Flashcards in Exam 2...Cardiac Deck (80):
S/S of cardiovascular disease
abdominal distention (spleen/liver enlargement)
episodes of paroxysms of pain or pressure in the anterior chest when the need for O2 exceeds the supply.
Caused by atherosclerosis.
May produce pain or other symptoms varying in severity from mild indigestion to a choking or heavy sensation.
Pain is often retrosternal and may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms.
DM may not have pain due to neropathy.
ECG may show T-wave inversion and ACS is ruled out via labs.
exposure to cold
eating a heavy meal
**unstable angina is not associated with these triggers - it may occur at rest and is most worrisome.
predictable and consistent pain that occurs on exertion and is relieved by rest or nitroglycerin
AKA "pre-infarction" or "crescendo"
Symptoms increase in frequency and severity and may not be relieved by rest or nitroglycerin - requires medical intervention.
Intractable or refractory angina
Severe incapacitating chest pain
AKA "Prinzmetal's" has pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm.
objective evidence of ischemia (such as an ECG with stress test) but patient denies pain
Coronary Artery Disease (CAD)
the most prevalent type of cardiovascular disease in adults.
Atherosclerosis, an abnormal accumulation of lipid or fatty substances and fibrous tissue in the lining of arterial walls reduce blood flow and trigger an inflammatory response altering the structural and biochemical properties of arterial walls. It may be a result of smoking, HTN, or poor diet and exercise.
Cardiac Biomarker Analysis
CK, CK-MB, myoglobin, troponin T, and troponin I leak into interstitial spaces of myocardium and are carried into circulation by the lymphatic system. Abnormally high levels of these substances indicate necrosis of myocardial cells from ischemia or trauma - gold standard in diagnosing MI.
Cholesterol (s risk of developing atherosclerosis.
Brain/B-type Natriuretic Peptide
Regulates BP and fluid volume; useful for prompt diagnosis of heart failure (BNP greater than 110) in settings such as emergency departments.
protein produced by the liver in response to systemic inflammation, a key component of atherosclerosis progression. Elevation of this protein places patients at risk for recurrent cardiac event.
An amino acid linked to the development of atherosclerosis which damages endothelial lining and promotes thrombus formation. Elevated levels may indicate CAD, stroke or peripheral vascular disease. A 12 hour fast is necessary for this test.
Determines the size, contour, and position of the heart; reveals calcifications and demonstrates physiologic alterations in pulmonary circulation; verifies correct placement of pacemakers and pulmonary artery catheters.
X-ray imaging that allows visualization of the heart on a screen showing cardiac and vascular pulsations and unusual cardiac contours; useful for guiding the insertion of catheters during cardiac procedures.
a graphic representation of the electrical currents of the heart. The standard ECG uses 12 leads, sued to diagnose dysrhythmias, conduction abnormalities, chamber enlargement, ischemia, injury or infarction. A 15 lead adds leads across right precordium and is used for early diagnosis of right or left ventricular infarction. An 18 lead adds posterior leads and is used for early diagnosis of myocardial ischemia and injury. Hardwire monitoring is used to continuously observe for dysrhythmias and conduction disorders using one or two leads on patients on bed rest, while telemetry uses a battery operated transmitter to wirelessly observe ambulatory patients.
an exercise test that shows compromised blood flow to the myocardium and resulting ischemia when the demand for oxygen is increased. It helps determine the presence of CAD, the cause of chest pain, the functional capacity of the heart after an MI or heart surgery,, effectiveness of medications, dysrhythmias that results from exercise and helps physicians create specific physical fitness goals.
Exercise stress testing
uses a treadmill or stationary bike to increase the patient's target heart 80-90% and is then terminated, if not sooner due to chest pain, fatigue, dysrhythmias, an ST-elevation or a decrease in pulse rate or BP. If any of these occur the test is positive and a cardiac cath is scheduled. No eating, smoking or caffeine 4 hours before the test.
Pharmacological stress testing
is similar to other stress testing only the heart rate is increased using vasodilating agents as opposed to physical exertion. Dipyridamole/Persantine & adenosine/Adenocard mimic the effects of exercise and last 15-30 minutes.
Ultrasound used to measure EF and examine the size, shape and motion of cardiac structures; particularly useful in diagnosing pericardial effusions, determining chamber size, etiology of heart murmurs & elevation of heart valves. Noninvasive; takes 30 to 45 minutes.
