Cardiovascular Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Risk factors for atherosclerosis

A
HTN
HLD
DM
Smoking
FHx
Sedentary lifestyle and poor diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atherosclerosis role in AAA

A

a main risk factor (smoking biggest risk factor)

Plaque compresses underlying media -> problem with nutrient and waste diffusion

  • > degeneration and necrosis of media
  • > arterial wall weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyperhomocysteinemia clinical significance and treatment

A

risk factor for CVA, PVD, coronary heart dz

Tx: B6, B12, folic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathogenesis of atherosclerosis

A
  1. endothelial dysfunction (caused by HTN, HLD, DM, Smoking) leads to increased vascular permeability, leukocyte adhesion, and thrombosis
  2. Accumulation of lipoproteins - in vessel wall, mostly LDL
  3. Monocyte adhesion to the endothelium: migration of the monocytes into the intima and then transformation of these cells into macrophages and foam cells
  4. Factor release: activated platelets, macrophages, inflammatory mediators, cytokines
  5. Smooth muscle cell proliferation: migraiton of sm.m. cells into intima, deposition of elastin and collagen
  6. Lipid accumulation occurs extracelularly and within macrophages and smooth muscle cells -> bulging atherosclerotic plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical presentation of atherosclerosis

A

most asx

Angina
Claudication of LE
Stroke sxs
HTN
retinal changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diagnostic tests for atherosclerosis

A
Exercise stress test - best initial test
Nuclear stress test
Stress test with echo
Pharmacologic stress test
PET myocardial imaging test
Coronary angiogram - gold standard
Ankle brachial pressure index
Carotid U/S
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Exercise stress test in atherosclerosis

A

best initial test to assess stable angina or worsening SOB with exertion or fatigue with exertion

Positive: CP, dizziness, claudication, decreased BP, ST changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Nuclear stress test in atherosclerosis

A

Test to assess myocardial profusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stress test with Echo in atherosclerosis

A

assess wall motion abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pharmacologic stress test in atherosclerosis

A

uses cardiac inotrope/chronotrope (dobutamine) or vasodilator (adenosine or dipyridamole) in place of exercise

caution with vasodilators in asthmatics and hypotensive patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Positron emission tomography (PET) myocardial imaging in atherosclerosis

A

assess heart perfusion defects - lights up with adequate perfusion, black if not perfusing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Coronary angiogram in atherosclerosis

A

gold standard test

Assess degree of coronary artery occlusion - more invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ankle brachial pressure index

A

Pt supine, ankle BP/brachial BP
assess peripheral artery disease
abnormal if less than 0.9 -> stress test or angiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Carotid ultrasound in atherosclerosis

A

assess carotid stenosis leading to TIA or stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of atherosclerosis

A
Stop tobacco use
Normalize BP
Control hyperglycemia
Control hypercholesterolemia
Low-fat diet
exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chylomicrons

A

lipoprotiens absorbed from gut travel to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

VLDL

A

produced by liver, high in TGs

can become IDL and LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HDL

A

produced by liver

take up cholesterol deposited by LDL particles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

LDL

A

high in cholesterol
made from VLDL

taken up into cells by endocytosis - part of atherogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Secondary causes of hypercholesterolemia

A
T2DM
Excess etOH
Primary biliary cholangitis
CKD
Hypothyroidism
Medications: oral estrogens, thiazide diruetics, B-blockers, atypical antipsychotics (clozapine, olanzapine), protease inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Xanthoma

A

deposits of lipid in tendons and under skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Xanthelasma

A

deposits of lipid around eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Arcus senilis

A

deposits of lipids in the periphery of the corneas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment of hypercholesterolemia

A

Goal: reduce risk of atherosclerosis and pancreatitis (TGs)

Lifestyle modifications:
Wt loss
aerobic exercise
diet
smoking cessation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

2013 AHA/ACC guidelines for treating hypercholesterolemia - who gets treated?

A

Clinical atherosclerotic CV dz (ASCVD) - need mod-high intensity statin:

  • ACS
  • MI
  • stable or unstable angina
  • Revascularization procedures
  • Stroke or TIA
  • Peripheral artery disease

