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MCC Part 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Autoregulation pathway of BP re: increased CO?

A

increased CO -> increased MAP - detected by aortic and carotid baroreceptors ->vasodilation -> reduced TPR = reduced CO

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2
Q

Pathway of pressure natriuresis (increased MAP)?

A

increased MAP -> increased renal perfusion = increased GFR = reduced aldosterone -> increase Na and H2O excretion (natriuresis)

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3
Q

Equation for BP

A

BP = CO x SVR

CO = HR X SV
MAP = dBP + 1/3 pulse pressure
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4
Q

RAAS pathway

A 
JG cells produce renin
renin = angiotensinogen -> angiotensin I
ACE = angiotensin I -> angiotensin II
ang II = aldosterone production, systemic vasoconstriction, vasoconstriction of afferent and efferent arterioles 
aldosterone = Na reabsorption
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5
Q

Causes of primary HTN?

A
  • lifestyle
  • medication
  • family history/ genetics
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6
Q

Causes of secondary HTN?

A
  • endocrine (aldosterone, glucocorticoid, hyperthyroid, hyperparathyroid, chatecholamines)
  • CKD (including PCKD)
  • vascular (coarctation of aorta, renal artery stenosis)
  • OSA
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7
Q

Rx than can induce HTN?

A
  • NSAIDs
  • corticosteroids
  • exogenous androgens/ estrogens
  • liquorice root (aldosterone-like), antidepressants
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8
Q

Will BP cuff that is too small over or under estimate BP?

A
  • small = overestimate BP
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9
Q

Exam for end organ damage?

A
  • fundoscopy (copper wiring, cotton wool spots, AV nicking, papilledema)
  • signs LVH (loud S2, S4, sustained apex beat)
  • signs CHF (elevated JVP, S3, lung crackles, ascites, leg edema)
  • peripheral vascular exam (pulsatile abdo mass, no peripheral pulses)
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10
Q

Lab investigations with HTN?

A
  • UA and Cr (CKD)
  • electrolytes (hypoK with hyperaldosteronism)
  • fasting glucose and lipid profile (CV risk)
  • 12-lead ECG (LVH, prior MI)
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11
Q

Workup secondary causes HTN?

A

endocrine
- TSH, PTH, 24h urine metanephrines, aldosterone, renin, aldosterone/renin ratio, 24h urine free cortisol, dexamethasone suppression test

ckd
- serum Cr and estimated GFR

vascular

  • trans thoracic echo, CT or MR angiography (coarctation)
  • captopril renal scan, abdo US with doppler, MRI (renal artery stenosis)

osa
- sleep study

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12
Q

Dx HTN

A
  • BP >140/90 on 3 occasions (or if end organ damage, kidney disease, DM)
  • at least 1 home, ambulatory or 24h BP monitoring recommended
    OR single measurement >180/90

office >140/90
ambulatory/home >135/85
24h average >130/80

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13
Q

Classify HTN

A

normal <120/80

preHTN 120-139/ 80-89

stage 1 HTN 140-159/ 90-99

stage 2 HTN >160//>100

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14
Q

Target organ damage from HTN

A
  • cerebrovascular disease
  • hypertensive retinopathy
  • HF
  • CAD
  • CKD
  • peripheral arterial disease
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15
Q

Tx HTN

A

Lifestyle

  • Na <1.8g/d
  • weight loss
  • EtOH reduction
  • exercise
  • diet

target <140/90
DM target <130/80

first line rx

  • thiazide diuretics
  • ACEi/ARBs (non-black pt)
  • long acting CCB
  • b-blocker (<60yr)
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16
Q

AntiHTN for DM?

A

ACEI or ARB

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17
Q

AntiHTN for asthma?

A

CCB (nondihydropyridine)

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18
Q

AntiHTN for prior MI?

A

ACEI, b-blocker

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19
Q

AntiHTN for angina?

A

b-blocker, long acting CCB

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20
Q

AntiHTN for CKD?

A

ACEI, ARB (caution)

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21
Q

AntiHTN for CHF?

A

ACEI, b-blocker, aldosterone antagonist

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22
Q

AntiHTN for migraines?

A

b-blocker, long acting CCB

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23
Q

AntiHTN for raynaud, coronary spasm?

A

long acting CCB

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24
Q

Which anti-HTN causes dry cough? Why?

A
  • ACEI -> bradykinin related
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25
Q

Define hypertensive urgency

A
  • severely elevated BP (>180/120) without progressive target organ dysfunction
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26
Q

Define hypertensive emergency

A
  • severely elevated BP PLUS evidence of impending or progressive target organ dysfunction
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27
Q

How to tissues maintain perfusion relatively constant with increased BP?

A
  • arterial and arteriolar vasoconstriction -> prevents pressure being transferred to smaller, more distal vessels
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28
Q

How do arteries and capillaries becomes damaged with severe HTN?

A
  • autoregulation fails = increased arteriole and capillary pressure = damage vascular wall, disruption of endothelium (breakthrough vasodilation)
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29
Q

How does RAS exacerbate HTN?

A
  • renin-angiotensin increases BP -> natriuresis and renal vascular injury -> increased renin which increases angiotensin II = HTN exacerbated
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30
Q

Mechanism HTN medication causes ischemic damage?

A
  • rx can cause BP autoregulation curve to shift and respond at lower BP = ischemic damage

Q = P/R
- if reduce P with rx but R same = reduce flow = ischemia

autoregulaiton -> artery and arteriole vasodilation -> tissue perfusion maintained during rx HTN

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31
Q

Cause of severe essential HTN?

A
  • often medication noncomplicance or acute drug withdrawal
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32
Q

Case of secondary HTN emergency/urgency?

A
  • acute renal failure
  • renovascular HTN (CHF + HTN)
  • thyrotoxicosis
  • medication-related (cocaine, MAOI + tyramine food)
  • advanced CKD with volume overload
  • pheochromocytoma
  • pregnancy
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33
Q

What is likely dx with arm-arm different >20/10?

A
  • aortic dissection
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34
Q

Investigations with HTN emergency/ urgency?

A
  • CBC, lytes, urea, Cr, UA, troponin, LFTs
  • CXR, ECG
  • CT head if six HTN encephalopathy, stroke
  • CT angio or TEE if sx aortic dissection

secondary causes
- toxicology, TSH, urine for metanephrines, b-hCG

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35
Q

Urgently drop BP in hypertensive urgency and emergency?

A

No - no evidence for aggressive drop with urgency

Drop aggressively and admit to ICU if emergency

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36
Q

How much do you want to reduce BP in HTN emergency?

A
  • 25% in first hour
  • gradually after first hour
    risk organ hypoperfusino with sudden fall in BP

target 160/100 in initial 6-24h then add PO

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37
Q

Rx HTN emergency?

