Exam 2 Flashcards

(312 cards)

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
ACC/AHA Classification Guidelines
``` 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 ```
26
HTN Diagnostic Tests
CBC, urinalysis, Blood chem (glucose, Ca, creatinine, electrolytes, GFR), TSH, lipid profile, EKG, echo, urine albumin
27
Treatment for Elevated BP
Lifestyle changes, reassess in 3-6 months
28
Treatment for Stage 1 HTN
if 10 year risk >10% or already have CVD/DM/CKD: lifestyle changes and meds if NOT: lifestyle changes
29
Treatment for Stage 1 HTN
if 10 year risk >10% or already have CVD/DM/CKD: lifestyle changes and meds (1 month f/u) if NOT: lifestyle changes
30
Treatment for Stage 2 HTN
Lifestyle changes and meds (1 month f/u)
31
ACC/AHA BP Goal of <130/80
Ischemic heart disease, heart failure w/ reduced EF, CKD, DM
32
HTN treatment in pregnancy
Methyldopa, nifedipine, labetalol | NO ACE/ARB/DRI
33
Poor outcomes of HTN
CVD, HF, LVH, ischemic stroke, intracerebral heme, CKD, peripheral artery disease, retinopathy
34
Indicators of poor prognosis
high pulse pressure, men >55 women >65
35
Benefits of HTN Therapy
``` Reduce risk of MI by 20-25% Stroke by 35-40% HF >50% CKD ```
36
Resistant Hypertension
failure to achieve goal BP in pt adhering to full-dose treatment of 3 drug regimen (or at goal w/ 4)
37
Causes of resistant HTN
Improper BP reading, volume overload, drug induced, obesity, excess alcohol
38
Cholesterol
Helps form steroid hormones and bile acids
39
Triglycerides
helps transfer energy from food to cells
40
Lipoproteins
how lipids are transported Low density: more triglycerides (bad) High density: more apoproteins (good)
41
Cholesterol Transport Steps
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
42
Total cholesterol (equation)
HDL+VLDL+LDL | VLDL and LDL are calculated not measured, we measure total, HDL and triglycerides (VLDL=tri/5)
43
Cardiovascular Disease
Fatty material collected in arterial walls hardening over time, started by excess cholesterol
44
Plaque Formation Cascade
LDL oxidation>macrophages create foam cells>endothelial dysfunction>vasoconstriction/plaque formation
45
CV Risk factors (modifiable)
HTN, DM, Dyslipidemia, CKD, obesity, smoking, HDL
46
CV risk factors (non-modifiable)
Age (M>45 F>55), sex, fam hx of premature heart disease (M<55 F<65)
47
CVD Risk Calculators
Coronary Framingham risk score (10 year risk MI/death) | ACC/AHA risk estimator plus (risk of heart disease and stroke)
48
Hyperlipidemia Physical
Most asymptomatic | Rare findings: xanthomatous tendons, corneal arcus, lipemia retinalis, xanthelasma, eruptive xanthomas
49
Low Intensity Statins
``` <30% LDL lowering simvastatin 10mg Pravastatin 10-20 Lovastatin 20 Fluvastatin 20-40 ```
50
Moderate Intensity Statins
``` 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 ```
51
High Intensity Statins
>50% LDL lowering Atorvastatin 40-80 Rosuvastatin 20-40
52
Cholesterol Screening/goals
Adults 20+ | LDL <70mg/dL (but nothing set in stone)
53
Statin Benefit Groups
1- 2dary prevention in patients w/ CVD 2- severe hyperholesterolemia (LDL>190) 3- DM patients 4- Primary prevention based on risk
54
Secondary Prevention w/ CVD (statin guidelines)
Goal is to reduce LDL w/ HIGH INTENSITY statin | if very high risk (multiple major cardiac events) add non-statin to lower LDL more
55
Severe Hypercholesterolemia
LDL>190 | High Intensity Statin (if tolerated)
56
Patients w/ DM (statin guidelines)
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
57
HMG-CoA Reductase Inhibitors MOA
-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%
58
HMG-CoA Reductase Inhibitors Contraindications
Pregnancy/breastfeeding, acute liver disease, elevated LFTs
59
HMG-CoA Reductase Inhibitors Side effects
Myalgias, myopathy, rhabdomyolysis, hepatotoxicity (rare), DM
60
Cholesterol Absorption Inhibitor MOA/use
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%
61
Cholesterol Absorption Inhibitor Contraindications
hepatic impairment, don't use with fibrates
62
PCSK9 Inhibitor
Alirocumab, evolocumab monoclonal antibodies block PCSK9 effect of degrading LDL receptors Lowers LDL 50-60% Very expensive, consider for familial hypercholesterolemia
63
Fibric acid Derivatives
Gemfibrozil, fenofibrate Reduced synthesis/increased breakdown of VLDL Drug of choice for TG>500 (decreases 40%)
64
Fibric Acid Derivatives Side effects/contraindications
SE: cholelithiasis, hepatitis, myositis Contras: liver disease/impairment, gallbladder disease, caution with pregnancy/renal impairment DO NOT USE WITH STATINS
65
Bile Acid Binding Resins MOA
Cholestyramine, colesevelam, colestipol Bind bile in intestine ONLY LIPID LOWERING SAFE IN PREGNANCY LDL decrease 15-25%
66
Bile Acid Binding Resins Side effects/Contraindications
SE: GI symptoms Contras: GI obstruction, hypertriglyceridemia, pancreatitis
67
Niacin
Reduces production of VLDL Long acting better tolerated-less flushing HDL increase 25-35%
68
Niacin Side effects/Contraindications
SE: flushing Contras: liver disease, peptic ulcers Caution with: pregnancy, gout, DM
69
Familial Hypercholesterolemia
LDL receptors absent or dysfunctional
70
Metabolic Syndrome
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)
71
Hypertriglyceridemia
Mild 200-499 mg/dL Moderate >500 Increased risk of pancreatitis Severe >1000: milky white serum, acute pancreatitis
72
ATP3 HCL Guidelines (9 steps)
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
73
