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
Define hypertensive urgency
- severely elevated BP (>180/120) without progressive target organ dysfunction
26
Define hypertensive emergency
- severely elevated BP PLUS evidence of impending or progressive target organ dysfunction
27
How to tissues maintain perfusion relatively constant with increased BP?
- arterial and arteriolar vasoconstriction -> prevents pressure being transferred to smaller, more distal vessels
28
How do arteries and capillaries becomes damaged with severe HTN?
- autoregulation fails = increased arteriole and capillary pressure = damage vascular wall, disruption of endothelium (breakthrough vasodilation)
29
How does RAS exacerbate HTN?
- renin-angiotensin increases BP -> natriuresis and renal vascular injury -> increased renin which increases angiotensin II = HTN exacerbated
30
Mechanism HTN medication causes ischemic damage?
- 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
31
Cause of severe essential HTN?
- often medication noncomplicance or acute drug withdrawal
32
Case of secondary HTN emergency/urgency?
- acute renal failure - renovascular HTN (CHF + HTN) - thyrotoxicosis - medication-related (cocaine, MAOI + tyramine food) - advanced CKD with volume overload - pheochromocytoma - pregnancy
33
What is likely dx with arm-arm different >20/10?
- aortic dissection
34
Investigations with HTN emergency/ urgency?
- 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
35
Urgently drop BP in hypertensive urgency and emergency?
No - no evidence for aggressive drop with urgency | Drop aggressively and admit to ICU if emergency
36
How much do you want to reduce BP in HTN emergency?
- 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
37
Rx HTN emergency?
- labetalol first line (except CHF) - nitroprusside (caution CKD and increased ICP) - nitroglycerine (use in coronary schema and HF) - hydralazine (use for eclampsia)
38
Define chronic HTN in pregnancy
- HTN prior to pregnancy - before 20wk GA - persists >12 wk postpartum
39
Define gestational HTN
- new onset HTN after 20wk GA | - without proteinuria
40
Define preeclampsia
- new HTN | - proteinuria (>300mg/24h) after 20wk GA
41
Define chronic HTN with superimposed preeclampsia
- new (or 2-3x increased) proteinuria, thrombocytopenia, elevated AST/ALT after 20wk GA - in women with preexisting HTN before 20wk GA
42
Define transient HTN in pregnancy
- postpartum return to normal BP by 12wk postpartum | - increased risk of HTN in future pregnancies
43
What fails to invade the myometrial portion of the uterus in preeclampsia?
- cytotrophoblast
44
Where is earliest pathological change with preeclampsia?
uteroplacental circuation
45
What happens to vessels in placenta with preeclampsia?
- vessels narrow (tortuous vascular channels don't develop) causing placental hypo perfusion
46
What happens in ischemic placenta?
- release of pro inflammatory cytokines and mediators of oxidative stress -> increase capillary permeability and activate endothelial cells and coagulation system - > preeclampsia
47
Sx preeclampsia?
- visual change - new headache - epigastric or RUQ pain - rapidly progressive peripheral edema - rapid weight gain
48
What is indicated by rollover test (>15mmHg rise in dBP from left lateral decubitus to supine)?
Preeclampsia
49
Lab testing with pregnancy HTN?
- 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)
50
How do you assess fetus with maternal HTN?
- NST or BPP
51
Management HTN pregnancy?
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
52
Safe anti-HTN in pregnancy
- labetalol (or other beta-blocker except atenolol) - methyldopa (mild, s/e common) CI - ACEI/ ARBS - aldosterone antagonist - > fetal renal abnormalities and death
53
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?
heart failure
54
Systolic vs. diastolic HF?
- low LV ejection fraction in systolic HF
55
Low output vs. high output HF?
- low BP, organ hypo perfusion in low output
56
Congestive vs. dry HF?
- pulmonary edema, orthopnea, ascites, leg deem in congestive
57
Left vs. right sided HF
- pulmonary edema in left sided | - ascites, leg edema in right sided
58
Acute decompensated vs. chronic HF
- rapid (<2wk) sx progression in acute
59
Causes of mortality with HF?
- arrhythmia 40% - worsening HF 40% - other 20%
60
Is ischemic or HTN most common cause of HF?
