Cardiovascular diseases and cardiac rehab Flashcards
artherosclerosis
disease of lipid laden plaques (lesions) affecting moderate and large size arteries
thickening and narrowing of the intimal layer of the blood vessel wall from focal accumulation of lipids, platelets, monocytes, plaque and other debris
part of CAD that leads to ischemia to the myocardium that can progress to injury and/or death
acute coronary syndrome (ACS)/ Coronary artery disease (CAD)
arthersclerotic disease; ranges from angina to infarction to sudden cardiac death
-leading cause of death in US
imbalance of myocardial oxygen supply and demand resulting in ischemic chest pain
symptoms present when lumen is 70% occluded
3 common presentations but may also have silent ischemia diagnosed by presence of a new pathologic Q wave
- most common in patients with diabetes, patients may have ischemia without any symptoms
- subacute occlusions may also produce no symptoms
1- angina
2-MI
3-heart failure
4-sudden death, usually due to significant ischemia or ventricular arrhythmia
angina pectoris
chest pain or pressure due to ischemia; may be accompanied by Levine’s sign- clenches fist over sternum
represents imbalance in myocardial oxygen supply and demand; brought on by:
- increased demands on heart: exertion, emotional stress, smoking, extremes of temperature (*cold), overeating, tachyarrhythmias
- vasospasm- may be present at rest
women more often describe sensations of discomfort, crushing, pressing and bad ache when referring to angina
with angina, patients often describe SOB, fatigue, diaphoresis and weakness as symptoms of ACS
older adults present more often with atypical symptoms (absence of chest pain): dyspnea, diaphoresis, nausea and vomiting and syncope
types of angina
1- stable:
- classic exertion angina occurring during exercise
- occurs at a predictable RPP
- relieved with rest and/or nitroglycerin
2-unstable (preinfarction, crescendo angina)
- coronary insufficiency at any time w/out precipitating factors or exertion
- chest pain increases in severity, frequency and duration; refractory to treatment
- increases risk for MI or lethal arrhythmia; pain is difficult to control
3-variant (Prinzmetal’s angina)
- caused by vasospasm of coronary arteries in the absence of occlusve disease
- responds well to nitroglycerin or calcium channel blocker long term
myocardial infarction
prolonged ischemia, injury and death of an area of the myocardium caused by occlusion of one or more of the coronary arteries
precipitating factors:
- atherosclerotic heart disease with thrombus formation
- coronary vasospasm or embolism
- cocaine use
Impaired ventricular function results in:
- decreased SV, CO and EF
- increased EDVP
electrical instability: arrhythmias, present in injured and ischemic areas
zones of infarction
zone of infarction:
- consists of necrotic, non contractile tissue
- electrically inert
- ECG: pathological Q waves
zone of injury:
- area immediately adjacent to central zone
- tissue is non contractile
- cells undergoing metabolic changes
- electronically unstable
- ECG: elevated ST segments in leads over injured area
zone of ischemia:
- outer area
- cells also undergoing metabolic changes
- electrically unstable
- ECG: T wave inversion
sites of coronary artery occlusion
R coronary A:
- inferior MI, RA, RV infarction, disturbances of upper conduction system
- blockage could result in arrhythmias, which can be fatal
L coronary A:
- supplies anterior, superior and lateral walls of the LV and the inter ventricular septum
- blockage usually causes LV failure, which leads to pulmonary edema
Circumflex A:
- lateral MI
- ventricular ectopy
L anterior descending A:
- anterior MI
- disturbances of lower conduction system
heart failure
clinical syndrome in which the heart is unable to maintain adequate circulation of the blood to meet the metabolic needs of the body
1- L sided heart failure
2- R sided heart failure
3-Biventricular failure
4- compensated heart failure
associated symptoms:
- muscle wasting
- myopathies
- osteoporosis
pathophysiology:
- decreased CO
- elevated end diastolic pressures (preload)
- tachycardia
- contractile deficiency (decreased SV and contractile force)
- impaired ventricular function
Left sided heart failure
(congestive heart failure, CHF)
characterized by pulmonary congestion, edema and low CO due to backup of blood from the LV to the LA and lungs.
