Chapter 11b Part 2 – Cardiovascular Physiology

1. Hypertension (Many questions from hypertension slide on exam) – primary and secondary hypertensiona. Primary or essential

i. We don’t know the causeii. Primary hypertension

1. Diet a. Like eating salty food can increase blood pressure because Na is important

ion for action potential for depolarization phase of cell. 2. Obesity

a. Sometimes obese people are healthier than skinny peopleb. Associated with endocrine hormone disorder

i. People with type II diabetes already have hormonal disorder3. Stress

a. Mother of all diseases and disordersb. Increases cortisol hormone level

i. Excess cortisol increases systolic and diastolic pressuresc. It increases TPR (total peripheral resistance that exists in capillaries).

i. Increased TPR by cortisol increases blood pressure because blood pressure = (cardiac output) x TPR

1. Increased TPR can cause hypertension and increased cardiac output

ii. Cardiac output 1. Amount of blood ejected into aorta by left ventricle

contraction per minute2. Close to 5 liters per minute. 3. Amount of blood body receives per minute

4. Overstimulation of sympathetic systema. By over secretion of NE which stimulates alpha I causing vasoconstriction

5. Hypernatremia a. Excess sodium in blood b. Causes overactivation and depolarization of cell

i. Opening of calcium channels and calcium enters into cell after depolarization.

ii. Calcium binds troponin C and leads to muscle contractioniii. Smooth muscle contraction means constriction of blood vessel

1. This increases blood pressure which causes hypertension6. Deficiency of natural vasodilator

a. Our body produces prostaglandin and bradykinin vasodilators that cells secrete and they relax blood vessel

b. Secondary hypertensioni. We know the cause and can treat itii. Adrenal gland this gland is main problem for secondary hypertension

1. Located above the kidney and it has two partsa. Adrenal medulla Center of adrenal medulla

i. Secretes1. Norepinephrine (noradrenaline) (NE)*2. Epinephrine (adrenaline) (E)*

ii. When secreted by neurons we call them neurotransmittersiii. Innervation

1. By preganglionic fiber of sympathetic system secretes Achb. Adrenal Cortex

i. Secretes 1. Aldosterone*2. Cortisol*3. Androgen*

2. All hormones secreted by adrenal medulla or cortex are involved in blood pressure3. Hypertension caused by tumor in adrenal medulla, cortex, or adrenal gland4. Disorders of adrenal gland

a. Due to i. Tumor in adrenal glandii. Tumor in cortex or medulla

iii. Infection in adrenal glandiv. Manipulation of tissue during surgery. v. Autoimmune disease

vi. Endocrine hormone disordersvii. Specific tumor that produces any of the previous hormones

5. 4 Important blood pressure hormones from adrenal gland (aldosterone, cortisol, )a. Aldosterone

i. Is sensitive to low blood sodium and low blood pressureii. Process

1. When blood pressure is low, this leads to secretion of an enzyme called renin from kidney tissue

2. Renin converts the protein from liver called angiotensin into angiotensin 1 (AgI)

3. We have enzyme ACE (angiotensin converting enzyme) which converts AgI into AgII which acts as vasoconstrictor and stimulates secretion of aldosterone from adrenal cortex

4. Blood carries aldosterone to nephron tubule5. Aldosterone binds to receptor on nephron tubule 6. After binding, the capillary starts to absorb sodium chloride

(NaCl) and water increases blood pressure and sodium7. 2nd function of aldosterone secretes potassium into urine

iii. Summary of aldosterone function

1. Aldosterone is sensitive to low blood pressure and low blood sodium

2. Blood sodium increases by absorption of NaCl and blood pressure increases by absorption of water into blood stream by capillary.