A
  • labetalol first line (except CHF)
  • nitroprusside (caution CKD and increased ICP)
  • nitroglycerine (use in coronary schema and HF)
  • hydralazine (use for eclampsia)
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38
Q

Define chronic HTN in pregnancy

A
  • HTN prior to pregnancy
  • before 20wk GA
  • persists >12 wk postpartum
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39
Q

Define gestational HTN

A
  • new onset HTN after 20wk GA

- without proteinuria

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40
Q

Define preeclampsia

A
  • new HTN

- proteinuria (>300mg/24h) after 20wk GA

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41
Q

Define chronic HTN with superimposed preeclampsia

A
  • new (or 2-3x increased) proteinuria, thrombocytopenia, elevated AST/ALT after 20wk GA
  • in women with preexisting HTN before 20wk GA
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42
Q

Define transient HTN in pregnancy

A
  • postpartum return to normal BP by 12wk postpartum

- increased risk of HTN in future pregnancies

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43
Q

What fails to invade the myometrial portion of the uterus in preeclampsia?

A
  • cytotrophoblast
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44
Q

Where is earliest pathological change with preeclampsia?

A

uteroplacental circuation

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45
Q

What happens to vessels in placenta with preeclampsia?

A
  • vessels narrow (tortuous vascular channels don’t develop) causing placental hypo perfusion
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46
Q

What happens in ischemic placenta?

A
  • release of pro inflammatory cytokines and mediators of oxidative stress -> increase capillary permeability and activate endothelial cells and coagulation system
  • > preeclampsia
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47
Q

Sx preeclampsia?

A
  • visual change
  • new headache
  • epigastric or RUQ pain
  • rapidly progressive peripheral edema
  • rapid weight gain
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48
Q

What is indicated by rollover test (>15mmHg rise in dBP from left lateral decubitus to supine)?

A

Preeclampsia

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49
Q

Lab testing with pregnancy HTN?

A
  • urinalysis: 24h urine protein, urine dip (>300 = preeclampsia)
  • CBC + peripheral blood smear, Hgb, LDH, hepatoglobin (anemia, with schistocytes, increased LDH and low hepatoglobin = hemolysis from severe preeclampsia)
  • platelet (low = severe preeclampsia)
  • Cr, uric acid (elevated = severe preeclampsia)
  • AST, ALT (elevated = severe preeclampsia)
  • PT, PTT, fibrinogen (elevated PT, PTT, and low fibrinogen = severe preeclampsia resulting in DIC)
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50
Q

How do you assess fetus with maternal HTN?

A
  • NST or BPP
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51
Q

Management HTN pregnancy?

A

chronic - anti-HTN

gestational - antiHTN (BP >160/110); fetal well being assessed; deliver if term

preeclampsia- delivery (definitive tx)

  • fetal well-being and lung maturity: betamethasone 12mg IM x2 q12h if <34wk GA
  • anticonvulsant - during labor, planned delivery or corticosteroid administration -> Magnesium sulphate 4-6g IV over 20min then 2g/h infusion
  • antiHTN - often avoided, may alter uteroplacental blood flow
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52
Q

Safe anti-HTN in pregnancy

A
  • labetalol (or other beta-blocker except atenolol)
  • methyldopa (mild, s/e common)

CI

  • ACEI/ ARBS
  • aldosterone antagonist
  • > fetal renal abnormalities and death
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53
Q

What is the inability of the heart to supply the circulatory needs of the body or the ability to do so only at higher than normal filing pressures?

A

heart failure

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54
Q

Systolic vs. diastolic HF?

A
  • low LV ejection fraction in systolic HF
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55
Q

Low output vs. high output HF?

A
  • low BP, organ hypo perfusion in low output
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56
Q

Congestive vs. dry HF?

A
  • pulmonary edema, orthopnea, ascites, leg deem in congestive
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57
Q

Left vs. right sided HF

A
  • pulmonary edema in left sided

- ascites, leg edema in right sided

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58
Q

Acute decompensated vs. chronic HF

A
  • rapid (<2wk) sx progression in acute
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59
Q

Causes of mortality with HF?

A
  • arrhythmia 40%
  • worsening HF 40%
  • other 20%
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60
Q

Is ischemic or HTN most common cause of HF?

A
  • ischemic (prior MI or severe CAD) is most common cause

- HTN is second most common cause

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61
Q

Sx HF

A
  • SOB
  • fatigue
  • orthopnea
  • PND
  • peripheral edema (leg edema, ascites)
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62
Q

Investigation HF

A
  • CBC, lytes, Cr, transferrin saturation (serum iron/ TIBC), ferritin, TSH
  • ECG
  • CXR
  • transthroacic echocardiogram
  • B-type natriuretic peptide (BNP) or NT-proBNP
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63
Q

Tx wet and warm HF

A
  • diurectics

- vasodilators (IV nitroglycerine or nitropatch)

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64
Q

Tx dry and warm HF (well compensated)

A
  • optimize chronic HF therapies (incl BB)
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65
Q

Tx dry and cold HF (over diuresis)

A
  • reduce/hold diuretic

- carful volume replacement

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66
Q

Tx wet and cold HF (advanced)

A
  • inotropes
    +/- invasive hemodynamic monitoring (PA catheter)
  • philosophy of care of transplant assessment
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67
Q

Do increased perfusion and increased congestion result in wet and warm HF or wet and cold HF?

A

wet and warm

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68
Q

Increased perfusion and reduced congestion = _ HF?

A

dry and warm

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69
Q

Increased congestion and reduced perfusion = _ HF?

A

wet and cold

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70
Q

Tx chronic HF?

A
  • ACEI if LVEF <40% (ARB if ACEI intolerant or hydralazine/ isosorbide denitrate)
  • beta blocker if LVEF <40%
  • aldosterone antagonist (spironolactone) if NYHA II-IV symptoms, LVEF <35%

life-prolonging devices (LVEF <35% with medical rx)?

  • cardiac resynchronization therapy (prolonged QRS)
  • implantable cardioverter defibrillator

+/- digoxin
treat comorbidities (HTN, lipids, DM, etc)
vaccinate - yearly influenza, q5yr S. pneumonia

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71
Q

Classification of:

  • enalapril
  • lisinopril
  • perindopril
  • ramipril
A

ACEI

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72
Q

Classification of:

  • bisoprolol
  • carvedilol
  • metoprolol
A

B-blocker

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73
Q

Classification of:

  • spironolactone
  • eplerenone
A

Aldosterone antagonist

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74
Q

Classification of:

  • candesartan
  • valsartan
A

ARB

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75
Q

Classification of:

- hydralazine

A

Vasodilator

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76
Q

Classification of:

  • verapamil
  • diltiazam
A

Non-DHP CCB

cardiac effect

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77
Q

Classification of:

  • nifedipine
  • amlodipine
A

DHP CCB

vascular > cardiac effect

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78
Q

NYHA functional classification of HF

A
  1. limitation of physical activity
  2. degree of comfort at rest
  3. sx with ordinary physical activity
    Class I-IV
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79
Q

What is a physiologic state of overwhelming reduction in systemic tissue perfusion leading to a change in tissue O2? What can result?