LDL >190
T1 or T2DM ages 40-75
10 yr ASCVD risk >7.5% ages 40-75

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Causes of Angina

A

Decreased O2 supply: atherosclerosis obstructing blood flow, shock, hypoxemia, anemia, prinzmetal angina

Increased O2 demand: vigorous exertion, tachycardia, htn, ventricular hypertrophy, increased catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clinical features of angina

A

chest discomfort/pressure - left sided or midsternal, radiates to back, jaw, or left arm

diaphroesis
SOB
Palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Atypical sxs of angina

A

older patients, females, DM pts

Abdominal pain, exercise intolerance, worsening generalized fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Stable angina

A

predictable CP that resolved with rest
No initiation of CP at rest

Dx: stress test - cardiac enzymes always normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Unstable angina

A

Unpredictable chest pain that can occur at rest
Pain more severe and lasts longer
1/3 will have MI within 3 years

Dx:
Give aspirin and transport to ED
ECG and cardiac enzymes initially normal, sometimes ST depression
Stress test or cardiac cath when stable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MI

A

occlusion of coronary vessels d/t thrombus formation following a plaque rupture

Pressure sensation radiates to jaw or left arm

Tachycardia, diaphoresis, N/V, impending doom

Possible new S3, S4, or systolic murmur

Abnormal cardiac enzymes - trp I most specific (elevates within 4 hours, lasts 2 weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

STEMI vs NSTEMI

A

ECG gold standard within 6 hrs of sxs

STEMI: ST elevation, cardiac cath to locate occlusion, new LBBB

NSTEMI: no ST elevation, cardiac cath to locate occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Evolution of MI on ECG

A

Acute: ST elevates - tomb stoning (also seen with prinzmetal angina)

Hours: ST elevated, R wave decreases, Q wave appears

Day 1-2: T wave inverts, Q wave deepens

Days later: ST normal, T wave inverted

Weeks later: ST normal, T wave normal, Q wave persists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Anterior wall MI on ECG

A

V2-V5 - LAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Septal wall MI on ECG

A

V1-3 - LAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Inferior wall MI on ECG

A

II, III, aVF - posterior descending a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Lateral wall MI on ECG

A

I, aVL, V5, V6 - LAD or circumflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Prinzmetal angina (Variant angina)

A

Coronary artery vasospasm
RF: smoking
More often younger pt, fewer CAD RFs

CP at rest - midnight to morning, lasts 5-15 min

Dx: recurrent CP at rest, transient ST elevation, no sign of high grade coronary artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

DDX for CP

A
MSK
Costochondritis
GERD
Esophageal spasm - nitrates relieve spasms
Cocaine
hyperventilation
Herpes zoster
aortic stenosis
trauma
PE
pneumonia
pericarditis
pancreatitis
angina
aortic dissection
aortic aneurysm
Infarction
Neuropsych dz - depression, anxiety
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Indications for CABG

A

> 50% stenosis in left main artery

3 vessel disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Complications of MI

A

arrhythmia d/t electrical irritability - Vfib MC and lethal

LVF and pulmonary edema - decreased heart function

Cardiogenic shock - high risk of mortality

Ventricular free wall rupture -> tamponade

Papillary muscle rupture -> severe MR

Interventricular septal rupture -> VSD

Aneurysm formation 2/2 scar tissue

Fibrinous pericarditis - friction rub 3-5 days after MI

Dressler syndrome - autoimmune pericarditis weeks after MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Equations for Cardiac output

A

CO = SV x HR

SV= EDV - ESV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Factors determining stroke volume

A

Preload
Afterload
Myocardial contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Preload

A

stretch of myocytes at the end of diastole

influenced by EDV and venous return

Increase intravascular volume increases preload
Dehydration decreases preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Afterload

A

pressure against which the ventricles contract to eject blood

influenced by aortic pressure

after load and stroke volume inversely related, lower after load allows more blood to get out of the ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Myocardial contractility influences

A

catecholamines, intracellular Ca2+, extracellular Na+

Independent of pre- and after-load

Increase calcium = increased contractility

Low extracellular sodium makes for higher intracellular calcium, increasing contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Fick principle

A

CO = (rate of O2 consumption)/(Ao2 - Vo2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does exercise change cardiac output?

