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Foundations 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Thiazide Diuretics

A

Hydrochlorothiazide
Side effects: low electrolytes/hypercalcemia, sexual dysfunction, gout, DM, dyslipidemia

contraindications: hypersensitivity to sulfas

Good for blacks and elderly

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2
Q

Loop diuretics

A

Furosemide
Side effects: hypokalemia/other electrolytes, DM, HCL, sexual dysfunction

Poor antihypertensive, use for kidney disease pts

Good for blacks and elderly

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3
Q

Potassium Sparing Diuretics

A

Triamterene
Side effects: hyperkalemia, nephrolithiasis, renal dysfunction

  • weak antihypertensive-wont combine with ace, arb, dry or K supps
    contraindications: kidney disease, renal failure, hyperkalemia

Good for blacks and elderly

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4
Q

Aldosterones

A

Spironolactone
Side effects: hyperkalemia, gynecomastia

Potassium sparing

Contraindications: renal impairment, DM, hyperkalemia

*not first line

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5
Q

Calcium Channel Blockers

A

-dipines (and verapamil/diltiazem-non dihydropyridines)

Inhibits calcium influx to muscle cells inhibiting contraction>vasodilation>reduced PVR

Side effects DHP: edema, headache, flushing-change drug if these happen

Side effects non-DHP: bradycardia, constipation, gingival hyperplasia, worsening heart failure

Good for blacks and elderly

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6
Q

Ace-Inhibitors

A

-prils
inhibit RAAS, stimulate bradykinin (vasodilation)

Side effects: cough, hyperkalemia, angioedema, acute renal failure

Contraindications: pregnancy, angioedema, renal artery stenosis

Bad for blacks and elderly
Good for CKD, DM, HF, post-MI

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7
Q

ARBs

A

-sartan
Inihbit RAAS binding with ACEs

Side effects: hyperkalemia, angioedema, acute renal failure

Good for CKD, DM, HF

Contraindications: pregnancy, renal artery stenosis

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8
Q

Direct Renin Inhibitors

A

Aliskiren
inhibits renin reducing angiotensin 1/2 and aldosterone

Side effects: hyperkalemia, renal impairment, hypersensitivity reactions

DONT combine with ACE or ARB in kidney impairment

Contraindications: use with ACE/ARB, pregnancy

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9
Q

Beta Blockers

A

-lol
Cardioselective (B1)/noncardioselective (B1/B2)

blocks catecholamines at B adrenoreceptors>decreased cardiac output/decreased PVR/decreased renin

Side effects: exercise intolerance, fatigue, bradycardia, depression, exacerbate airway/peripheral vascular diseases

Caution with respiratory diseases
avoid abrupt cessation

Contraindications: AV block, cardiogenic shock, heart failure, hypotension

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10
Q

Central Alpha Agonists

A

Clonidine (patch), Methyldopa (okay for pregnancy)

Stimulate adrenergic receptors reducing CNS sympathetic outflow

Only used for difficult to treat pts (3+ meds already)

Side effects: bradycardia, orthostatic hypotension, dizziness, rebound HTN, anticholinergic side effects
Methyldopa effects: hepatitis, hemolytic anemia, fever

Avoid abrupt cessation

Contraindications: methyldopa in liver disease

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11
Q

Alpha Blockers

A

-zosin
Targets a1 receptors on vascular smooth muscle>PVR decrease>decreased BP

Side effects: orthostatic hypotension, dizziness, reflex tachycardia

Not for monotherapy
Helpful for BPH

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12
Q

ACC/AHA Guidelines

A

BP goal <130/80

NO ACE/ARB or DRI if pregnant

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13
Q

Hypertensive Emergencies

A

180/120
Urgency if asymptomatic

Emergency if associated with acute end-organ damage

Reduce BP quickly (160/100), but too quickly could cause cerebral/MI ischemia or infarct (no more than 25% w/in 1 hour)

NO NIFEDIPINE, treat w/ rest and diuretic

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14
Q

Statins

A

Secondary prevention, severe hypercholesterolemia (LDL>190), DM, primary prevention based on risk

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15
Q

Primary Hypertension

A

Primary=90-95% of cases
controlled by SNS, RAAS, plasma volume (kidneys)
Genetic and environmental factors

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16
Q

Non-reversible risks for Elevated blood pressure

A

Age, race (black highest risk), family history, dyslipidemia, diabetes, personality traits (hostility, impatience)

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17
Q

Reversible risks for Elevated blood pressure

A

Smoking, diet, excess alcohol (>2/day women, >3/day men), obesity, physical inactivity

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18
Q

Secondary Hypertension

A

compare clinical presentations
Renal disease, medication induced, thyroid/parathyroid, sleep apnea, pheochromocytoma, coarctation of aorta, aldosteronism, renovascular disease, cushings

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19
Q

When to suspect secondary HTN

A

Young onset, diastolic onset >50 years, target organ damage at presentation, signs of secondary hen, poor response to therapy

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20
Q

End organ damage exam findings

A

Headache (cerebral heme/stroke), transient weakness/blindness (retinopathy),
Neck: thyroid/carotid abnormalities
Resp: rhonchi/rales
Abdomen: renal masses, renal bruits, femoral pulses
Neuro: visual disturbance, focal weakness, confusion
CV: displaced PMI, ECG changes, S4 gallop, bruits, edema

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21
Q

HTN Screening

A

All adults 18+
18-39 every 3-5 years if no risk
40+ or high risk every year

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22
Q

HTN Diagnosis

A

2 or more proper BP readings at separate visits

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23
Q

HTN Classifications ACC/AHA

A 
Normal <120/<80
Prehtn 120-129/<80
Stage 1: 130-139/<80
Stage 2: >140/>90
General goal: 130/80
Diabetic/renal disease goal: 130/80
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24
Q

HTN Classifications JNC

A 
Normal <120/<80
Prehtn 120-139/80-89
Stage 1: 140-159/90-99
Stage 2: >160/>100
General goal: 140/90
Diabetic/renal disease goal: 130/80
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25
Q

ACC/AHA Classification Guidelines

A 
Normal <120/<80
Elevated 120-129/<80
Stage 1: 130-139/80-89
Stage 2: >140/>90
Goal 130/80 w/ meds
<140/90 w/out meds
>60 w/ systolic don't drop diastolic below 55-609
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26
Q

HTN Diagnostic Tests

A

CBC, urinalysis, Blood chem (glucose, Ca, creatinine, electrolytes, GFR), TSH, lipid profile, EKG, echo, urine albumin

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27
Q

Treatment for Elevated BP

A

Lifestyle changes, reassess in 3-6 months

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28
Q

Treatment for Stage 1 HTN

A

if 10 year risk >10% or already have CVD/DM/CKD: lifestyle changes and meds
if NOT: lifestyle changes

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29
Q

Treatment for Stage 1 HTN

A

if 10 year risk >10% or already have CVD/DM/CKD: lifestyle changes and meds (1 month f/u)
if NOT: lifestyle changes

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30
Q

Treatment for Stage 2 HTN

A

Lifestyle changes and meds (1 month f/u)

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31
Q

ACC/AHA BP Goal of <130/80

A

Ischemic heart disease, heart failure w/ reduced EF, CKD, DM

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32
Q

HTN treatment in pregnancy

A

Methyldopa, nifedipine, labetalol

NO ACE/ARB/DRI

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33
Q

Poor outcomes of HTN

A

CVD, HF, LVH, ischemic stroke, intracerebral heme, CKD, peripheral artery disease, retinopathy

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34
Q

Indicators of poor prognosis

A

high pulse pressure, men >55 women >65

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35
Q

Benefits of HTN Therapy

A 
Reduce risk of
MI by 20-25%
Stroke by 35-40%
HF >50%
CKD
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36
Q