A

Hypotension
- reversible at early stage
Cellular O2 deprivation -> cellular hypoxia
- ion pump dysfunction across cell membrane
- intracellular edema
- intracellular contents leak into extracellular space
- intracellular pH derangement

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80
Q

Causal conditions of hypotension?

A

Distributive (reduced SVR)
- sepsis, anaphylaxis, other

Reduced CO (increased SVR)

  • hypovolemia
  • cardiac dysfunction -> intrinsic vs. extrinsic (obstructive)
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81
Q

What is Beck’s triad?

A
  • muffled heart sounds
  • jugular venous distention
  • hypotension
  • > cardiac tamponade (+ pulses paradoxus)
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82
Q

5 common features of shock?

A
  • hypotension (sBP <90 or drop >40 in sBP)
  • cool, clammy skin (except distributive shock)
  • oliguria (<0.5mL/kg/h)
  • change in mental status (agitation -> confusion -> obtundation)
  • metabolic acidosis

other: tachycardia, orthostatic hypotension, poor skin turgor, reduced sweat, dry mucous membranes

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83
Q

Hypotension workup

A
  • CBC, lytes, LFT, Cr clearance, amylase/lipase, fibrinogen degradation product, lactate, cardiac enzymes, ABG, toxicology, CXR, ECHO, EKG, troponin, pro-BNP, UA
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84
Q

Acute tx hypotension/shock

A

ABCs, airway, 100% O2, two large bore IVs

  • Trandeleberg position to increase venous return, cerebral profusion
  • automatic BP monitor, pulse O2, cardiac monitoring
  • dx cause of shock
  • ICU admission if IV vasopressors needed or refractory hypoTN
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85
Q

Dx

  • dry conjunctiva and mucous membrane
  • reduced JVP
  • tachycardia
  • tachypnea, Kussmaul breathing
  • abdo tender, distended, no bowel sounds, pulsatile masses
  • cold clammy skin
  • agitation, confusion, delirium, obtunded, coma
  • bright red blood per rectum, melena, occult blood in stool

Workup? Causes?

A

Hypovolemic shock

CBC, lytes, BUN, Cr, amylase, lipase, lactate
AXR, UA

Hemorrhage, third space loss, GI fluid loss

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86
Q

Dx

  • scleral icterus
  • increased JVP, pulsus parvus et tardus (AS)
  • arrhythmia, tachy/bradycardia, S3 gallop, ventricular heave, murmur, rub, distant heart sounds, pulsus paradoxus
  • crackles (CHF), no breath sounds, rub
  • distended abdomen (hepatic congestion)
  • agitation, confusion, delirium, obtundation, coma
  • hemorrhoids

Workup? Causes?

A

Cardiogenic shock

CBC, lytes, BUN, Cr, D-dimer, cardiac enzymes, ABG, toxicology screen
CXR, EKG, PCWP in ICU

Ischemic/dilated cardiomyopathy, arrhythmia, mechanical (valvular - AS), PE, TP, tamponade

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87
Q

Dx

  • flushy/ swollen face, angioedema
  • reduced JVP, delayed carotid, meningeal sign
  • tachycardia
  • shallow breaths
  • abdo tenderness, distension, rebound tenderness, absent bowel sounds, pulsatile masses
  • skin warm, hyperaemic, rashes, petechia, urticarial, cellulitis
  • agitation, confusion, delirium, obtundation, coma, spinal cord injury
  • reduced anal tone

Workup? Causes?

A

Distributive shock

CBC with differential, lytes, lactate, toxicology screen, amylase, lipase, blood culture
spinal X-ray, EKG, ECHO
cardiac enzymes, TSH, procalcitonin

Sepsis, anaphylaxis, neurogenic, spinal shock

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88
Q

Variable to assess preload?

A

PCWP

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89
Q

Variable to assess pump function?

A

CO

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90
Q

Variable to assess after load?

A

SVR

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91
Q

Variable to assess tissue perfusion?

A

mixed venous O2 saturation

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92
Q

Targets for tx hypovolemic shock (non-hemorrhagic and hemorrhagic)?

A 
nonhemorrhagic 
- bolus 1-2L crystalloid (NS, RL)
sBP >90
MAP >60
urine output >0.5mL/kg/h

hemorrhagic

  • transfuse + crystalloid
  • hemoglobin >80-90 (Hat 30-35%)
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93
Q

Acidosis, hypothermia and hypocalcemia can happen with what treatment?

A
  • massive transfusion
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94
Q

Septic shock management

A
  • bolus 2-6L crystalloid/colloid to target CVP 8-12mmHg
  • vasoactive agents for sBP>90 and MAP >65
  • organ perfusion: RBC transfusion and inotropes pro
  • empiric broad spectrum abx ASAP (pip-taco, imipenem)
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95
Q

Management neurogenic shock?

A
  • methylprednisolone 30mg/kg over 15min then infusion 5.4 mg/kg/h x24h
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96
Q

Management carcinogenic shock?

A
  • underlying cause
  • optimize volume status
  • add/substitute inotropes for hypo perfusion
  • treat arrhythmias
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97
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

NE

A

vasopressor
CO +
SVR +++
HR +

alpha adrenergic agonist, mild B1 adrenergic agonist

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98
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

Dopamine

A

vasopressor
CO ++
SVR +++ (low dose can decrease)
HR +++

dopamine agonist and B1 agonist at intermediate-high doses

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99
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

Phenylephrine

A

vasopressor
CO -
SVR +++
HR -

pure alpha adrenergic agonist

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100
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

Vasopressin

A

vasopressor
CO -
SVR ++
HR -

ADH analog - vasoconstriction

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101
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

Epinephrine

A

vasopressor
CO +++
SVR +++
HR +++

alpha and beta adrenergic agonist

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102
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

dobutamine

A

inotrope
CO +++
SVR -
HR ++

strong beta1 adrenergic agonist

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103
Q

Vasopressor or inotrope? Act on CO/ SVR/ HR?

milrinone

A

inotrope
CO +++
SVR decreased
HR +

phosphodiesterase (PD3) inhibitor with positive inotropic and vasodilatory action

104
Q

Define anaphylaxis

A

IgE mediated, immediate hypersensitive allergic reaction to protein substances

105
Q

Ag exposure cascade

A
  • mast cell -> stimulation by cell-bound IgE cross linking with Ag -> degranulation
  • complement proteins -> anaphylatoxins C3a, C4a, C5a -> degranulation
  • arachidonic acid -> precursor to PGs, prostacyclin, thromboxjnes and LTs -> degranulation

degranulation = released mediators from mast cells and basophils promote synthesis of other active substances

106
Q

Are these mediators initial or late?

