PANCE Prep- Cardiology Part 2 Flashcards

1
Q

What creates S1, S2, S3, S4 and what disease are associated with them

A

S1- MV and TV closure (loudest at apex)
S2- AV and PV closure (loudest at base)
S3- rapid passive ventricular filling
-LVSF, normal in kids

S4- atrial contraction into the ventricles
-HTN, LVH, AS, normal in kids

Split S2: delayed PV closure

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2
Q

What murmurs radiate and to where?

A

AS- carotids
AR- LUSB
MS- none
MR- axilla

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3
Q

What positions increase murmur intensities?

What positions decrease murmur intensities?

A
  1. increase venous return increases ALL murmurs except HCM–> squatting, leg raise, lying down
  2. Right sided murmurs increase w/ inspiration
  3. Left sided murmurs increase w/ expiration
  4. Hand grips increases afterload–> increases regurg murmurs (AR and MR)
  5. decreasing venous returns decreases all murmurs except HCM–> valsalva, standing
  6. Amyl nitrate decreases afterload–> decreased regurg murmurs (AR and MR)
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4
Q

Complications of AS

A

think AS Complications

  1. Angina (increased O2 demand but fixed CO due to obstructed LVoutlow
  2. Syncope w/ exertion
  3. CHF
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5
Q

Systolic ejection murmur, crescendo-decrescendo murmur heard at RUSB that radiates to carotids

  • pulsus parvus et tardus: small, delayed carotid pulse
  • Narrowed pulse pressure***
A

AS

DX: Echo, EKG: LVH

TX: surgery

  • no medical therapy is truly effective
  • AVOID physical exertion/venodilators (nitrates) neg. inotropes (CCB, BB)
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6
Q

diastolic, decresendo, blowing murmur at LUSB

  • bounding pulses*
  • wide pulse pressure*
  • Hill’s sign: popliteal artery systolic pressure > brachial artery by 60mmHg
  • Water Hammer pulse- swift upstroke and rapid fall of radial pulse accentuated w/ wrist elevation
  • Corrigans pulse- similar to water hammer pulse but in referringto carotid artery
A

AR

DX: Echo

TX:

  1. surgery
  2. afterload reduction with vasodilators (ACEI, ARBs, Nifedipine, Hydralazine)
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7
Q

-Ruddy flushed cheeks with facial pallor
-dyspnea
-early-mid diastolic rumble at apex esp. in LLD position
-Prominent S1 and opening snap
+/- afib

A

MS MC caused by rheumatic heart disease by far

DX: echo, ekg- LAE +/- afib

TX: surgery

  1. meds-does not alter need for surgery
    - loop diuretics and Na restriction (if congestion)
    - BB, digoxin if Afib
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8
Q
  • Dyspnea, +/- afib
  • blowing holosystolic murmur at apex w/ radiation to axilla
  • widely split S2
  • hyerdynamic LV on echo
A

MR *MC cause is MVP and ischemia

DX: echo

TX: surgery
2. meds- vasodilators to decrease afterload (ACEI, hydralazine) decrease preload (diuretics), digoxin if afib

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9
Q

MVP is usually asymptomatic but some may experience:

A

autonomic dysfunction: anxiety, atypical CP, palps–> then tx w/ BB but otherwise no tx is needed

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10
Q

harsh midsystolic ejection cresc-decrecendo murmur at LUSB radiates to neck
-systolic ejection click

A

PS *almost always congenital

TX: balloon valvuloplasty

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11
Q

brief decrescendo early diastolic murmur at LUSB with full inspiration (Graham Steell murmur)

A

PR *almost always congenital

TX: none needed- well tolerated

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12
Q

mid-diastolic murmur heard at LLSB at 4th ICS

  • opening snap
  • can lead to RHF
A

TS

TX: surgery
2. meds- diuretics and na restriction

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13
Q

holosystolic blowing high pitched murmur at subxyphoid area (L mid sternal border)
-Carvallo signs- increased murmur intensity w/ inspiration

A

TR

TX: surgery
2. meds- diuretics

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14
Q
describe the pathophysiology of 
AS
MS
AR
MR
A

AS: LV outflow obstruction–> fixed CO
-increased afterload–> LVH
MS: Obstruction of flow from LA to LV–> increased LAE andLA pressure–> PHTN
AR: back flow from aorta to LV–> LV volume overload
MR: back flow from LV into LA–> LV volume overload–> decreased CO

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15
Q

common causes of secondary HTN

A

*consider if BP is refractory to antihypertensives or severly elevated

  1. Renovascular (MC): renal artery stenosis
  2. Fibromuscular dysplasia
  3. atherosclerosis
  4. Endocrine: primary hyperaldosteronism, PCC, Cushings
  5. Coarc, OSA, ETOH, OCPs
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16
Q