Resistant Hypertension

A

failure to achieve goal BP in pt adhering to full-dose treatment of 3 drug regimen (or at goal w/ 4)

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37
Q

Causes of resistant HTN

A

Improper BP reading, volume overload, drug induced, obesity, excess alcohol

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38
Q

Cholesterol

A

Helps form steroid hormones and bile acids

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39
Q

Triglycerides

A

helps transfer energy from food to cells

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40
Q

Lipoproteins

A

how lipids are transported
Low density: more triglycerides (bad)
High density: more apoproteins (good)

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41
Q

Cholesterol Transport Steps

A

1-made in liver, taken from food
2-loaded into VLDL w/ triglycerides>bloodstream
3-VLDL transformed into LDL after dropping off triglycerides in tissues, LDLs deliver cholesterol to cells
4-excess LDLs trigger plaque formation
5-HDLs remove excess cholesterol from blood/cells
6-HDL collects cholesterol from plaques
7-HDLs can add cholesterol back to VLDL, turning them into LDLs
8-liver removes LDLs from blood and converts cholesterol into bile acid and eliminates it

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42
Q

Total cholesterol (equation)

A

HDL+VLDL+LDL

VLDL and LDL are calculated not measured, we measure total, HDL and triglycerides (VLDL=tri/5)

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43
Q

Cardiovascular Disease

A

Fatty material collected in arterial walls hardening over time, started by excess cholesterol

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44
Q

Plaque Formation Cascade

A

LDL oxidation>macrophages create foam cells>endothelial dysfunction>vasoconstriction/plaque formation

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45
Q

CV Risk factors (modifiable)

A

HTN, DM, Dyslipidemia, CKD, obesity, smoking, HDL

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46
Q

CV risk factors (non-modifiable)

A

Age (M>45 F>55), sex, fam hx of premature heart disease (M<55 F<65)

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47
Q

CVD Risk Calculators

A

Coronary Framingham risk score (10 year risk MI/death)

ACC/AHA risk estimator plus (risk of heart disease and stroke)

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48
Q

Hyperlipidemia Physical

A

Most asymptomatic

Rare findings: xanthomatous tendons, corneal arcus, lipemia retinalis, xanthelasma, eruptive xanthomas

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49
Q

Low Intensity Statins

A 
<30% LDL lowering
simvastatin 10mg
Pravastatin 10-20
Lovastatin 20
Fluvastatin 20-40
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50
Q

Moderate Intensity Statins

A 
30-49% LDL lowering
Atorvastatin 10-20
Rosuvastatin 5-10
Simvastatin 20-40
Pravastatin 40-80
Lovastatin 40-80
Fluvastatin 40-80
Pitvastatin 1-4
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51
Q

High Intensity Statins

A

> 50% LDL lowering
Atorvastatin 40-80
Rosuvastatin 20-40

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52
Q

Cholesterol Screening/goals

A

Adults 20+

LDL <70mg/dL (but nothing set in stone)

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53
Q

Statin Benefit Groups

A

1- 2dary prevention in patients w/ CVD
2- severe hyperholesterolemia (LDL>190)
3- DM patients
4- Primary prevention based on risk

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54
Q

Secondary Prevention w/ CVD (statin guidelines)

A

Goal is to reduce LDL w/ HIGH INTENSITY statin

if very high risk (multiple major cardiac events) add non-statin to lower LDL more

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55
Q

Severe Hypercholesterolemia

A

LDL>190

High Intensity Statin (if tolerated)

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56
Q

Patients w/ DM (statin guidelines)

A

40-70 years old: moderate intensity statin
Consider high intensity if multiple high risk factors
Add ezitimibe if 10 year risk >20%

20-39 years old-consider statin, make decision w/ patient

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57
Q

HMG-CoA Reductase Inhibitors MOA

A

-statins
Inhibit rate-limiting enzyme in formation of cholesterol
Reduces fatal/non-fatal MI, incidence of CVA and all cause mortality

Decreased LDL 20-55%, increases HDL 5-15%, TG decrease 7-30%

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58
Q

HMG-CoA Reductase Inhibitors Contraindications

A

Pregnancy/breastfeeding, acute liver disease, elevated LFTs

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59
Q

HMG-CoA Reductase Inhibitors Side effects

A

Myalgias, myopathy, rhabdomyolysis, hepatotoxicity (rare), DM

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60
Q

Cholesterol Absorption Inhibitor MOA/use

A

Ezetimibe

Decreases absorption of cholesterol in sm intestine, up regulates LDL receptors

Add to statin when LDL>70 in very high risk CVD

LDL decrease 15-20%

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61
Q

Cholesterol Absorption Inhibitor Contraindications

A

hepatic impairment, don’t use with fibrates

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62
Q

PCSK9 Inhibitor

A

Alirocumab, evolocumab

monoclonal antibodies block PCSK9 effect of degrading LDL receptors
Lowers LDL 50-60%

Very expensive, consider for familial hypercholesterolemia

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63
Q

Fibric acid Derivatives

A

Gemfibrozil, fenofibrate

Reduced synthesis/increased breakdown of VLDL

Drug of choice for TG>500 (decreases 40%)

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64
Q

Fibric Acid Derivatives Side effects/contraindications

A

SE: cholelithiasis, hepatitis, myositis
Contras: liver disease/impairment, gallbladder disease, caution with pregnancy/renal impairment
DO NOT USE WITH STATINS

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65
Q

Bile Acid Binding Resins MOA

A

Cholestyramine, colesevelam, colestipol
Bind bile in intestine

ONLY LIPID LOWERING SAFE IN PREGNANCY
LDL decrease 15-25%

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66
Q

Bile Acid Binding Resins Side effects/Contraindications

A

SE: GI symptoms

Contras: GI obstruction, hypertriglyceridemia, pancreatitis

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67
Q

Niacin

A

Reduces production of VLDL
Long acting better tolerated-less flushing
HDL increase 25-35%

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68
Q

Niacin Side effects/Contraindications

A

SE: flushing
Contras: liver disease, peptic ulcers
Caution with: pregnancy, gout, DM

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69
Q

Familial Hypercholesterolemia

A

LDL receptors absent or dysfunctional

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70
Q

Metabolic Syndrome

A

3 of the following: central obesity (>40”men >35” women, high BP (130/80), high TG(>150), low HDL (<40M <50F), insulin resistance (glucose >100)

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71
Q

Hypertriglyceridemia

A

Mild 200-499 mg/dL
Moderate >500 Increased risk of pancreatitis
Severe >1000: milky white serum, acute pancreatitis

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72
Q

ATP3 HCL Guidelines (9 steps)

A

1-Obtain fasting lipid profile (9-12hr)
2-ID presence of atherosclerotic disease that confers high risk for CHD
3-determine presence f major risk factors (smoking, hen, HDL<40, fam hx, men>45 women >55
4-assess 10 year risk w/ framingham
5-determine risk category
6-Initiate therapeutic lifestyle changes if LDL high
7-consider drug therapy
8-identify metabolic syndrome (treat after 3 months if present)
9-treat high TG/low HDL

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73
Q

Acute Coronary Syndrome Therapy

A

M-morphine
O-oxygen
N-nitroglyceride
A-aspirin

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74
Q

Angina

A

Clinical syndrome characterized by chest, jaw, shoulder or arm discomfort attributable to coronary ischemia

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75
Q

NSTEMI/STEMI

A

angina with elevated cardiac biomarkers indicating MI with or without ST segment deviation

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76
Q

MI Symptoms

A

Symptoms of ischemia, new ST segment changes/LBBB, pathological Q waves, new loss of viable myocardium, identification of thrombus