- histamine, tryplase, PGs, LTs, platelet activating factor

A

initial minutes

107
Q

Are these mediators initial or late?

- cytokines (IL4, IL13, TNF)

A

hours later - released by same cells as early mediators

108
Q

What is an anaphylactoid reaction?

A
  • non IgE mediated
  • direct release of mediators from mast cells
  • immune complex/complement mediated
  • arachidonic acid metabolism modulator
  • multiple/ unknown mechanisms
109
Q

Management anaphylactic reaction?

A
  • ABCs
  • IV access, O2, cardiac monitoring, pulse O2
  • intubate if stridor, altered mental status, resp arrest
  • hypotension - 1-2L bolus +/- vasopressors
  • epinephrine 0.3-0.5mg IM 5min
  • antihistamine (diphenhydramine) and IV corticosteroid (methylprednisolone)
    +/- H2 receptor blocker (ranitidine)
  • mild bronchospasm = nebulizer salbutamol (2.5-5mg)

observe 8hr -> biphasic reaction

110
Q

What is test to sx anaphylaxis?

A 
Clinical diagnosis!
Based on 1/3 criteria
- acute onset
- 2+ sx after exposure to Ag
- reduced BP
111
Q

Pathophys of angina?

A

MOD exceeds myocardial O2 supply -> stimulation of chemosensitive and mechanoreceptive receptors of unmyelinated cardiac nerve cells -> angina

112
Q

WHO MI criteria?

A

2 out of 3:

  • chest pain
  • ECG-ST changes, T wave inversions
  • increased cardiac enzymes
113
Q

What causes downsloping or horizontal ST depression?

A

ischemia

114
Q

What causes ST elevation or T wave inversion?

A

infarction

115
Q

Likely dx?

  • substernal pressure (+/- radiation to neck/ jaw/ shoulders/ L arm)
  • with exertion/ stress
  • relieved with rest (5-10min) or nitroglycerin (immediate)
A

typical angina

2 out of 3 sx = atypical angina
0 or 1 out of 3 = non cardiac pain

116
Q

What can you hear on cardiac exam with angina?

A

S4 with chest pain due to impaired myocardial relaxation from schema

117
Q

Angina workup

A
  • resting ECG (may see ST)
  • depression (ischemia) or Q waves
  • cardiac enzymes - negative
  • exercise stress test
118
Q

Positive exercise stress test?

A

> 1mm ST depression with exercise (85% age-predicted maximal [220-age]HR) = +

119
Q

What are causes of increased MOD (e.g. causing chest pain)?

A
  • increased HR
  • increased myocardial contractility
  • increased myocardial work -> increased MOD
  • increased after load + increased preload -> increased wall tension
120
Q

Dx?

- new or rapidly worsening pattern of typical angina that severely limits usual activities or occurs at rest

A

unstable angina

121
Q

Dx?
- sudden, severe chest pain pressure lasting >30min and associated with diaphoresis, nausea, malaise, sense of impending doom

A

NSTEMI/STEMI

122
Q

Why can you hear new systolic murmur with ACS?

A
  • in MI = mitral regurgitation due to papillary muscle dysfunction
123
Q

ACS workup

A
  • ECG

- cardiac enzymes

124
Q

Dx?

  • very severe, sudden onset sharp/tearing pain in chest and/ or back (mid scapular)
  • HTN or hypotension
  • asymmetric BP/ pulses in upper extremities (>20 mmHg difference)
A

aortic dissection

hypotension from tamponade or AI in ascending aortic dissection

125
Q

Workup aortic dissection

A

CXR - widened mediastinum, pleural effusion
Contrast CT - identifies true lumen from false lumen (no contrast in false lumen)
TEE - assess pericardium, AI and safe in renal failure (no contrast)
MRI - gold standard, time consuming

126
Q

Dx

  • sudden, pleuritic pain and shortness of breath
  • often unilateral
  • unilateral reduced breath sounds on exam with hyper-resonance on percussion

Imaging?

A

tension pneumothorax

CXR - mediastinal shift, distinct pleural lining -> confirm with expiratory views

127
Q 
Dx
- sudden, pleuritic pain with severe SOB
\+/- syncope
- tachypnea, tachycardia
- may hear loud S2, feel parasternal heave or new RUSB systolic murmur
A

PE

  • S2= pulmonic component
  • parasternal heave = RV pressure overload
  • RUSB systolic murmur = pulmonary insufficiency from pulmonary HTN = Graham Steel murmur
128
Q

PE workup?

A
  • d-dimer: high false positive rate
  • ECG: sinus tachycardia +/- t wave inversion in V1-V3 from RV strain (S1, Q3, T3) pattern
  • ABG: hypoxemia with A-a gradient
  • Imaging: V/Q scan, contact CT chest, angiogram is confirmatory
129
Q

Define aortic dissection

A

tear in aortic intima = blood accumulation in false lumen

130
Q

Causes of pericarditis

A
  • infectious
  • post-MI (acute vs. subacute -> subacute is autoimmune aka Dressler syndrome)
  • uremic
  • CT disease
131
Q

Life threatening causes of chest pain?

A
  • angina
  • ACS
  • aortic dissection
  • tension pneumo
  • PE
132
Q

Management stable angina?

A
  • Nitroglycerine 0.4mg SL q5min x3
  • ASA 81mg
  • high dose statin (Lipitor, Crestor)
  • antianginal medications: b-blocker (1st line), CCBs, long acting nitrates
  • lifestyle
  • stress test
  • high risk = coronary angiography
133
Q

Does PCI improve MI occurrence or death or help with symptom relief of stable angina?

A
  • symptom relief

- does not prevent MI or death in stable angina

134
Q

Treatment offered to pt with prognosis-altering CAD, pt refractory to medication?

A

CABG

135
Q

What is similar in all cases of ACS re: pathophys?