3. Excretes potassium into urine. 4. In this manner, aldosterone increases sodium in blood and

increases blood pressure.5. Aldosterone increase absorption of H+ into urine and secretion

of bicarbonate into blood (HCO3-)

iii. Common Causes of secondary hypertension1. (1st cause) Overstimulation of ACE (angiotensin converting enzyme)

a. Treatmenti. You have to block the angiotensin converting enzyme by medicine

called Captopril1. Captopril and Ramipril are ACE inhibitor

2. (2nd cause) Over secretion of angiotensin 2 a. Leads to hypertension because AgII acts as vasoconstrictor and stimulates

aldosterone secretion from adrenal cortex. b. Treatment

i. Use AgII blocker which is called Valsartan3. (3rd cause) Over secretion of aldosterone

a. You need to block aldosterone receptor by medicine called Spironolactonei. Spironolactone is an aldosterone receptor blocker and you can

control hypertension with it4. (4th cause) Over secretion of calcium hypercalcemia

a. You need calcium channel blocker Use Benidipine or Felodipine5. (5th cause) Due to heart problem

a. You have to go for beta I blocker use Propranolol6. (6th cause) Kidney does not have normal filtration rate

a. Urine production of kidney decreases blood volume and blood pressure.i. Kidney produces urine and eliminates extra fluid our body has and

our body uses kidney to adjust blood volume. b. When kidney cannot work, you have to use diuretic such as

Hydrochlorothiazide this accelerates urination. 7. (7th cause) Cushing’s syndrome - disorder of adrenal cortex

a. Due to i. Tumorii. Infection

b. Patient has increased aldosterone, cortisol, and androgen hormones. i. Cortisol

1. Controls stress

2. Increases appetite3. Maintain blood glucose4. Suppresses inflammation5. Is immunosuppressant suppresses immune system

ii. Androgen1. When female has puberty, 1st hormone to become active is

androgen.2. First sign of puberty in female is axillary hair growth due to

androgen.3. Facial acne is also from androgen. 4. In male very little androgen is produced

c. Signs and symptomsi. Increase of all 3 previously mentioned hormones androgen,

aldosterone, cortisolii. Aldosterone increases blood sodium level and blood pressure

1. Patient has hypernatremia increased blood sodiumiii. Hypertension due to high aldosteroneiv. Patient has all signs of hypertension

1. Headache2. Vomiting3. Anxiety4. Sleep disorder5. Noe bleed6. Sometimes sweating

v. Obesity due to high cortisol since it stimulates appetitevi. Hyperglycemia due to excess cortisolvii. Affected immune system

viii. Effects of increased cortisol1. Central obesity

a. Fat buildup in face, belly, and in shoulder region b. Thinner upper and lower limb c. Because cortisol increases appetite and excess cortisol

breaks down proteins in patient’s body, especially the skeletal muscles which are full of protein. This causes thinner upper and lower limbs.

2. Changes texture of skin causes stretch marks in abdominal skin because cortisol affects collagen in skin

a. Skin becomes fragile3. Cortisol increases systolic and diastolic pressure4. Increases TPR which is in capillaries because they have…

a. Smaller diameterb. More intersectional area

5. Cortisol increases blood pressure because of high systolic, diastolic, and TPR

ix. Female patient has facial hair because high androgen levelsd. Treatment

i. If tumor, remove tumor from glandii. If infection, treat infection

iii. Treatment depends on type of problem in gland8. (8th cause) Hyperaldosteronism excess aldosterone

a. Causei. Tumor of aldosterone producing cells in adrenal cortex

1. Patient only has increased aldosterone level because of tumorb. Other name of hyperaldosteronism is Conn’s disease

i. Signs and symptoms1. Patient has hypernatremia increased sodium in blood (Na+)2. Hypokalemia low level of potassium (K+)3. Hypertension4. Headache5. Vomiting6. Nosebleed7. Increased blood volume8. Sometimes patient has muscle spasm due to continuous

depolarization of cells a. This is due to increased sodium hypernatremia.