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77
Q

Etiologies of Acute Coronary Syndrome

A

Coronary artery obstruction/atherosclerosis, vasospasm, coronary embolism, dissection, metabolic demand

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78
Q

Coronary Artery Disease Risk Factors

A

M>F, age, CKD, DM, HCL, HTN, PAD, tobacco, fam hx

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79
Q

MI EKG Evolution

A

Peaked T waves>ST seg elevation>Q wave formation>T wave inversion

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80
Q

MI Initial Diagnostic Studies

A

EKG, Cardiac biomarkers (CK, CK-MB, troponin), CBC, BMP, coag panel, cholesterol levels, BNP, Chest XR

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81
Q

Other causes of Elevated Troponin

A

Tachy/bradyarrhythmias, cardiogenic, hypovolemic or septic shock, severe anemia, heart failure, pulmonary embolism, renal failure

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82
Q

Cardiac Enzyme Time Frames

A

CK-MB: rises 3-4h, peaks 12-24h, normalizes 1-3 days

Troponin: rises 3-6h, peaks 12-24h, normalizes 7-14 days

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83
Q

TIMI Risk Score

A

1 point for each: >65years old, >3 CAD risk factors, known CAD, aspirin use in last 7 days, severe angina, ST changes, positive cardiac biomarker
3-4 intermediate risk
>5 high risk

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84
Q

Acute Coronary Syndrome Medications

A

Oxygen, anti-platelet, statins (high intensity 6-12 months), Nitroglycerin (IV or sublingual), Analgesics (IV morphine-NO NSAIDs), beta blockers (w/in 24 hours), ACE, ARB, Aldosterone Antagonist

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85
Q

Anti-platelet Therapy for ACS/STEMI

A 
Aspirin (all pts w/ suspicion of ACS, continue forever)
P2Y12 Inhibitor (Clopidogrel-in addition to aspirin for 12 months)
GP IIb/IIa Inhibitors (inhibit platelet aggregation)
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86
Q

Anticoagulation Therapies

A

Recommended in addition to dual anti-platelet
Indirect Thrombin Inhibitors: UFH bolus, Enoxaparin, Fondaparinux
Direct Thrombin Inhibitors: Bivalirudin, Argatroban

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87
Q

Calcium Channel Blockers (ACS)

A

Not used often (-pyridines)

Used for ongoing angina

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88
Q

Final Risk Stratification

A

Stress testing recommended in low/intermediate risk patients (perfusion better than echo)
Should have 2 negative troponins, w/in 72 hours of onset
recommended as first line

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89
Q

Who should get Stress Test

A

Abnormal baseline ECG: baseline ST abnormalities, bundle branch block/conduction delays, LV hypertrophy, paced rhythm, pre-excitation, digoxin

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90
Q

Percutaneous Coronary Intervention

A

Cather in leg>aorta stops at L coronary artery, contrast injected and Xray done to find stenosis

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91
Q

Vessels Used in CABG

A

Internal thoracic artery best for LAD grafts

Great saphenous vein used commonly

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92
Q

Infarction Complications

A

Arrhythmias and conduction abnormalities (sinus bradycardia, SVT, PVC/vtach/vfib, heart blocks, heart failure/shock, mechanical defects, inflammation (pericarditis)

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93
Q

Heart Failure

A

Inability of heart to pump in proportion to the metabolic demand of the body
Can result from structural or functional disorders, impairs preload/afterload and results in hypervolemia

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94
Q

Systolic Heart Failure

A

Reduced ejection fraction (<60%), results in eccentric remodeling

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95
Q

Diastolic Heart Failure

A

Normal/preserved ejection fraction, altered ventricular compliance>high filling pressure, results in concentric remodeling

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96
Q

Systolic HF Classification

A

Depressed myocardial contractility: Cardiac ischemia (#1), severe hypertension (#2), aortic stenosis, valvular regurgitation, dilated cardiomyopathy

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97
Q

Diastolic HF Classification

A

Abnormal diastolic relaxation/filling (stiff): hypertrophic/restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis, LVH

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98
Q

Ejection Fraction

A

% of blood ejected during systole in relation to end-diastolic volume
Normal 50-57%
Borderline 41-49%
Low<40

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99
Q

Most common cause of HF

A

Left sided heart failure

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100
Q

ACC/AHA Heart Failure Classifications

A

Based on STRUCTURE
A: High risk w/out structural disease
B: Structural disease w/out symptoms of HF
C: Structural disease with prior/current symptoms
D: Refractory HF requiring intervention

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101
Q

New York HA Heart Failure Classifications

A 
Based on Symptoms
I: Asymptomatic
II: Symptomatic w/ moderate exertion
III: Symptomatic w/ minimal exertion
IV: Symptomatic at rest
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102
Q

Left Ventricular Failure Signs/Symptoms

A

Pulmonary issues

Dyspnea, fatigue, weight gain, pulmonary crackles/wheezing, Elevated JVP, edema, S3/4 gallop

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103
Q

Right Ventricular Failure Signs/Symptoms

A

Peripheral signs

Edema, hepatomegaly, anasarca (full body edema), elevated JVP, S3 gallop, ascites

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104
Q

S3 Gallop

A

Early diastole, congestive heart failure (Kentucky)

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105
Q

S4 Gallop

A

Late Diastole, diastolic failure and noncompliant ventricle

Tennessee

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106
Q

Heart Failure Diagnostic Studies

A

CBC (anemia), CMP (electrolytes, renal/hepatic), thyroid, iron studies, biopsy, BNP, EKG (S1Q3T3), pulse O (<92), ABG (metabolic acidosis), chest Xray, echo (most useful), cardiac Cath

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107
Q

B-type Natriuretic Peptide

A

Hormone released from ventricles in response to ventricular volume expansion and pressure overload
<100 noHF
100-400 iffy
>400 consistent with HF

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108
Q

2 most important things to do in HF

A

Reduce BP and heart rate (decrease cardiac workload)`

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109
Q

Initial treatment of HF

A

diuretic and ACE

can use B blockers later, NO CCB

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110
Q

Diuretics in HF

A

Decrease preload, monitor renal function and electrolytes (for hyper/hypokalemia)
Loop diuretics better in severe, given IV when acute

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111
Q

Potassium sparing diuretics in HF

A 
Spirinolactone/eplerenone inhibit aldosterone
Indicated for NYHA class III/IV with LVEF <35% or HF/LVEF<40%
Monitor for hyperkalemia
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112
Q

ACE-I in Heart Failure

A

Vascular dilation by reducing preload and after load
First line or added to diuretics
Start w/ low dose
Don’t use w/ renal artery stenosis

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113
Q

ARBs in Heart Failure

A

block vasoconstrictors that contribute to impairment of LV function
Useful for patients that can’t use ACEs

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114
Q

B Blockers in Heart Failure

A

ALL patients w/ stable HF from LV systolic dysfunction

all asymptomatic with EF<40% and all patients with MI

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115
Q

Digoxin in Heart Failure

A

Relieves symptoms, increases contractility
inhibits Na/K/ATPase pump
Used if diuretics, ACEs and B blockers don’t work

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116
Q

HF treatment in Black patients

A

B blockers and ACEs first line
Vasodilators (hydralazine/isosobide dinitrate) part of standard therapy w/ class 2/3/4 symptoms
Angiotensin 2 antagonists for pts who can’t take ACEs

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117
Q

Nitroglycerin

A

Venous dilator, reduces preload

topical or IV

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118
Q

Implantable Cardioverter-Defibrillator (ICD)

A

Monitors rate and rhythm, corrects arrhythmias
Previous MI and EF<30%
Patients with EF<35% and NYHA class 2/3
Life expectancy >1 year

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119
Q

Pacemaker

A

Symptomatic NYHA class 3/4 with EF<35% and QRS >130 despite medications

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120
Q

Poor Prognosis in HF

A

need for hospitalization, noncompliance, age, gender, race, cause

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121
Q

Valvular Stenosis

A

Pressure overload on upstream cardiac and vascular structures (valve doesn’t open easily)

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122
Q

Valvular Regurgitation

A

Volume overload and dilation of chambers over time

back flow when valve is normally closed

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123
Q

Symptoms of Valvular Heart Disease

A

SOB, dyspnea on exertion, palpations, syncope, edema, weakness, fatigue
Good reasons for echo!

