inflammation*, smoking, HTN, DM, ↑ lipids, ↑ homocystine, autoimmune, infection (chlamydia, herpes viruses)
 Ischemic events
 Coronary heart disease, myocardial infarction, stroke
 Rx: treat ischemia, exercise, smoking cessation, control hypertension and DM, reducing LDL cholesterol
 Cholesterol <200, LDL <100, HDL >40
 Drugs to ↓ lipidemia
Aneurysm
 Local dilation or outpouching of a vessel wall or cardiac chamber
 Aorta very susceptible ¾ are abdominal
 Causes:
 Atherosclerosis, plaque erodes vessel wall
types of aneurysms
 True aneurysm involve all three layers
 Fusiform – saccular
 False aneurysm
 Only intima (inner) layer as in leak between vascular graft and artery
 Dissecting
 Wall of an artery dissects longitudinally
 Surgical emergency
Aortic aneurysms
 Often asymptomatic until rupture
 Risks: Age, atherosclerosis, HTN, tobacco, white race, family, males, Marfan’s syndrome, trauma
 Treatment
 Surgical – graft for greater than 5 cm
 Endovascular surgery
Venous thromboembolism (Deep vein thrombosis)
 Triad of Virchow
• Venous stasis, endothelial injury, hypercoagulability (Factor V Leiden, antithrombin III, Protein C or Protein S deficiencies)
 Risk factors: surgery (esp. hips & knees), immobility, cancer, pregnancy, postpartum, oral contraceptive, HRT
 S/S, Dx: unilateral leg swelling, pain,
 Dx: US, venous duplex
 Rx: anticoagulation, bedrest
Thrombus
 Blood clot that remains fixed to a vessel wall
 Detached thrombus = thromboembolus
 Tend to form at areas of inflammation
• Surgery, trauma, infection, plaque
 Veins – thrombophlebitis
 Valvular thrombi – endocarditis & RHD
 Rx: anticoagulants
Embolus
 Bolus of matter: thrombus, air, amniotic fluid, fat, bacteria, cancer cells
 Pulmonary embolus
 From venous circulation to lungs
 Systemic (arterial) embolus originates in L ♥ from MI, ♥ failure, endocarditis, dysrhythmias
 Causes ischemia, infarction, sepsis, stroke
Varicose Veins
Varicose Veins
 Blood pooling " distended, tortuous, palpable veins
• Trauma to saphenous vein / valvular damage
• Prolonged standing
Gravity and i muscle pump
Raynaud disease
characterized by attacks of vasospasm in the small arteries & arterioles of the fingers and less commonly in te toes, primary artery disease
 Raynaud’s (primary)
 Unknown origin
 Vasospastic attacks 2° to cold, emotions
 Raynaud’s (secondary)
 2° to systemic diseases
• Collagen vascular (scleroderma), lupus, and rheumatoid arthritis
 Vasospasm – mostly fingers
 Pallor, cyanosis, numbness, cold sensation followed by rubor, throbbing, paresthesias
 Rx: SSRI, vasodilators, reserpine, Ca++ channel blockers
Superior vena cava syndrome
 Compression of the SVC causing venous distention of the head and upper extremities
 Bronchogenic cancer (75%), lymphoma, metastases, pacemaker insertion, long-term CV catheter
 R mainstem bronchus abuts the SVC which is easily compressed by tumor, lymph node growth
 S/S: edema, fullness, tightness of collars, rings, HA, visual disturbances, respiratory distress, purple skin coloration
 Rx: diuretics, steroids, anticoagulants prn, stent placement
Pericardial tamponade
 Fluid in the pericardium creates enough pressure to cause cardiac compression
 S/S: * pulsus paradoxus – BP during expiration > BP during inspiration by >10mm Hg, muffled ♥ sounds, DOE, dull CP
 Causes: uremia with LV failure, ♥ surgery, radiation to chest
 Rx: pericardiocentesis
Acute pericarditis
 inflammation of the two layers of the thin, sac-like membrane that surrounds the heart
 Commonly caused by infection, uremia, neoplasm, surgery, trauma
 S/S: severe chest pain that worsens with respiratory movements or lying down
 Low grade fever, tachycardia, friction rub (sandpaper)
 Rx: treat cause
Endocarditis
 Heart valve vegetation which h risk of embolus
 Must have invasion of blood stream
 Staph aureus*, strep viridans
 Portal of entry
 Low host resistance, high virulence
 Risks: overt infection, IV drug abuse, surgical or dental procedure, mechanical heart valves, long term catheters, valvular disease, ♥ surgery
 “classic” findings: fever, murmur, petechiae
 Rx: IV to oral abx for 4 – 6 wks
 Valvular stenosis
 Blood can not flow forward, chamber “in front of” the valve has h workload
 Valvular regurgitation (insufficiency)
 Cusps fail to close completely, some blood leaks back
 Eventually " heart failure
Anaphylactic shock
 Widespread hypersensitivity
 Penicillin, latex & food allergies, venoms, pollens
 Alteration same as neurogenic, ↓ tissue perfusion
 Extensive immune & inflammatory response
 Bronchoconstriction, urticaria (hives), edema, hypotension
 Remove stimulus, epinephrine, steroids, volume
Cardiogenic shock
 ↓ CO & tissue hypoxia with adequate intravascular volume