Patient has rigid muscles and muscle spasmc. Treatment

i. Remove tumor and replace hormone9. (9th cause) Pheochromocytoma

a. Causei. Specific adrenaline and noradrenaline producing tumor in adrenal

medullab. Signs and symptoms

i. Adrenaline and noradrenaline increased in blood ii. Noradrenaline can act as neurotransmitters

1. High level causes sweating and hypertension because of alpha I receptors

2. Increases heart rate3. Increased contractility of myocardium due to beta I receptors4. Patients may have heart disease/problem due to

overactivation of beta Iiii. Signs and symptoms of hypertension

1. Sweating due to alpha I receptors2. No hypernatremia

a. Since we don’t have high level of aldosterone3. No hypokalemia

a. Since adrenaline and noradrenaline are not involved in potassium

iv. Treatment1. Remove tumor 2. May have to remove adrenal medulla and replace hormones

10. (10th cause) Kidney diseasea. Cause

i. Any disease in kidneyii. Having cyst in kidney

iii. Polycystic kidney diseaseiv. Endocrine hormone disorder type I or II diabetesv. Blockage of artery supplying the kidney

b. Kidney is for filtration and production of urinec. Goal of urine is to adjust blood volume d. Signs and symptoms

i. Any disease that leads to accumulation of glucose in nephron which destroys nephron (nephropathy).

1. This leads to decreased renal filtration rate (less urination) which means body can’t control blood volume. This increases blood pressure and causes hypertension and edema

e. Treatmenti. Give diuretic (hydrochlorothiazide) to accelerate urination and

decrease blood volume and blood pressure11. (11th cause) Some drugs can cause hypertension

a. Corticosteroid same as cortisoli. Increases systolic and diastolic pressure and TPRii. Taking corticosteroids such as cortisone, prednisone, hydrocortisone

1. When patient has local inflammation of skin or dermatitis they can use cortisol steroids

2. Dermatitis due to autoimmune disease use cortisol to control skin inflammation

3. Long term cortisol steroid usea. Long term, taking cortisol causes…b. Hypertensionc. Weight gain obesityd. Hyperglycemia

i. Due to cortisol which maintains blood glucose level

e. Affects immune systemb. Other medicines

i. Nonsteroidal anti-inflammatory drug1. Not steroid by suppresses inflammation such as aspirin

ii. Aspirin is an acid and it can affect blood vessel wall1. Anything that leads to destruction, constriction, or obstruction

of blood vessel leads to hypertensioniii. Pills to lose weight can have side affect

1. It destroys wall of blood vessels and gives hypertensioniv. Overactivation of sympathetic system

1. Maybe tumor of lateral horn of spinal cord center for ANS2. Overactivation leads to over secretion of NE from

postganglionic fiber which leads to hypertension (from alpha 1)

12. (12th cause) Preeclampsia hypertension due to pregnancya. Pregnancy itself means big hormonal change. b. Pregnancy can change levels of thyroid and sex hormones. c. These changes can affect wall of blood vessels and at end of pregnancy

causing hypertensiond. Hypertension is not good for you or child since it has risk for abortione. You need strict diet of not salty foods, carbs, or sugar during pregnancyf. Pregnant female can’t take medicine to control blood pressure because it can

give side effect so control diet instead13. (13th cause) Coarctation of aorta congenital problem of aorta

a. Right after arch of aorta, we have narrow part (boxed in picture) which leads to increasing the blood pressure in head and neck

b. Arch of aorta has three branchesi. Two of the branches take blood to inside the skull (brain) we call

them internal carotid artery1. Because of congenital problem, we have hypertension in

internal carotid artery that gives some branch to cerebral arteries. It increases the pressure in head and neck.