occurs with:
- insult to the LV from myocardial disease
- excessive workload of the heart (HTN, valvular disease or congenital defects)
- cardiac arrhythmias or heart damage
S&S of pulmonary congestion
- dyspnea, dry cough
- orthopnea
- paroxysmal nocturnal dyspnea
- pulmonary rales, wheezing
S&S of low CO:
- hypotension
- tachycardia
- lightheaded/dizzy
- cerebral hypoxia: irritability, restless, confusion, impaired memory, sleep disturbances
- fatigue, weakness
- poor exercise tolerance
- enlarged heart on chest x-ray
- S3 heart sound, possible S4
- murmurs of mitral or tricuspid regurgitation
Right sided heart failure
reduced venous return to the heart from the systemic circulation due to failure of RV; increased pulmonary artery pressures with peripheral edema
characterized by:
- increased pressure load on the RV with higher pulmonary vascular pressures
- mitral valve disease, or chronic lung disease (cor pulmonale)
- produces hallmark signs of jugular vein distention and peripheral edema
S&S:
- dependent edema
- weight gain
- ascites (abnormal abdominal fluid retention)
- liver engorgement (hepatomegaly)
- anorexia, nausea, bloating
- cyanosis
- R upper quadrant pain
- jugular vein distension
- R sided S3 heart sounds
- murmurs of pulmonary or tricuspid insufficiency
Biventricular failure
severe LV pathology producing back up into the lungs, increased PA pressure and RV signs of HF
compensated heart failure
heart returns to functional status with reduced CO and exercise tolerance
control is achieved through:
- physiological compensatory mechanisms: SNS stimulation, LV hypertrophy, anaerobic metabolism, cardiac dilatation, arterial vasoconstriction
- medial therapy
cor pulmonale
failure or hypertrophy of RV resulting from disorders of the lungs, pulmonary vessels or chest wall
the lung pathology (chronic bronchitis or emphysema) produces pulmonary artery HTN that creates a problem for the RV
usually chronic, but may be acute and reversible
treatment for heart CHF
bed rest
diuretics
sodium restriction
measures to improve myocardial contractility and correction of arrhythmias
meds: 1-Digitalis (digoxin) -increases cardiac pumping ability -decreases HR 2- diuretics (lasix) -decrease vascular fluid volume -decrease preload and after load -control HTN
ACE inhibitors
Quinipril (accupril) Captopril (capoten) Enalopril (vasotec) Lisinopril (zestril) Fosinopril (monopril) benazepril (lotensin)
Inhibit conversion of angiotensin I to angiotension II (inhibits vascular smooth muscle contraction)
- decreases Na retention and peripheral vasocontriction in order to decrease BP
- also prevents the inactivation of bradykinin (a vasodilator)
- result is arteriolar vasodilation, decreased peripheral resistance and increased flow
usually the 1st step in managing LV failure
can be used with diuretics and calcium channel blockers (for HTN, never for CHF or angina)
side effects:
- nonproductive dry cough
- decreased taste perception
adverse effects:
- excessive hypotension
- hyperkalemia
- angioedema
May react with diuretics and cause hypotension.
-with potassium sparing diuretics, the problem may be hyperkalemia
step 2 with CHF is use of diuretics, especially loop diuretics (lasix)
step 3 with CHF is use of nonselective beta blocker and selective alpha 1 adrenergic blocker (carvedilol)
step 4: digoxin- when there is systolic dysfunction and arrhythmias
nitrates
nitroglycerin
decreasepreload through peripheral vasodilation
- reduce myocardial oxygen demand
- reduce chest discomfort (angina)
- may also dilate coronary arteries, improve BF
side effects:
- dizziness
- flushing and headache
- reflex tachycardia
beta blockers and calcium channel blockers may also be used for angina
beta-adrenergic blocking agents
Non-selective beta-blockers:
-propanolol (inderl)
-nadolol (corgard)
penbutolol (levatol)
**-olol
Selective beta blockers (beta-1)
- lopressor
- atenolol
- beta1 receptors in the heart
- beta2 receptors in the lungs and some arterioles
“anti-hypertensives”
- reduce myocardial demand by reducing HR and contractility and SV
- control arrhythmias, chest pain
- reduce BP
should be avoided with certain kinds of angina, all COPD, and DM
patients should never suddenly discontinue use of BB since there a risk of sudden death from anginal attack
side effects:
- sleep disturbances
- mental status changes- depression, disorientation