Acute Coronary Syndrome Therapy
M-morphine O-oxygen N-nitroglyceride A-aspirin
74
Angina
Clinical syndrome characterized by chest, jaw, shoulder or arm discomfort attributable to coronary ischemia
75
NSTEMI/STEMI
angina with elevated cardiac biomarkers indicating MI with or without ST segment deviation
76
MI Symptoms
Symptoms of ischemia, new ST segment changes/LBBB, pathological Q waves, new loss of viable myocardium, identification of thrombus
77
Etiologies of Acute Coronary Syndrome
Coronary artery obstruction/atherosclerosis, vasospasm, coronary embolism, dissection, metabolic demand
78
Coronary Artery Disease Risk Factors
M>F, age, CKD, DM, HCL, HTN, PAD, tobacco, fam hx
79
MI EKG Evolution
Peaked T waves>ST seg elevation>Q wave formation>T wave inversion
80
MI Initial Diagnostic Studies
EKG, Cardiac biomarkers (CK, CK-MB, troponin), CBC, BMP, coag panel, cholesterol levels, BNP, Chest XR
81
Other causes of Elevated Troponin
Tachy/bradyarrhythmias, cardiogenic, hypovolemic or septic shock, severe anemia, heart failure, pulmonary embolism, renal failure
82
Cardiac Enzyme Time Frames
CK-MB: rises 3-4h, peaks 12-24h, normalizes 1-3 days | Troponin: rises 3-6h, peaks 12-24h, normalizes 7-14 days
83
TIMI Risk Score
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
84
Acute Coronary Syndrome Medications
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
85
Anti-platelet Therapy for ACS/STEMI
``` 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) ```
86
Anticoagulation Therapies
Recommended in addition to dual anti-platelet Indirect Thrombin Inhibitors: UFH bolus, Enoxaparin, Fondaparinux Direct Thrombin Inhibitors: Bivalirudin, Argatroban
87
Calcium Channel Blockers (ACS)
Not used often (-pyridines) | Used for ongoing angina
88
Final Risk Stratification
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*
89
Who should get Stress Test
Abnormal baseline ECG: baseline ST abnormalities, bundle branch block/conduction delays, LV hypertrophy, paced rhythm, pre-excitation, digoxin
90
Percutaneous Coronary Intervention
Cather in leg>aorta stops at L coronary artery, contrast injected and Xray done to find stenosis
91
Vessels Used in CABG
Internal thoracic artery best for LAD grafts | Great saphenous vein used commonly
92
Infarction Complications
Arrhythmias and conduction abnormalities (sinus bradycardia, SVT, PVC/vtach/vfib, heart blocks, heart failure/shock, mechanical defects, inflammation (pericarditis)
93
Heart Failure
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
94
Systolic Heart Failure
Reduced ejection fraction (<60%), results in eccentric remodeling
95
Diastolic Heart Failure
Normal/preserved ejection fraction, altered ventricular compliance>high filling pressure, results in concentric remodeling
96
Systolic HF Classification
Depressed myocardial contractility: Cardiac ischemia (#1), severe hypertension (#2), aortic stenosis, valvular regurgitation, dilated cardiomyopathy
97
Diastolic HF Classification
Abnormal diastolic relaxation/filling (stiff): hypertrophic/restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis, LVH
98
Ejection Fraction
% of blood ejected during systole in relation to end-diastolic volume Normal 50-57% Borderline 41-49% Low<40
99
Most common cause of HF
Left sided heart failure
100
ACC/AHA Heart Failure Classifications
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
101
New York HA Heart Failure Classifications
``` Based on Symptoms I: Asymptomatic II: Symptomatic w/ moderate exertion III: Symptomatic w/ minimal exertion IV: Symptomatic at rest ```
102
Left Ventricular Failure Signs/Symptoms
Pulmonary issues | Dyspnea, fatigue, weight gain, pulmonary crackles/wheezing, Elevated JVP, edema, S3/4 gallop
103
Right Ventricular Failure Signs/Symptoms
Peripheral signs | Edema, hepatomegaly, anasarca (full body edema), elevated JVP, S3 gallop, ascites
104
S3 Gallop
Early diastole, congestive heart failure (Kentucky)
105
S4 Gallop
Late Diastole, diastolic failure and noncompliant ventricle | Tennessee
106
Heart Failure Diagnostic Studies
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
107
B-type Natriuretic Peptide
Hormone released from ventricles in response to ventricular volume expansion and pressure overload <100 noHF 100-400 iffy >400 consistent with HF
108
2 most important things to do in HF
Reduce BP and heart rate (decrease cardiac workload)`
109
Initial treatment of HF
diuretic and ACE | can use B blockers later, NO CCB
110
Diuretics in HF
Decrease preload, monitor renal function and electrolytes (for hyper/hypokalemia) Loop diuretics better in severe, given IV when acute
111
Potassium sparing diuretics in HF
``` Spirinolactone/eplerenone inhibit aldosterone Indicated for NYHA class III/IV with LVEF <35% or HF/LVEF<40% Monitor for hyperkalemia ```
112
ACE-I in Heart Failure
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
113
ARBs in Heart Failure
block vasoconstrictors that contribute to impairment of LV function Useful for patients that can't use ACEs
114
B Blockers in Heart Failure
ALL patients w/ stable HF from LV systolic dysfunction | all asymptomatic with EF<40% and all patients with MI
115
Digoxin in Heart Failure
Relieves symptoms, increases contractility inhibits Na/K/ATPase pump Used if diuretics, ACEs and B blockers don't work
116
HF treatment in Black patients
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
117
Nitroglycerin
Venous dilator, reduces preload | topical or IV
