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
Etiology of HTN, secondary causes: neurogenic
Brain tumor Autonomic dysfunction Sleep apnea Intracranial HTN
26
Etiology of HTN, secondary causes: drugs and toxins
``` Alcohol Cocaine Cyclosporin, tacrolimus NSAIDs Erythropoietin Adrenergic meds Decongestants containing ephedrine Herbal remedies containing licorice or ephedrine Nicotine ```
27
Etiology of HTN, secondary causes: other causes
``` Hyperthyroidism and hypothyroidism Hypercalcemia Hyperparathyroidism Acromegaly OSA Pregnancy-induced ```
28
Pathophys of heart failure
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
Etiology of heart failure: underlying causes of systolic heart failure
``` CAD DM HTN Valvular heart disease Arrhythmia Infections and inflammation Peripartum cardiomyopathy Congenital heart disease Drugs Idiopathic cardiomyopathy Rare conditions ```
30
Etiology of heart failure: underlying causes of diastolic heart failure
``` CAD DM HTN Valvular heart disease HCM Restrictive cardiomyopathy Constrictive pericarditis ```
31
How should BP be checked on the first visit?
Check in both arms and in one leg to avoid missing the dx of coarctation of aorta or subclavian artery stenosis
32
PE of hypertension- what to check?
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
Workup of HTN
``` UA Fasting BG or A1c Hct Serum sodium Potassium Creatinine Calcium Lipid profile ```
34
Workup of HTN based on suspected secondary causes: chronic kidney dz
Estimated GFR
35
Workup of HTN based on suspected secondary causes: coarctation of the aorta
CTA
36
Workup of HTN based on suspected secondary causes: Cushing syndrome; other states of glucocorticoid excess
Dexamethasone suppression test
37
Workup of HTN based on suspected secondary causes: drug-induced/drug-related HTN
Drug screening
38
Workup of HTN based on suspected secondary causes: pheochromocytoma
24-hr urinary metanephrine and normetanephrine
39
Workup of HTN based on suspected secondary causes: primary aldosteronism, other states of mineralcorticoid excess
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
Workup of HTN based on suspected secondary causes: renovascular HTN
Doppler flow u/s MRA CTA
41
Workup of HTN based on suspected secondary causes: sleep apnea
Sleep study with oxygen saturation
42
Workup of HTN based on suspected secondary causes: thyroid/parathyroid dz
TSH | Serum parathyroid hormone level
43
What is the criterion standard for the evaluation of renal and pulmonary causes of HTN?
Digital subtraction angiography with arterial injection of radiocontrast dye
44
What is the main indication for echo in HTN?
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
Nonpharm tx of HTN
Moderate reduction in salt DASH diet Reduce alcohol consumption Wt loss and exercise
46
Pharmacologic tx of HTN
Initiate ACE/ARB, BB or CCB, thiazide diuretic If not working, titrate up to max dose Still not working, add another agent
47
Meds used to treat dyslipidemia
``` 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
What is usually first-line pharmacotherapy for dyslipidemia?
Statins
49
MOA of statins
Inhibit HMG-CoA reductase, which is the rate-limiting step in cholesterol biosynthesis
50
Long-term effects of statins
Reduce ASCVD, mortality | Effect seen across age, genders, disease states
51
Most common SEs of statins
``` Constipation Abdominal pain Diarrhea Dyspepsia Nausea ```
52
Who is more likely to have myopathy with statins?
Small body frame Multisystem dz Perioperative periods Taking interacting meds/substances
53
Other AEs of statins
Elevation in LFTs Increased BG/A1c Cognitive impairment Pregnancy category X
54
Monitoring of statins
LFT | CK
55
Which statins are preferred in renal impairment?
Atorvastatin | Fluvastatin
56
What is contraindicated with statins?
Gemfibrozil
57
Grapefruit juice and statins
Only drink <8 oz grapefruit juice daily or 1/2 grapefruit
58
Which statins are better at preventing myalgia?
Pravastatin and pitavastatin | Rosuvastatin
59
Use of ezetimibe
Mostly used in combo with a statin | Shown a reduction in ASCVD events s/p MI when combined with moderate intensity statin
60
CIs of ezetimibe
Acute liver dz or persistent elevations in LFTs