A

1st: increased stroke volume

later - increased heart rate - which sustains increased cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Mean arterial pressure equations

A

MAP = CO - TPR (total peripheral resistance)

MAP = 2/3 DBP + 1/3 SBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Pulse pressure equation

A

PP = SBP - DBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

LV ejection fraction

A

Normal 55-75%

EF = SV/EDV = (EDV-ESV)/EDV

52
Q

Causes of systolic heart failure

A

Systolic heart failure - CO doesn’t meet systemic demands

Increased preload
Increased after load
Decreased contractility
Brady or tachycardia

High output conditions:

  • decreased O2 carrying capacity (anemia)
  • Increased metabolic demand (hyperthyroidism, beriberi (thiamine deficiency))
53
Q

Causes of diastolic heart failure

A

Filling problem

LVH - 2/2 chronic htn -> S4, S3, summation gallop

Hypertrophic cardiomyopathy
Restrictive cardiomyopathy

54
Q

Hypertrophic cardiomyopathy (HOCM)

A

AD
Chaotic, disordered hypertrophy of the LV myocytes with interstitial fibrosis - muscle fibers oriented in different directions

Hypertrophy of the inter ventricular septum -> LV outflow tract obstruction

Clinical features:

  • Exertional syncope, dyspnea, CP
  • Sudden cardiac death in a young athlete
  • Systolic murmur (like AS), LOUDER with Valsalva (decreased preload), SOFTER with squatting (increased after load)
  • Forceful, enlarged apical impulse - silver dollar sized

Dx: ECHO

Tx: B-blocker (decrease HR, prolong diastole); restrict physical exertion
AVOID volume depletion, NO diuretics

55
Q

Dilated cardiomyopathy

A

MC
Dilation of ventricles -> systolic dysfunction

Clinical features:

  • fatigue, dyspnea, systolic dysfunction
  • S3
  • Systolic and diastolic murmurs - leaflets separate
  • CXR: globular heart

Tx: diuretics, ACE inhibitors, B-blockers

56
Q

Causes of dilated cardiomyopathy

A
Ischemic heart disease!
Idiopathic
etOH
Cocaine
Doxorubicin
Coxsackie virus B
Myocarditis
HIV
Chagas disease (Trypanosoma cruz)
Beriberi (thiamine deficiency) - wet = edema
Hemochromatosis (most commonly causes dilated CM)
Pregnancy - "permpartum CM"
57
Q

Restrictive cardiomyopathy

A

Least common CM

Ventricular walls become stiff and noncompliant -> diastolic dysfunction

Causes: usually d/t infiltration of the myocardium

  • Sarcoidosis
  • Amyloidosis
  • Hemochromatosis (less likely than dilate)

Clinical features:
Right-sided heart failure - edema, JVD, ascites

Diagnosis: ECHO, myocardial bx

Tx: identify and tx underlying cause; Diuretics, ACE-i, B-blockers

58
Q

Symptoms of left heart failure

A

Left = lungs

DOE
Orthopnea
Paroxysmal nocturnal dyspnea
Rales (crackles)
Displaced PMI
S3 heart sound - apex
59
Q

Causes of left heart failure

A

Ischemic heart disease

HTN

60
Q

Symptoms of right heart failure

A

JVD
Hepatomegaly
Lower extremity edema

61
Q

Causes of right heart failure

A

Left heart failure
Valvular heart disease
COPD -> cor pulmonale
Pulmonary hypertension

62
Q

Tests used to diagnosis CHF

A
ECHO
BNP
CXR
Cardiac enzymes
ECG
63
Q

BNP and how to interpret

A

Hormone produced in response to ventricular stretch -> vasodilation and urinary excretion of Na+ and H2O (little)

BNP less than 100 - r/o CHF
BNP 100-400 - indeterminate
BNP >400 indicates CHF

64
Q

CXR in CHF

A
Cardiomegaly
Pulmonary edema
Cephalization of pulmonary vasculature - bigger in upper lungs, normally hard to see
Kerley B lines - peripheral, lower lungs
Pleural effusion
65
Q

Treatment of acute decompensated CHF presenting with pulmonary edema

A

NOLIP

Nitrates - redistributes blood outside pulmonary vasculature

O2 - only if hypoxemic

Loop diuretic - takes long time to work d/t low CO = low kidney perfusion, only help volume overload

