Physilogy Exam 3 Cardiovascular Physiology B

Cardiac Output

amount of blood ejected into aorta per min, 5 liters/ min

Systemic Circulation

carries oxygenated blood to body and returns deoxygenated blood back to heart

Pulmonary Circulation

carried oxygen depleted blood to lungs and then oxygenated blood back to heart

Arteries

deliver oxygenated blood to tissues, thick walled, smooth muscle, high pressure

Capillaries

no smooth muscle, has pores for absorption of nutrients and gas exchange

Arteries and Arterolies are innervated by what?

Alpha 1 receptors (constrict arterioles), beta 2 causes vasodilation

highest to lowest pressure in arteries (w #s)

aorta (100 mmHg) → arteries (50 mmHg) → arterioles + capillaries (20 mmHg) → veins (SVC + IVC) (4 mmHg)

Why does the aorta have such high pressure?

Because the blood is coming directly from the left ventricle which is very strong

Why do capillaries have such low pressure?

Because they are so small and have many intersectional areas which shows resistance to blood flow

Total Peripheral Resistance

resistance of arteries and capillaries to blood flow, exist in capillaries and arterioles

Venules

formed from merged capillaries, collects deoxygenated blood

Veins

thin walled, low pressure

What are veins innervated by?

A1 recepetors

velocity of blood flow

depends on cross sectional area, slows down in arteries and capillaries

Blood flow (cardiac output)

depends on total peripheral resistance and cardiac output, in arteries and capillaries

Resistance

depends on viscosity of blood (^ viscosity → blood is concentrated → resistance ^), small diamters and length of blood vessels

Capacitance

depends on thickness of walls and elastic fibers → thicker ^, elastic fiber ^ → capacitance low

Which has more capacity arteries or veins?

Veins due to more elastic fiber in the artery which occupies internal environment making capacity smaller

Systolic Pressure

pressure in ventricle after contraction and ejection of cardiac ouput

Diastolic pressure

pressure in ventricle in relaxation phase and recieving blood

Pulse pressure

difference between systolic and diastolic pressure

order of highest to lowest pressures (arteriole, ventricular, atrial, venous)

ventricular > arteriole > veinous > atrial

Primary Hypertension

do not know exact cause, but if cardiac output or TPR is increased it will increase blood pressure.

blood pressure (what and equation)

pressure that comes to wall of blood vessels, cardiac ouput x TPR

Any factors that lead to …, …, … lead to hypertension

vasoconstriction, vasobstruction (too many RBCs and calcium creat blocks), vasodestruction (too much glucose destroys blood vessels)

Secondary Hypertension Causes - adrenal gland disorder

secretes aldastrone through renin converting angiotensin → angiotensin 1 and angiotensin converting enzyme → angiotensin 2 which is a vasoconstrictor. Increases BP and aldastrone secretion which is carried to kidney, binds to receptor causes expression of K+ and H+ into urine → over secretion of aldastrone increases blood sodium, blood pressure, and K+ in urine.

Secondary Hypertension Causes- Cushing’s Syndrome

over production of cortisol secreted from adrenal cortex, if too much can cause increase in TPR and systolic + diastolic which leads to hypertension. S/S: blood sodium ^, bicarbonate ^, blood K+ low, obesity, weak immune system, hyperglycemia, facial hair growth (female), irregular menstruation/ovulation/fertility

Secondary Hypertension Causes- Conn’s Disease

specific tumor of aldastrone producing cells, BP ^, blood K+ low

Secondary Hypertension Causes- Pheochromocytoma

tumor causes adrenaline and noradrenaline hormones ^, S/S: excess sweating, arrythmia

Secondary Hypertension Causes- Kidney Disease

excess glucose can destroy renal artery and kidneys, BP ^

Secondary Hypertension Causes- Drugs

synthetic cortisol in long term

Secondary Hypertension Causes- Coarction of aorta

congenital defect, arch of aorta becomes narrow, low BP in femoral artery, risk of rupture of arteries in head, neck, brain → hypertension in head

Secondary Hypertension Causes- Preeclampsia

hypertenion due to pregnancy

Secondary Hypertension Causes- Thyroid and parathyroid problems

T3 +T4 hormones controls body metabolism and temp, ^ sensitivity of alpha 1 and beta 1 to norepinephrine, adrenaline causes ^ HR, excess sweating by alpha 1, vasoconstriction, hyperthyroidism patient has hypertenion and palpitation, PTH causes calcium ^ if below 10 mg (hyperparathyroidism → hypercalcemia → hypertension)

Hormones involved in Secondary Hypertension (8)

cortisol, aldasterone, norepinephrine, epinephrine, T3, T4, Parathyroid hormone, calcium (ion, hypercalemia)

Drugs to treat High Blood Pressure

ACE inhibitors- Captopril, Ramipril

Angiotension 2 receptor blockers- Valsartan

Diuretics (dec BP, ^ urination)- hydrochlorothiazide

Calcium Channel blockers- felodipine, benidipine

Beta- adrenergic blocking agents- propranolol

Alpha 1 blocker- Prazosin

Aldosterone Receptor Blocker- spironolactone

P wave

atrial depolarization/contraction, .08- .1 seconds

PR Interval

depolarization of AV node, .12 to .20 seconds

if PR interval is less than .2 seconds what does it mean

AV conduction block

QRS complex

ventricular depolarization/contraction, .06 to .1 seconds

Ectopic Foci

abnormal QRS, post myocardial infarction there is irritated tissue that can send signals to other area of heart after depolarization

ST segment

ventricles completely depolarized/ contracted, now ready for relaxation phase

depressed or elevated St segment can mean

sign of myocardial infarction

T wave

relaxation phase of ventricles

U wave

continuation of T wave

QT interval

time for both ventricular depolarization/contraction and repolarization/relaxation to occur, .2 - .4 seconds

prolonged QT interval can be

tachyarrhythmias

Cardiac action potentials: Ventricles, atria and purkinje system - phase 0

sodium enters cell

Cardiac action potentials: Ventricles, atria and purkinje system - phase 1

potassium leaves cell

Cardiac action potentials: Ventricles, atria and purkinje system - phase 2

calcium enters

Cardiac action potentials: Ventricles, atria and purkinje system - phase 3

potassium leaves

Cardiac action potentials: Ventricles, atria and purkinje system - phase 4

potassium reaches equilibrium potential → -85mv

Cardiac action potentials: SA and AV node - phase 0

calcium enters cell

Cardiac action potentials: Sinoatrial node - phase 3

potassium leaves

Cardiac action potentials: Sinoatrial node - phase 4

few sodium ions enter cell

Absolute refractory period

if there is a second stimulus during phase 0, membrane cannot except it or show reaction

Effective refractory period

if there is secon stimulus to cell membrane during phase 1 and 2 that stimulus is effective but membrane cannot show reaction

relative refractory period

if there is a second stimulus to cell membrane during phase 3 membrane accepts it and shows a reaction