Cardio part 2 Flashcards

1
Q

Pathophys of premature ventricular contractions

A

Suggested mechanisms are reentry, triggered activity, and enhanced automaticity

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2
Q

Etiology of premature ventricular contractions

A
Cardiac:
Acute MI or myocardial ischemia
Myocarditis
Cardiomyopathy
Myocardial contusion
Mitral valve prolapse
Other causes:
Hypoxia and/or hypercapnia
Medications
Illicit substances
Hypomagnesemia, hypokalemia, hypercalcemia
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3
Q

Hx of PVCs

A

Pts are usually asymptomatic
Paplpitations and neck and/or chest discomfort
Pt may report feeling that his or her heart stops after a PVC
Pts with frequent PVS or bigeminy may report syncope
Long runs of PVCs can result in hypotension
Exercise can increase or decrease the PVC rate

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4
Q

PE of PVCs

A

BP- frequent PVCs may result in hemodynamic compromise
Pulse- ectopic beat may produced a diminished or absent pulse
Hypoxia may precipitate PVCs- check pulse oximetry
Cardiac findings- Cannon A waves may be observed in the jugular venous pulse
Cardiopulmonary- Elevated BP and S4 or S3 and rales are important clues to the cause and clinical significance of PVCs
Neuro- Agitation and findings of sympathetic activation suggest that catecholamines may be the cause of the ectopy

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5
Q

PVCs workup

A
In young, healthy pts without concerning concomitant sx, labs are not typically necessary
Otherwise:
Serum electrolyte levels
Drug screen
Drug levels
Echo
EKG
Holter monitor
Exercise stress testing used complementary to Holter monitoring
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6
Q

Tx of PVCs

A

In absence of cardiac disease, no tx needed
Otherwise:
Establish telemetry and IV access, initiate oxygen, and obtain 12-lead
Treat the underlying cause of hypoxia
Treat any drug toxicity
Correct electrolyte imbalances
BBs with those who have sustained an MI
Amiodarone
In PVCs from the right or left ventricular outflow tract that occur in structurally nl hearts, catheter ablation

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7
Q

Hx of congestive heart failure- what to ask

A
Ask about the following:
Myopathy
Previous MI
Valvular heart dz, familial heart dz
Alcohol use
HTN
DM
Dyslipidemia
Coronary/peripheral vascular dz
Sleep-disordered breathing
Collagen vascular dz, rheumatic fever
Pheochromocytoma
Thyroid dz
Substance abuse
Hx of chemo/radiation to the chest
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8
Q

Hx of left-sided heart failure

A
Exertional dyspnea
Orthopnea
PND
Dyspnea at rest
Acute pulmonary edema
CP/pressure
Palpitations
Anorexia
Nausea
Wt loss
Bloating
Fatigue
Weakness
Oliguria
Nocturia
Cerebral sx of varying severity
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9
Q

Cerebral sx of congestive heart failure

A
Confusion
Memory impairment
Anxiety
HAs
Insomnia
Bad dreams or nightmares
Rarely, psychosis with disorientation, delirium, or hallucinations
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10
Q

PE of congestive heart failure

A

Obvious dyspnea during and immediately after moderate activity
Dyspneic when lying flat without elevation of the head for more than a few minutes
Chronic severe heart failure- malnourished and sometimes even cachectic
Exophthalmos
Severe tricuspid regurgitation
Visible pulsation of the eyes and of the neck veins
Severe- central cyanosis, icterus, and malar flush
Stroke volume reduced
Pulse may be weak, rapid, and thready
Ascites
Tachycardia
Diaphoresis
Pallor
Peripheral cyanosis with pallor and coldness of the extremities
Obvious distention of the peripheral veins
Rales
JVD
Kussmal’s sign
Hepatojugular reflux
Hepatomegaly- right sided
S3 gallop

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11
Q

Stage A heart failure

A

At high risk for heart failure but do not have structural heart disease or sx of heart failure
Treat HTN
Encourage smoking cessation
Treat lipid d/os
Encourage regular exercise
Discourage alcohol intake and illicit drug use

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12
Q

Stage B heart failure

A

Asymptomatic, with LV dysfunction from peveious MI, LV remodeling form LV hypertrophy, and asymptomatic valvular dysfunction
Treat with Stage A tx
ACE/ARB and/or BB