118
Implantable Cardioverter-Defibrillator (ICD)
Monitors rate and rhythm, corrects arrhythmias Previous MI and EF<30% Patients with EF<35% and NYHA class 2/3 Life expectancy >1 year
119
Pacemaker
Symptomatic NYHA class 3/4 with EF<35% and QRS >130 despite medications
120
Poor Prognosis in HF
need for hospitalization, noncompliance, age, gender, race, cause
121
Valvular Stenosis
Pressure overload on upstream cardiac and vascular structures (valve doesn't open easily)
122
Valvular Regurgitation
Volume overload and dilation of chambers over time | back flow when valve is normally closed
123
Symptoms of Valvular Heart Disease
SOB, dyspnea on exertion, palpations, syncope, edema, weakness, fatigue Good reasons for echo!
124
Valvular Disease Tests
EKG, CXR, Echo (transthoracic unless obese), blood cultures (if possible endocarditis), cardiac cath
125
AHA/ACC Valvular Classifications
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
Mitral Stenosis Causes
Rheumatic fever*, congenital, systemic disease
127
Mitral Stenosis signs/symptoms
Dyspnea, orthopnea, left HF, hoarseness, endocarditis, LA dilation High thromboembolic risk w/ afib Apical diastolic thrill (purring cat)
128
Mitral Stenosis murmur
Opening snap, low pitched rumbling mid-diastolic in left lateral decubitus, best with bell
129
Mitral Stenosis Tests
EKG (a-fib) CXR (LA enlargement) Echo (gradients across valve (LA>LV)
130
Mitral Stenosis Treatment
Diuretics, B blockers, warfarin for symptoms | Balloon valvuloplasty in mod-severe or valve replacement
131
Mitral Valve Prolapse
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
Mitral Valve Prolapse Murmur
Mid-systolic clicks, late systolic murmur
133
Mitral Regurgitation
Acute: ruptured chord tendinae Chronic: annular and LV dilation Dilated LV, increased preload, decreased afterload Asymptomatic>exertion dyspnea, fatigue, left HF
134
Mitral Regurgitation Murmur
Holosystolic, apical blowing murmur the radiates to axilla, associated with thrill S3 gallop
135
Mitral Regurg Tests
EKG (normal initially>afib, LAE, LVH, RVH) CXR (cardiomegaly) Echo Cardiac Cath (if possible sx)
136
Mitral Regurg Treatment
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
Acute Mitral Regurg Murmur/treatment
Holosystolic murmur at apex, radiates to axilla or back | IV nitroglycerin, IABP as bridge to surgery for repair/replacement
138
Aortic Stenosis
"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
Aortic Stenosis Signs/Symptoms
Asymptomatic for decades | Angina, dyspnea, syncope, delayed carotid pulse
140
Aortic Stenosis Murmur
harsh systolic crescendo-decrescendo at right sternal border radiating to neck, can have thrill
141
Aortic Stenosis Tests
EKG Echo (characterization, LV size/thickness/EF) Caution with stress testing Cardiac cath if possible sx
142
Aortic Stenosis Treatment
No medications help Control BP in asymptomatic transcatheter replacement if not sx candidate avoid hypotension
143
Chronic Aortic Regurgitation
^ end diastolic volume, ^wall stress/cardiac output, ^afterload/worse CO Asymptomatic>dyspnea>LHF Water hammer pulse
144
Chronic Aortic Regurgitation Murmur
Blowing diastolic decrescendo at left sternal base | Austin flint: mid-late diastolic rumble at apex (severe AR)
145
Chronic Aortic Regurgitation Tests
EKG CXR (cardiomegaly, dilated aortic knob) Echo
146
Chronic Aortic Regurgitation Treatment
SX if symptomatic or >5cm | Vasodilators, CCB, ACE, B blockers (decrease rate of root enlargement)
147
Acute Aortic Regurgitation
True emergency-loss of LV compensatory mechanisms, can't adapt to increased diastolic filling
148
Acute Aortic Regurgitation Signs/symptoms
Sudden hemodynamic deterioration weakness, mental status change, severe dyspnea, diaphoresis, syncope, chest pain (aortic dissection), cool extremities Quickly progresses to hemodynamic collapse
149
Acute Aortic Regurgitation Tests
EKG (nonspecific ST changes, sinus tach) CXR (widened mediastinum, palm edema or normal) Echo TEE and blod cultures if endocarditis suspected
150
Acute Aortic Regurgitation Treatment
SURGICAL EMERGENCY Stabilize hemodynamic w/ vasodilators, IV inotropes B blockers if aortic dissection
151
Tricuspid Stenosis
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
Tricuspid Regurgitation
Volume overload of RV, increased systemic venous pressures ad RHF Caused by dilated right ventricle, connective tissue diseases, trauma
153
Tricuspid Regurg Symptoms
RHF, hepatic congestion and peripheral edema, increased JVP
154
Tricuspid Regurg Murmur
Pansystolic at 3-4th intercostal space at left sternal border, increases with inspiration
155
Tricuspid Regurg Tests/Treatment
EKG (nonspecific, RBBB, afib) Echo Treat RHF (diuretics, ACEs), Sx if already going in for other cause
156
Pulmonary Stenosis
``` Congenital Cyanosis, RHF, dyspnea Murmur: harsh systolic crescendo-decrescendo at 3-4 ICS EKG/echo rarely requires intervention ```
157
Cardiomyopathy
Abnormality of heart muscle, can be ischemic, hypertensive or valvular
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3 Main Types of Cardiomyopathy
Dilated (most common), hypertrophic (#1 cause of sudden death in athletes <35) and restrictive (least common)
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Dilated Cardiomyopathy
Ventricular enlargement w/out hypertrophy, systolic dysfunction, interstitial and endocardial fibrosis Usually gradual onset
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Causes of Dilated Cardiomyopathies