- ischemic (prior MI or severe CAD) is most common cause | - HTN is second most common cause
61
Sx HF
- SOB - fatigue - orthopnea - PND - peripheral edema (leg edema, ascites)
62
Investigation HF
- CBC, lytes, Cr, transferrin saturation (serum iron/ TIBC), ferritin, TSH - ECG - CXR - transthroacic echocardiogram - B-type natriuretic peptide (BNP) or NT-proBNP
63
Tx wet and warm HF
- diurectics | - vasodilators (IV nitroglycerine or nitropatch)
64
Tx dry and warm HF (well compensated)
- optimize chronic HF therapies (incl BB)
65
Tx dry and cold HF (over diuresis)
- reduce/hold diuretic | - carful volume replacement
66
Tx wet and cold HF (advanced)
- inotropes +/- invasive hemodynamic monitoring (PA catheter) - philosophy of care of transplant assessment
67
Do increased perfusion and increased congestion result in wet and warm HF or wet and cold HF?
wet and warm
68
Increased perfusion and reduced congestion = _ HF?
dry and warm
69
Increased congestion and reduced perfusion = _ HF?
wet and cold
70
Tx chronic HF?
- 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
71
Classification of: - enalapril - lisinopril - perindopril - ramipril
ACEI
72
Classification of: - bisoprolol - carvedilol - metoprolol
B-blocker
73
Classification of: - spironolactone - eplerenone
Aldosterone antagonist
74
Classification of: - candesartan - valsartan
ARB
75
Classification of: | - hydralazine
Vasodilator
76
Classification of: - verapamil - diltiazam
Non-DHP CCB | cardiac effect
77
Classification of: - nifedipine - amlodipine
DHP CCB | vascular > cardiac effect
78
NYHA functional classification of HF
1. limitation of physical activity 2. degree of comfort at rest 3. sx with ordinary physical activity Class I-IV
79
What is a physiologic state of overwhelming reduction in systemic tissue perfusion leading to a change in tissue O2? What can result?
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
80
Causal conditions of hypotension?
Distributive (reduced SVR) - sepsis, anaphylaxis, other Reduced CO (increased SVR) - hypovolemia - cardiac dysfunction -> intrinsic vs. extrinsic (obstructive)
81
What is Beck's triad?
- muffled heart sounds - jugular venous distention - hypotension - > cardiac tamponade (+ pulses paradoxus)
82
5 common features of shock?
- 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
83
Hypotension workup
- CBC, lytes, LFT, Cr clearance, amylase/lipase, fibrinogen degradation product, lactate, cardiac enzymes, ABG, toxicology, CXR, ECHO, EKG, troponin, pro-BNP, UA
84
Acute tx hypotension/shock
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
85
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?
Hypovolemic shock CBC, lytes, BUN, Cr, amylase, lipase, lactate AXR, UA Hemorrhage, third space loss, GI fluid loss
86
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?
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
87
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?
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
88
Variable to assess preload?
PCWP
89
Variable to assess pump function?
CO
90
Variable to assess after load?
SVR
91
Variable to assess tissue perfusion?
mixed venous O2 saturation
92
Targets for tx hypovolemic shock (non-hemorrhagic and hemorrhagic)?
``` 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%)
93
Acidosis, hypothermia and hypocalcemia can happen with what treatment?
- massive transfusion
94
Septic shock management
- 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)
95
Management neurogenic shock?
- methylprednisolone 30mg/kg over 15min then infusion 5.4 mg/kg/h x24h
96
Management carcinogenic shock?