A
  • intra-coronary thrombosis
136
Q

UA vs. NSTEMI vs. STEMI

A

UA

  • sub-total occlusion by intra-coronary thrombus
  • myocardial ischemia but no infarction

NSTEMI

  • subtotal occlusion by intra-coronary thrombus
  • myocardial infarction (non-transmural)

STEMI

  • total occlusion by intra-coronary thrombus
  • large, transmural infarction (if flow not immediately restored)
137
Q

Management ACS

A
  • stabilize and monitor: O2, IV access, cardiac monitoring, ASA 160mg PO, 12lead EKG
  • SL nitroglycerine or IV; morphine for pain
  • serial cardiac enzymes (repeat 6h)
138
Q

Management UA/NSTEMI

A

medical + RF tx

  • ASA 160mg load then 81mg daily
  • anti platelet (clopidogrel) x1yr
  • anticoagulant (LMWH unless GFR <30) x48-72h
  • high dose statin (crestor, lipitor) x life
  • b-blocker (metoprolol, bisoprolol) x1yr or longer
  • ACEI (ramipril, lisinopril, coversly) x1yr or longer
  • revascularize with PCI or CABG
  • invasive - coronary angiography/ echo
  • conservative - stress test/ echo, with coronary angiography if high risk stress test or EF <40%
139
Q

TIMI risk score for UA/NSTEMI

A 
age >65 = 1
>CAD RF = 1
Known CAD = 1
ASA in past 7d = 1
Recent severe angina = 1
troponin + = 1
ST deviation >0.5mm = 1

risk score /7

140
Q

STEMI management

A
  • urgent repercussion with primary PCI or thrombolysis (high risk from MI = PCI; high risk bleeding = PCI; time delay >60-90min to cath lab favours thrombolysis)
  • dual anti platelet (ASA + clopidogrel) and anticoagulant (LMWH, heparin)
  • ongoing cardiac monitoring in CCU for arrhythmia, recurrent CP
  • coronary angiography in next 6-24h if thrombolysis; if unsuccessful then emergency rescue PCI
  • optimize medical therapy and RFs
141
Q

Aortic dissection types

A

De Bakey

  • type I - proximal dissection
  • type II - proximal dissection (isolated)
  • type III - distal dissection

Stanford

  • type A = proximal dissection
  • type B = distal dissection

proximal dissection - surgical root repalcement
distal dissection = medical management

142
Q

Management aortic dissection

A
  • medical therapy, continuous BP monitoring in ICU
  • IV anti-HTN
  • HR aggressively controlled with b-blockers to reduce shear stress on tidal tear
  • pain control with morphine
143
Q

Dx

  • pulses paradoxus
  • tachycardia
  • hypotension
  • muffled heart sounds
  • bottle shaped heart on CXR
A

pericardial tamponade

144
Q

Management Pericarditis

A

r/o pericardial tamponade and secondary causes

  • echocardiogram to assess size of effusion
  • viral/idiopathic: NSAIDs, colchicine, corticosteroids (if refractory)
  • large effusion/tamponade: pericardiocentesis
  • recurrent large effusion/ tamponade: pericardial window
145
Q

What is most common rhythm in sudden cardiac death?

A

VF

146
Q

Management of cardiac arrest (in hospital)

A
  • responsiveness/ confirm lack of pulse
  • call for help
  • BLS
  • check heart rhythm, ensure IV access
  • ACLS guidelines
147
Q

Management asystole/PEA

A
  • CPR
  • epinephrine 1mg IV q3-5min

5Hs + Ts (reversible causes)

  • hypoxia
  • hypo/hyperK
  • hypo/hyperglycemia
  • hypovolemia
  • hypothermia
  • H+ (acidosis)
  • tension pneumo
  • tamponade
  • toxins
  • thromboembolism (PE)
  • thrombosis (MI)
148
Q

Management VF/ pulseless VT

A
  • defibrillate 200J (biphasic) WITH CPR
  • epinephrine 1mg IV q3-5min
  • amiodarone 300mg IV if VF/ pulseless VT persists/ returns after 3 shocks
    consider hypoMg and hypoK
149
Q

Management stable severe tachycardia (VT or SVT)

A
  • sx hypoperfusion -> present = cardioversion
  • 12lead ECG if stable
  • adenosine if regular HR
  • irregular HR and a fib likely then give b-blocker, CCB or digoxin
150
Q

Management severe bradycardia

A
  • sx hypo perfusion -> atropine 1mg if present
  • transcutaneous pa king or IV dopamine/ epinephrine (stimulate escape rhythm)
    consider hyperK
151
Q

Is mild therapeutic hypothermia a treatment option post-arrest?

A

Yes

  • if GCS <14 and not rapidly improving, downtime 10min -1h, VT or VF initial rhythm or no CI to cooling
  • > improves long term neurologic outcomes
152
Q

Define syncope

A
  • transient loss of consciousness due to global cerebral hypoperfusion
153
Q

Equation for CO

A

CO = HR x SV

154
Q

What 3 main factors determines SV?

A
  • proload
  • afterload
  • contractility
155
Q

What is ventricular volume at end of diastole?

A

Preload

- increased preload = increased SV

156
Q

What is Starling law of heart?

A
  • energy of contraction of muscle is proportional to initial length of muscle fiber
157
Q

What is resistance to vernacular ejection?

A

Afterload
- caused by resistance to flow in systemic circulation
= SVR

158
Q

What refers to degree of active constriction of vessels (mainly veins) which affects return of blood to the heart?

A

vascular capacitance

159
Q

Increacred intravascular volume increases what?

A

increases vascular capacitance which increases preload

160
Q

Ddx syncope

A

neurocardiogenic (most common, often benign)

  • vasovagal
  • situational
  • carotid sinus hypersensitivity
  • orthostatic

cardiac

  • bradyarrhythmia
  • tachyarrhythmia
  • obstructive

psychogenic
- hyperventilation, panic disorder, malingering

cerebrovascular
- vertebrobasilar insufficiency, subclavian steal syndrome, carotid artery disease, bilateral TIA

pseudosyncope (no cerebral hypo perfusion)

  • seizure
  • hypoglycaemia
  • hypoxia
  • drug intoxication
161
Q

Describe auto regulation of cerebral blood flow

A

increased vasodilators -> reduced cerebral arteriolar resistance -> reestablish cerebral blood flow

constriction of systemic vasculature of skin, splanchnic bed, muscles -> diverts blood to brain

increased sympathetic output -> increased contractility and peripheral resistance -> increased arterial pressure

162
Q

Workup neuro causes syncope?

A
  • heat CT
  • EEG
  • cerebral flow studies (Doppler)
163
Q

Workup sudden dyspnea, risk PE with syncope?

A

V/Q scan
spiral CT
-> anticoagulate

164
Q

Workup cardiac cause of syncope?

A
  • CXR
  • CCU admission
  • echocardiogram
  • cardiac enzymes (r/o MI)
  • perfusion test
  • functional assessment
    +/- CTA

tx re: etiology

165
Q

Workup unexplained syncope with abnormal EKG, hx of CAD?

A
  • holter monitor
  • loop monitor
  • electrophysiology study
  • tilt table test
  • ECHO
  • consider cardiology consult/EP, psychiatry
166
Q

Standard investigation syncope?

A

ECG
CBC, lytes, urea, glucose/ chemstrip, Cr

  • postural BP
167
Q

Where are central pulses assessed? What are they assessed for?

A
  • carotid and/or femoral arteries

- palpated for amplitude, contour, upstroke

168
Q

Where are peripheral pulses assessed?

