Cardio 4

Front 1

When is immediate treatment indicated in htn?

Back 1

Defn of hypertensive emergency: i)>220/120 ii)end organ damage.

Front 2

What is hypertensive urgency? what do you do?

Back 2

i)>220/120 w/o end organ damage. ii)attempt to lower BP over 24 hours

Front 3

In HTN, what end organ damage do you need to assess?

Back 3

i)eyes: papilledema ii)CNS: a)altered mental status or intracranial hemorrhage. b)encephalopathy: suspect if BP >240/140 w/confusion. iii)kidneys: RF or hematuria iv)heart: USA; MI; CHF w/pulm edema; dissection. v)lungs: pulm edema

Front 4

What are causes of htnive emergency?

Back 4

i)noncompliant w/meds ii)cushings iii)coke or speed iv)hyperaldo v)eclampsia vi)vasculitis vii)EtOH w/drawal

Front 5

What are clinical features of htnive emergency?

Back 5

i)altered mental status ii)visual disturbance iii)severe H/A

Front 6

What are the steps if pt presents w/H/A and very high BP?

Back 6

i)lower BP w/antihtnive ii)order CT: r/o intracranial bleed (SAH). iii)if --, do an LP

Front 7

What is general guideline for HTNive emergency? If severe (DBP>130) or if htnive enceph? What is treat for not immed danger or HTN urgency?

Back 7

i)lower arterial BP by 25% in 1-2 hrs: get out of danger and reduce slowly. ii)IV nitroprusside, labetalol, nitro iii)oral agents; lower BP w/in 24 hrs for urgency

Front 8

What are risk factors for dissection?

Back 8

i)Chronic HTN * ii)trauma iii)bicuspid AV iv)coarct v)pregnant

Front 9

What are the 2 types of dissection?

Back 9

i)Type A (prox): asc aorta (including retrograde extension from descending aorta). ii)Type B: distal (descending)

Front 10

How does type A dissection present vs type B? What are other clinical features?

Back 10

Both are ripping/stabbing pain: i)type A: Ant CP ii)Type B: Back. iii)most are hypertensive, some hypo. iv)pulse or BP asymmetry b/w limbs. v)neurologic (hemiplegia, hemianesthesia) b/c of carotid obstruction.

Front 11

How do you DX dissection?

Back 11

i)CXR w/widened mediastinum ii)TEE and CT (MRI good but takes too long.) TEE good b/c portable for ER. iii)angiography pre-SX for extent

Front 12

Treatment of dissection?

Back 12

i)NO thrombolytics (if misDX as AMI). ii)Control BP: IV B block (decr HR and decr force of LV ejection); IV nitroprusside to lower BP<120. iii)Type A=sx; type B=medical

Front 13

Where are AAA usually? What are risks? x3. What is risk for thoracic aneurysm?

Back 13

i)AAA b/w renal arteries and iliac bifurc. ii)trauma, HTN, vasculitis iii)syphilis and Marfans

Front 14

How would a non ruptured AAA present?

Back 14

i)asympto, found on ab exam ii)sense of fullness iii)if pain: throbbing in hypogastrium and lower back iv)expansion and impending rupture sxs: i)sudden pain radiating to butt or groin ii)Grey Turners (ecchymosis on back and flanks) and Cullen's: ecchymosis around umbilicus

Front 15

How does rupture of AAA present?

Back 15

i)triad: ab pain, hypotension, palpable pulsatile ab mass: need laparotomy. ii)N/V iii)hemorrhage signs

Front 16

How to DX aneurysm? x3

Back 16

i)*U/S ii)CT, but only for stable pts. iii)Xray: quick and if calcified can measure diameter, but not sensitive (no r/o)

Front 17

How to treat unruptured and ruptured aneurysms?