__ is 2nd MC cause of ESRD is US

A

HTN

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17
Q

describe the different grades of retinopathy

A

I: arterial nicking
II: AV nicking
III: hemorrhages and soft exudates
IV: papilledema

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18
Q

what is the initial tx of choice for uncomplicated HTN

A

thiazide diuretics

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19
Q

SE of:

  1. Thiazide diuretics
  2. Loop diuretics
  3. K sparing diuretics
A
  1. Thiazide diuretics: HypoK+, HypoNa+, HyperCa++, Hyperglycemia, Hyperuricemia (caution w/ gout)
  2. Loop diuretics: HypoK+, HypoNa+, HypoCa++, metabolic akalosis, Ototoxicity,
    * CI: sulfa allergy
  3. K sparing diuretics: HyperK*, gynecomasia
    * CI: renal failure
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20
Q

When is it best to use ACEI for HTN and what are their SE

A
  1. Hx of DM, nephropathy or CHF, post MI–> renoprotective**

SE:

  1. hypotension w/ first dose
  2. azotemia/RI
  3. HyperK+
  4. Cough/angioedema
  5. hyperuricemia
    * CI: pregnancy
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21
Q

What are the 2 types of CCBs?

A

Dihydropyridines: potent vasodilator w/ little or no effect on cardiac contractility or conduction
ex. Nifedipine and amlodipine

Non-dihydropyridines: affects cardiac contractility and conduction

  • used w/ HTN w/ concomitant Afib and used for raynauds
    ex. verapamil, diltiazem
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22
Q

SE of CCBs

A

HA, dizziness, LH, flushing, peripheral edema,
Verapamil: constipation

CI: 2nd and 3rd Heart block, CHF

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23
Q

SE of BB

A

fatigue, depression, impotence, masked sympathetic sx of hypoglycemia (caution w/ diabetics)

  • may worsen PVD or raynauds
  • CI: 2/3 Heart block, asthma, decompensated HF
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24
Q