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13
Q

Stage C heart failure

A
Structural heart disease and current or previous sx of heart failure
Treat like stage A
ACEI/ARBs
BBs
ARNIs
Ivabradine
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14
Q

Stage D heart failure

A

Pts have refractory heart failure that requires specialized interventions
Tx for stage A, B, C
Heart transplantation or placement of an LV assist device in eligible pts
Pulmonary catheterization
Options for end of life care

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15
Q

Workup of congestive heart failure

A
CBC
Serum electrolyte levels
Renal and liver function studies
Assessment for iron deficiency
BNP or NT-proBNP
ABG
EKG
CXR
Echo
MUGA
CT or MRI
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16
Q

Tx of congestive heart failure

A
Encourage physical activity
Sodium restriction
Fluid restriction
Diuretics for symptomatic relief
ACE
ARBs
Hydralazine and nitrates to improve sx or for those who can't tolerate ACE/ARB or as add-on
Beta-adrenergic blockers
Aldosterone antagonists as adjunct
Digoxin
Anticoagulants
Inotropic agents
Pacemakers
Cardiac resynchronization therapy
ICDs
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17
Q

RFs for CAD

A
Age >45 years in men
Age >55 years in women
FHx of early heart disease
Lipoprotein a levels
Low HDL
HLD
HTN
Cigarette smoking
DM
Obesity
Lack of physical activity
Metabolic syndrome
Mental stress
Depression
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18
Q

Primary prevention of CAD- statin therapy

A

Statin therapy is appropriate for

  • Those with clinical ASCVD
  • Those with primary elevations of LDL of 190 or greater
  • Those aged 40-75 yrs old with DM and LDL levels of 70-89 without clinical ASCVD
  • Those without clinical ASCVD or DM aged 40-75 years who have LDL level of 70-189 as well as an estimated 10-year ASCVD risk of 7.5% or higher
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19
Q

Primary prevention of CAD- other measures

A
BP control
Antioxidants
ASA
Smoking cessation
Dietary modifications
Physical activity
Wt management
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20
Q

Pathophys of HTN

A

Multifactorial
Multiple factors modulate the BP, including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation

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21
Q

Etiology of HTN

A

Primary- from environmental or genetic causes

Secondary

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22
Q

Etiology of HTN, secondary causes: kidney

A
Polycystic kidney disease
CKD
Urinary tract obstruction
Renin-producing tumor
Liddle syndrome
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23
Q

Etiology of HTN, secondary causes: vascular

A

Coarctation of aorta
Vasculitis
Collagen vascular dz

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24
Q

Etiology of HTN, secondary causes: endocrine

A
Exogenous: steroids, oral contraceptive use, NSAIDs
Endogenous:
Primary hyperaldosteronism
Cushing syndrome
Pheochromocytoma
Congenital adrenal hyperplasia
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25
Q

Etiology of HTN, secondary causes: neurogenic

A

Brain tumor
Autonomic dysfunction
Sleep apnea
Intracranial HTN

26
Q

Etiology of HTN, secondary causes: drugs and toxins

A
Alcohol
Cocaine
Cyclosporin, tacrolimus
NSAIDs
Erythropoietin
Adrenergic meds
Decongestants containing ephedrine
Herbal remedies containing licorice or ephedrine
Nicotine
27
Q

Etiology of HTN, secondary causes: other causes

A
Hyperthyroidism and hypothyroidism
Hypercalcemia
Hyperparathyroidism
Acromegaly
OSA
Pregnancy-induced
28
Q

Pathophys of heart failure

A

Adaptations:
-Frank-Starling mechanism, where an increased preload helps to sustain cardiac performance
-Alterations in myocyte regeneration and death
-Myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented
-Activation of neurohumoral systems, such as RAAS, sympathetic nervous system
Angiotensin II
Myocytes and myocardial remodeling
Activation of atrial natriuretic peptide and B-type natriuretic peptide
LV chamber stiffness

29
Q

Etiology of heart failure: underlying causes of systolic heart failure

A
CAD
DM
HTN
Valvular heart disease
Arrhythmia
Infections and inflammation
Peripartum cardiomyopathy
Congenital heart disease
Drugs
Idiopathic cardiomyopathy
Rare conditions
30
Q

Etiology of heart failure: underlying causes of diastolic heart failure

A
CAD
DM
HTN
Valvular heart disease
HCM
Restrictive cardiomyopathy
Constrictive pericarditis
31
Q

How should BP be checked on the first visit?

