Cardiovascular #2 (vein disorders, CMP, vascular assessment) Flashcards

1
Q

Causes of cardiomyopathy

A

Primary-unknown
Secondary- secondary to another disease process.
Known causes: HTN, chronic etoh intoxication, pregnancy, tumors/post radiation, infections, genetics, valvular disease.

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2
Q

3 major types of cardiomyopathy

A

Dilated (congestive)
Hypertrophic (thickened muscle wall-thin chamber
Restrictive-wall stiffened so there is decrease in motion.

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3
Q

Dilated Cardiomyopathy (DCM)

A

Most common type of CM

  • often occurs after infectious myocarditis; possible autoimmune process
  • characterized by inflammation & rapid degeneration of myocardial fibers. Ventricular dilation.
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4
Q

Characteristics of DCM

A
  • dilated, enlarged ventricles
  • decreased muscle wall thickness
  • systolic dysfunction–decreased cardiac output
  • Atria enlarge
  • stasis of blood in Left ventricle. –embolic episodes, increased heart pressure, pulmonary & vascular congestion.
  • Cardiomegaly from ventricular dilation.–contractile dysfunction. BP normal to low.
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5
Q

Symptoms of DCM

A
  • Activity intolerance, fatigue, weakeness
  • dyspnea at rest, PND, orthopnea
  • dry cough
  • palpitations
  • abdominal bloating, anorexia, N/V
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6
Q

Signs of DCM

A
  • Irregular HR, S3/S4, murmur
  • Crackles
  • Edema, weak peripheral pulses, pallor
  • hepatomegaly, JVD, emboli
  • BP below normal
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7
Q

Diagnostic studies for DCM

A
  • patient history

- Endocardiogram & ECG, endomyocardial biopsy, CXR, labs

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8
Q

Treating and Managing DCM

A

-Treat underlying cause, palliative not curative
GOAL: enhance contractility & decrease afterload…Focus is improving cardiac output
-Automatic implantable cardiac defibrillator, NAS diet, rest & avoid exertion and stress, avoid etoh, heart transplant.

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9
Q

Medications for DCM

A

-nitrates, loop diuretics, ACE inhibitors, beta blockers, anticoagulants, antidysrhythmias

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10
Q

Hypertrophic Cardiomyopathy (HCM)

A
  • Most common cause of sudden death in otherwise healthy young people.
  • 1/2 genetic cause
  • More common in men 30-40 yrs
  • Usually diagnosed in athletes in late adolescence or early adulthood (Af. Amer.)
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11
Q

Characteristics of HCM

A
  • Massive ventricular hypertrophy
  • rapid, forceful LV contraction
  • impaired relaxation of ventricles (LV stiff) (diastolic dysfunction)
  • Enlarged ventricular septum blocks blood flow from LV to aorta –obstruction of aortic outflow-decreased cardiac output.
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12
Q

Symptoms of HCM

A
  • Asymptomatic to sudden death
  • Exertional dyspnea, exercise makes symptoms worse.
  • chronic fatigue
  • Angina, dizziness, syncope
  • dysrhythmias, palpitations
  • HF-PND
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13
Q

Diagnosing HCM

A

PRIMARY: echocardiogram

  • history & physical
  • ECG, CXR
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14
Q

Medically Managing of treatment

A

-improve ventricular filling by
-reduce ventricular contractility
-relieve LV outflow obstruction
meds–BB, CCB, anti coags, anti dysrhyths

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15
Q

Surgical therapy –HCM

A
  • for severe symptoms not relieved with medications
  • to relieve aortic obstruction from hypertrophic ventricles
  • ventriculomyopathy
  • myectomoy
  • percutaneous transluminal septal myocardial ablatio (decrease outflow obstruction)
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16
Q

Restrictive Cardiomyopathy (RCM)

A

Least common form

  • unknown etiology-myocardial fibrosis, hypertrophy, infiltration, secondary to radiation or disease
  • ventricles stiff and resist filling (impaired diastolic filling & stretch, filling pressures increase, decreased CO, HF and mild ventricular hypertrophy
17
Q

Symptoms of RCM

A
  • exercise intolerance, fatigue
  • dyspnea, orthopnea
  • syncope, Angina, palpitations
  • HF, SOB, JVD
  • peripheral edema / ascites, hepatomegaly
  • RUQ fullness and discomfort
18
Q

Managing RCM

A

GOAL: to diminish HF, improve diastolic filling, treat underlying diseases
-avoid strenuous activity, dehydration, increases in systemic vascular resistance
meds-treat HF, dysrhythmias, prophylactic antibiotics