ABCD PIG Alcohol, Beriberi (thiamine deficiency), Coxsackie B or Chagas, Drugs (adriamycin/cocaine), Pregnancy, Idiopathic (50%)/infection, Genetic
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Types of Dilated Cardiomyopathy
Hypertensive, ischemic, alcoholic, permpartum, Takotsubo
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Hypertensive Cardiomyopathy
Concentric LVH "hypertensive heart disease" Due to uncontrolled/sustained HTN over long period of time
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Ischemic Cardiomyopathy
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
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Alcoholic Cardiomyopathy
Prolonged QTc | Treat outcome with abstinence, but can't reverse
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Permpartum Cardiomyopathy
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
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Takotsubo Cardiomyopathy
"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
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Dilated Cardiomyopathy Signs/Symptoms
Edema w/ pitting, abdominal pain, nausea, congestive cough, fatigue, weakness, JVD, hypoxia (clubbing) Sleeps w/ lots of pillows Pulmonary congestion
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Dilated Cardiomyopathy Diagnostics
``` CBC (anemia) CMP (electrolytes, liver, kidney) Thyroid, BNP CXR (cardiomegaly, R pleural effusion, Kerley Bs Echo ECG (conduction delays( Cardiac Cath (Gold standard) ```
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Dilated Cardiomyopathy Treatment
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)
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Hypertrophic Cardiomyopathy
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
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HCM Risk Factors for Sudden Cardiac Death
History of syncope, family hx, gene mutations, LV wall thickness >30mm, young age (<30)
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Hypertrophic Cardiomyopathy Signs/Symptoms
Fatigue, dyspnea, angina, palpitations, syncope, orthopnea, dizziness Double apical pulse, S2 splitting, S3/S4 gallop
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Hypertrophic Cardiomyopathy Murmur
Systolic ejection crescendo-decrescendo at apex and left sternal border Increases w/ decrease in preload
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Hypertrophic Cardiomyopathy Tests
Transthoracic echo for diagnosis* | 24-48 hour ECG, exercise BP testing
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Hypertrophic Cardiomyopathy Management
Risk stratification every 12-24 hours, low-moderate exercise, avoid volume depletion
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Hypertrophic Cardiomyopathy Treatment
1st line: B blockers w/ symptomatic arrhythmias; amiodarone w/ICD; anticoags w/ afib If Bblockers dont work>CCB>Disopyramide Septal myectomy or ablation
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Restrictive Cardiomyopathy
``` 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 ```
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Restrictive Cardiomyopathy Signs/Symptoms
SOB, fatigue, autonomic neuropathy w/ amyloidosis, edema w/ pitting, hepatomegaly, ascites, JVD, cardiac cachexia, day bruising, Kussmaul Sign
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Restrictive Cardiomyopathy Tests
*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)
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Restrictive Cardiomyopathy Management/Treatment
B blockers, CCB (increase filling time), diuretics (reduce preload), ACE/ARB in amyloidosis, anticoags, pacemakers, LVAD
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Cardiac Amyloidosis
Mulitsystem deposition of amyloid fibrils | A systemic disease w/ cardiac infiltration
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Myocarditis
Inflammation of myocardium, usually manifests in healthy patient, rapidly progressive and acute Classification based on time course
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Myocarditis Epidemiology
Idiopathic in 50%, viral is most common, autoimmune, exogenous and genetic/environmental postpartum mortality rates up tp 50%
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Myocarditis Signs/Symptoms
Heart failure w/out underlying dysfunction, recent URI/flu-like symptoms, edema, S3 gallop, tachycardia
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Myocarditis Tests
``` Endomyocardial Biopsy Gold standard ECG Echo Cardiac MR Titers ```
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Myocarditis Management
Supportive care, serial assessment codetermine recovery, consider transplant if severe
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Syncope
Sudden, transient, complete loss of consciousness and postural tone with spontaneous recovery attributed to cerebral hypoperfusion
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Pre-syncopal Symptoms
``` Lightheaded/dizzy Tunnel vision "Graying out"/facial pallor Altered consciousness Palpitations Generalized weakness Tremulousness Nausea ```
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Medications that cause Syncope
Anti-hypertensives, anti-depressants, anti-anginals, narcotics, muscle relaxers, anti-ED, alcohol, rec drugs
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Orthostatic BP