Back 17

i)unruptured: a)>5cm (nl 2cm) or symptoms: SX w/synth graft placement. b)<5: imaging for follow up but small ones can rupture. Need to consider age, other illnesses, and risk of SX. ii)SX for ruptured

Front 18

What is Peripheral Vascular dz (Chronic aortic insuff)? What is do these pts usually have coexisting? Which arteries are affected? What is px?

Back 18

i)occlusive atherosclerotic dz of lower ext. ii)coexisting PVD (CHF, h/o MI, DM, etc). iii)SF femoral *; popliteal A. iv)intermittent claudication is good PX; rest pain or ischemic ulcers bad PX

Front 19

What are sxs of intermittent claudication? Sxs of rest pain? What are signs?

Back 19

i)cramping leg pain reproduced by same walking distance; pain relieved by rest. ii)felt at night over distal metatarsals; standing or legs over bed help. Afraid of gangrene w/o intervention. iii)muscle atrophy; decr hair growth, thick toenails; ischemi ulceration (toes) that is 2ndary to trauma and doesn't heal; gangrene/tissue infarction.

Front 20

What is leriche's syndrome?

Back 20

i)atheromatous occlusion of distal aorta just above bifurc: b/l claudication, impotence, absent/dim femoral pulses

Front 21

How to DX PVD? x3

Back 21

i)Ankle to Brachial index (ABI)-> systolic BP at ankle/sys BP at arm (nl is 1; rest pain is <.4; claud: <.7). ii)pulse volume recordings: assesses perfusion->large wave form means lots of blood/heart beat and measure down the leg. iii)arteriography: gold std for DX and locating PVD; only needed if revasc SX intended.

Front 22

How to treat PVD? meds vs SX and their indications

Back 22

i)SX: ind if rest pain, ulcers, severe SXs refrac to conserv tx. Can bypass graft or angioplasty (balloon). ii)ASA; no smoke; graduated walking program; foot care (esp DM); reduce atherosclerosis

Front 23

What is main cause of acute arterial occlusion? Where is it usually? What are the sources?

Back 23

i)embolization ii)femoral artery iii)Heart (afib*); post MI; endocarditis iv)aneurysms v)atheromatous plaque

Front 24

What are the clinical features of AAO? x6

Back 24

6 P's: i)Pain: acute, very severe and need to sit or lie ii)pallor iii)poikilothermy iv)paralysis v)paresthesias vi)pulselessness (doppler)

Front 25

How to DX AAO?x3 (acute arterial occlusion)

Back 25

i)arteriogram to define site ii)EKG for MI, AFib iii)echo: evaluate valves, clot, MI

Front 26

How to treat AAO?

Back 26

i)1st: assess viability of tissue->sk m can tolerate 6 hrs of ischemia; if paralysis/paresthesia: amputation ii)immediate anticoag iii)embolectomy via cutdown and fogarty balloon->bypass if doesn't work. Or Intraarterial thrombolytics.

Back 31

i)If SF venous system is patent, no erythema, pain, cords b/c blood drains from the patent veins

Front 32

What are classic findings of DVT? How is sn and sp?

Back 32

i)all are low sn and sp. ii)pain and swelling better w/rest and elevation iii)Homan's (calf pain w/dorsiflex) iv)fever v)cord

Front 33

How to DX DVT? x3

Back 33

i)*Doppler w/duplex US: initial test, noninvasive. High sn/sp for popliteal/femoral, not distal (calf). ii)*VenographyL: most accurate test of calf veins, but invasive. iii)D dimer: high sn but low sp: used to r/o w/doppler

Front 34

How to interpret tests for DVT depending on pretest probability?

Back 34

i)intermediate to high: U/S if +, then start anticoag. if non diagnostic, repeat q2-3 days x 2 weeks. ii)low pretest: U/S is --: no anticoag but observe and repeat US in 2 days

Front 35

What are complications of DVT x3

Back 35

i)PE ii)postthrombotic syndrome (CVI): get ambulatory HTN iii)phlegmasia cerulea dolens: severe leg edema blocks blood, so impaired sensory and motor fcn: need venous thrombectomy

Front 36

What is treatment for DVT?