 Dyspnea, tachycardia, hypotension, ↑ SVR, ↓ EF & tissue perfusion
 Heart failure – any kind
 Occurs with MI, ischemia, infection, drug toxicity
 Mortality of 70%
Hypovolemic shock
 Loss of blood/ fluid
 Hemorrhage, burns, diaphoresis, DM, DI, emesis, diuresis in large amounts
 S/S: ↓ BP, ↑ HR & SVR (compensatory), oliguria, poor skin turgor, thready pulse,
 ↓ mental status
 peripheral vasoconstriction
 R-A-A, ADH activation
 Rx: Fluid replacement
Neurogenic shock
 Vasogenic shock
 Vasodilation, ↑ parasympathetic or ↓ sympathetic stimulation
 * ↓ SVR, hypotension, bradycardia
 Loss of vascular tone, blood volume the same
 Causes: injury to spinal cord or medulla, depressive drugs, anesthesia
Septic shock
 Component of systemic inflammatory response syndrome (SIRS)
 Infection →bacteremia →sepsis →septic shock →multiple organ dysfunction (MODS)
 Endotoxins act as triggers for a cascade
 Vasopressors to support hypotension
 Acidosis, oliguria, change in mental status
 Low BP, low SVR, systemic edema, GI abnormality, ARDS
 Common in ICU, 40% mortality
Multiple organ dysfunction syndrome (MODS)
 50-90% mortality
 Sepsis, septic shock most common causes
 Dysfunction of two or more organ systems
 Risks: age > 65, organ dysfunction, bowel infarction, steroids, multiple blood transfusion, chronic disease, delayed resuscitation, severe tissue injury (more, p. 698)
 First organ to be affected: Lung – adult respiratory distress syndrome (ARDS)
 Renal, liver, GI, hematologic, cardiac, CNS
Myocardial infarction: define, what causes the cardiac dysfunction? Which lab tests and diagnostics are performed..how is diagnosis made?
 Necrosis following blood flow interruption. EKG changes with 30-60 sec of hypoxia
 Pain not relieved by nitrates, heavy, crushing, radiating
 “silent” in elderly and DM
 N/V, diaphoresis
 Dysrhythmias, heart failure

 Dx: EKG, serial enzymes, troponin
 “cardiac profile”
 Rx: thrombolytic therapy, heparin, percutaneous transluminal coronary intervention (PTCI)
 Sudden cardiac death related to
 Ischemia
 LV dysfunction
Electrical instability
 Myocardium has it’s own conduction system, concentrated at certain sites called nodes
 Heart can beat without nervous innervation (automaticity)
 SA node – pacemaker of the ♥ " AV node " Bundle of HIS" bundle branches " Purkinje fibers
Rheumatic fever or heart disease
 After upper respiratory infection with Group A beta-hemolytic streptococcus
 Untreated" RHD
 Also infects joints, skin, nervous system
 Children 5 – 15 yrs
 Genetic, *immune
 Destruction of MV & AV, atrial fibrillation
 High recurrence rate
Acute Rheumatic fever
 Carditis
 Valve dysfunction, murmur
 Pericardial effusion
acute reumatic fever
 Polyarthritis
 Acute, migratory, > than 1 joint
acute rheumatic fever
 Chorea
 St Vitus dance: aimless, involuntary movements
acute rheumatic fever
 Erythema marginatum
 Truncal rash, erythematous
 macules, transitory, h with heat
Systolic, Primary, Secondary hypertension
 Consistent elevation of BP often “silent”
 3rd leading cause of death
 Increases incidence MI, ♥ failure, stroke, kidney disease
 Risks include: genetics, nicotine, older age, obesity, heavy ETOH, gender (women>50), black race, h Na+, glucose intolerance
 From h in peripheral resistance, h blood volume or both
 Sustained pressure damages arterial walls, h inflammation
 Primary (essential, idiopathic) HTN (92-95%)
 Genetic, environmental factors
 Neural, hormonal i.e. sympathetic stim, R-A-A system, Na+ retention,
 Insulin resistance and endothelial dysfunction
 Secondary HTN is caused by systemic diseases such as:
 Renal disease
 Adrenal tumors
 Cortex – aldosterone
 Medulla – pheochromocytoma
 Drugs: BCP, steroids, antihistamines
 Can be reversed
 Isolated systolic HTN
 S >140, D < 90, * widening PP
 Rigidity of aorta, changes in A0 valve, age >65
Congestive heart failure
 Impaired ability of myocardial fibers to contract (systolic failure) or to relax (diastolic failure)
 Pressure reflected back into pulmonary circulation
 Rales, SOB
 Rx: diuretics, ACE inhibitors, β blockers, digoxin, daily weights
Atrial fibrillation
 No p waves, atrial rate 300 – 600 bpm
 Atria fibrillate or quiver
 Ventricular rate varies and is irregular– called ventricular response
 Rx: Cardioversion – timed electrical shock to the heart
 Drug therapy
 Digoxin, β blockers, CCB and others
 ANTICOAGULATION

 Causes
 Idiopathic  Thyroid disorders, valve disease, hypertension, sick sinus syndrome, pericarditis, lung disease, and congenital heart defects and others
Cardiomyopathy
 Affects the myocardium and leads to diminished cardiac performance
 Result of ischemic changes, HTN, infectious disease, toxins, connective tissue disease, nutritional deficiencies, metabolic disorders