good HTN med to use w/ BPH

A

A1 blockers
prazosin
terazosin
doxazosin

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25
What antihypertensive med should you use to treat HTN w/ comorbid: 1. afib 2. angina 3. post MI 4. Systolic HF 5. DM 6. isolated HTN in elderly 7. BPH 8. AA 9. Gout
1. afib: BB or CCB 2. angina: BB or CCB 3. post MI: BB or ACEI 4. Systolic HF: ACEI, ARB, BB, diuretic 5. DM: ACEI 6. isolated HTN in elderly: diuretic 7. BPH: a1 blocker 8. AA: thiazide, CCB 9. Gout: CCB, Losartan (only ARB that doesn't cause hyperuricemia)
26
Tx of Hypertensive Urgency
decrease BP by 25% over 24-48 hrs using oral meds -clonidine or captopril *Goal BP to = 160/100mmHg
27
Tx goals of hypertensive emergency
decrease BP by 25% in first hr then additional 5-15% over next 23 hrs using IV agents UNLESS: 1. ischemic stroke: only lower if >/=185/110mmHg for tpa candidiates or if >/=220/120 for non candidates 2. Aortic dissection: BP often reduced to 100-120 SBP w/in 20 min
28
What meds should you use for HTN emergency w/ neurologic sx (HTN encephalopathy, heorrhagic stroke, or ischemic stroke)
Nicardipine or labetalol
29
What meds should you use for HTN emergency w/ cardiovascular sx 1. Aortic dissection: 2. ACS: 3. Acute HF:
1. Aortic dissection: BB- esmolol, labetolol 2. ACS: nitroglycerin, BB (esmolol, metoprolol) 3. Acute HF: Nitroglycerin, furosemide
30
Indication for statins
1. 40-75y/o with DM 1 or 2 2. 40-75y/o w/o CV risk factors but 7.5% or greater for having MI or CVA w/ in 10 yrs 3. 21y/o or older w/ LDL 190 or higher 4. s/s clinical atherosclerotic CV disease
31
Best meds to: 1. lower LDL 2. Lower TG 3. Increase HDL
1. lower LDL: Statins 2. Lower TG: Fibrates 3. Increase HDL: Niacin
32
what is the only med that is safe in pregnancy to help tx hyperlipidemia
Bile acid sequestrants (cholestyramine, colestipol, colesevelam) *may increase TGs
33
what valve is MC affected in infective endocarditis
MV **TV is most commonly affected for LV drug users
34
MC organisms that cause endocardititis
SBE: strep viridan ABE: staph aureus IVDU: MRSA Men w/ h/o GI/GU procedures: Enterococci Others: HACEK organisms (gram neg) (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Klingella)
35
s/s of endocarditis
1. Fever 2. ECG conduction abnormalites 3. Janeway lesions: painless erythematous macules on palms and soles 4. Roth spots: retinal hemorrhages w/ pale centers, Petechiae 5. Osler nodes: tender nodules on pads of digits 6. Splinter hemorrhages of prox. nail beds
36
How do you dx Endocarditis
1. Blood cultures: 3 sets at least 1 hr apart if pt is stable 2. EKG (prone to arrhythmias) 3. Echo/TEE 4. CBC: leukocytosis, anemia: increased ESR/RF MODIFIED DUKE CRITERIA *2 major OR 1 major + 3 minor OR 5 minor Major: 1. 2+ blood cultures 2. + echo 3. new valvular regurg Minor: 1. Predisoping condition (abnormal valves, IVDU, indwelling cath) 2. Fever 3. Vascular and embolic phenomena: Janeway, septic arterial or pulm. emboli 4. Immunologic phenomona: Osler nodes, Roth, + RF, 5. + blood culture 6. + echo (worsening of existing murmur)
37
Empiric therapy for endocarditis for someone with: 1. Acute (native valve) 2. Subacute (native valve) 3. Prosthetic valve 4. Fungal
1. Acute (native valve)- Nafcillin + Gentamicin or vanco + Gentamicin (if MRSA suspected) 2. Subacute (native valve)- PCN or Ampicillin + Gentamicin (Vanco if IVDU) 3. Prosthetic valve- Vanco+ Gentamicin + Rifampin (for s. aureus) 4. Fungal- Amphotericin B * DURATION= 4-6 weeks * Gentamicin= gram neg coverage * PCN and Vanco= gram pos. coverage
38
When is endocarditis prophylaxis indicated and what is it?
1. Prosthetic (artificial) heart valve 2. Hear repair using prosthetic material (nots stents) 3. Hx of endocarditis 4. Congenital Heart disease 5. Cardiac valvulopathy in transplanted heart Use: Amox. 2g 30-60min prior or Clindamycin 600mg if allergy
39
- LE pain/discomfort brought on by exercise or walking and relieved w/ rest - Claudication (buttock, thigh, calf) - Impotence - Decreased femoral pulses - atrophic skin changes, dusky red w/ dependency, lateral malleolar ulcers
PAD DX: 1. ABI: +PAD if ABI <0.90 2. Arteriography (gold standard) 3. hand held doppler- used in ED TX: 1. Platelet inhibitor: Cilostazol mainstay of tx*, ASA, plavix 2. Revascularization: PTA ,bypass, endarterectomy 3. Supportive: exercise
40
Where do AAA typically occur and what measurement is considered aneurismal
infrarenally >3.0cm (>5cm = increased risk of rupture)
41
How do you dx AAA
DX: 1. Abdominal US- best initial test for suspected AAA and for monitoring progression in size 2. CT: best for thoracic aneurysms and for further eval of known AAA 3. Angiography- gold standard
42
How do you treat AAAs
1. 5.5cm or greater OR >0.5cm expansion in 6 months= immediate surgical repair even if asymptomatic 2. >4.5cm= vascular surgeon referal 3. 4-4.5cm= monitor by US q6months 4. 3-4cm= monitor by US q1yr *BB reduces shearing forces and risk of rupture
43
What is an aortic dissection and where is it is the worst place to have?