Inotropic drugs - Dobutamine, milrinone - not first line d/t increased mortality

Positioning - pool blood in legs

66
Q

Drugs proven to reduce mortality in CHF

A

ACE inhibitors - decrease preload and after load, increase CO
-candesartan and valsartan if intolerant to ACE-i d/t cough

B-blockers - bisoprolol, carvedilol, extended-release metoprolol

  • prevents cardiac remodeling
  • Avoid with acute decompensated CHF

Aldosterone antagonists - spironolactone, eplerenone
-Start after ACE-i and B-blocker

67
Q

Drugs used for symptom relief in chronic CHF

A

Loop diuretics - decrease preload, fluid overload

Digoxin - improve contractility

Vasodilators - isosorbide dinitrate, hydrazine (decreased mortality in AA)

68
Q

Cardiac resynchronization therapy

A

Pacemaker leads in each ventricle -> synchronized ventricular contraction

Can improve mortality and reduce sxs in patients with LVEF at or below 35%

69
Q

Pulmonary capillary wedge pressure (PCWP) is a good approximation of what other pressures?

A

LA pressure

LV diastolic pressure

70
Q

Two most common sites of pulmonary artery catheter placement

A

L subclavian v.

Right internal jugular v.

71
Q

Causes of myocarditis

A

MC- viruses: parvovirus B19, coxsackie, echoviruses, adenovirus, EBV, CMV, influenza

Trypanosoma cruz - Chagas disease

Drug toxicity - chloroquine, PCNs, sulfonamides, cocaine, radiation, cyclophosphamide, doxorubicin, daunorubicin

72
Q

Clinical features in myocarditis

A
Asx -> sudden death
fatigue
CP
HF sxs - edema, SOB
palpitations
fever
S3 or S4
Signs of CHF - edema, pulmonary rales, JVD
73
Q

Diagnostic tests in myocarditis

A

ECG: normal or signs of MI - ST elevation, Q waves; peripheral or ectopic beats

Cardiac enzymes - normal or elevated - troponin I

CXR: CM or pulmonary congestion

ECHO: impaired ventricular function

Cardiac magnetic resonance (CMR) - detect inflammatory hyperemia, edema, myocyte necrosis

Definitive dx: endomyocardial bx - cx and viral PCR

74
Q

Chagas disease

A

Trypanosoma cruz

MEGA -3

cardioMEGAly
MEGAesophagus
MEGAcolon

75
Q

Treatment of myocarditis

A
treat underlying cause - abx for bacterial
Stop offending agents
Tx any significant arrhythmias
Tx HF sxs
\+/- immunosuppressant agents

Supportive treatment - usually viruses

76
Q

Acute rheumatic fever causes

A

2-4 weeks after untreated group A strep pharyngitis - 3%

Due to autoantibodies that attack heart and joints - sterile vegetations

MC: MV>AV>TV=PV

77
Q

Diagnosis of acute rheumatic fever

A

JONES criteria
-Hx of recent strep and 2 major or 1 major and 2 minor

Major: JONES

  • Joints - polyarthritis - hot swollen
  • Heart - pancarditis, pericarditis, endocarditis, myocarditis
  • Nodules - subcutaneous on extensor surfaces - painless, back wrist, elbow, anterior knee
  • Erythema marginatum - painless, trunk or medial limbs; multiple lesions with central clearing
  • Sydenham chorea

Minor: PEACE

  • Previous rheumatic fever
  • ECG with PR prolongation
  • Arthralgias
  • CRP and ESR elevation (nonspecific)
  • Elevated temperature
78
Q

Diagnostic testing for acute rheumatic fever

A

Elevated ESR and CRP
Elevated WBC
90% ASO titer

79
Q

Treatment for acute rheumatic fever

A

NSAIDs - joint inflammation
Corticosteroids - carditis severe
B-lactams (PCN) - ongoing infection

80
Q

Endocarditis ppx prior to surgery or dental procedure - patient population and tx

A

Prosthetic cardiac valve
Previous infective endocarditis
Congenital heart disease - unrepaired cyanotic defect, palliative shunts, repaired with prosthetic device/material
Cardiac transplant with cardiac valvuloplasty