A
  • radial, brachial, popliteal, posterior tibialis, dorsalis pedis
169
Q

Ddx peripheral pulse deficit?

A
  • dissection
  • aortic coarctation
  • peripheral vascular disease
170
Q

What is laminar flow re: pulses?

A
  • laminar flow aka streamline flow occurs when a fluid flows in parallel layers, with no disruption between the layers
  • no current perpendicular to the direction of flow
171
Q

Is laminar flow high or low momentum of diffusion? Convection? Pressure and velocity?

A

High momentum of diffusion
Low momentum of convection
Constant pressure and velocity

172
Q

What is flow regime characterized by chaotic, stochastic property changes?

A

Turbulent flow

- includes low momentum diffusion, high momentum convection, and rapid variation of pressure and velocity

173
Q

Types of abnormal pulses?

A
  • small and weak
  • large and bounding
  • Bisferiens pulses
  • pulses alternans
174
Q

Does increase velocity cause laminar or turbulent flow?

A
  • turbulent flow
  • very low speed = blood flow laminar
  • increase in velocity (narrowing blood vessels or increase flow rate) = turbulent flow
175
Q

Ddx unequal or delayed pulses

A
  • obstructive arterial disease (atherosclerosis)
  • aortic disease
  • Takayasu arteritis
176
Q

Ddx rhythm irregular/ too fast/ too slow

A
  • tachycardia
  • bradycardia
  • arrhythmia
177
Q

Dx

  • alternating weak and strong pulses with fixed cycle length
  • present in systolic dysfunction/low EF
A

Pulses alternans

178
Q

Dx

  • biphasic pulse
  • present in: AS plus AI, severe AI, HOCM
A

pulses bisferiens

179
Q

Dx

  • double peak, with weaker second beat
  • present in: low arterial pressure/ PVR, very low EF, post AVR
A

dicrotic pulse

180
Q

Dx

  • slow rising, typically with an ascending notch
  • present in aortic stenosis
A

Anacrotic pulse/ pulsus parvus et tardus

181
Q

Dx

  • rapid pulse then sudden collapse
  • present in aortic insufficiency
A

Corrigan pulse (water hammer/ collapsing)

182
Q

Dx

  • exaggerated inspiratory decrease in arterial pulse amplitude
  • present in cardiac tamponade, asthma, hypovolemic shock
A

Pulsus paradoxus

183
Q

What is ankle-brachial index?

A
  • grading of peripheral vascular disease
    ++ calcified vessels
    1-1.3 normal ABI
    low = peripheral vascular disease
184
Q

What does brachio-femoral delay indicate?

A

coarctation of aorta

185
Q

Define dyslipidemia

A
  • one of more alterations in serum lipids (elevated fasting TC, LDL, TG, apoB, low HDL)
  • increase risk of CVD -> atherosclerosis
186
Q

What elevates LDL levels?

A

increased VLDL or reduced LDL catabolism

187
Q

What does reverse cholesterol transport?

A

HDL

188
Q

What changes occur in atherosclerosis?

A
  • changes in blood vessel wall -> lipid deposition and cell proliferation
    = narrow lumen and thrombus formation
189
Q

High risk (FRS >20%) management and target?

A

Treatment
LDL <2mmol/L or >50% reduction win LDL-C
apoB <0.8g/L

190
Q

Moderate risk (FRS 10-19%) management and target?

A

Treatment if LDL-C <3.5 mmol/L, TC/HDL-C ratio >5, hs-CRP >2mg/L (men >50, women >60)

Target <2mmol/L LDL or >50% reduction LDL-C
apo-B <0.8g/L

191
Q

Low risk (FRS <10%) management and target?

A

Treatment if LDL-C <5mmol/L

Target >50% reduction in LDL-C

192
Q

Who gets a screening fasting lipid profile?

A
  • men >40yr and postmenopausal women (or >50yr)
  • kids with fam hx hypercholesterolemia or chylomicronemia
  • adults with RF: DM, smoker, HTN. BMI >27, family history of premature CAD, signs of hyperlipidemia, evidence of atherosclerosis, CT disease (RA, SLE, psoriasis), HIV on HAART, GFR <60, erectile dysfunction
193
Q

What provides 10yr risk of CAD events based on RF (age, gender, TC, HDL-C, sBP, smoker, DM)?

A

Framingham risk score

194
Q

What is similar to FRS but includes high-sensitivity CRP and family history of parent having MI <60yr?

A

Reynold’s risk score

195
Q

Key points on physical exam for pt with hyperlipidemia?

A
  • tendon xanthomas (high LDL-C)
  • eruptive xanthomas (high TG-C)
  • xanthelasma
  • corneal arcus (ring-like appearance on cornea)
196
Q

Drugs to treat lipid abnormalities?

A

HMG-CoA (simvastatin)

  • reduces LDL
  • inhibits cholesterol synthesis, up regulates LDL receptors
  • s/e myopathy and hepatic dysfunction

Fibrates (gemfibrozil)

  • reduce Tg through VLDL
  • inhibits VLDL production
  • s/e nausea, abdo discomfort, gallstone, myopathy

Niacin

  • reduce LDL through VLDL
  • inhibits VLDL production
  • s/e flushing, hyperglycaemia, pruritus, gout, elevated liver function enzymes

Bile-acid binding resins (cholestyramine)

  • depletes bile acids, up regulates LDL receptors
  • s/e constipation, abdo discomfort, may bind other rx

Inhibitors of intestinal sterol absorption (ezetimibe)

  • reduced LDL by preventing dietary cholesterol absorption
  • s/e reversible impairment in hepatic function
197
Q

Mitral stenosis, prosthetic mitral valve, short PR interval -> causes loud or soft S1 or S2?

A

Loud S1

198
Q

Mitral regurgitation, COPD, long PR interval -> causes loud or soft S1 or S2?

A

Soft S1

199
Q

HTN, aortic sclerosis, prosthetic aortic valve -> causes loud or soft S1 or S2?

A

Loud S2

200
Q

Hypotension, severe aortic stenosis, HF/ low cardiac output -> causes loud or soft S1 or S2?

A

Soft S2

201
Q

What causes split S2 (often heard LUSB)?

A
  • normal (physiologic) due to pulmonary valve closure (p2) being slightly delayed after aortic closure (a2) during inspiration
  • exaggerated:
    delayed P2 with RBBB, PE;
    early A2 with VSD, mitral regurgitation
  • fixed, split S2 with ASD
  • paradoxical split (P2 before A2): LBBB, RV pacemaker
202
Q

Etiologies S3?

A

low pitched sound just after S2 caused by large volume of blood entering ventricle in early diastole

  • dilated cardiomyopathy with volume overload
  • mitral/tricuspid regurgitation
  • occasionally young athlete (hyper dynamic hearts)
203
Q

Etiologies S4?