- underlying cause - optimize volume status - add/substitute inotropes for hypo perfusion - treat arrhythmias
97
Vasopressor or inotrope? Act on CO/ SVR/ HR? | NE
vasopressor CO + SVR +++ HR + alpha adrenergic agonist, mild B1 adrenergic agonist
98
Vasopressor or inotrope? Act on CO/ SVR/ HR? | Dopamine
vasopressor CO ++ SVR +++ (low dose can decrease) HR +++ dopamine agonist and B1 agonist at intermediate-high doses
99
Vasopressor or inotrope? Act on CO/ SVR/ HR? | Phenylephrine
vasopressor CO - SVR +++ HR - pure alpha adrenergic agonist
100
Vasopressor or inotrope? Act on CO/ SVR/ HR? | Vasopressin
vasopressor CO - SVR ++ HR - ADH analog - vasoconstriction
101
Vasopressor or inotrope? Act on CO/ SVR/ HR? | Epinephrine
vasopressor CO +++ SVR +++ HR +++ alpha and beta adrenergic agonist
102
Vasopressor or inotrope? Act on CO/ SVR/ HR? | dobutamine
inotrope CO +++ SVR - HR ++ strong beta1 adrenergic agonist
103
Vasopressor or inotrope? Act on CO/ SVR/ HR? | milrinone
inotrope CO +++ SVR decreased HR + phosphodiesterase (PD3) inhibitor with positive inotropic and vasodilatory action
104
Define anaphylaxis
IgE mediated, immediate hypersensitive allergic reaction to protein substances
105
Ag exposure cascade
- 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
Are these mediators initial or late? | - histamine, tryplase, PGs, LTs, platelet activating factor
initial minutes
107
Are these mediators initial or late? | - cytokines (IL4, IL13, TNF)
hours later - released by same cells as early mediators
108
What is an anaphylactoid reaction?
- non IgE mediated - direct release of mediators from mast cells - immune complex/complement mediated - arachidonic acid metabolism modulator - multiple/ unknown mechanisms
109
Management anaphylactic reaction?
- 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
What is test to sx anaphylaxis?
``` Clinical diagnosis! Based on 1/3 criteria - acute onset - 2+ sx after exposure to Ag - reduced BP ```
111
Pathophys of angina?
MOD exceeds myocardial O2 supply -> stimulation of chemosensitive and mechanoreceptive receptors of unmyelinated cardiac nerve cells -> angina
112
WHO MI criteria?
2 out of 3: - chest pain - ECG-ST changes, T wave inversions - increased cardiac enzymes
113
What causes downsloping or horizontal ST depression?
ischemia
114
What causes ST elevation or T wave inversion?
infarction
115
Likely dx? - substernal pressure (+/- radiation to neck/ jaw/ shoulders/ L arm) - with exertion/ stress - relieved with rest (5-10min) or nitroglycerin (immediate)
typical angina 2 out of 3 sx = atypical angina 0 or 1 out of 3 = non cardiac pain
116
What can you hear on cardiac exam with angina?
S4 with chest pain due to impaired myocardial relaxation from schema
117
Angina workup
- resting ECG (may see ST) - depression (ischemia) or Q waves - cardiac enzymes - negative - exercise stress test
118
Positive exercise stress test?
>1mm ST depression with exercise (85% age-predicted maximal [220-age]HR) = +
119
What are causes of increased MOD (e.g. causing chest pain)?
- increased HR - increased myocardial contractility - increased myocardial work -> increased MOD - increased after load + increased preload -> increased wall tension
120
Dx? | - new or rapidly worsening pattern of typical angina that severely limits usual activities or occurs at rest
unstable angina
121
Dx? - sudden, severe chest pain pressure lasting >30min and associated with diaphoresis, nausea, malaise, sense of impending doom
NSTEMI/STEMI
122
Why can you hear new systolic murmur with ACS?
- in MI = mitral regurgitation due to papillary muscle dysfunction
123
ACS workup
- ECG | - cardiac enzymes
124
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)
aortic dissection hypotension from tamponade or AI in ascending aortic dissection
125
Workup aortic dissection
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
Dx - sudden, pleuritic pain and shortness of breath - often unilateral - unilateral reduced breath sounds on exam with hyper-resonance on percussion Imaging?
tension pneumothorax CXR - mediastinal shift, distinct pleural lining -> confirm with expiratory views
127
``` Dx - sudden, pleuritic pain with severe SOB +/- syncope - tachypnea, tachycardia - may hear loud S2, feel parasternal heave or new RUSB systolic murmur ```
PE - S2= pulmonic component - parasternal heave = RV pressure overload - RUSB systolic murmur = pulmonary insufficiency from pulmonary HTN = Graham Steel murmur
128
PE workup?
