Cardiovascular #2 (vein disorders, CMP, vascular assessment) Flashcards
Causes of cardiomyopathy
Primary-unknown
Secondary- secondary to another disease process.
Known causes: HTN, chronic etoh intoxication, pregnancy, tumors/post radiation, infections, genetics, valvular disease.
3 major types of cardiomyopathy
Dilated (congestive)
Hypertrophic (thickened muscle wall-thin chamber
Restrictive-wall stiffened so there is decrease in motion.
Dilated Cardiomyopathy (DCM)
Most common type of CM
- often occurs after infectious myocarditis; possible autoimmune process
- characterized by inflammation & rapid degeneration of myocardial fibers. Ventricular dilation.
Characteristics of DCM
- 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.
Symptoms of DCM
- Activity intolerance, fatigue, weakeness
- dyspnea at rest, PND, orthopnea
- dry cough
- palpitations
- abdominal bloating, anorexia, N/V
Signs of DCM
- Irregular HR, S3/S4, murmur
- Crackles
- Edema, weak peripheral pulses, pallor
- hepatomegaly, JVD, emboli
- BP below normal
Diagnostic studies for DCM
- patient history
- Endocardiogram & ECG, endomyocardial biopsy, CXR, labs
Treating and Managing DCM
-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.
Medications for DCM
-nitrates, loop diuretics, ACE inhibitors, beta blockers, anticoagulants, antidysrhythmias
Hypertrophic Cardiomyopathy (HCM)
- 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.)
Characteristics of HCM
- 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.
Symptoms of HCM
- Asymptomatic to sudden death
- Exertional dyspnea, exercise makes symptoms worse.
- chronic fatigue
- Angina, dizziness, syncope
- dysrhythmias, palpitations
- HF-PND
Diagnosing HCM
PRIMARY: echocardiogram
- history & physical
- ECG, CXR
Medically Managing of treatment
-improve ventricular filling by
-reduce ventricular contractility
-relieve LV outflow obstruction
meds–BB, CCB, anti coags, anti dysrhyths
Surgical therapy –HCM
- for severe symptoms not relieved with medications
- to relieve aortic obstruction from hypertrophic ventricles
- ventriculomyopathy
- myectomoy
- percutaneous transluminal septal myocardial ablatio (decrease outflow obstruction)
Restrictive Cardiomyopathy (RCM)
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
Symptoms of RCM
- exercise intolerance, fatigue
- dyspnea, orthopnea
- syncope, Angina, palpitations
- HF, SOB, JVD
- peripheral edema / ascites, hepatomegaly
- RUQ fullness and discomfort
Managing RCM
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
Surgical Treatment- Cardiac transplatation
-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
Heart transplantation surgery
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
Heart transplant: post op
- first year death due to acute rejection and infection
- infection is the primary complication
- grading rejection and guiding treatment by endomyocardial biopsy
Primary complication of heart transplant
Infection
Artificial heart
-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
Infective endocariditis (IE)/ Bacterial Endocarditis
- 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
Two forms of IE
subacute and acute
Subacute IE
Occurs in existing diseases valves, sicker longer
Acute IE
Affects healthy valves, rapidly progresses
-fatal unless treated with antibiotics
Patho of IE
- 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
Symptoms of IE
- nonspecific, multiple organ
- low grade fever
- flu-like s
Peripheral Arterial disease (PAD)
- 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
Risk factors for PAD
- cigarette smoking
- hyperlipidemia
- HTN
- diabetes
- family hx
PAD: atherosclerosis
- 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
Common Arterial disease sites
- disease occurs in segments of artery between areas of healthy artery
- s/s begin when occlusion 60-75% and depend on site of disease
PAD definition
Primarily affects LEs
- chronic, slow, progressive
- non-diabetic pts: femoral and popliteal
- diabetics: anterior and posterior tibials, peroneal
Symptoms of PAD
- 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)
Signs of PAD
- 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
Complications of PAD
- decreased arterial blood flow
- non-healing ulcers over bony prominences
- gangrene then amputation
Diagnostics for PAD – non invasive
- Doppler ultrasound
- duplex imaging
- segmental blood pressures
- ankle brachial index
Diagnostics for PAD – invasive
-angiography and MRA –location/extent of disease, good pre-op