2. Patient has risk for…a. Intracranial hemorrhageb. Rupture of blood vesselsc. Hypertensiond. Headachee. Comaf. Inflammation in braing. Edemah. It can affect different parts of braini. Low blood pressure in femoral arteryj. Weak pulse

k. Insufficient blood supply to lower limb and abdominal cavity

c. Treatmenti. Remove that part of aorta surgically

14. (14th cause) Some hormone disorders can cause hypertension a. Thyroid (T3 and T4)

i. Because T3 and T4 increase sensitivity of alpha 1 and beta 1 adrenergic receptors to NE

ii. Hyperthyroidism leads to overstimulation of alpha 1 (vasoconstriction) and increases blood pressure and patient has hypertension, palpitation, heart problem (beta 1 overactivation)

iii. Other function of thyroid hormones1. Control body metabolism2. Excess leads to losing weight3. Less hormone leads to obesity4. Excess thyroid causes sweating (alpha 1 overstimulation)5. Patient has palpitation, hypertension 6. Increase oxygen consumption7. Control heart function8. Control blood pressure9. Control memory and learning10. Controls development of CNS and bone in fetus11. Deficiency of T3 and T4 in pregnancy leads to mental

retardation, bone growth retardation, hypotension, bradycardia

12. Increase lipolysis breaks down fat13. Controls glucose metabolism such as increasing

gluconeogenesis (formation of new glucose from fatty acids, lactic acid, amino acid, glycerol)

14. Increase glycogenolysis (breaks down glycogen into glucose) and gluconeogenesis

15. Controls protein degradation and synthesisb. Parathyroid hormone (PTH)

i. Secreted by Parathyroid (PT) glandii. Sensitive to hypocalcemia low level of calcium

iii. Normal blood calcium range is 10 mg/dliv. When blood calcium is low, PTH is active which increases blood

calcium level, v. Hyperparathyroidism lead to hypercalcemia

vi. Calcium is important for contraction of smooth muscle of blood vessels

1. Hypercalcemia causes hypertension

vii. Deficiency of calcium leads to heart diseaseviii. Calcium is important for formation of bone

1. PTH is important hormone which converts inactive form of vitamin D to active form of vitamin D. Vitamin D increases vitamin C, which increases calcium absorption by bone tissue.

ix. PTH removes calcium from bone and releases into blood stream. In this way, PTH increases blood calcium level.

x. Signs and symptoms of hypertension1. Headache2. Vomiting3. Nose bleeding4. Local hemorrhage due to rupture of blood vessels5. Sweating (alpha 1)6. Palpitation (beta 1)7. Anxiety8. Sleep disorder9. Dizziness vertigo10. Respiratory problem11. Weakness

xi. Treatment1. Drugs which treat these were already talked about

2. Cardiac electrophysiologya. Electrocardiogram (EKG/ECG)

i. Sequence of waves in EKG1. 1st wave P way

a. Depolarization of atriab. 1st half of P wave depolarization and contraction of right atriumc. 2nd half of P wave depolarization and contraction of left atriumd. Duration of P wave Between 0.08 to 0.1 seconds

i. P wave for contraction of both atria2. Repolarization and relaxation of atria doesn’t have any specific signs in EKG

Maybe it is part of the beginning of QRS complex. 3. 2nd wave QRS complex - contains Q, R, and S wave

a. Depolarization and contraction of ventriclesi. Ventricular contraction occurs very rapidly very short duration of

QRS complexb. Duration of QRS Between 0.06 to 0.1 seconds.c. Repolarization of atria probably buried in QRS complex

4. 3rd wave T wavea. For ventricular repolarization (relaxation)

5. 4th wave U wavea. Sometimes present

b. Represents remnants of ventricular repolarization (relaxation)c. Prominent U waves indicate pathological conditions affecting repolarization

of ventriclesii. Ectopic foci

1. Abnormal pacemaker sites within heart (outside of SA node) that display automaticity leads longer QRS complex

2. After treatment of myocardial infarction, some cells spontaneously have depolarization in ventricle tissue called ectopic foci