- 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
Define aortic dissection
tear in aortic intima = blood accumulation in false lumen
130
Causes of pericarditis
- infectious - post-MI (acute vs. subacute -> subacute is autoimmune aka Dressler syndrome) - uremic - CT disease
131
Life threatening causes of chest pain?
- angina - ACS - aortic dissection - tension pneumo - PE
132
Management stable angina?
- 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
Does PCI improve MI occurrence or death or help with symptom relief of stable angina?
- symptom relief | - does not prevent MI or death in stable angina
134
Treatment offered to pt with prognosis-altering CAD, pt refractory to medication?
CABG
135
What is similar in all cases of ACS re: pathophys?
- intra-coronary thrombosis
136
UA vs. NSTEMI vs. STEMI
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
Management ACS
- 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
Management UA/NSTEMI
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
TIMI risk score for UA/NSTEMI
``` 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
STEMI management
- 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
Aortic dissection types
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
Management aortic dissection
- 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
Dx - pulses paradoxus - tachycardia - hypotension - muffled heart sounds - bottle shaped heart on CXR
pericardial tamponade
144
Management Pericarditis
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
What is most common rhythm in sudden cardiac death?
VF
146
Management of cardiac arrest (in hospital)
- responsiveness/ confirm lack of pulse - call for help - BLS - check heart rhythm, ensure IV access - ACLS guidelines
147
Management asystole/PEA
- 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)
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Management VF/ pulseless VT
- 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
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Management stable severe tachycardia (VT or SVT)
- 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
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Management severe bradycardia
- sx hypo perfusion -> atropine 1mg if present - transcutaneous pa king or IV dopamine/ epinephrine (stimulate escape rhythm) consider hyperK
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Is mild therapeutic hypothermia a treatment option post-arrest?
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
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Define syncope
- transient loss of consciousness due to global cerebral hypoperfusion
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Equation for CO
CO = HR x SV
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What 3 main factors determines SV?
- proload - afterload - contractility
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What is ventricular volume at end of diastole?
Preload | - increased preload = increased SV
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What is Starling law of heart?
- energy of contraction of muscle is proportional to initial length of muscle fiber
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What is resistance to vernacular ejection?
Afterload - caused by resistance to flow in systemic circulation = SVR
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What refers to degree of active constriction of vessels (mainly veins) which affects return of blood to the heart?
vascular capacitance
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Increacred intravascular volume increases what?
increases vascular capacitance which increases preload
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Ddx syncope
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
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Describe auto regulation of cerebral blood flow
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
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Workup neuro causes syncope?
- heat CT - EEG - cerebral flow studies (Doppler)
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Workup sudden dyspnea, risk PE with syncope?
V/Q scan spiral CT -> anticoagulate
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Workup cardiac cause of syncope?
- CXR - CCU admission - echocardiogram - cardiac enzymes (r/o MI) - perfusion test - functional assessment +/- CTA tx re: etiology
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Workup unexplained syncope with abnormal EKG, hx of CAD?
- holter monitor - loop monitor - electrophysiology study - tilt table test - ECHO - consider cardiology consult/EP, psychiatry
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Standard investigation syncope?
ECG CBC, lytes, urea, glucose/ chemstrip, Cr - postural BP
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Where are central pulses assessed? What are they assessed for?
- carotid and/or femoral arteries | - palpated for amplitude, contour, upstroke
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Where are peripheral pulses assessed?
- radial, brachial, popliteal, posterior tibialis, dorsalis pedis
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Ddx peripheral pulse deficit?
- dissection - aortic coarctation - peripheral vascular disease
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What is laminar flow re: pulses?
- 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
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Is laminar flow high or low momentum of diffusion? Convection? Pressure and velocity?
High momentum of diffusion Low momentum of convection Constant pressure and velocity
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What is flow regime characterized by chaotic, stochastic property changes?
Turbulent flow | - includes low momentum diffusion, high momentum convection, and rapid variation of pressure and velocity
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Types of abnormal pulses?
- small and weak - large and bounding - Bisferiens pulses - pulses alternans
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Does increase velocity cause laminar or turbulent flow?