Transesophageal Echo (TEE)
a small ultrasound transducer is passed through the mouth and esophagus providing higher quality imaging with more clarity. The first-line diagnostic tool is sued for diagnosing CVD such as HF, valvular heart disease, dysrhythmias and more. Complications such as impaired swallowing are uncommon.
Invasive diagnostic procedure in which radiopaque arterial and venous catheters are introduced into selected blood vessels of the right and left sides of the heart. The catheter is guided by fluoroscopy and inserted most commonly percutaneously. Pressures and oxygen saturation levels in all four heart chambers are measured. Diagnostic cardiac caths are commonly performed on an outpatient basis and require 2-6 hours of bed rest afterwards.
Cardiac cath is usually performed with angiography, in which a contrat agent is injected into the vascular system to outline the heart and its blood vessels.
CAD effects on the renal system
Nocturia is common in HF; decreased blood flow to kidneys = decreased renal perfusion and decreased uring output (oliguria); diuretic use; dialysis; renal failure
CAD effects on neuro system
Thrombi and emboli may cause cerebral infarction; inability to follow simple commands post-op up to 6 hours; confusion; light-headedness; weakness on one side of the body.
CAD effects on respiratory system
impaired gas exchange; orthopnea; decreased ventilations/ventilation assistance; increase in mucus production; crackles cough won't clear; wheezes; low O2 saturation; PND & coug
percent of end diastolic volume ejected with each heart beat (normal 55-65% from left ventricle; less than 40% indicates decreased left ventricle function & HF)
Cardiac Output (CO)
amount of blood pumped by ventricle in liters per minute (5-6 L/min is normal for adults)
SV x HR = CO
Stroke volume (SV)
amount of blood ejected with each heartbeat (70 mL from left ventricle) Affected by preload, afterload & contractility.
degree of stretch of cardiac muscle fibers at end of diastole; amount of blood in ventricles prior to contraction.
Resistance to ejection of blood from ventricle; affected by systemic vascular resistance & pulmonary vascular resistance; amount of blood left in ventricles after contraction.
Heart Failure (HF)
the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygenation and nutrition. Characterized by signs of fluid overload or inadequate tissue perfusion. The term HF indicates myocardial disease in which there is a problem with contraction of the heart (systolic dysfunction), or filling of the heart (diastolic dysfunction, less common). Sometimes it is reversible but most of the time it is a lifelong progressive condition managed with lifestyle changes and medications.
S/S left sided heart failure
fatigue, pulmonary congestions, dyspnea, cough, SOB, crackles, low O2 sats, S3 ventricular gallop, paroxysmal nocturnal syndrome, oliguria, altered digestion, dizziness, light-headedness, confusion, restlessness, anxiety, cool clammy skin, pallor, palpitations, and weak thready pulses.
S/S of right sided HF
fatigue, JVD, ascites, dependent edema, anorexia and nausea, weakness and weight gain, hepatomegaly and RUQ tenderness, and liver engorgement or dysfunction.
Class 1 HF (NYHA)
ordinary physical activity does NOT cause undue fatigue, dyspnea, palpitations or chest pain. NO pulmonary congestion or peripheral hypotension. Patient is considered asymptomatic without limitations of ADL's. Prognosis is good.
Class 2 HF (NYHA)
Slight limitations of ADL's. Patient reports no symptoms at rest but increased physical activity will cause symptoms. Basilar crackles and S3 murmur may be detected. Prognosis is good.
Class 3 HF (NYHA)
Marked limitation on ADL's. Patient feels comfortable at rest but less than ordinary activity causes symptoms. Prognosis is fair.
Class 4 HF (NYHA)
Symptoms of cardiac insufficiency at rest. Prognosis is poor.
HF Assessment & Diagnostic findings
echo usually performed to confirm diagnosis, identify underlying cause and determine EF. ECG also performed. Labs include electrolytes, BUN, creatinine, thyroid-stimulating hormone, CBC, routine analysis & BNP. Cardiac stress testing or cath may also be performed to determine whether or not CAD or ischemia are playing a role.
goal is to relieve symptoms, improve function and quality of life and extend survival- eliminate etiologic contributory factors such as uncontrolled HTN, optimize pharmacologic regiments, reduce workload of the heart by reducing preload and afterload, promote a healthy lifestyle and prevent episodes of acute HF.