Tx: amox 2 g x1 30-60 min prior to procedure

No longer recommended if hx of rheumatic HD unless previous endocarditis

81
Q

Endocarditis vegetation composition

A

platelets, fibrin, microorganisms, inflammatory cells

82
Q

Risk factors for endocarditis

A
Damaged heart valves - rheumatic HD, congenital HD
IV drug users
poor dentition
age >60 yo
Male
83
Q

Presentation of endocarditis

A

Fever, malaise, weakness, anorexia, new heart murmur, wt loss

Jane way lesions - contender, erythematous macule on palms and soles - septic emboli

Osler nodes - tender nodules on fingers and toe pads; caused by immune complexes (also in lupus and disseminated gonococcal infections)

Roth spots - retinal hemorrhages with pale centers - immune complexes

Splinter hemorrhages - nonspecific

Conjunctival hemorrhages

84
Q

Bacterial causes of endocarditis

A
S. aureus - 31%
Viridan group Strep 17% - assoc with dental procedures
Enterococci 11%
Coagulase-negative staph 11%
S. bovis 7%

HACEK

  • Haemophilus spp
  • Actinobacillus
  • Cardiobacterium
  • Eikenella
  • Kingella

Culture negative - intracellular

  • Coxiella burnetii - Q fever
  • Bartonella spp. - cat scratch
  • Brucella spp - unpasturized milk, zoonotic
85
Q

Complications of endocarditis

A

severe damage to endocardium and valves -> valve repair/replace

Septic emboli - Right side -> PE; Left side -> stroke, spleen, kidney, anywhere

86
Q

Duke criteria

A

Endocarditis - definitive dx - positive culture/histo of vegetation

Clinical criteria - 2 major; 1 major 3 minor; 5 minor

Major:
Serial blood cultures positive
Vegetations or cardiac abscesses on ECHO - TEE
New valve regurgitaiton - MC MR
Blood cx positive for Coxiella burnetii (closely associated)

Minor:
Predisposing heart condition or IV drug use
Temp >38C
Vascular phenomenon - arterial emboli, conjunctival hemorrhages, Janeway lesions
Immunologic phenomenon - glomerulonephritis, Osler nodes, roth spots
Positive cx not meeting requirements for major criteria
Serologic evidence of infection without positive cx

87
Q

Empiric antibiotic most often used for infective endocarditis

A

Vancomycin until sensitivities back

4-6 weeks

88
Q

Nonbacterial thrombotic endocarditis (marantic)

A

Occurs on non-damaged valves - sterile vegetations

Associated with:
sepsis, pregnancy - hyper coagulable states
venous catheters
mutinous adenocarcinoma

89
Q

Libman-Sacks endocarditis

A

Associate with SLE
both sides of the valve
Due to deposition of immune complexes

90
Q

Chronic constrictive pericarditis

A

Scarred, fibrous pericardium becomes rigid -> decreased diastolic filing and cardiac output

Risk factors: cardiac surgery, radiation

Presentation:
HF sxs - DOE, fatigue, peripheral edema
Physical exam: JVD, Kussmaul’s sign (JVD with inspiration)

Confirm with ECHO - thickening of pericardium, most ventricle filling in early diastole

CXR: calcification of pericardium - specific, not sensitive

Tx: pericardiectomy - high mortality - 10%

91
Q

Conditions with Kussmaul’s sign

A

JVD with inspiration - impaired RV relaxation and filling

Restrictive CM
RV infarction
tricuspid stenosis
massive PE
right sided CHF
Chronic constrictive pericarditis
92
Q

Left atrial myxoma

A

MC cardiac tumor in adults
75-80% left atrium
ball valve - obstruct blood flow into LV -> syncope

Physical exam: rarely - early diastolic “tumor plop”

Dx: ECHO

Tx: surgical resection

93
Q

Atrial fibrillation Risk factors

A
Hyperthyroidism
pulmonary dz
CAD
HTN
anemia
valvular disease
pericarditis
Rheumatic HD
sepsis
alcoholism
94
Q

Afib

A

rapid, irregularly irregular rhythm
ECG: no distinct p waves

asx or SOB, CP, palpitations, irregularly irregular pulse

95
Q

Afib managment

A

Acute: new onset less than 48 hours - electrocardioversion

Chronic:
-evaluate for thumbs with TEE
Anticoagulate with heparin and warfarin
Rhythm control with sotalol or amiodarone -> sinus rhythm
Rate control with B-blockers, NDP CCBs or digoxin