- cold extremities
**patients taking BB- can’t use HR to determine exercise tolerance **
Calcium channel blockers
procardia
norvasc
cardizem
verapamil
inhibit flow of calcium ions decrease HR decrease contractility dilate coronary arteries reduce BP control arrhythmias chest pain
side effects:
- significant bradycardia
- peripheral vasodilation can cause flushing, headache, ankle swelling, and reflex tachycardia
drug interactions:
- verapamil can result in digoxin toxicity
- verapamil and BB together can cause cardiac depression and AV block
anti-arrhythmics
numerous drugs, 4 main classes
alter conductivity
restore normal heart rhythm
control arrhythmias
improve cardiac output
ex:
- quinidine (ACE)
- procanamide
digitalis
cardiac glycosides
increases contractility and decreases HR
mainstay in the treatment of CHF (digoxin (lanoxin))
used as step 4 with CHF when there is a systolic dysfunctional and arrhythmias
increases the force of contraction of cardiac muscle without increasing oxygen demand
-EF may increase
adverse effects
-toxicity (signs: cardiac arrhythmia, anorexia, nausea, vomiting, mental status change (hallucinations, blurred vision))
PT** watch for digoxin toxicity
diuretics
THIAZIDES
furosemide (lasix)
hydrochlorothizide (esidrix)
- decrease myocardial work (reduce preload and aferload)
- control HTN
- inhibit tubular reabsorption of sodium and chloride in the kidney, which in turn, inhibits water reabsorption and increases urine volume–>ultimate result is decreased vascular resistance
thiazides should NOT be used with the elderly or anyone with renal dysfunction
side effects:
- hyperglycemia especially with diabetes
- hypokalemia
- hyperuricemia- too much uric acid- gout
- increase in LDL
- hypercalcemia
drug interactions:
- increases lithium reabsorption, which can increase lithium blood levels and result in lithium toxicity
- digoxin toxicity
Loop diuretics (furosemide (lasix), bumex, edecrin)
- inhibit sodium and chloride reabsorption in the lop of Henle
- more effective than thiazides
- may be used with elderly
potassium sparing diuretics:
-weak diuretics that prevent hypokalemia
aspirin
decreases platelet aggregation
may prevent myocardial infarction
used in treatment of angina, CAD and to prevent MI
shouldn’t be used after acute injury since it prolongs clotting
alpha adrenergic blockers
alpha 1 blockers: prazosin (minipress)
-blocks alpha1 receptors in smooth muscle allowing arterial and venous vasodilation
side effects:
- syncope
- headache
- palpitations
alpha 2 blockers (clonidine (catapress))
-stimulate alpha 2 receptors in the brainstem, which decrease sympathetic NS signals with resulting decreased HR, peripheral resistance and BP
side effects:
- dry mouth
- sedation
- depression
vasodilators
hydralazine (apresoline)
used in combo with ACE inhibitors ad have increased survival with CHF
can also be used with beta blockers to treat HTN
side effects:
- GI disturbances
- headache
- flushing
- nasal congestion
activity restriction with acute MI
activity can be increased once the acute MI has stopped (peak in cardiac troponin levels)
limited to 5 METs or 70% of age predicted HRmax for 4-6 weeks following MI
activity restriction with acute heart failure
oxygen demand should not be increased in patients in acute or decompensated heart failure
gradual increase while monitoring hemodynamic response to activity
surgical interventions for heart disease
1- percutaneous transluminal coronary angioplasty (PTCA)
2- intravascular stents
3- coronary artery bypass graft (CABG)
4- transplantation
5- ventricular assist device
percutaneous transluminal coronary angioplasty
PTCA
under fluoroscopy, surgical dilation of blood vessel using a small balloon tipped catheter inflated inside the lumen
relieves obstructed blood flow in acute angina or acute MI
results in improved coronary BF, improved LV function, anginal relief
intravascular stents
an endoprosthesis (pliable wire mesh) implanted postangioplasty to prevent restenosis and occlusion in coronary or peripheral arteries
often coated in medication to prevent thrombosis
coronary artery bypass graft
CABG
surgical circumvention of an obstruction in a coronary artery using an anastomosing graft (saphenous vein, internal mammary artery)
multiple grafts may be necessary
results in improved coronary BF, improved LV function, anginal relief