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124
Q

Valvular Disease Tests

A

EKG, CXR, Echo (transthoracic unless obese), blood cultures (if possible endocarditis), cardiac cath

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125
Q

AHA/ACC Valvular Classifications

A

Stage A: at risk for valvular disease
Stage B: mild-moderate valvular disease, asymptomatic
Stage C: severe w/out symptoms (C1 normal LV function, C2 abnormal LV function/decreased EF)
Stage D: symptomatic valvular disease

126
Q

Mitral Stenosis Causes

A

Rheumatic fever*, congenital, systemic disease

127
Q

Mitral Stenosis signs/symptoms

A

Dyspnea, orthopnea, left HF, hoarseness, endocarditis, LA dilation
High thromboembolic risk w/ afib
Apical diastolic thrill (purring cat)

128
Q

Mitral Stenosis murmur

A

Opening snap, low pitched rumbling mid-diastolic in left lateral decubitus, best with bell

129
Q

Mitral Stenosis Tests

A

EKG (a-fib)
CXR (LA enlargement)
Echo (gradients across valve (LA>LV)

130
Q

Mitral Stenosis Treatment

A

Diuretics, B blockers, warfarin for symptoms

Balloon valvuloplasty in mod-severe or valve replacement

131
Q

Mitral Valve Prolapse

A

Most common mitral regurg, lengthened or ruptured chord tendinae
Asymptomatic, young, skinny female pts w/ skeletal deformity or marfans/ehlers-danlos
Treat w/ B blockers

132
Q

Mitral Valve Prolapse Murmur

A

Mid-systolic clicks, late systolic murmur

133
Q

Mitral Regurgitation

A

Acute: ruptured chord tendinae
Chronic: annular and LV dilation
Dilated LV, increased preload, decreased afterload
Asymptomatic>exertion dyspnea, fatigue, left HF

134
Q

Mitral Regurgitation Murmur

A

Holosystolic, apical blowing murmur the radiates to axilla, associated with thrill
S3 gallop

135
Q

Mitral Regurg Tests

A

EKG (normal initially>afib, LAE, LVH, RVH)
CXR (cardiomegaly)
Echo
Cardiac Cath (if possible sx)

136
Q

Mitral Regurg Treatment

A

No meds will prevent progression

Sx repair>replacement, can do trans catheter for primary or for mod/severe that can’t undergo open sx

137
Q

Acute Mitral Regurg Murmur/treatment

A

Holosystolic murmur at apex, radiates to axilla or back

IV nitroglycerin, IABP as bridge to surgery for repair/replacement

138
Q

Aortic Stenosis

A

“graying of the heart”, impaired or preserved LVEF
Risk factors: bicuspid aortic valve, rheumatic fever
LVH > LAH, oxygen demand outweighs supply
“fixed cardiac output”

139
Q

Aortic Stenosis Signs/Symptoms

A

Asymptomatic for decades

Angina, dyspnea, syncope, delayed carotid pulse

140
Q

Aortic Stenosis Murmur

A

harsh systolic crescendo-decrescendo at right sternal border radiating to neck, can have thrill

141
Q

Aortic Stenosis Tests

A

EKG
Echo (characterization, LV size/thickness/EF)
Caution with stress testing
Cardiac cath if possible sx

142
Q

Aortic Stenosis Treatment

A

No medications help
Control BP in asymptomatic
transcatheter replacement if not sx candidate
avoid hypotension

143
Q

Chronic Aortic Regurgitation

A

^ end diastolic volume, ^wall stress/cardiac output, ^afterload/worse CO
Asymptomatic>dyspnea>LHF
Water hammer pulse

144
Q

Chronic Aortic Regurgitation Murmur

A

Blowing diastolic decrescendo at left sternal base

Austin flint: mid-late diastolic rumble at apex (severe AR)

145
Q

Chronic Aortic Regurgitation Tests

A

EKG
CXR (cardiomegaly, dilated aortic knob)
Echo

146
Q

Chronic Aortic Regurgitation Treatment

A

SX if symptomatic or >5cm

Vasodilators, CCB, ACE, B blockers (decrease rate of root enlargement)

147
Q

Acute Aortic Regurgitation

A

True emergency-loss of LV compensatory mechanisms, can’t adapt to increased diastolic filling

148
Q

Acute Aortic Regurgitation Signs/symptoms

A

Sudden hemodynamic deterioration
weakness, mental status change, severe dyspnea, diaphoresis, syncope, chest pain (aortic dissection), cool extremities
Quickly progresses to hemodynamic collapse

149
Q

Acute Aortic Regurgitation Tests

A

EKG (nonspecific ST changes, sinus tach)
CXR (widened mediastinum, palm edema or normal)
Echo
TEE and blod cultures if endocarditis suspected

150
Q

Acute Aortic Regurgitation Treatment

A

SURGICAL EMERGENCY
Stabilize hemodynamic w/ vasodilators, IV inotropes
B blockers if aortic dissection

151
Q

Tricuspid Stenosis

A

RARE
Rheumatic valve disease most common cause
Leads to systemic venous congestion, worsened by exercise/inspiration
Murmur: diastolic over left sternal border w/ inspiration
EKG and echo
Sx treatment

152
Q

Tricuspid Regurgitation

A

Volume overload of RV, increased systemic venous pressures ad RHF

Caused by dilated right ventricle, connective tissue diseases, trauma

153
Q

Tricuspid Regurg Symptoms

A

RHF, hepatic congestion and peripheral edema, increased JVP

154
Q

Tricuspid Regurg Murmur

A

Pansystolic at 3-4th intercostal space at left sternal border, increases with inspiration

155
Q

Tricuspid Regurg Tests/Treatment

A

EKG (nonspecific, RBBB, afib)
Echo
Treat RHF (diuretics, ACEs), Sx if already going in for other cause

156
Q

Pulmonary Stenosis

A 
Congenital
Cyanosis, RHF, dyspnea
Murmur: harsh systolic crescendo-decrescendo at 3-4 ICS
EKG/echo
rarely requires intervention
157
Q

Cardiomyopathy

A

Abnormality of heart muscle, can be ischemic, hypertensive or valvular

158
Q

3 Main Types of Cardiomyopathy

A

Dilated (most common), hypertrophic (#1 cause of sudden death in athletes <35) and restrictive (least common)

159
Q

Dilated Cardiomyopathy

A

Ventricular enlargement w/out hypertrophy, systolic dysfunction, interstitial and endocardial fibrosis
Usually gradual onset

160
Q

Causes of Dilated Cardiomyopathies

A

ABCD PIG
Alcohol, Beriberi (thiamine deficiency), Coxsackie B or Chagas, Drugs (adriamycin/cocaine), Pregnancy, Idiopathic (50%)/infection, Genetic

161
Q

Types of Dilated Cardiomyopathy

A

Hypertensive, ischemic, alcoholic, permpartum, Takotsubo

162
Q

Hypertensive Cardiomyopathy

A

Concentric LVH
“hypertensive heart disease”
Due to uncontrolled/sustained HTN over long period of time