tear in the innermost layer of aorta (intima) | 65% ascending= highest mortality
44
What are risk factors of aortic dissections
1. HTN 2. age 50-60 (M>F) 3. vasculitits 4. collagen disorders
45
Tx of aortic dissections
Surgical if: (A needs surgery ASAP) 1. Acute proximal (Type A or I II) 2. acute distal (type III) w/ complications Medical management w/ esmolol., labetolol (SBP 100-120 and pulse <60) if: 1. descending if no complications (B or III) * could use sodium nitroprusside added if needed
46
- superficial migratory thrombophlebitis - claudication/ distal extremity ischemia - raynauds phenomenon - STRONG ASSOCIATION W/ SMOKING
Thromboangiitis obliterans (Buerger's disease) DX: aortography- occlusive lesions of small and medium vessels- corkscrew collaterals (Gold standard) 2. abnormal Allen test (occlude radial and/or ulnar arteries) TX: 1. STOP smoking (only definitive management of Buerugers) 2. Wound care 3. CCB
47
What is virchows triad
increased risk of PVD ( hypercoagulablility) 1. Intimal damage 2. stasis 3. hypercoagulability (ex. FVL)
48
what is the hypercoagulability work up?
1. Factor V Leiden (MC) 2. Prothrombin gene mutation 3. Protein C and S def. 4. Antiphospholipid Ab 5. Lupus 6. Factor VII def.
49
How do you dx and tx DVT
DX: Venous duplex (1st line) 2. d-dimer +/- Wells criteria 3. Venography (gold standard) TX: 1. Heparin (unfractionated heparin or LMWH (lovenox) --> Warfarin (overlap w/ heparin for at least 5 days)
50
what is the MOA, duration of action, antidote, and SE of LMWH
- MOA: potentiates antithrombin III - Duration of action: 12 hrs - Antidote: protamine sulfate - SE/CI: renal failure, thrombocytopenia
51
what is the MOA, duration of action, antidote, and SE of unfractionated heparin
- MOA: potentiates antithrombin III, inhibits thrombin and other coag. factors - Duration of action: 1hr - Antidote: protamine sulfate - SE: thrombocytopenia
52
- leg pain worse w/ prolonged standing/sitting, foot dependency - improves w/ elevation and walking - brownish hyperpigmentation - medial malleolus ulcer - pitting edema, stasis dermatitis
Chronic venous insufficiency
53
How to measure orthostatic hypotension
2-5 min of quiet standing after a 5 minute period of being supine there is either: 1. fall is SBP 20mmHg or more AND/OR 2. fall in DBP 10mmHg or more * HR usually increases on standing- absence of increase is associated with autonomic dysfunction - increase in HR >15 may be due to hypovolemia
54
Describe the 4 types of shock
1. Hypovolemic: loss of blood or fluid volume (increase PVR and HR to maintain CO) 2. Cardiogenic: primary myocardial dysfunction- reduced CO 3. Obstructive: extrinisic or intrinsic obstruction to circulation (tamponade) 4. distribution: maldistribution of blood flow from essential organs to nonessential organs
55
Management of Shock
``` ABC's Airway Breathing Circulation Delivery of oxygen Endpoint resusication ```
56
- Pale, cool mottled skin - Prolonged capillary refill - Decreased skin turgor, dry mucous membranes - 2/2 hemorrhage, vomiting, diarrhea, severe burns - CO: decreased, PCWP: DECREASED, SVR: Increased
hypovolemic shock
57
- Severe respiratory distress - Cool clammy skin - 2/2 MI, myocarditis, valvular disease, cardiomyopathy, arrhythmia - -CO: decreased, PCWP: INCREASED, SVR: Increased
Cardiogenic shock
58
- Severe respiratory distress - Cool clammy skin - 2/2 tamponade, PE, tension pneumo, aortic dissection - CO: decreased, PCWP: INCREASED, SVR: Increased
Obstructive shock
59
Describe the 4 types of Distributive shock
1. Septic- severe host immune response- vasodilate 2. Neurogenic- sympathetic blockade- unopposed vagal tone on vessels--> vasodilate 3. Anaphylactic- IgE mediated HSN rxn w/ histamine release- vasodilation and cap. permeability 4. Hypoadrenal- decreased corticosteroid and mineralocorticoid activity
60
- Increased CO*** - Warm, flushed extremities and skin - Brisk cap refill - Bounding pulses, WIDE pulse pressure
Septic shock (only shock w/ increased CO)
61
How do you treat hypovolemic shock
1. ABCDEs 2. volume resuscitation: crystalloids (NS or lactated ringer 3-4L) 3. control hemorrhage source and prevent hypothermia
62
How do you treat cardiogenic shock
1. O2, isotonic fluids (avoid aggressive IV fluid tx- use smaller amounts of fluids*)-- ONLY shock where large amounts of fluids are not given 2. Inotropic support: dobutamine, epi 3. tx underlying cause
63
How do you treat obstructive shock
1. O2, isotonic fluids, inotropic support: dobutamine, epi, | 2. tx underlying cause
64
How do you tx septic shock
1. broad spectrum IV abx 2. IV fluid resuscitation: NS or LR 3. Vasopressors
65
How do you tx anaphylactic shock
1. Epi 2. Airway managment 3. Antihistamine (diphenhydramine or Ranitidine) 4. IV fluids 5. Observe patient for 4-6hrs
66
how do you tx adrenal insufficiency (Addisonian crisis) shock?
Hydrocortisone 100mg IV
67
What type of antibiotic interacts with statins and what does it increase the patients risk of?
statin + macrolides (clarithromycin) *prolonged QT interval, myopathy and rhabdomyolysis