>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
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Syncope Diagnostics
Echo, holter/external loop/external patch ECGs, telemetry, ICD, EP study, stress test, chest imaging, tilt table test
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Types of Syncope
Vasovagal Situational Carotid Sinus Syndrome
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Vasovagal Syncope
"common faint", short duration, usually solitary attacks Triggers: heat, standing, physical exertion Treatment: avoid triggers, education, salt/water intake
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Situational Syncope
post-micturition, cough, swallow, defecation, emotional state, pain
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Carotid Sinus Syndrome
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
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Bradyarrythmia
``` 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) ```
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Tachyarrhythmias
Supraventricular tachycardia, wolff Parkinson white, afib, vtach/torsades de pointes
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Obstructive Cardiovascular Syncope
Aortic stenosis most common (^LV pressure>decreased SVR>decreased BP/syncope) Aortic dissection, HCM, pulmonary embolus, cardiac tamponade, ischemia, pulmonary HTN
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Obstructive Cardiovascular Syncope treatment
Pacemaker, anti-arrhythmics, fluid for preload
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Psychogenic Causes of Syncope
Conversion disorder, pseudo-syncope (arm-drop test), pseudo-seizures (jerking, lateral tongue biting>seizure)
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San Francisco Syncope Rule
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
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Canadian Syncope Arrhythmia Risk Score
Goal is to identify small set of patients who suffer arrhythmia or death w/in 30 days of ED visit for syncope
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Syncope Positions
``` If supine/sitting>cardiogenic If changing position>orthostatic If prolonged standing>vasovagal No prodrome>arrhythmia Prodrome>vasovagal ```
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Life Threatening Syncope Causes
Cardiac Acute severe hemorrhage (ectopic pregnancy, ovarian cyst, ruptured aneurysm, etc) Pulmonary embolism (+hemodynamic instability) Subarachnoid hemorrhage (+headache) Stroke, seizure, head injury
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Shock
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
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Systemic tissue perfusion
MAP=COxSVR (when either is decreased so is perfusion
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Shock Stages
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
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Arterial Lines
Radial, brachial or femoral arteries; recurrent ABGs | Don't use for meds
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Central Lines
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)
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Central Venous Pressure
5-15mmHg | near right atrium, correlates to preload or volume status
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Swan-Ganz Catheter
Enters heart through SVC>R atrium>r ventricle>palm artery | Best for cardiogenic shock
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Clinical Presentation of Shock
hypotension (<90 or decrease >40), tachycardia (except neurogenic shock), oliguria, mental status changes, metabolic acidosis
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Hypovolemic Shock
Inadequate volume>decreased CO and O2 delivery | Blood loss or fluid loss (trauma/bleed, burns, pancreatitis)
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Pathophysiology of Hypovolemic Shock
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
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Hypovolemic Shock Presentation
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
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Hypovolemic Shock Diagnostics
CBC, CMP, PT/INR, lactate (increases), ABG, CXR/CT, abdominal XR/CT
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Hypovolemic Shock Management
``` Replace volume (saline, albumin/colloid, blood), monitor response (urine output, perfusion, etc) Vasopressors if severe ```
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Cardiogenic Shock
Decreased CO due to pump failure | Caused by ischemia, valvular heart disease, arrhythmias, Obstructive* (tamponade, pneumothorax, palm embolism)
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Pathophysiology of Cardiogenic Shock
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)
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Presentation of Cardiogenic Shock
Chestpain, dyspnea, palpitations, fatigue | Tachy, hypotension, cool clammy extremities, JVP, muffled heart sounds, new murmur, deviated trachea, crackles in lungs
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Cardiogenic Shock Diagnostics
CBC, CMP, Cardiac enzymes, ABG, EKG (MI, arrhythmia), CXR, echo (ejection fraction), Chest CT
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Cardiogenic Shock Management