Treat systolic HF.
Decrease BP & afterload, relieving progression and S/S of HF.
Treat ACE resistant pts w/ cough.
Decrease BP & afterload, relieving progression and S/S of HF
Treat systolic HF.
Dilate blood vessels and decrease afterload decreasing S/S of HF and improving exercise capacity.
Treat fluid overload.
Decrease fluid volume overload decreasing S/S of HF.
Calcium Channel Blockers
Treat diastolic HF.
Vasodilation and reduction of systemic vascular resistance.
Improves contractility decreasing S/S of HF; most common form of HF treatment at one time.
Effects of different types of diuretics on the body.
Diuretics remove extracellular fluid by increasing the rate of urine produced in patients with fluid overload. Most effective if patient remains supine for 1-2 hours after taking them. Side effects may include electrolyte imbalances, symptomatic hypotension, hyperuricemia & gout and ototoxicity. Diuretics are hard on the kidneys and may cause cardiorenal syndrome. Avoiding excess fluid intake (no more than 2 qt/day) and limiting sodium reduces the need for diuretics.
Usually first line treatment. Lasix is an example of a loop diuretic. It inhibits sodium and chloride reabsorption mainly in the ascending loop of Henle. Serum potassium must be closely monitored since it causes an increase in the excretion of potassium. May be part of dual therapy for severe HF patients unresponsive to single therapy treatment.
Metolazone is an example of a thiazide diuretic. It inhibits sodium and chloride reabsorption in the early distal tubules. Serum potassium must be closely monitored since it causes an increase in the excretion of potassium. May be part of dual therapy for severe HF patients unresponsive to single therapy treatment.
Spironolactone is a potassium sparing diuretic that blocks the effects of aldosterone in the late distal tube and collecting duct. It reduces mortality and morbidity in patients with moderate to severe HF. Serum creatinine and potassium levels must be monitored.
Control fluid overload
Restricting fluid & sodium intake
Sleeping with extra pillows
breathing techniques and positioning
Promote physical activity
30 minutes a day such as walking with a 5 minute warm-up; avoid extreme weather; wait 2 hours after meals; stop if SOB, pain or dizziness occure.
Prioritizing activities; eating small frequent meals; pacing yourself throughout the day.
maintain adequate oxygenation; identify stress triggers; identify coping mechanisms & support systems; relaxation techniques; screening for depression; encouragement; decision-making skills; self-power; questions & communication.
Lifestyle changes r/t activity and exercise; diet changes; smoking cessation; medication administration; how to identify and handle a HF re-occurrence or worsening HF s/s and unnecessary hospitalizations; when to contract a health professional; family involvement/teaching; home health care referrals; tele-health; advance directives.
Presentation of pericardial effusion
an increase over 20 mL fluid in the pericardial sac which leads to elevated pressure in all heart chambers, decreased venous return due to arterial compression & inability of ventricles to distend & fill adequately. S/S include feeling of pressure/fullness within the chest or substantial or ill-defined pain; engorged neck veins; SOB; low BP; pulsus paradoxus (abnormal difference of at least 10 MM Hg in systolic heart during exhalation & the point it is heard at inhalation); distant, muffled heart sounds.
recurring inflammation of arteries and veins of extremities resulting in thrombus formation and occlusion of vessels. It is believed to be an autoimmune vasculitis occurring mostly in men between 20 and 35. Heavy smoking or chewing tobacco is a causative agent.
Peripheral arterial disease: arterial insufficiency. Affects men more then women; obstructive lesions commonly confined to arteries from the aorta down (legs), although the arms may be affected. THE HALLMARK SIGN IS Intermittent claudication, a cramping, aching weakness that occurs with activity and is relieved with rest, occurring distal to the area of occlusion. Pain worsens at night and is so excruciating it is unrelieved by opiods. Elevating or horizontal placement increases the pain and dependent positioning relieves it. LIMBS PRESENT COLD, NUMB AND PALE, BRUITS MAY BE AUSCULTATED AND PULSES MAY BE DIMINISHED, ABSENT, OR UNEQUAL IN EXTREMITIES. THERE IS DEPENDENT RUBOR WITH DRY SHINY SKIN, LOSS OF HAIR, THICK RIGID NAILS, AND DEEP ULCERS THAT MAY REACH JOING SPACES AND TURN GANGRENE. patients are encouraged to walk at least 3x/week, stop smoking, and lose weight.