96
Q

Atrial flutter

A

re-entrant rhythm in right or left atrium - can degenerate to afib
ECG - sawtooth pattern, >150bpm

Risk: CAD, CHF, COPD, valve dz, pericarditis

Sxs: Asx or palpitations, syncope

Tx: rate control - b-blockers, CCB; cardioversion - electrical or chemical; catheter ablation

97
Q

PVCs

A

causes: hypoxemia, abnl electrolytes, hyperthyroidism, caffeine

Clinical: asx or palpitations, syncope, sensation of skipped, heavy, or dramatic beat

ECG: wide QRS

Tx: none if healthy - b-blockers in CAD

More than 3 in a minute concerning for other ventricular arrhythmias

98
Q

V-tach

A

sustain -> vfib

ECG: series of 3 or more PVCs, HR of 160-240

Tx: electrocardioversion, followed by antiarrhythmic medication
Recurrent -> internal defibrillator

Clinical: asx if brief -> palpitations, syncope, hypotension

99
Q

Torsades de pointes

A

ECG: vtach with sine wave

Tx: IV magnesium rapid bolus -> lidocaine, phenytoin

100
Q

Vfib

A

lack of ordered ventricular contractions leading to NO cardiac output

ECG: erratic, no identifiable p waves or QRS

Tx: CPR, immediate shock

101
Q

Treatable causes leading to a code - H’s

A

Hypovolemia -> rapid volume resuscitation through multiple IV sites and/or central lines

Hypoxemia -> correct via intubation, chest tube, or O2

H+ (acidosis) -> IV push 1-2 amps bicarbonate (common in prolonged code)

Hyperkalemia -> CaCl2 IV push, bicarbonate, insulin/glucose (common in prolonged resuscitation due to acidosis)

Hypoglycemia -> 1 amp D50 IV push - always check finger stick

Hypothermia -> warming

102
Q

Treatable causes leading to a code - T’s

A

Tamponade -> pericardiocentesis

Tension PTX -> needle decompression then chest tube

Thombus - MI -> cardiac cath or thrombolytic

Thombus - PE -> thrombolytic or thombectomy

Trauma -> follow ATLS protocols

Toxins

103
Q

Prehypertension vs hypertension BP readings

A

Pre: 120-139/80-89

htn: over 140/90

Diagnosis HTN after 3 separate occasions

104
Q

Complications of uncontrolled htn

A
atherosclerosis -> CAD, ischemic stroke
hemorrhagic stroke
LVH -> diastolic dysfunction
Thoracic aortic dissection
AAA
CKD (also can cause the htn)
hypertensive retinopathy (AV nicking, cotton wool spots, retinal hemorrhages-flame hem)
105
Q

Most likely cause of htn refractory to multiple meds? Next step to dx? tx options?

A

renal a. stenosis

  • over 50 - atherosclerosis
  • under 50, women - fibromuscular dysplasia of renal a (needs on string)

MRA of renal a. - best, least invasive
Spiral CT with con
renal a. duplex scan
renal arteriogram - gold standard, but invasive

Tx:
medical management - avoid ACE/ARBs if bilateral (decreased GFR and worsening renal fxn)
Angioplasty
Surgical revascularization - bypass

106
Q

Causes of secondary hypertension

A

renal a. stenosis

CKD or ESRD

Drugs - OCPs over 35, NSAIDs, antidepressants, glucocorticoids

Hypercortisolism - Cushing - dx: serum cortisol, serum ACTH, dexamethasone suppression test

Primary hyperaldosteronism - Conn -
Triad: htn + hypokalemia + metabolic alkalosis
Dx: high plasma aldosterone:plasma renin ratio

Pheochromocytoma:
episodic htn with diaphoresis, tachy, palpitations, HA
Dx: 24 hr urine catecholamines and metanephrins, CT abd

Hypo- or hyperthyroidism - dx TSH

Hyperparathyroidism - calcium drives sm.m. contraction -> peripheral vasoconstriction
Dx: serum calcium, PTH