Treat underlying problem, cardio consult, fluids (but be cautious) Inotropes (dobutamine first line), vasopressors, diuretics, anti-arrhythmics Last line: LVAD, ECMO, transplant
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Distributive (Vasodilatory) Shock
``` #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 ```
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Pathophysiology of Early Septic Shock
^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
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Pathophysiology of Late Septic Shock
Capillary leakage, loss of vascular tone>hypovolemia/hypotension>stimulates SNS>^HR/SVR Vasoconstriction compromises tissue perfusion aggravating cellular hypoxia>organ system malfunction
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Septic Shock Presentation
Fever, low BP, ^HR, warm extremities (early), confused Early (warm): ^ CO, decreased CVP/SVR Late (cold): ^SVR, decreased CO/CVP
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Septic Shock Diagnostics
CBC, CMP, Lactate (higher it is=worse), blood/urine cultures, ABG, CXR, other imaging
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Septic Shock Treatment
Goal directed Treat underlying problem/infection, broad spectrum antibx after culture, fluid resuscitation Vasopressors (norepinephrine first line), ventilator if needed
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Neurogenic Shock
Loss of sympathetic tone>vasodilation and hypotension (bradycardia+hypotension) Spinal cord injury/closed head trauma
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Pathophysiology of Neurogenic Shock
``` 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) ```
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Neurogenic Shock Presentation
low BP/HR, altered mental status, para/quadriplegic, altered senses depending on level, warm extremities, decreased sphincter tone
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Neurogenic Shock Diagnostics
CBC, CMP, Xrays (Cspine), head CT, spinal CT/MRI
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Neurogenic Shock Treatment
Address co-existing symptoms, fluids for hypovolemia, Neurosurgery consult
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PQRST Conductions
``` P-depolarization of atria (SA node) PR-AV node delay/ventricular filling QRS-depolarization of ventricles/pumping ST-repolarization starting T wave-ventricular repolarization ```
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Heart Rates
``` 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) ```
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Rhythm Disorder Signs/Symptoms
Fatigue,palpitations, syncope, dizziness | JVP
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Anti-arrhythmic Drugs
Na channel blockers, B blockers, K blockers, CCB, digoxin, adenosine
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Tachycardia
>100bpm, SA node | Secondary to another cause (fever, pain, anemia, hypovolemia, thyrotoxicosis, HF, etc); gradual onset
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Bradycardia
<60bpm Vagal influence/disease of SA node Normal for athletes/sleep Pacemakers
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Supraventricular Tachycardias
Must have a 12 lead EKG for diagnosis | PSVT, MAT, Afib, Aflutter, WPW
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Paroxysmal Supraventricular Tachycardia (PSVT)
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
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Multifocal Atrial Tachycardia (MAT)
``` seen wit Severe COPD 100-400bpm Intermittent/self-limiting, often confused with Afib May need BB or CCB No anti-coag ```
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Atrial Fibrillation
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
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A-fib Symptoms/Tests
Asymptomatic-heart failure: chest pain, fatigue, dyspnea, palpitations, syncope, HF, stroke symptoms "irregularly irregular" EKG: no distinct P waves, QRS variable/irregular
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A-fib Classifications
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"
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CHADSVASC
>2 qualify for anticoagulant (warfarin) 1=anti-platelet therapy recommended 0=no therapy Does not apply for valvular afib pas-automatically get warfarin
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A-fib treatment
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
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Atrial Flutter
"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
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Wolff Parkinson White
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
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Premature Ventricular Complexes
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
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1st Degree Atrioventricular Block
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"
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2nd Degree Atrioventricular Block Type 1
Wenckeback/Mobitz1 PR elongates until QRS is blocked Block within AV node, generally asymptomatic, benign "longer, longer, longer drop, now you have a wenckebach"
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2nd Degree Atrioventricular Block Type 2