- turbulent flow - very low speed = blood flow laminar - increase in velocity (narrowing blood vessels or increase flow rate) = turbulent flow
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Ddx unequal or delayed pulses
- obstructive arterial disease (atherosclerosis) - aortic disease - Takayasu arteritis
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Ddx rhythm irregular/ too fast/ too slow
- tachycardia - bradycardia - arrhythmia
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Dx - alternating weak and strong pulses with fixed cycle length - present in systolic dysfunction/low EF
Pulses alternans
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Dx - biphasic pulse - present in: AS plus AI, severe AI, HOCM
pulses bisferiens
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Dx - double peak, with weaker second beat - present in: low arterial pressure/ PVR, very low EF, post AVR
dicrotic pulse
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Dx - slow rising, typically with an ascending notch - present in aortic stenosis
Anacrotic pulse/ pulsus parvus et tardus
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Dx - rapid pulse then sudden collapse - present in aortic insufficiency
Corrigan pulse (water hammer/ collapsing)
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Dx - exaggerated inspiratory decrease in arterial pulse amplitude - present in cardiac tamponade, asthma, hypovolemic shock
Pulsus paradoxus
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What is ankle-brachial index?
- grading of peripheral vascular disease ++ calcified vessels 1-1.3 normal ABI low = peripheral vascular disease
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What does brachio-femoral delay indicate?
coarctation of aorta
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Define dyslipidemia
- one of more alterations in serum lipids (elevated fasting TC, LDL, TG, apoB, low HDL) - increase risk of CVD -> atherosclerosis
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What elevates LDL levels?
increased VLDL or reduced LDL catabolism
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What does reverse cholesterol transport?
HDL
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What changes occur in atherosclerosis?
- changes in blood vessel wall -> lipid deposition and cell proliferation = narrow lumen and thrombus formation
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High risk (FRS >20%) management and target?
Treatment LDL <2mmol/L or >50% reduction win LDL-C apoB <0.8g/L
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Moderate risk (FRS 10-19%) management and target?
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
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Low risk (FRS <10%) management and target?
Treatment if LDL-C <5mmol/L Target >50% reduction in LDL-C
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Who gets a screening fasting lipid profile?
- 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
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What provides 10yr risk of CAD events based on RF (age, gender, TC, HDL-C, sBP, smoker, DM)?
Framingham risk score
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What is similar to FRS but includes high-sensitivity CRP and family history of parent having MI <60yr?
Reynold's risk score
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Key points on physical exam for pt with hyperlipidemia?
- tendon xanthomas (high LDL-C) - eruptive xanthomas (high TG-C) - xanthelasma - corneal arcus (ring-like appearance on cornea)
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Drugs to treat lipid abnormalities?
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
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Mitral stenosis, prosthetic mitral valve, short PR interval -> causes loud or soft S1 or S2?
Loud S1
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Mitral regurgitation, COPD, long PR interval -> causes loud or soft S1 or S2?
Soft S1
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HTN, aortic sclerosis, prosthetic aortic valve -> causes loud or soft S1 or S2?
Loud S2
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Hypotension, severe aortic stenosis, HF/ low cardiac output -> causes loud or soft S1 or S2?
Soft S2
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What causes split S2 (often heard LUSB)?
- 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
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Etiologies S3?
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)
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Etiologies S4?
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
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What is a high pitched sound in early systole (after S1) heard in pt with bicuspid aortic (or pulmonic) valve?
ejection sound
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What is high pitched should in early diastole (after S1) heard in pt with rheumatic mitral (or tricuspid) disease?
opening sound
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What is high pitched sound in mid-systole, caused by bowing of a myxomatous mitral valve, heard in pt with mitral valve prolapse?
mid-systolic click
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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)?
Pericardial friction rub
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What is a sound caused by turbulent blood flow, which could be occurring between chambers of the heart or across narrowed arterial vessels?
Murmur
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Grade a murmur
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
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Are diastolic murmurs often innocent or pathologic?
Pathologic
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What cardiac issues is Marfan associated with?
MVP | aortic regurgitation
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What cardiac issue is Down syndrome associated with?
AVSD
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Where is it best to palpate for systolic heave?