Back 36

i)anticoag: heparin to PTT 1.5-2; continue for 48 hrs...warfarin: INR 2.5-3 after PTT 1.5; for 3-6 mths. ii)thrombolytic therapy (tPA): for massive PE, unstable, or RHF. iii)IVC filter placement: if high risk and C/I to other forms of prophylaxis. iv)prophylaxis after SX methods: a)mechanical: leg elevate, ambulate, stockings, leggings. b)heparin

Front 37

Where does chronic venous insuff (venous stasis DZ/postphlebitic syndrome) affect in venous systems? What is the pathophysiology?

Back 37

i)SF or deep or both ii)DVT is usually the cause: a)destroys valves in deep system so pressure from blood column to ankles. This damages perforating valves so no blood from SF to deep->amb HTN leading to edema and plasma proteins and RBCs into subQ tissues, giving brown induration and pigmentation of skin->get decreased cap blood flow and hypoxic tissues. Get tissue death-> ulcers from minor trauma

Front 38

What is presentation of CVI? x3

Back 38

i)swollen lower leg, worsened by sitting or inactive standing. Leg elev causes relief (opp for arterial insuff). ii)chronic: skin change: shiny, atrophic, cyanotic and brawny induration; iii)venous ulcers: above medial malleoulus and less pain than arterial insuff.

Front 39

What is management in CVI b/4 ulcer development? After ulcers develop?

Back 39

i)leg elevate above the heart periodically in a day b)avoid long standing/sitting c)elastic stockings. ii)a)wet to dry saline dressing daily x3 b)unna venous boot (external compression): change q 1 week. c)if no healing of ulcers w/unna boot: split thickness skin graft w/or w/o ligation of adjacent perf veins

Front 40

What is implicated in SF thrombophlebitis? Where does it occur in upper ext? In lower ext?

Back 40

i)virchow's triad ii)IV infusion iii)ass'd w/varicose veins (greater saph system); secondary to static blood flow in those veins.

Front 41

What do you think when SF thrombophlebitis occurs in diff location in short time? What is it due to usually?

Back 41

i)migratory thrombophlebitis ii)malignancy, usually of pancreas.

Front 42

what are clinical features of SF thrombophlebitis?

Back 42

i)pain, tenderness, induration, erythema along course of vein. ii)may feel cord

Front 43

How to treat SF thrombophlebitis? Localize vs severe?

Back 43

i)no anticoag: rarely causes PE. ii)localized: mild analgesic (ASA) and continue activity. iii)severe (pain and cellulitis): bed rest, elevation, hot compresses; ambulate w/stockings once sxs gone. ABx if purulent, and need drainage also.

Front 44

What is diff b/w thrombophlebitis and cellulitis and lymphangitis?

Back 44

i)more swelling and erythema in cellulitis and lymphangitis. ii)no palpable, indurated vein in c and l

Front 45

What are signs and sxs common to all types of shock?

Back 45

i)hypotension ii)oliguria iii)tachycardia iv)altered mental status

Front 46

What parameters is shock's effect assessed by? x3

Back 46

hemodynamic changes: i)CO ii)SVR iii)volume status: PCWP or JVP

Front 47

What history and PE findings suggest the cause of shock?

Back 47

i)fever and possible site of infection: septic ii)trauma, GI, bleeding, vomit, diarrhea: hypovolemic iii)JVD: cardiogenic iv)spinal injury or neuro deficits: neurogenic

Front 48

How to treat shock in first steps?

Back 48

Stabilize and determine cause i)ABCs*; 2 large bore, central line, arterial line. ii)fluid bolus usually iii)bloods: CBC, PT/PTT, lytes, renal fcn. iv)EKG, CXR v)continuous pulse oximetry vi)vasopressors

Front 49

When does cardiogenic shock occur and what is the defn?