Peripheral vascular disease: venous insufficiency. Venous blood flow can be reduced by thromboembolus obstruction, incompetent venous valves or by reduced effectiveness of the pumping action of surrounding muscles. This results in decreased venous blood flow, increased venous pressure & capillary hydrostatic pressure which leads to edema (pooling of blood). S/S include EDEMA, ACHING, CRAMPING, PIGMENTATION IN GAITER AREA, THICK TOUGH SKIN THAT MAY BE RED OR BLUE, AND SUPERFICIAL IRREGULAR ULCERS WITH RED TO YELLOW GRANULATION TISSUE.
BP is the produce of CO x peripheral resistance. HTN results form an increase in CO, an increase in peripheral resistance or both. Primary is high BP from an unidentifiable cause & secondary is high BP r/t an indentified cause.
Stage 1 HTN: 141-159/90-99
Stage 2 HTN: >160/>100
a hypertensive emergency exists when blood pressure reaches levels that are damaging organs. Hypertensive emergencies generally occur at BP levels exceeding 180 systolic or 120 diastolic, but can occur at even lower levels in patients whose blood pressure had not been previously high. S/S include chest or back pain, SOB, numbness/weakness, change in vision, difficulty speaking. HTN crisis may result in stroke, loos of consciousness, memory loss, MI, kidney or eye damage, aortic dissection, angina, PE & eclampsia.
BP severely elevated 180 or higher systolic and 110 or higher diastolic with no associated organ damage. S/S include headache, SOB, nosebleeds & severe anxiety. Treatment generally requires readjustment and/or additional dosing of oral medications, but most often does not necessitate hospitalization for rapid blood pressure reduction. A blood pressure reading of 180/110 or greater requires immediate evaluation, because early evaluation or organ function and blood pressure elevations at these levels is critical to determine the appropriate management.
diuretics, centrally-acting alpha 2 agonists, beta-blockers, alpha1-blockers, combined alpha and beta blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, calcium channel blockers & direct renin inhibitors.
HTN PT education: RISKS
smoking, dyslipidemia, DM, impaired renal function, obesity, physical inactivity, age > 55 for men and 65 for women, family history
HTN PT education: DIET
DASH diet rich in fruits, vegetables and low-fat dairy; reduce sodium to 2 grams a day
HTN PT education: Long term effects
HTN patients are at risk for heart disease, stroke, chronic kidney disease, peripheral arterial disease and retinopathy.
HTN PT education: lifestyle changes
maintain normal body weight; limit alcohol consumption of no more then 2 drinks per day; engage in regular aerobic activity 30 min/day.
The formation of a blood clot in a blood vessel. The vessel may be any vein or artery as, for example, in a DVT or a coronary artery thrombosis. The clot itself is termed a thrombus. If the clot breaks loose and travels through the bloodstream, it is a thromboembolism.
a result of poorly controlled HTN, blunt chest trauma or cocaine use, dissecting aortas are tears in the intima or media degenerates. This causes arteries branching from the involved area and aorta to shear and occlude. Severe ripping pain occurs suddenly and is often mistaken for an MI. They are 3x more common in men aged 50-70.
a localized sac or dilation formed at the weak point of the wall of an artery. Classified by shape or form, the most common types include saccular (projects from one side of the vessel) and fusiform (entire segment dilated). Most commonly a result of atherosclerotic changes, aneurysms can rupture leading to hemorrhage and death.
As the volume of blood returning to the heart increases, muscle fiber stretch also increases resulting in stronger contraction & greater stoke volume, and is maintained until the physiologic limit of the muscle is reached. Within limits, the greater the initial length or stretch of cardiac muscle sarcomeres(, the greater the degree of shortening, a result of increased interaction between thick and thin filaments within the cells.
atrial depolarization (contraction); first small hump in EKG
Ventricle depolarization/firing (spike in middle of EKG)
ventricular repolarization / rest (last small hump in EKG)
Area between S & T elevated
indicative of heart attack
P to R interval
time from beginning of atrial depolarization to the beginning of ventricular depolarization
S to T segment
period between ventricular depolarization and beginning of ventricular repolarization
Q to T interval
total time for ventricular depolarization and repolarization