163
Q

Ischemic Cardiomyopathy

A

Most common cause of HF due to systolic dysfunction
EF 35-40% from CAD (often after MI)
Treat w/ ASA, statin, B blocker, ACE, loop diuretic

164
Q

Alcoholic Cardiomyopathy

A

Prolonged QTc

Treat outcome with abstinence, but can’t reverse

165
Q

Permpartum Cardiomyopathy

A

Development of HF late in pregnancy or w/in 5 months of birth (LVEF <45%)
Risks: >30years, black, cocaine, multiple fetuses
Low chance of recurrence if recovered

166
Q

Takotsubo Cardiomyopathy

A

“broken heart syndrome”
Transient LV dysfunction appearing as systolic apical ballooning on echo
Physical/emotional stressors
Symptoms mimic MI, troponin 7X upper limit, ST elevation, decreased EF
Recovery 1-4 weeks
Treat w/ B blockers

167
Q

Dilated Cardiomyopathy Signs/Symptoms

A

Edema w/ pitting, abdominal pain, nausea, congestive cough, fatigue, weakness, JVD, hypoxia (clubbing)
Sleeps w/ lots of pillows
Pulmonary congestion

168
Q

Dilated Cardiomyopathy Diagnostics

A 
CBC (anemia)
CMP (electrolytes, liver, kidney)
Thyroid, BNP
CXR (cardiomegaly, R pleural effusion, Kerley Bs
Echo
ECG (conduction delays(
Cardiac Cath (Gold standard)
169
Q

Dilated Cardiomyopathy Treatment

A

Same as HF
ACE/ARB, B blockers (EF<40%, not with HR<50), aldosterone antagonists, diuretics, nitrates, anticoagulant (if afib, thrombi)
LVAD, ICD, heart transplant (Dilated CM=45% of all heart transplants in US)

170
Q

Hypertrophic Cardiomyopathy

A

Genetic disease of heart muscle
Unexplained LV hypertrophy w/out dilation or disease, LV hyper contractile with small cavity/lots of wall stress
high incidence of sudden cardiac death (leading in kids)
Systolic dysfunction

171
Q

HCM Risk Factors for Sudden Cardiac Death

A

History of syncope, family hx, gene mutations, LV wall thickness >30mm, young age (<30)

172
Q

Hypertrophic Cardiomyopathy Signs/Symptoms

A

Fatigue, dyspnea, angina, palpitations, syncope, orthopnea, dizziness
Double apical pulse, S2 splitting, S3/S4 gallop

173
Q

Hypertrophic Cardiomyopathy Murmur

A

Systolic ejection crescendo-decrescendo at apex and left sternal border
Increases w/ decrease in preload

174
Q

Hypertrophic Cardiomyopathy Tests

A

Transthoracic echo for diagnosis*

24-48 hour ECG, exercise BP testing

175
Q

Hypertrophic Cardiomyopathy Management

A

Risk stratification every 12-24 hours, low-moderate exercise, avoid volume depletion

176
Q

Hypertrophic Cardiomyopathy Treatment

A

1st line: B blockers w/ symptomatic arrhythmias; amiodarone w/ICD; anticoags w/ afib
If Bblockers dont work>CCB>Disopyramide
Septal myectomy or ablation

177
Q

Restrictive Cardiomyopathy

A 
Least common (5% of myopathies)
Non-dilated, non-hypertrophied ventricles with impaired LV filling leading to decreased cardiac output/bi-atrial enlargement (DIASTOLIC DYSFUNCTION)
Primarily idiopathic, Amyloidosis most common cause in US
178
Q

Restrictive Cardiomyopathy Signs/Symptoms

A

SOB, fatigue, autonomic neuropathy w/ amyloidosis, edema w/ pitting, hepatomegaly, ascites, JVD, cardiac cachexia, day bruising, Kussmaul Sign

179
Q

Restrictive Cardiomyopathy Tests

A

*must distinguish from constrictive pericarditis
Echo (front line), cardiac MRI, CBC w/ smear (eosinophilia), CMP, Iron tests, BNP, ECG (ST changes, afib, low voltage QRS)

180
Q

Restrictive Cardiomyopathy Management/Treatment

A

B blockers, CCB (increase filling time), diuretics (reduce preload), ACE/ARB in amyloidosis, anticoags, pacemakers, LVAD

181
Q

Cardiac Amyloidosis

A

Mulitsystem deposition of amyloid fibrils

A systemic disease w/ cardiac infiltration

182
Q

Myocarditis

A

Inflammation of myocardium, usually manifests in healthy patient, rapidly progressive and acute
Classification based on time course

183
Q

Myocarditis Epidemiology

A

Idiopathic in 50%, viral is most common, autoimmune, exogenous and genetic/environmental
postpartum mortality rates up tp 50%

184
Q

Myocarditis Signs/Symptoms

A

Heart failure w/out underlying dysfunction, recent URI/flu-like symptoms, edema, S3 gallop, tachycardia

185
Q

Myocarditis Tests

A 
Endomyocardial Biopsy Gold standard
ECG
Echo
Cardiac MR
Titers
186
Q

Myocarditis Management

A

Supportive care, serial assessment codetermine recovery, consider transplant if severe

187
Q

Syncope

A

Sudden, transient, complete loss of consciousness and postural tone with spontaneous recovery
attributed to cerebral hypoperfusion

188
Q

Pre-syncopal Symptoms

A 
Lightheaded/dizzy
Tunnel vision
"Graying out"/facial pallor
Altered consciousness
Palpitations
Generalized weakness
Tremulousness
Nausea
189
Q

Medications that cause Syncope

A

Anti-hypertensives, anti-depressants, anti-anginals, narcotics, muscle relaxers, anti-ED, alcohol, rec drugs

190
Q

Orthostatic BP

A

> 20mm drop in systolic or >10mm drop in diastolic
HR >20bpm also
Assess 3 minutes after supine to standing
Could be due to hypovolemia, meds, autonomic dysfunction
Treat with fluids, compression socks, 6-9g salt/day

191
Q

Syncope Diagnostics

A

Echo, holter/external loop/external patch ECGs, telemetry, ICD, EP study, stress test, chest imaging, tilt table test

192
Q

Types of Syncope

A

Vasovagal
Situational
Carotid Sinus Syndrome

193
Q

Vasovagal Syncope

A

“common faint”, short duration, usually solitary attacks
Triggers: heat, standing, physical exertion
Treatment: avoid triggers, education, salt/water intake

194
Q

Situational Syncope

A

post-micturition, cough, swallow, defecation, emotional state, pain

195
Q

Carotid Sinus Syndrome

A

Syncope associated by carotid sinus stimulation, usually older pts (shaving, tight collar, neck injury, etc)
Drop in BP >50 or sinus pressure >3 seconds
Diagnose w/ carotid massage

196
Q

Bradyarrythmia

A 
Sinus node dysfunction (sick sinus syndrome)-intermittent pause w/ alternating bradycardia and tachycardia>pacemaker
OR
AV block (2nd degree type 2 (mobitz), complete heart block)
197
Q

Tachyarrhythmias

A

Supraventricular tachycardia, wolff Parkinson white, afib, vtach/torsades de pointes

198
Q

Obstructive Cardiovascular Syncope

A

Aortic stenosis most common (^LV pressure>decreased SVR>decreased BP/syncope)
Aortic dissection, HCM, pulmonary embolus, cardiac tamponade, ischemia, pulmonary HTN

199
Q

Obstructive Cardiovascular Syncope treatment

A

Pacemaker, anti-arrhythmics, fluid for preload

200
Q

Psychogenic Causes of Syncope

A

Conversion disorder, pseudo-syncope (arm-drop test), pseudo-seizures (jerking, lateral tongue biting>seizure)