Back 49

i)heart can't generate suff CO to maintain perfusion ii)SBP<90; urine<20 mL/hr; adequate LV filling pressure

Front 50

What are causes of cardiogenic shock? x5

Back 50

i)after acute MI* ii)compression of heart: cardiac tamponade and tension pneumothorax iv)arrhythmia v)PE

Front 51

What is presentation of cardiogenic shock?

Back 51

i)typical findings of shock (altered mental status; pale cool skin; hypotensive; tachy). ii)engorged neck veins iii)pulm congestion

Front 52

How to DX cardiogenic shock. x3

Back 52

i)EKG: ST elevation suggesting acute MI or arrythmia is most common. ii)echo: mechanical compliations of MI, estimate EF, look for effusion iii)hemodynamic monitor w/swan-ganz: PCWP, pulm A pressure, CO, SVR. JVP/PCWP is only elevated in cardiogenic shock (adequate LV filling pressure).

Front 53

How to treat cardiogenic shock? x

Back 53

i)ABCs ii)ID and treat underlying cause (AMI, arrhyth, tamponade, valves iii)Vasopressors: DA*. Don't use afterload reducers (nitro, nitroprusside) b/c worsens hypotension. iv)IV fluids bad b/c LVP is increased. v)Give IABP: decr afterload, incr CO, decr O2 demand

Front 54

What are indications of IABP? x4

Back 54

i)angina refrac to medical therapy ii)mech complications of MI iii)cardiogenic shock iv)low CO states

Front 55

What are imp details of hypovolemic shock in px? x2

Back 55

i)rate of loss: slower loss means better compensatory mech. ii)sig med comorbidities (cardiac): unable to compensate physiologically in early stages of hypovolemic shock

Front 56

How to dx hypovolemic shock/

Back 56

i)clinical ii)Central venous line or pulm A catheter for hemodynamic monitoring. iii)decr CVP/PCWP, decr CO, incr SVR

Front 57

How to treat hypovolemic shock?

Back 57

i)ABCs (may need mechanical ventilation) ii)circulation: if hemorrhage, need direct pressure. iii)IV hydrate: Class I doesn't need; Class II benefits; class III/IV needs. If nonhemorrhagic (vol loss): lytes and soln

Front 58

What is the progression of stages in septic shock? x4

Back 58

i)SIRS (2 of these: fever or hypothermia, hyperventilate, tachycard, incr WBC). ii)sepsis iii)septic shock iv)multi-organ dysfcn.

Front 59

What are the hemodynamic changes in septic shock? x4

Back 59

i)decrease SVR b/c peripheral vasodilate (warm). ii)CO is normal or increased iii)PCWP is decreased. iv)EF decreased b.c decr reduced contractility

Front 60

What are clinical features of septic shock? x4

Back 60

i)manifestations of cause ii)hypothermia usually, but can be hyper iii)shock signs (oliguria, hypotension, lactic acidosis) iv)SIRS signs

Front 61

How to treat septic shock? x4

Back 61

i)IV ABx ii) drainage if need iii)fluids to increase mean BP iv)vasopressor: if hypotension persists despite IV fluid resus (DA first, then NE)

Front 62

what is neurogenic shock due to and what are causes (x3). how is it characterized?

Back 62

i)failure of SNS to maintain adquate vasc tone (symp denerv). ii)spinal cord injury, spinal anesthesia, pharm iii)peripheral vasodilation and decr SVR

Front 63

What is presentation of neurogenic shock? x4

Back 63

i)warm, well perfused skin ii)urine output low or normal iii)bradycardia and hypotension iv)CO normal, SVR low, PCWP low/nl

Front 64

Treat of neurogenic shock? x4

Back 64

i)IV fluids as mainstay ii)vasopressors cautiously: only to restore venous tone iii)supine or trendelenburg position iv)maintain body temp