Ch 35: Assessment of Cardiovascular Flashcards
Coronary arteries
Supply the heart muscle with blood. They originate on the aorta just beyond the aortic valve.
LMCA Left main coronary artery
LAD left anterior descending
LCX left circumflex Half of the AV node
RCA. right coronary artery, perfuses the right heart and inferior wall of the left heart. Supplies blood to the AV node in almost everyone, and half of the SA node
Blood flow to the heart occurs primarily during diastole. You must have a mean arterial pressure/MAP of at least 60.
Flow of blood through the heart
IVC & SVC > RA > tricuspid valve > RV > pulmonic valve > pulmonary artery > lungs > pulmonary veins > LA > mitral (bicuspid) valve > LV > aortic valve > aorta
Cardiac output
The heart rate x the stroke volume.
4 to 7 L per minute in adults
60 mL with each beat
Amount pumped by left ventricle
Heart rate
60-100
parasympathetic/vagus nerve slows it
Sympathetic increases it.
Epinephrine and norepinephrine stimulate it.
Betablockers block the sympathetic>slow the HR.
Ex. Metoprolol. Check HR and BP before giving
Stroke volume
Amount ejected from left ventricle with each beat
Preload: degree of myocardial fiber stretch at end of diastole, the volume contained in the ventricles at end of diastole.
Determined by amnt of blood returning to heart from venous and pulmonary system.
Sterlings law: more the heart is filled, the stronger is contracts.
Afterload: pressure resistance the ventricles must overcome to eject blood thru semilunar valves and into the blood vessels. Affected by arterial BP and diameter of blood vessels.
impedance: pressure needed to open aortic valve
Myocardial contractility: force of contraction increased by sympathetic stimulation, calcium release, positive inotropic drugs. Decreased by hypoxia and acidemia
Diastole
2/3 cardiac cycle
relaxation and filling of the atria and ventricles
passive
systole
contraction
emptying of atria and ventricles
Blood Pressure
Determined primarily by the quantity of blood flow or cardiac output as well as the resistance in the arterials. It equals cardiac output x peripheral vascular resistance
3 things regulate it:
ANS which excites or inhibits the sympathetic nervous system in response to chemo (peripheral respond to hypoxemia) (central receptors respond to hypercapnia and acidosis) and baro (respond to increased pressure) receptors
Kidneys which activate the renin-angiotensin-aldosterone system (Na and water retention, vasoconstriction)
Endocrine which releases hormones to stimulate the sympathetic nervous system
External factors: exercise, pain, stress, etc..
Systolic: pressure generated by LV to distribute blood into aorta during contraction
Diastolic: pressure against the arterial walls during relaxation
Changes with Aging
See pic 35-1
Calcification and degeneration of mitral and aortic valves
Pacemaker cells decreased, fewer muscle fibers, conduction time increases
Left ventricle increases in size, becomes stiff and less distensible, fibrotic changes decrease the speed of diastolic filling
Aorta thickens and stiffens, increased systolic BP, vascular resistance increases which leads to L/ventricle hypertrophy
Baro receptors become less sensitive.
Angina pain
Sudden, usually response to exertion, emotion, or extremes in temperature. Usually is squeezing, viselike pain. Substernal, may spread across the chest and back or down the arms. Usually the left side of the chest without radiation, my less than 15 minutes, relieved with rest, nitrate, or O2
Myocardial infarction pain
Severe, without any factors, often in early morning. Intense stabbing, viselike pain or pressure, severe. Substernal and may spread throughout the anterior chest into the arms, jaw, back, or down the arms. Continuous or no chest discomfort, relieved with morphine, cardiac drugs, and O2
Pericarditis pain
Sudden, sharp, stabbing, moderate to severe pain. Substernal, usually spreads to the left side for the back. It is intermittent. Relieved with sitting upright, analgesia, or anti-inflammatories.
Pleuropulmonary pain
Has a variable onset. A moderate ache worse on inspiration. In the lung fields. Continuous until the underlying condition is treated or the patient has rested
Esophageal/gastric pain
Variable onset. Squeezing, heartburn, variable severity. Substernal, may spread to the shoulders or the abdomen. Variable duration. May be relieved with antacid administration, food intake, or a sitting position
Anxiety pain
Variable, maybe in response to stress or fatigue. Dull ache to sharp stabbing. May be associated with numbness in fingers. Usually lasts 30 minutes or longer is relieved with opioids.
Classification of cardiovascular disease
See pic table 35-2
Class I: no limitations in activity, activity does not cause fatigue or pain
Class II: slight limitation, comfortable at rest, fatigue, palpitation, dyspnea, or pain with activity
Class III: marked limitations, comfortable at rest, little activity causes fatigue, pain, etc
Class IV: inability to carry on activities, anginal syndrome and cardiac insufficiency at rest, and activity causes discomfort
anascara
generalized edema
Postural - orthostatic hypotension
A decrease of more than 20 mm HG at the systolic pressure or more than 10 mm HG diastolic pressure, as well as a 10 to 20% increase in the heart rate.
Causes include cardiovascular drugs, blood volume decrease, prolonged bed rest, age-related changes, or disorders of the ANS
First measure when the patient is supine. After remaining in that position for three minutes, the patient changes position to sitting or standing. After the position change, wait for one minute before retaking the pulse and blood pressure. Note any dizziness.
Pulse pressure
The difference between systolic and diastolic values. Narrowed pressure is rarely normal and can be from increased peripheral vascular resistance, decreased stroke volume in patients with heart failure, hypovolemia, or shock. It can be from mitral stenosis or regurgitation.
An increased pulse pressure may occur in patients with a slow heart rate, aortic regurgitation, atherosclerosis, hypertension, and aging
Heart sounds
S1: 1st heart sound, closure of mitral and tricuspid AV valves. Listen at l/lower sternal border or apex
S2: 2nd heart sound, closure of aortic and pulmonic semilunar valves. Listen at base of heart during end of ventricular systole
Abnormal:
splitting of S2 - paradoxical splitting heard on expiration, early closure of pulmonic or late closure of aortic
Pericardial friction rub
Gallops.
Murmurs: turbulent blood flow
Diastolic filling sounds S3 & S4
S3 ventricular gallop during filling of ventricular diastole (pt on left side)
S4 atrial gallop
S3 and S4 together is called summation > severe heart failure, quadruple gallop
S4