201
Q

San Francisco Syncope Rule

A

Identifies low risk patients for short term serious outcomes who are unlikely to benefit from hospital admission
“CHESS”-if any are present consider admission
Congestive heart failure, Hematocrit <30%, Ecg abnormal, Shortness of breath, Systolic BP <90

202
Q

Canadian Syncope Arrhythmia Risk Score

A

Goal is to identify small set of patients who suffer arrhythmia or death w/in 30 days of ED visit for syncope

203
Q

Syncope Positions

A 
If supine/sitting>cardiogenic
If changing position>orthostatic
If prolonged standing>vasovagal
No prodrome>arrhythmia
Prodrome>vasovagal
204
Q

Life Threatening Syncope Causes

A

Cardiac
Acute severe hemorrhage (ectopic pregnancy, ovarian cyst, ruptured aneurysm, etc)
Pulmonary embolism (+hemodynamic instability)
Subarachnoid hemorrhage (+headache)
Stroke, seizure, head injury

205
Q

Shock

A

Inadequate systemic tissue perfusion>decreased O2 delivery>cellular hypoxia and metabolic malfunction
can result in cell death, end organ damage, multi-system organ failure and death

206
Q

Systemic tissue perfusion

A

MAP=COxSVR (when either is decreased so is perfusion

207
Q

Shock Stages

A

Pre-shock: “compensated shock”, tachycardia, peripheral vasoconstriction, decreased BP
Shock: “compensatory mechanism overwhelmed; tachy, dyspnea, metabolic acidosis, oliguria, confusion, clammy skin
End organ: irreversible organ damage, coma, death

208
Q

Arterial Lines

A

Radial, brachial or femoral arteries; recurrent ABGs

Don’t use for meds

209
Q

Central Lines

A

Delivery of caustic or critical meds, measurement of CVP (fluid status)
Triple/double lumen, dialysis catheters, swan-ganz catheter, PICC line (peripherally inserted central line cath.-venous pressures, multiple drugs, blood draws)

210
Q

Central Venous Pressure

A

5-15mmHg

near right atrium, correlates to preload or volume status

211
Q

Swan-Ganz Catheter

A

Enters heart through SVC>R atrium>r ventricle>palm artery

Best for cardiogenic shock

212
Q

Clinical Presentation of Shock

A

hypotension (<90 or decrease >40), tachycardia (except neurogenic shock), oliguria, mental status changes, metabolic acidosis

213
Q

Hypovolemic Shock

A

Inadequate volume>decreased CO and O2 delivery

Blood loss or fluid loss (trauma/bleed, burns, pancreatitis)

214
Q

Pathophysiology of Hypovolemic Shock

A

Decreased blood volume>decreased SV> decreased CO/BP>decreased O2 delivery, ^SVR to compensate for decreased CO
switch from aerobic to anaerobic metabolism, blood pushed to trunk body

215
Q

Hypovolemic Shock Presentation

A

Depends on amount and rate of loss
Hematemisis, hematochezia (bloody poop), melena, N/V/D, abdominal pain, trauma, post-op
Dry mouth, hypotension,tachycardia/pnea, cool/clammy extremities, low turgor, confused

216
Q

Hypovolemic Shock Diagnostics

A

CBC, CMP, PT/INR, lactate (increases), ABG, CXR/CT, abdominal XR/CT

217
Q

Hypovolemic Shock Management

A 
Replace volume (saline, albumin/colloid, blood), monitor response (urine output, perfusion, etc)
Vasopressors if severe
218
Q

Cardiogenic Shock

A

Decreased CO due to pump failure

Caused by ischemia, valvular heart disease, arrhythmias, Obstructive* (tamponade, pneumothorax, palm embolism)

219
Q

Pathophysiology of Cardiogenic Shock

A

Pump failure>decreased BP/CO>activation of SNS>decreased renal perfusion>sodium/fluid retention; sen=condary response=^filling pressures>volume overload in lungs>^SVR to compensate for decreased CO
CVP ^ (>5); CO decreased 1500); PCWP ^ (>5)

220
Q

Presentation of Cardiogenic Shock

A

Chestpain, dyspnea, palpitations, fatigue

Tachy, hypotension, cool clammy extremities, JVP, muffled heart sounds, new murmur, deviated trachea, crackles in lungs

221
Q

Cardiogenic Shock Diagnostics

A

CBC, CMP, Cardiac enzymes, ABG, EKG (MI, arrhythmia), CXR, echo (ejection fraction), Chest CT

222
Q

Cardiogenic Shock Management

A

Treat underlying problem, cardio consult, fluids (but be cautious)
Inotropes (dobutamine first line), vasopressors, diuretics, anti-arrhythmics
Last line: LVAD, ECMO, transplant

223
Q

Distributive (Vasodilatory) Shock

A 
#1 cause: Sepsis
Decreased SVR/vasodilation; Inadequate tissue perfusion/cellular hypoxia resulting from ^O2 demand from tissues to combat systemic infection/septic endotoxins
SALAD: sepsis, Adrenal insufficiency, Liver disease, Anaphylaxis, Drugs
224
Q

Pathophysiology of Early Septic Shock

A

^BP bc of O2 demands>vasodilation (decreased SVR)
When low BP detected>^HR/contractility/CO
Circulating endotoxins aggravate cellular hypoxia, exert toxic effects on soft tissues/organ

225
Q

Pathophysiology of Late Septic Shock

A

Capillary leakage, loss of vascular tone>hypovolemia/hypotension>stimulates SNS>^HR/SVR
Vasoconstriction compromises tissue perfusion aggravating cellular hypoxia>organ system malfunction

226
Q

Septic Shock Presentation

A

Fever, low BP, ^HR, warm extremities (early), confused
Early (warm): ^ CO, decreased CVP/SVR
Late (cold): ^SVR, decreased CO/CVP

227
Q

Septic Shock Diagnostics

A

CBC, CMP, Lactate (higher it is=worse), blood/urine cultures, ABG, CXR, other imaging

228
Q

Septic Shock Treatment

A

Goal directed
Treat underlying problem/infection, broad spectrum antibx after culture, fluid resuscitation
Vasopressors (norepinephrine first line), ventilator if needed

229
Q

Neurogenic Shock

A

Loss of sympathetic tone>vasodilation and hypotension (bradycardia+hypotension)
Spinal cord injury/closed head trauma

230
Q

Pathophysiology of Neurogenic Shock

A 
SNS responsible for release of epi/norepi which cause ^HR, myocardial contractility and peripheral vasoconstriction; disruption in SNS>unopposed parasympathetic action>hypotension with decreased SVR and normal-low HR
Decreased CO (<4), SVR (<1500) and CVP (<5)
231
Q

Neurogenic Shock Presentation

A

low BP/HR, altered mental status, para/quadriplegic, altered senses depending on level, warm extremities, decreased sphincter tone

232
Q

Neurogenic Shock Diagnostics

A

CBC, CMP, Xrays (Cspine), head CT, spinal CT/MRI

233
Q

Neurogenic Shock Treatment

A

Address co-existing symptoms, fluids for hypovolemia, Neurosurgery consult

234
Q

PQRST Conductions

A 
P-depolarization of atria (SA node)
PR-AV node delay/ventricular filling
QRS-depolarization of ventricles/pumping
ST-repolarization starting
T wave-ventricular repolarization
235
Q

Heart Rates

A 
300>150>100>75>60>50>43>37
Normal 60-100
SA node/sinus: 60-100
AV node: 40-60
Ventricular escape:20-40 (purkinjes)
236
Q