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"
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3rd Degree Block
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"
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Ventricular Tachycardia
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
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V-tach Diagnostics
Stable w/ normal vitals, hemodynamically unstable or pulseless Cardiac cath, QRS only thing on ECG big "saw-tooth"
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V-tach Treatment
Treat underlying | Long-term:B blockers, ICD implant, anti arrhythmic call 3 (sotalol/amiodarone), ablation if persistent
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Torsades de Pointes
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
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Torsades de Pointes Treatment
ACLS: if unstable-debibrillation; IV magnesium, IV B blocker Long term: B blockers, ICD Treat underlying causes/stop offending meds
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Ventricular Fibrillation
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
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V-fib Management
ACLS guidelines: ABCs, defibrillator/CPT, epi | Once resuscitated-hypothermia protocol (32-36*),EKG, echo, cardiac cath, ICD
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Sick Sinus Syndrome
Sinus node dysfunction (sinus arrest/pause, tachy-brady syndrome) Brady due to fibrosis/MI/meds Fatigue, dyspnea, dizziness, syncope *symptoms+EKG findings
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Sick Sinus Syndrome Treatment
Hospitalize | ACLS, atropine/dopamine/epi, transcutaneous/transvenous pacing, stop offending agents, pacemaker for bradycardia
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Accelerated Idioventricular Rhythm
Repetitive ventricular rhythm 60-100bpm | Accelerated ventricular focus faster than sinus node>assumes control, may be marker of repercussion
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Pacemakers
Used for anyone with bradycardia/conduction blocks | dual lead more common in older patients
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ICD
Shocks heart out of v-tach/v-fib etc | Used for cardiac arrest, systolic heart failure, EF 35-40%
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Acute Rheumatic Fever
Develops 1-5 weeks post strep in 5-15 Y.O. w/ risk of recurrence within 10 years, most mitral valve>aortic>tricuspid
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Diagnosis of rheumatic fever
Echo, ECG, ASO titer, CRP/ESR
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Treatment of rheumatic fever
Supportive care 1st line-Salicylates (then steroids if needed) for arthralgia Benzathine Penicillin IM inj.
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Rheumatic Heart Disease
Mitral 50-60%>aortic/mitral>aortic>tricuspid | 10-20 years after rheumatic fever
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Diagnosis of rheumatic heart disease
Transthoracic echo
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Treatment of rheumatic heart disease
Restrict activity, treat complications, prevent IE
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Infective Endocarditis
clin presentation/risk factors Present with fever, cough, dyspnea, arthralgia, diarrhea, back pain, regurgitant murmur, Osler nodes, Janeway lesions, Roth spots
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Etiology of Infective Endocarditis
Bacteria in bloodstream causes vegetations Native valve: S. aureus Prosthetic: S. aureus early, Strep late Drug users: S aureus>strep>enterococci
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Diagnosis of Infective Endocarditis
``` BLOOD CULTURES (2+) Echo (TTE or TEE), EKG, CXR ```
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Infective Carditis Risk Factors
Sex, age (>60), IV drug use, poor dentition, valvular disease, prosthetic valve, dialysis
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Treatment for Infective Endocarditis
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
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Duke criteria of Infective Endocarditis
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
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Acute Pericarditis
Inflammation of pericardial sac, most common pericardium disorder, commonly idiopathic or viral
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Acute Pericarditis Clinical Presentation
Chest pain* (sudden, anterior, sharp, improves leaning forward), fever, malaise, myalgia, dyspnea, tachypnea Friction rub at L sternal border
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Diagnosis of Acute pericarditis
``` ECG* (diffuse ST elevation, PR depression) CT w/ contrast MRI Biomarkers (tropinin^) New/worsening effusion* Friction rub* "swinging heart" ```
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Treatment of Acute Pericarditis
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
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Pericardial Effusion
Fluid in pericardium exceeds 15-50mL, usually due to injury to pericardium Other causes: idiopathic, infectious, malignancy, post-op, autoimmune, drugs
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Pericardial Effusion Presentation