Left parasternal area - typically in right ventricular enlargement or pulmonary HTN
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What and where is the apex beat?
- 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)
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What produces S1?
mitral valve closes (and tricuspid valve)
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What produces S2?
AV valve closure
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How do you describe a murmur?
- 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)
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Ddx mid systolic murmur
- AS - Ao valve sclerosis - PS - increased semilunar blood flow - innocent mid systolic murmur
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Ddx later systolic murmur
- mitral valve prolapse - tricuspid valve prolapse - papillary muscle dysfunction
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Ddx holosystolic murmur
- MR - TR - VSD
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Ddx continuous murmur
PDA
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Ddx early diastolic murmur
- AR | - PR
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Ddx mid diastolic murmur
- MS - TS - atrial myxoma
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Ddx late diastolic murmur?
- complete heart block
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Workup murmur?
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
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Mitral stenosis - etiology - sx and physical exam - investigations - management
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
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Mitral regurgitation - etiology - sx and physical exam - investigations - management
- 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
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Mitral valve prolapse - etiology - sx and physical exam - investigations - management
- 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
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Aortic stenosis - etiology - sx and physical exam - investigations - management
- 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)
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Hypertrophic cardiomyopathy - etiology - sx and physical exam - investigations - management
- 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
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Aortic insufficiency - etiology - sx and physical exam - investigations - management
- 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
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Define palpitations
unpleasant awareness of the heartbeat; rapid, forceful or irregular
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What is normal SA pacemaker function and impulse propagation?
- 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
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Mechanism of arrhythmia?
- 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)
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Ddx palpitations
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
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How does parasympathetic stimulation reduce pacemaker current to reduce HR?
via vagus nerve
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How does sympathetic stimulation increase SA node automaticity and increase rate of pacemaker depol to increase HR?
b1 adrenergic receptor stimulation
238
Investigations for palpitations?
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
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Dx, acute/long-term rx? | Unstable arrhythmia
VT, VF, rarely AF/SVT acute - defibrillation or cardioversion long-term - AICD for unstable VT or VF
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Acute/long-term rx? | VT (stable), SVT
12-lead ECG then cardioversion long-term - cardiologist tx - meds, RF ablation, ICD
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Acute/long-term rx? | - sinus tachycardia
treat underlying cause long-term - n/a
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Acute/long-term rx? | ectopic atrial tachycardia
b-blocker or CCB long-term - b-blocker or CCB - RF ablation if meds fail
243
Acute/long-term rx? | PSVT (AVNRT or AVRT)
- vagal maneuvers, adenosine long-term - b-blocker, CCB if no accessory pathway (delta wave) - RF ablation
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Acute/long-term rx? | atrial fibrillation
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
Acute/long-term rx? | atrial flutter
- b-blocker, CCB, digoxin long-term - b-blocker, CCB, +/- digoxin - RF ablation often needed as HR control can be difficult
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Acute/long-term rx? | - multifocal atrial tachycardia
- b-blocker or CCB long-term - b-blocker or CCB - RF ablation of AV node + pacemaker if meds fail
247
Is ventricular tachyarrhytmia narrow or wide QRS complex?
Wide | - narrow = SVT
248
Ddx SVT with regular P wave morphology
- 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
Ddx SVT with irregular P wave morphology
- AFL if F waves at 300 bpm - no P or fibrillation = AF - multifocal atrial tachycardia if >3 morphology
250
Ddx ventricular tachyarrhytmia
- 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
What can cause fatigue/palpitations, HF (HR >110 persistently), stroke?
A fib
252
When acute cardioversion be done for AF?
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
Is rate or rhythm control better for long-term AF management?
Both equal for risk of death or stroke
254
When do you anticoagulant pt with A fib?
CHADS2-Vasc score >=2 (men with scores >=1) | - daily ASA if pt not receiving chronic anticoagulant
255
What is CHADS2 score? What does it estimate?
Estimate yearly CVA risk in AF ``` CHF = 1 HTN = 1 Age >75yr = 1 DM = 1 Hx stroke = 2 ```
256
What is CHADS2-Vasc score? What does it estimate?
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 ``` /9