Rhythm Disorder Signs/Symptoms

A

Fatigue,palpitations, syncope, dizziness

JVP

237
Q

Anti-arrhythmic Drugs

A

Na channel blockers, B blockers, K blockers, CCB, digoxin, adenosine

238
Q

Tachycardia

A

> 100bpm, SA node

Secondary to another cause (fever, pain, anemia, hypovolemia, thyrotoxicosis, HF, etc); gradual onset

239
Q

Bradycardia

A

<60bpm
Vagal influence/disease of SA node
Normal for athletes/sleep
Pacemakers

240
Q

Supraventricular Tachycardias

A

Must have a 12 lead EKG for diagnosis

PSVT, MAT, Afib, Aflutter, WPW

241
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A

Narrow complex, 150-250 bpm; QRS<120ms
Sudden onset/termination, few seconds-few hours
Indication of structural disease
Symptoms: palpitations, diaphoresis, dyspnea dizziness, chest discomfort
Treatment: valsalva, carotid sinus massage; adenosine, IV CCB/BB (esmolol), ablation

242
Q

Multifocal Atrial Tachycardia (MAT)

A 
seen wit Severe COPD
100-400bpm
Intermittent/self-limiting, often confused with Afib
May need BB or CCB
No anti-coag
243
Q

Atrial Fibrillation

A

Most common chronic arrhythmia, often paroxysmal
Can cause intracardiac clots due to atrial stasis
Risk factors: alcohol/holiday heart, pericarditis, chest trauma, thyroid disorders, sleep apnea, pulmonary disease, age, meds

244
Q

A-fib Symptoms/Tests

A

Asymptomatic-heart failure:
chest pain, fatigue, dyspnea, palpitations, syncope, HF, stroke symptoms
“irregularly irregular”
EKG: no distinct P waves, QRS variable/irregular

245
Q

A-fib Classifications

A

Paroxysmal: terminates spontaneously or w/in 7 days w/ treatment
Persistent: fails to terminate after 7 days
Longstanding persistent: longer than 12 months
Permanent: agreed to stop treatment, adopt “rate control”

246
Q

CHADSVASC

A

> 2 qualify for anticoagulant (warfarin)
1=anti-platelet therapy recommended
0=no therapy
Does not apply for valvular afib pas-automatically get warfarin

247
Q

A-fib treatment

A

Acute: rate control (diltiazem, esmolol, digoxin, amiodarone), cardioversion for unstable, anticoags
Long term: antiarrhythmic drugs, ablation, surgical Maze; BB, CCB, digoxin, pacemaker, AV node ablation

248
Q

Atrial Flutter

A

“saw tooth pattern” on ECG leads 2, 3, VF
2:1, 3:1 or 4:1 conduction pattern, atrial rate 300bpm, ventricular 150bpm
Presents same as Afib
Treat with anticoags, cardioversion

249
Q

Wolff Parkinson White

A

Pre-excitation syndrome; accessory pathways between atrium and ventricles
Short PR interval, wide QRS, delta wave
Syndrome when SVT develops
Presents and treat like PSVT, but avoid CCB and B blockers
Catheter ablation to block pathways

250
Q

Premature Ventricular Complexes

A

Early V depolarization>wide QRS without p wave, can be bigeminal or trigeminal
Palpitation most common symptom
Irregular pulse, work with holder monitor
Treatment: Blockers/CCB, antiarrhythmics (sotalol), ablation

251
Q

1st Degree Atrioventricular Block

A

PR >200ms
all impulses conducted to ventricles, benign, asymptomatic, no treatment; avoider blockers
“if R is far from P then you have a first degree”

252
Q

2nd Degree Atrioventricular Block Type 1

A

Wenckeback/Mobitz1
PR elongates until QRS is blocked
Block within AV node, generally asymptomatic, benign
“longer, longer, longer drop, now you have a wenckebach”

253
Q

2nd Degree Atrioventricular Block Type 2

A

Fixed PR, dropped QRS; more than 1 blocked p wave in a row, originates in Bundle of His
Malignant/emergent-pacemaker indicated, atropine to increase HR
“If some Ps just don’t go through then you have a Mobitz type 2”

254
Q

3rd Degree Block

A

Complete heart block-no conduction from atria to ventricles; Ps separate from QRS, atrial rate faster than ventricular
Presents w/ syncope, SOB, HF, fatigue
Medical emergency>pacemaker asap
Atropine to increase HR
“If Ps and Qs just don’t agree then you have a 3rd degree”

255
Q

Ventricular Tachycardia

A

Wide QRS complex, 160-200bpm
Syncope, dizziness, palpitations, chest pain
Sustained: over 30 seconds in duration
Nonsustained: more than 3 beats but <30s before spontaneous termination

256
Q

V-tach Diagnostics

A

Stable w/ normal vitals, hemodynamically unstable or pulseless
Cardiac cath, QRS only thing on ECG big “saw-tooth”

257
Q

V-tach Treatment

A

Treat underlying

Long-term:B blockers, ICD implant, anti arrhythmic call 3 (sotalol/amiodarone), ablation if persistent

258
Q

Torsades de Pointes

A

Polymorphic VT
“twisting of the point”-twisted/prolonged QRS, can occur in complete heart block
Requires emergency cardioversion, can lead to sudden cardiac death
magnesium to treat after cardioversion
Presents with syncope

259
Q

Torsades de Pointes Treatment

A

ACLS: if unstable-debibrillation; IV magnesium, IV B blocker
Long term: B blockers, ICD
Treat underlying causes/stop offending meds

260
Q

Ventricular Fibrillation

A

No discernible activity, 200-300bpm
Pulseless, quick death unless resuscitated (progresses to systole)
Requires emergent defibrillation
CAD most common cause (65-70%)
Focus is on rapid resuscitation>prevent anoxic brain injury

261
Q

V-fib Management

A

ACLS guidelines: ABCs, defibrillator/CPT, epi

Once resuscitated-hypothermia protocol (32-36*),EKG, echo, cardiac cath, ICD

262
Q

Sick Sinus Syndrome

A

Sinus node dysfunction (sinus arrest/pause, tachy-brady syndrome)
Brady due to fibrosis/MI/meds
Fatigue, dyspnea, dizziness, syncope
*symptoms+EKG findings

263
Q

Sick Sinus Syndrome Treatment

A

Hospitalize

ACLS, atropine/dopamine/epi, transcutaneous/transvenous pacing, stop offending agents, pacemaker for bradycardia

264
Q

Accelerated Idioventricular Rhythm

A

Repetitive ventricular rhythm 60-100bpm

Accelerated ventricular focus faster than sinus node>assumes control, may be marker of repercussion

265
Q

Pacemakers

A

Used for anyone with bradycardia/conduction blocks

dual lead more common in older patients

266
Q

ICD

A

Shocks heart out of v-tach/v-fib etc

Used for cardiac arrest, systolic heart failure, EF 35-40%

267
Q

Acute Rheumatic Fever

A

Develops 1-5 weeks post strep in 5-15 Y.O. w/ risk of recurrence within 10 years, most mitral valve>aortic>tricuspid

268
Q

Diagnosis of rheumatic fever

A

Echo, ECG, ASO titer, CRP/ESR

269
Q

Treatment of rheumatic fever

A

Supportive care
1st line-Salicylates (then steroids if needed) for arthralgia
Benzathine Penicillin IM inj.