Asymptomatic Chest pain/pressure/discomfort, syncope, light-headed, palpitations, respiratory Friction rup, JVP, tachycardia, decreased lung sounds, weak pulse, edema, cyanosis, pulses paradoxus
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Pericardial Effusion Diagnostics
``` ECG (low voltage, tachycardia, alternates/swinging heart) CXR (cardiomegaly) Echo (choice test) CT Pericardiocentesis ```
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Pericardial Effusion Treatment
Observation Treat underlying cause NSAID +/- colchicine if pericarditis involved
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Chronic Pericardial Effusion
Present for 3+ months Often asymptomatic, can cause cardiac tamponade randomly Pericardiectomy if reaccumulation of fluid
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Hemorrhagic Pericardial Effusion
Blood fills pericardial space instead of serous fluid | Malignancy most common cause (breast cancer)
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Cardiac Tamponade
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
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Cardiac Tamponade Presentation
Dyspnea*, fatigue, syncope, chest discomfort, edema, tachypnea, Beck's Triad Tachycardia, friction rub, cold clammy extremities
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Beck's Triad
Hypotension, JVP, muffled heart sounds
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Cardiac Tamponade Diagnosis
``` CLINICAL ECG: tachycardia, low voltage CXR: cardiomegaly Echo: must be done for hemodynamic significance Labs-for underlying disorders ```
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Cardiac Tamponade Treatment
STAT cardio consult, echo guided pericardioentesis or sx drainage
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Constrictive Pericarditis
Scarring/loss of elasticity, filling volume restricted decreased stroke volume/cardiac output
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Constrictive Pericarditis Presentation
Symptoms of heart failure* (edema, anasarca) diminished cardiac output, chest pain JVP*, Kussmauls sign, pericardial "knock" (right before S3)
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Constrictive Pericarditis Diagnosis
``` ECG (ST/T wave changes) CXR: pericardial calcification* Echo CT Cardiac cath BNP (increased) ```
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Constrictive Pericarditis Treatment
Try conservative 2-3 months (diuretics) | Pericardiectomy is only definitive treatment
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Aortic Aneurysm
Localized dilation of aorta including all 3 layers of vessel | Most common infrarenally>ascending thoracic (usually due to cystic medial necrosis)
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Aortic Aneurysm Presentation
Asymptomatic Chest/abdominal/back pain Hoarseness, respiratory, extremity pain Triad: hypotension, abdominal/back pain and pulsatile abdominal mass>ruptured AAA
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Aortic Aneurysm Diagnosis
Chest/abdominal x-ray Ultrasound CT/MRI w/ angio-assess size and location
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Aortic Aneurysm Treatment
Immediate surgical intervention for rupture Suggested sx repair for >5.5cm, symptomatic or rapidly growing Risk factor modifications, BP control
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Acute Arterial Occlusion
Sudden cessation fo blood supply due to thrombus or embolus
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Arterial Emboli
Most originate in heart (a-fib, MI, debris from prosthetic valves) Can be malignancy or Antiphospholipid antibody syndrome (appears in pregnancy)
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Acute Arterial Occlusion Presentation
Ranges from claudication-paralysis can be sudden and dramatic in healthy patient 6 P's: paresthesia, pain, pallor, pulseless, paralysis, poikilothermic (change in temp)
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Acute Arterial Occlusion Diagnosis/Treatment
Diagnosis: Ultrasound, CTA, MRA Treatment: IV heparin, thrombolytic meds, revascularization sx
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Varicose Veins
Dilated, elongated tortuous subcutaneous veins; valvular incompetence in perforating veins of legs ^ with age, pregnancy, female, hereditary, obesity
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Varicose Veins Exam
Tortuous veins, dermatitis, hyperpigmentation, edema, ulcers, infection Ultrasound
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Varicose Vein Treatment
Leg elevation, compression socks, weight loss Topical corticosteroids, antibiotics if infection present Sclerotherapy (ablation), laser treatment, surgery (phlebotomy)
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Deep Vein Thrombosis
Clot forms in deep vein of legs, thighs or pelvis | Virchow's Triad (venous stasis, vessel wall injury, coagulation abnormality)
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DVT Presentation
Swelling, pain and discoloration of leg, 1-2cm circumferential difference Positive Homan's sign Pulmonary embolism symptoms
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DVT Diagnosis
Venous ultrasound* | Contrast venography
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DVT Treatment
Anticoags for 3, 6 or 12 months Low molecular-weight heparin IV heparin Oral anticoagulant (warfarin 10mg/day