Coarctation of aorta
-BP high in arms, low in legs; weak dorsals pedis pulses
Dx: ECHO

OSA - Dx: polysomnography

107
Q

Hypertensive urgency vs emergency

A

BP >180/120

urgency- no sxs, no end organ damage

emergency - end organ damage
-renal dz, AMS, papilledema, retinal vascular changes, unstable angina, MI, aortic dissection, pulmonary edema

108
Q

Treatment of hypertensive urgency

A

Goal:
reduce BP to 160/100 initially
Reduce MAP no more than 25% in first 2-3 hours - risk ischemia

IV drugs:
Nitroprusside
Labetalol
Nicardipine
Clonidine
Captopril
Enalapril
109
Q
JNC8 bp goals:
Gen pop under 60
Adults with CKD
Adults with DM
Gen pop over 60 no CKD, no DM
A

less than 140/90 for:
Gen pop under 60
Adults with CKD
Adults with DM

less than 150/90 for:
Gen pop over 60 no CKD, no DM

110
Q

Aortic dissection - mechanism, risk, features and dx

A

Tear in intimate of aorta -> blood dissects into media -> forms false lumen

Risk factors:
HTN
Dz weakening aorta - Marfans, Ehlers-Danlos, syphilis

Features:
Severe, sharp or tearing CP radiating to back
May cause syncope, TIA or decreased peripheral pulses

Dx:
Normal ECG
Widening mediastinum on CXR
Best test: CT chest with contrast - two lumens; classify as Stanford A (involves ascending aorta) or Stanford B (distal to L. subclavian A)

111
Q

Aortic dissection - management

A

Stabilze BP with beta-blockers - decreases slope of rise in BP - anti-impulse treatment

Morphine for pain control

Stanford A - emergency surgical repair - high risk

Stanford B - treat medically unless LE ischemia, uncontrolled pain

112
Q

AAA - risk factors, features, dx, screening

A

Focal dilation of the abdominal aorta, distal to renal a.

Risk:
Tobacco use
Age >55
Male
Caucasian
Atherosclerosis
HTN
FHx

Features:
Asx - possible abd/lower back pain
Exam: pulsatile abdominal mass, abdominal bruit
Ruptured AAA: hypotension, severe abd pain, pulsatile mass

Dx:
Best first test: abd u/s
CT or MRI with con

Screen: one time abd u/s all men 65-75 with hx of smoking

113
Q

Indication for repair of AAA

A

Diameter > 5.5 cm in men or >5 cm in women
Increase in diameter by more than 0.5 cm in 6 mo - should be having abd u/s q6mo

Symptomatic - tenderness, pain in abdomen or back

114
Q

Peripheral artery disease (PAD) - risk, features, dx

A

Atherosclerosis of peripheral arteries - legs

Risk:
Smoking
HTN
DM
HLD

Claudication - exertion leg pain improves with rest
Non-healing foot ulcers
Erectile dysfunction
Skin changes - dry, shiny skin, decreased hair growth on legs
decreased pulses in legs

Dx:
ABI ratio - ankle SBP to brachial SBP
-ABI >= 0.9 normal; less than 0.9 = vascular insufficiency; less than 0.4 = severe disease
U/S or CT angiogram or MRA
Arteriogram
115
Q

Management of peripheral artery disease

A

Conservative medical management:

  • smoking cessation
  • Glucose and BP control
  • Daily exercise to increase collateral flow
  • Cilostazol - improves blood flow to LE and decreases claudication via arteriovasodilation; more effective than pentoxifylline (makes RBC more flexible); contra in HF d/t increased mortality
  • daily aspirin or clopidogrel to reduce CV events
  • Statin to reduce CV events, increase pain-free walking distance

If not responding to medical management -> angioplasty, bypass grafting, or amputation
-may have concurrent CAD

116
Q

DVT - risk, features, dx, tx

A

Blood clot developing in deep vein - usually LE

Risk: -virchow’s triad

  • Hemostasis - immobilization from illness, surgery, travel
  • Hypercoagulability - inherited, cancer, high estrogen states (pregnancy, OCPs)

Features:
Often asx
Pain, warmth, and/or swelling in LE -calf
Homan’s sign - pain with dorsiflexion, found in less than 1/3