A

low pitched sound just before S1, caused by late filling into a stuff ventricle

  • left ventricular hypertrophy (from HTN or hypertrophic cardiomyopathy)
  • ischemia
  • aortic stenosis
204
Q

What is a high pitched sound in early systole (after S1) heard in pt with bicuspid aortic (or pulmonic) valve?

A

ejection sound

205
Q

What is high pitched should in early diastole (after S1) heard in pt with rheumatic mitral (or tricuspid) disease?

A

opening sound

206
Q

What is high pitched sound in mid-systole, caused by bowing of a myxomatous mitral valve, heard in pt with mitral valve prolapse?

A

mid-systolic click

207
Q

What is classically a biphasic or triphasic scratching sound with systolic and diastolic components, caused by pericardial inflammation and rubbing between the visceral and parietal pericardium (best heard when pt leaning forward)?

A

Pericardial friction rub

208
Q

What is a sound caused by turbulent blood flow, which could be occurring between chambers of the heart or across narrowed arterial vessels?

A

Murmur

209
Q

Grade a murmur

A

Graded according to intensity (loudness)

Grade I - very faint, heard only when tuned in
Grade II - faint but can be identified after placing stethoscope on chest
Grade III - moderately loud
Grave IV - loud with palpable thrill
Grade V - very loud, with thrill, may be heard with stethoscope partly off chest
Grade VI - very loud, with thrill, heard without stethoscope

210
Q

Are diastolic murmurs often innocent or pathologic?

A

Pathologic

211
Q

What cardiac issues is Marfan associated with?

A

MVP

aortic regurgitation

212
Q

What cardiac issue is Down syndrome associated with?

A

AVSD

213
Q

Where is it best to palpate for systolic heave?

A

Left parasternal area - typically in right ventricular enlargement or pulmonary HTN

214
Q

What and where is the apex beat?

A
  • most inferolateral cardiac impulse palpated on chest
  • should be in 4th intercostal space, in left midclavicular line
    displaced if inferior or lateral to this = left ventricular enlargement (LVH also noted by sustained impulse)
215
Q

What produces S1?

A

mitral valve closes (and tricuspid valve)

216
Q

What produces S2?

A

AV valve closure

217
Q

How do you describe a murmur?

A
  • intensity (loudness /6)
  • timing (re: systolic/diastolic)
  • shape (crescendo, decrescendo, holosystolic, etc)
  • location (aortic, pulmonic, tricuspid, mitral area)
  • radiation (carotids, apex, back)
  • pitch (low = bell, high = diaphragm)
  • quality (harsh, blowing, musical)
  • dynamic maneuver (handgrip, valsalva)
218
Q

Ddx mid systolic murmur

A
  • AS
  • Ao valve sclerosis
  • PS
  • increased semilunar blood flow
  • innocent mid systolic murmur
219
Q

Ddx later systolic murmur

A
  • mitral valve prolapse
  • tricuspid valve prolapse
  • papillary muscle dysfunction
220
Q

Ddx holosystolic murmur

A
  • MR
  • TR
  • VSD
221
Q

Ddx continuous murmur

A

PDA

222
Q

Ddx early diastolic murmur

A
  • AR

- PR

223
Q

Ddx mid diastolic murmur

A
  • MS
  • TS
  • atrial myxoma
224
Q

Ddx late diastolic murmur?

A
  • complete heart block
225
Q

Workup murmur?

A

ECHO (for all new systolic murmurs >=3/6; all diastolic murmurs; all murmurs with other sx cardiac disease)
CXR
ECG
cardiac catheterization
cardiology consult for pathologic murmurs

226
Q

Mitral stenosis

  • etiology
  • sx and physical exam
  • investigations
  • management
A

Rheumatic heart disease, claficiation of leaflets

Sx - malar flush, AF, CHF

  • mid-diastolic rumbling after OS at apex
  • loud P2
  • OS after S2
  • low pitch tapping apex beat, thrill
  • LLD position = increased murmur

Inv

  • ECHO
  • R heart cath - measure pulmonary pressures, PCWP
  • CXR - LA, LV enlargement
  • ECG - P mitral +/- AF

Tx

  • medical - b-blocker and diuretics
  • anticoagulate pt in AF
  • surgical - balloon valvoplasty
227
Q

Mitral regurgitation

  • etiology
  • sx and physical exam
  • investigations
  • management
A
  • myxomatous degeneration
  • ischemic heart disease, infective endocarditis, rheumatic heart disease, dilatation of LV

Sx - CHF (SOB, fatigue, leg deem, pulmonary deem, orthopnea, PND)

  • high pitch holosystolic murmur at apex, radiates to axilla
  • laterally displaced apex beat, parasternal heave
  • handgrip = increases

Inv

  • ECHO - color doppler = back flow from LV to LA
  • ECG - P mitral, LVH +/- AF
  • CXR - LA, LV nelargement
  • Cath - can quantify regurgitation with LV contrast

Tx

  • acute/hypotensive: IABP and surgery
  • normotensive: nitroprusside, ACEI, hyralazine
  • anticoagulation if AF
  • surgery - repair vs. replacement
228
Q

Mitral valve prolapse

  • etiology
  • sx and physical exam
  • investigations
  • management
A
  • myxomatous degeneration (genetic variants of fibrillar, elastin, collagen I and II)
    f: m = 3:1

Sx - usually asx, may lead to MR

  • mid-systolic click
  • late systolic murmur

Inv

  • ECHO - thickened prolapsing valve +/- mitral regurgitation anatomy, regurgitant flow
  • ECG - PACs, PVCs

Tx
- no tx unless mitral regurgitation

229
Q

Aortic stenosis

  • etiology
  • sx and physical exam
  • investigations
  • management
A
  • calcification of aortic valve
  • bicuspid aortic valve, rheumatic heart disease

Sx - angina, CHF, syncope/ SCD

  • mid-systolic, crescendo-decrescendo murmur at LUSB, radiating to carotids
  • weak pulse with slow upstroke (pulsus parvus and tardus)
  • soft S2
  • sustained apical beat

Inv

  • ECHO - measure transoartic gradient
  • Cath - measure pullback gradient across aortic valve
  • ECG: LVH
  • CXR - cardiomegaly

Tx

  • avoid after load reducers (fixed after load from AS) and b-blockers (fixed stroke volume, may depend on HR for CO)
  • surgery - valve replacement (transcatheter valve if poor surgical candidate)
230
Q

Hypertrophic cardiomyopathy

  • etiology
  • sx and physical exam
  • investigations
  • management
A
  • mutation in genes that code for characteristics of heart muscle

sx- angina, CHF, syncope/SCD

  • mid-systolic crescendo-decrescendo murmur at LUSB
  • biphasic pulse
  • increases with standing (from squat)