A

Check in both arms and in one leg to avoid missing the dx of coarctation of aorta or subclavian artery stenosis

32
Q

PE of hypertension- what to check?

A

Do a fundoscopic exam
Palpate all peripheral pulses
Absent, weak, or delayed femoral pulses suggests coarctation of the aorta or severe peripheral vascular dz
Examine the neck for carotid bruits, distended veins, or enlarged thyroid gland
Careful cardiac examination

33
Q

Workup of HTN

A
UA
Fasting BG or A1c
Hct
Serum sodium
Potassium
Creatinine
Calcium
Lipid profile
34
Q

Workup of HTN based on suspected secondary causes: chronic kidney dz

A

Estimated GFR

35
Q

Workup of HTN based on suspected secondary causes: coarctation of the aorta

A

CTA

36
Q

Workup of HTN based on suspected secondary causes: Cushing syndrome; other states of glucocorticoid excess

A

Dexamethasone suppression test

37
Q

Workup of HTN based on suspected secondary causes: drug-induced/drug-related HTN

A

Drug screening

38
Q

Workup of HTN based on suspected secondary causes: pheochromocytoma

A

24-hr urinary metanephrine and normetanephrine

39
Q

Workup of HTN based on suspected secondary causes: primary aldosteronism, other states of mineralcorticoid excess

A

Plasma aldosterone to renin activity ratio
If abnl, refer for further eval such as saline infusion to determine if aldosterone levels can be suppressed, 24-hr urinary aldosterone level, and specific mineralocorticoid tests

40
Q

Workup of HTN based on suspected secondary causes: renovascular HTN

A

Doppler flow u/s
MRA
CTA

41
Q

Workup of HTN based on suspected secondary causes: sleep apnea

A

Sleep study with oxygen saturation

42
Q

Workup of HTN based on suspected secondary causes: thyroid/parathyroid dz

A

TSH

Serum parathyroid hormone level

43
Q

What is the criterion standard for the evaluation of renal and pulmonary causes of HTN?

A

Digital subtraction angiography with arterial injection of radiocontrast dye

44
Q

What is the main indication for echo in HTN?

A

Eval for end-organ damage in a pt with borderline-high BP

Presence of left ventricular hypertrophy despite nl or borderline-high BP measurements

45
Q

Nonpharm tx of HTN

A

Moderate reduction in salt
DASH diet
Reduce alcohol consumption
Wt loss and exercise

46
Q

Pharmacologic tx of HTN

A

Initiate ACE/ARB, BB or CCB, thiazide diuretic
If not working, titrate up to max dose
Still not working, add another agent

47
Q

Meds used to treat dyslipidemia

A
HMG-CoA reductase inhibitors (statins)
Cholesterol absorption inhibits
Bile acid resins
Niacin
Fibrates
Long-chained omega 3 fatty acids
PCSK-9 inhibitors
Lomitapide
Mipomersen
48
Q

What is usually first-line pharmacotherapy for dyslipidemia?

A

Statins

49
Q

MOA of statins

A

Inhibit HMG-CoA reductase, which is the rate-limiting step in cholesterol biosynthesis

50
Q

Long-term effects of statins

A

Reduce ASCVD, mortality

Effect seen across age, genders, disease states

51
Q

Most common SEs of statins

A
Constipation
Abdominal pain
Diarrhea
Dyspepsia
Nausea
52
Q

Who is more likely to have myopathy with statins?

A

Small body frame
Multisystem dz
Perioperative periods
Taking interacting meds/substances

53
Q

Other AEs of statins

A

Elevation in LFTs
Increased BG/A1c
Cognitive impairment
Pregnancy category X

54
Q

Monitoring of statins

A

LFT

CK

55
Q

Which statins are preferred in renal impairment?

A

Atorvastatin

Fluvastatin

56
Q

What is contraindicated with statins?

A

Gemfibrozil

57
Q

Grapefruit juice and statins

A

Only drink <8 oz grapefruit juice daily or 1/2 grapefruit

58
Q

Which statins are better at preventing myalgia?

A

Pravastatin and pitavastatin

Rosuvastatin

59
Q

Use of ezetimibe

A

Mostly used in combo with a statin

Shown a reduction in ASCVD events s/p MI when combined with moderate intensity statin

60
Q

CIs of ezetimibe

A

Acute liver dz or persistent elevations in LFTs