3. This depolarization can send signal to other part of ventricles or even atrium4. In EKG, we see normal P, Q, R, and S, T, P, Abnormal QRS, then T. Post myocardial

infarction appears as abnormal QRS in EKG. iii. PR interval

1. Depolarization of AV node a. AV node connects and transfers the signals from atrium to ventricle

2. Duration should be 0.12 to 0.20 seconds3. Longer than 0.2 seconds shows that there is a problem in AV node and

interruption between atrium and ventricle which is called AV node block or AV conduction block.

a. AV block there is no perfect connection between atrium and ventricleiv. ST segment

1. Means ventricle has already had (completed) contraction and is ready for relaxation phase

2. Clinical point: depressed or elevated ST segment a. Positive sign for myocardial infarctionb. This means there is a problem in myocardial tissue that cannot complete

normal contractility phasev. QT interval

1. From start of QRS to end of T wave2. Show ventricular contraction and relaxation depolarization and repolarization3. High heart rates (tachyarrhythmias) ventricular contraction duration shortens

which leads to shortened QT intervals

b. Conduction system in hearti. Sinoatrial node (SA node)

1. Locationa. In superior vena cava

2. Normal pacemaker of the heartii. Atrioventricular node (AV node)

1. Located on right atrium in atrial sectum2. AV carries signal to ventricles and gives signal to bundle of His

iii. Bundle of His (AV bundle)1. This bundle becomes left and right branches

iv. Bundle of branches (right and left)1. After left and right branches, we have Purkinje fibers

v. Purkinje fibers1. These fibers penetrate myocardial tissue and controls contractivity of myocardium

c. Cardiac action potentialsi. Action potential in heart is a little different from neuronsii. Two groups

1. 1st group: Action potential for ventricles, atria, and Purkinje fibera. 5 steps

i. Phase 0 depolarization phase1. We have opening of sodium channels. 2. Sodium (Na+) enters into cell leads to depolarization

ii. Phase 1 initial repolarization1. Sodium channels are closed 2. Just few potassium channels open and few potassium ions

leave the cell (small potassium outflow)iii. Phase 2 repolarization plateau

1. Suddenly opening of calcium channels and calcium enters into cell

2. Outward current of K+ and inward current of Ca2+ approximately equal stable plateau of membrane potential

iv. Phase 3 repolarization, hyperpolarization1. Fast opening of potassium channels and potassium leaves the

cell2. This causes repolarization phase3. Not enough for hyperpolarization though because it needs to

reach equilibrium potential = -85 mV. v. Phase 4 resting membrane potential

1. After equilibrium potential for potassium, closure of potassium channels and potassium equilibrium potential is completed

2. 2nd group: Action potential of SA (pacemaker of heart) and AV nodea. No phase 1 and 2b. Phase 0 depolarization

i. Depolarization of tissue by opening of calcium channels. ii. Ca2+ is important of depolarization of SA and AV node

1. Ventricles, atria, and Purkinje fibers use Na+ for depolarizationc. Phase 3 repolarization

i. Then repolarization occurs which is due to opening of potassium channels and potassium outflow

d. Phase 4 slow depolarizationi. Sodium channels open sodium enters cell

d. Conduction velocityi. Time required for excitation to spread through cardiac tissueii. Slowest in AV node

iii. Fastest in Purkinje systeme. Excitability

i. Ability of cardiac cell to initiate action potentialsii. Absolute refractory period (ARP)

1. When there is second stimulus during phase 0 (depolarization phase), the cell membrane cannot accept that stimulus and cannot show a reaction

iii. Effective refractory period (ERP)1. If second stimulus during phase 1 and 2 (initial repolarization), cell membrane CAN

accept 2nd stimulus but cannot show any reaction. 2. Effective stimulus but no reaction

iv. Relative refractory period (RRP)1. Second stimulus during phase 3 which is repolarization phase, cell membrane

accepts stimulus and it shows reaction to stimulus.