270
Q

Rheumatic Heart Disease

A

Mitral 50-60%>aortic/mitral>aortic>tricuspid

10-20 years after rheumatic fever

271
Q

Diagnosis of rheumatic heart disease

A

Transthoracic echo

272
Q

Treatment of rheumatic heart disease

A

Restrict activity, treat complications, prevent IE

273
Q

Infective Endocarditis

A

clin presentation/risk factors
Present with fever, cough, dyspnea, arthralgia, diarrhea, back pain, regurgitant murmur, Osler nodes, Janeway lesions, Roth spots

274
Q

Etiology of Infective Endocarditis

A

Bacteria in bloodstream causes vegetations
Native valve: S. aureus
Prosthetic: S. aureus early, Strep late
Drug users: S aureus>strep>enterococci

275
Q

Diagnosis of Infective Endocarditis

A 
BLOOD CULTURES (2+)
Echo (TTE or TEE), EKG, CXR
276
Q

Infective Carditis Risk Factors

A

Sex, age (>60), IV drug use, poor dentition, valvular disease, prosthetic valve, dialysis

277
Q

Treatment for Infective Endocarditis

A

Usually vancomycin 4-6 weeks (table for more)
SX if fungus, prosthetic infection, emboli, abscess
Prophylaxis: amoxicillin 2mg for prosthetic valves, Congential HD, dental/resp tract procedures

278
Q

Duke criteria of Infective Endocarditis

A

Major: 2 pos cultures, endocardial involvement on echo, new murmur
Minor: fever, vascular findings, immuno findings, 1 pos culture
Need 2 major or 1 major+3 minor or 5 minor

279
Q

Acute Pericarditis

A

Inflammation of pericardial sac, most common pericardium disorder, commonly idiopathic or viral

280
Q

Acute Pericarditis Clinical Presentation

A

Chest pain* (sudden, anterior, sharp, improves leaning forward), fever, malaise, myalgia, dyspnea, tachypnea
Friction rub at L sternal border

281
Q

Diagnosis of Acute pericarditis

A 
ECG* (diffuse ST elevation, PR depression)
CT w/ contrast
MRI
Biomarkers (tropinin^)
New/worsening effusion*
Friction rub*
"swinging heart"
282
Q

Treatment of Acute Pericarditis

A

NSAIDS (Ibu 600-800 TID, taper) +/- colchicine (0.6-1.2x2 on day 1, then based on weight)
Glucocorticoids if can’t take NSAIDS
Treatment up to 2 weeks
Activity restriction

283
Q

Pericardial Effusion

A

Fluid in pericardium exceeds 15-50mL, usually due to injury to pericardium
Other causes: idiopathic, infectious, malignancy, post-op, autoimmune, drugs

284
Q

Pericardial Effusion Presentation

A

Asymptomatic
Chest pain/pressure/discomfort, syncope, light-headed, palpitations, respiratory
Friction rup, JVP, tachycardia, decreased lung sounds, weak pulse, edema, cyanosis, pulses paradoxus

285
Q

Pericardial Effusion Diagnostics

A 
ECG (low voltage, tachycardia, alternates/swinging heart)
CXR (cardiomegaly)
Echo (choice test)
CT
Pericardiocentesis
286
Q

Pericardial Effusion Treatment

A

Observation
Treat underlying cause
NSAID +/- colchicine if pericarditis involved

287
Q

Chronic Pericardial Effusion

A

Present for 3+ months
Often asymptomatic, can cause cardiac tamponade randomly
Pericardiectomy if reaccumulation of fluid

288
Q

Hemorrhagic Pericardial Effusion

A

Blood fills pericardial space instead of serous fluid

Malignancy most common cause (breast cancer)

289
Q

Cardiac Tamponade

A

Compression due to increased pericardial pressure, reducing diastolic compliance>reduced CO and BP
Acute: within minutes due to trauma/rupture etc
Subacute: days to weeks-neoplastic, uremic, idiopathic

290
Q

Cardiac Tamponade Presentation

A

Dyspnea*, fatigue, syncope, chest discomfort, edema, tachypnea, Beck’s Triad
Tachycardia, friction rub, cold clammy extremities

291
Q

Beck’s Triad

A

Hypotension, JVP, muffled heart sounds

292
Q

Cardiac Tamponade Diagnosis

A 
CLINICAL
ECG: tachycardia, low voltage
CXR: cardiomegaly
Echo: must be done for hemodynamic significance
Labs-for underlying disorders
293
Q

Cardiac Tamponade Treatment

A

STAT cardio consult, echo guided pericardioentesis or sx drainage

294
Q

Constrictive Pericarditis

A

Scarring/loss of elasticity, filling volume restricted decreased stroke volume/cardiac output

295
Q

Constrictive Pericarditis Presentation

A

Symptoms of heart failure* (edema, anasarca)
diminished cardiac output, chest pain
JVP*, Kussmauls sign, pericardial “knock” (right before S3)

296
Q

Constrictive Pericarditis Diagnosis

A 
ECG (ST/T wave changes)
CXR: pericardial calcification*
Echo
CT
Cardiac cath
BNP (increased)
297
Q

Constrictive Pericarditis Treatment

A

Try conservative 2-3 months (diuretics)

Pericardiectomy is only definitive treatment

298
Q

Aortic Aneurysm

A

Localized dilation of aorta including all 3 layers of vessel

Most common infrarenally>ascending thoracic (usually due to cystic medial necrosis)

299
Q

Aortic Aneurysm Presentation

A

Asymptomatic
Chest/abdominal/back pain
Hoarseness, respiratory, extremity pain

Triad: hypotension, abdominal/back pain and pulsatile abdominal mass>ruptured AAA

300
Q

Aortic Aneurysm Diagnosis

A

Chest/abdominal x-ray
Ultrasound
CT/MRI w/ angio-assess size and location

301
Q

Aortic Aneurysm Treatment

A

Immediate surgical intervention for rupture
Suggested sx repair for >5.5cm, symptomatic or rapidly growing

Risk factor modifications, BP control

302
Q

Acute Arterial Occlusion

A

Sudden cessation fo blood supply due to thrombus or embolus

303
Q

Arterial Emboli

A

Most originate in heart (a-fib, MI, debris from prosthetic valves)
Can be malignancy or Antiphospholipid antibody syndrome (appears in pregnancy)

304
Q

Acute Arterial Occlusion Presentation

A

Ranges from claudication-paralysis
can be sudden and dramatic in healthy patient
6 P’s: paresthesia, pain, pallor, pulseless, paralysis, poikilothermic (change in temp)

305
Q

Acute Arterial Occlusion Diagnosis/Treatment

A

Diagnosis: Ultrasound, CTA, MRA
Treatment: IV heparin, thrombolytic meds, revascularization sx

306
Q

Varicose Veins

A

Dilated, elongated tortuous subcutaneous veins; valvular incompetence in perforating veins of legs
^ with age, pregnancy, female, hereditary, obesity

307
Q

Varicose Veins Exam

A

Tortuous veins, dermatitis, hyperpigmentation, edema, ulcers, infection
Ultrasound

308
Q

Varicose Vein Treatment

A

Leg elevation, compression socks, weight loss
Topical corticosteroids, antibiotics if infection present
Sclerotherapy (ablation), laser treatment, surgery (phlebotomy)

309
Q

Deep Vein Thrombosis

A

Clot forms in deep vein of legs, thighs or pelvis

Virchow’s Triad (venous stasis, vessel wall injury, coagulation abnormality)

310
Q

DVT Presentation

A

Swelling, pain and discoloration of leg, 1-2cm circumferential difference
Positive Homan’s sign
Pulmonary embolism symptoms

311
Q

DVT Diagnosis

A

Venous ultrasound*

Contrast venography

312
Q

DVT Treatment

A

Anticoags for 3, 6 or 12 months
Low molecular-weight heparin
IV heparin
Oral anticoagulant (warfarin 10mg/day

Foundations 2 (4 decks)

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