19
Q

Surgical Treatment- Cardiac transplatation

A

-transfer of the heart from one person to another (refractory end stage HF, CMP, inoperable CAD)
Thorough evaluation, transplant list and wait- home or hospital
recipient must match with donors body/heart sixe, ABO blood typer

20
Q

Heart transplantation surgery

A

Max time from harvest to transplant: optimal 4 hours

  • patient placed on cardiopulmonary bypass machine
  • donor heart replaces recipients heart and trimmed to match
  • immunosuppressive therapy
21
Q

Heart transplant: post op

A
  • first year death due to acute rejection and infection
  • infection is the primary complication
  • grading rejection and guiding treatment by endomyocardial biopsy
22
Q

Primary complication of heart transplant

A

Infection

23
Q

Artificial heart

A

-possible help for short term survival in pt with end-stage HF- experimental
-designed to minimize coagulation (lifelong)
-motor driven pumping system : internal/external batteries
-artificial ventricles
-no immunosuppressant needed
-electronic abdominal monitor adjusts HR based on activity of pt
-external battery pack: 6-8h power; recharges during sleep
two types: cardiowest, abioCor

24
Q

Infective endocariditis (IE)/ Bacterial Endocarditis

A
  • infection or inflammatory process of inner layer of heart and heart valves
  • classified by cause of affected site
    • IV drug abuse IE, fungal IE, prosthetic valve endocarditis
25
Q

Two forms of IE

A

subacute and acute

26
Q

Subacute IE

A

Occurs in existing diseases valves, sicker longer

27
Q

Acute IE

A

Affects healthy valves, rapidly progresses

-fatal unless treated with antibiotics

28
Q

Patho of IE

A
  • Causative organisms: bacterial, fungal, viruses
  • Organisms infiltrate damaged heart valves & endothelial surfaces
  • circulating organisms attach to roughened endocardium
  • form colonies-vegetation
  • vegetation may break off into circulation, emboli
  • vegetation may spread and damage heart valves
29
Q

Symptoms of IE

A
  • nonspecific, multiple organ
  • low grade fever
  • flu-like s
30
Q

Peripheral Arterial disease (PAD)

A
  • progressive narrowing and degeneration of arteries
  • affects upper and lower extremities
  • risk increases w/ age
  • ATHEROSCLEROSIS LEADING CAUSE
  • typically appears @ ages 60-80s
  • prevalence similar in men and women
  • strongly rt other CV disease
31
Q

Risk factors for PAD

A
  • cigarette smoking
  • hyperlipidemia
  • HTN
  • diabetes
  • family hx
32
Q

PAD: atherosclerosis

A
  • gradual thickening and narrowing of arterial lumen
  • theory: begins w/ inflammation or endothelial injury
  • more commonly affects certain portions of arterial tree
  • Commonly affected arteries: coronary, carotid, iliac, femoral, popliteal, tibial
33
Q

Common Arterial disease sites

A
  • disease occurs in segments of artery between areas of healthy artery
  • s/s begin when occlusion 60-75% and depend on site of disease
34
Q

PAD definition

A

Primarily affects LEs

  • chronic, slow, progressive
  • non-diabetic pts: femoral and popliteal
  • diabetics: anterior and posterior tibials, peroneal
35
Q

Symptoms of PAD

A
  • Factors: site obstruction, amount of collateral circulation
  • intermittent claudication: pain w/ exercise, resolves with rest, reproducible
  • impotence
  • Paresthesia-numbness or tingling in toes/feet
  • Neuropathy: shooting/burning pain, loss of pressure, loss of deep pain sensation, injuries often go unnoticed by pt (more common in diabetes)
36
Q

Signs of PAD

A
  • thin, shiny, and taut skin
  • loss of hair on the lower legs
  • diminished or absent pedal, popliteal, or femoral pulses
  • pallor of foot with leg elevation
  • reactive hyperemia of foot w/ dependent position –> dependent rubor
  • pain at rest–occurs in forefoot or toes, aggravated by limb elevation, occurs from insufficient blood flow, occurs more often at night
37
Q

Complications of PAD

A
  • decreased arterial blood flow
  • non-healing ulcers over bony prominences
  • gangrene then amputation
38
Q

Diagnostics for PAD – non invasive

A
  • Doppler ultrasound
  • duplex imaging
  • segmental blood pressures
  • ankle brachial index
39
Q

Diagnostics for PAD – invasive

A

-angiography and MRA –location/extent of disease, good pre-op