Inv

  • ECHO - severe global or regional hypertrophy
  • ECG - LVH, Q waves, T wave abnormalities
  • Holter, exercise stress test - risk stratify

Tx

  • medical - b-blocker, no competitive sports
  • anticoagulant - if AF
  • ICD if high risk SCD
  • surgery - septal ablation (EtOH) or myomectomy if refractory sx
231
Q

Aortic insufficiency

  • etiology
  • sx and physical exam
  • investigations
  • management
A
  • aortic root dilatation (Marfan, HTN, idiopathic)
  • bicuspid aortic valve, aortic dissection, syphilis

sx- angina, CHF
- 3 murmurs: high-pitched, blowing decrescendo diastolic murmur at LLSB; mid-systolic murmur at base; Austin Flint - low pitched

Inv

  • ECHO - regurgitant flow from aorta to LV, LV dilated
  • ECG - LAD, LVH
  • Cath - quantity regurgitation with aortic root contrast injection

Tx

  • acute/ hypotensive: inotropes (dobutamine) +/- vasodilators (nitroprusside)
  • chronic: b-blockers (Marfan), vasodilators (hydralazine, nifedipine, ACEI), diuretics +/- digoxin
  • surgery - valve and/or root replacement
232
Q

Define palpitations

A

unpleasant awareness of the heartbeat; rapid, forceful or irregular

233
Q

What is normal SA pacemaker function and impulse propagation?

A
  • spontaneous depol of SA node -> atrial depol (P wave) -> impulse propagates slowing through AV node with normal delay in reaching His bundle (PR segment) -> impulse travels rapidly vis Purkinje fibres of bundle branches, reaching ventricular myocardium
234
Q

Mechanism of arrhythmia?

A
  • reentry (perpetual loop/ short circuit is formed, often due to additional conduction pathway)
  • automaticity (focus other than SA node)
  • triggered activity/ after depolarizations (oscillations in membrane voltage after preceding impulse, which can trigger depol)
235
Q

Ddx palpitations

A

Cardiac

  • arrhythmia - SVT, PACs, PVCs
  • structural heart disease

Psych
- anxiety, panic, stress

Endocrine
- hyperthyroidism, hypoglycaemia, pheochromocytoma

Medications
- caffeine, nicotine, sympathomimetics

High output state
- anemia, pregnancy, fever, exercise, Paget disease

236
Q

How does parasympathetic stimulation reduce pacemaker current to reduce HR?

A

via vagus nerve

237
Q

How does sympathetic stimulation increase SA node automaticity and increase rate of pacemaker depol to increase HR?

A

b1 adrenergic receptor stimulation

238
Q

Investigations for palpitations?

A

Vitals
Cardiac exam
ECG - rhythm strips and 12 lead
Labs - CBC, lytes, TSH (r/o anemia, hypo/hyperK, hyperthyroidism)
+/- trans thoracic echo to r/o structural heart disease
- ambulatory monitoring if dx unclear to capture event

239
Q

Dx, acute/long-term rx?

Unstable arrhythmia

A

VT, VF, rarely AF/SVT

acute
- defibrillation or cardioversion

long-term
- AICD for unstable VT or VF

240
Q

Acute/long-term rx?

VT (stable), SVT

A

12-lead ECG then cardioversion

long-term
- cardiologist tx - meds, RF ablation, ICD

241
Q

Acute/long-term rx?

- sinus tachycardia

A

treat underlying cause

long-term
- n/a

242
Q

Acute/long-term rx?

ectopic atrial tachycardia

A

b-blocker or CCB

long-term

  • b-blocker or CCB
  • RF ablation if meds fail
243
Q

Acute/long-term rx?

PSVT (AVNRT or AVRT)

A
  • vagal maneuvers, adenosine

long-term

  • b-blocker, CCB if no accessory pathway (delta wave)
  • RF ablation
244
Q

Acute/long-term rx?

atrial fibrillation

A

b-blocker, CCB, digoxin
- rarely cardio version if unstable

long-term

  • anticoagulation for most
  • rate control: b-blockers, CCB, digoxin
  • rhythm control: antiarrhythmics +/- RF ablation
245
Q

Acute/long-term rx?

atrial flutter

A
  • b-blocker, CCB, digoxin

long-term

  • b-blocker, CCB, +/- digoxin
  • RF ablation often needed as HR control can be difficult
246
Q

Acute/long-term rx?

- multifocal atrial tachycardia

A
  • b-blocker or CCB

long-term

  • b-blocker or CCB
  • RF ablation of AV node + pacemaker if meds fail
247
Q

Is ventricular tachyarrhytmia narrow or wide QRS complex?

A

Wide

- narrow = SVT

248
Q

Ddx SVT with regular P wave morphology

A
  • sinus tach, sinoatrial node reentrant tacky if upright P before QRS
  • AT if no sinus before QRS
  • AVNRT if no P
  • AVNRT, AVRT, non paroxysmal junctional tachycardia if retrograde P waves
  • AFL if F waves at 300 bpm
249
Q

Ddx SVT with irregular P wave morphology

A
  • AFL if F waves at 300 bpm
  • no P or fibrillation = AF
  • multifocal atrial tachycardia if >3 morphology
250
Q

Ddx ventricular tachyarrhytmia

A
  • PVC if QRS >12s, bizarre QRS morphology or LBBB/ RBBB pattern
  • VT if 3+ consecutive ventricular rate >100/min; rate 120-300 bpm; AV dissociation, capture beats, fusion beats, L axis deviation, mono/biphasic QRS in V1 with RBBB; concordance V1-V6
  • VF if no true QRS complex
251
Q

What can cause fatigue/palpitations, HF (HR >110 persistently), stroke?

A

A fib

252
Q

When acute cardioversion be done for AF?

A

Yes, if <48hr

  • when >48h or uncertain onset then anticoagulant x3-4wk or transesophageal echo (visualize LAA) to prevent CVA
  • unless urgently required, i.e. patient unstable
253
Q

Is rate or rhythm control better for long-term AF management?

A

Both equal for risk of death or stroke

254
Q

When do you anticoagulant pt with A fib?

A

CHADS2-Vasc score >=2 (men with scores >=1)

- daily ASA if pt not receiving chronic anticoagulant

255
Q

What is CHADS2 score? What does it estimate?

A

Estimate yearly CVA risk in AF

CHF = 1
HTN = 1
Age >75yr = 1
DM = 1
Hx stroke = 2
256
Q

What is CHADS2-Vasc score? What does it estimate?

A

Estimates yearly CVA risk in AF

CHF = 1
HTN = 1
Age 65-75 = 1
Age >75 = 2
DM = 1
Stroke (or TIA) = 2
Vascular disease (MI, PAD, aortic plaque) = 1
Sex (female) = 1

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MCC Part 1 (22 decks)

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