Dx:
Positive D-dimer (also high in post op) - negative r/o
Best test: doppler u/s of extremity

Tx:
elevate leg
Anticoagulate - LMWH (enoxaparin) or unfractionating heparin -> warfarin x3 mo
If anticoagulant contraindicated (high fall risk) - IVC filter

117
Q

Treatment of varicose veins

A

Weight reduction, avoid prolonged standing, leg elevation
Compression stockings
Sclerotherapy - inject substance to cause injury and thrombosis
Thermal ablation - laser
Surgery ligation of long saphenous v or short saphenous v - lose option for CABG

118
Q

Giant cell arteritis (temporal arteritis)

A

Large vessel vasculitis

elderly woman
Associated with polymyalgia rheumatica (PMR)
HA, tenderness of temples, jaw claudication
Transient or permanent vision loss

Histo: granulomas - multinucleate giant cells
Elevated ESR - normal r/o
Definitive dx: temporal a. bx

Tx: prednisone 1-2 mo, with long taper 9-12 mo; don’t delay start, risk blindness
Aspirin
Calcium, vit D to reduce risk of osteoporosis due to steroids

119
Q

Takayasu arteritis

A

Large vessel vasculitis - arch of aorta and major branches off arch

Asian woman - 10-40 yo

Cerebrovascular ischemia, coronary ischemia, syncope, vertigo
Poor pulses in UE - pulseless disease

Tx: glucocorticoids

120
Q

Kawasaki disease (mucocutaneous lymph node syndrome)

A

Medium vessel vasculitis

Asian infant, kid
“CRASH and Burn”
Conjunctivitis - b/l non exudative, painless
Rash on trunk
Adenopathy of cervical LN
Strawberry tongue and diffuse erythema of mucous membranes
Hands and feet - edema with induration, erythema or desquamation
Fever - >40 C or 104 lasting at least 5 days

coronary artery aneurysm within weeks of illness onset - risk rupture or thrombosis -> MI

Tx: IVIG within first 10 days of illness
High dose aspirin until 48 hr after fever resolution
Low dose aspirin until inflammatory markers (platelets, ESR) return to normal (usually 6 weeks)
ECHO in acute phase and 6-8 weeks later

Steroids NOT indicated, no benefit

121
Q

Polyarteritis nodosa

A

Necrotizing inflammation of small and medium sized arteries -> ischemia

  • Kidneys, GI tract
  • SPARES lungs

Associated with Hep B/C - Hep with renal dz - proteinuria, hematuria

ANCA negative

Angiography - aneurysms in affected organs

122
Q

Thormboangiitis obliterates (Buerger disease)

A

Small/medium sized arteries and veins

Heavy smoker, young male 30-40s

Ischemia of digits, Raynaud’s

Tx: stop smoking

123
Q

Henoch-Schonlein purpura (IgA vasculitis)

A

Small vessel vasculitis

Kids - recent URI, strep
Palpable purpura of LE
Arthritis and arthralgia
Abd pain d/t intestinal hemorrhage
Renal dz (IgA nephropathy) - microscopic hematuria, mild proteinuria

Tx: hydration, pain control

124
Q

Mixed cyroglobulinemia syndrome (essential mixed cyroglobulinemia)

A

Small vessel vasculitis

Polyclonal IgG and IgM against IgGs precipitate out at cool temps

Associated with Hep C

Melzer’s triad: palpable purpura, weakness (peripheral neuropathy), arthralgia

Raynauds
Liver involvement (hep C)

20-30% kidney dz - hematuria, proteinuria

125
Q

Granulomatosis with polyangiitis (Wegners)

A

Granulomas in:
Lung - pulmonary nodules, infiltrates, hilar LAD
Upper airway - ENT, soft palate
Kidneys

c-ANCA + (PR3-ANCA)

Dx: Kidney or lung bx

Tx: steroids and cyclophosphamide

126
Q

Eosinophili granulomatosis with polyangiitis (Chrug-Strauss)

A

Allergic!
Assoc with asthma

Lung dz - opacities, nodules
Upper airway disease
Skin - tender skin nodules, palpable purpura
20% renal involvement

Histo: Eosinophilic inflammation + granulomas on lung bx

p-ANCA + (MPO-ANCA)
Eosinophilia