75B_Ms_Test1_Cardiac System, Assessment, Htn _Chapter 31,32,33

Front 1

Structure of the heart

Back 1

_chambers:4(LR atriums, LR ventricals), thoracix(betw.lung)
_layers:inner(endocardium), midd(myocardium),outter(epicardium)
_Pericardial sac:inner layers:visceral; outer layers:parietal.
_Pericadial fluid in sac=lubricant:allow movement of H. when it beat.
_Septum: divide L & R atrial & ventrical.
_Apex(PMI:point of proximal impluse)=apical pulse.Apex beat=beat of L ventrical.
_Notes:
+Atrial myocardium THINNER than Ventrical.
+L ventrical(pump blood to systemnic sys) 3* THICKER than R ventrical

Front 2

Blood flow

Back 2

super/inferior vene cava(deoxygenated blood)=>R.atrium=>(tricuspid valve/artrial ventricular valve)=>R. ventrical=>Pul.arteries(only arteries have deoxygenated blood in the body)=>lung(exchange gas=>oxygenated blood)=>pul.vein (only vein in the body carries oxygenated blood)=>L.artrium=>(mitral valve)=>L.ventrical=>(pul./aortic valve)=>tissues (systemic circulation)

Front 3

Valves:4_keep blood flow in forward direction

Back 3

_ atrialventricular valve(AV)/tricuspid & mitral valve: prevent blood regurgitation/back flow into R. atrium or L.ventrical.

_Pulmonary/Aortic valve(Semilunar Valves) prevent blood back to the L.ventrical.

Front 4

Electrical conduction Sys.
Sequences & Problem

Back 4

E.impulse: SA node(R.atrium)=> AV node(R.atrium near R ventrical)=>
pause briefly (allow R.atrium contract/empty or filling up R.ventricular before it contract)=>travel to bundle of his(along intraventricular septum, by way of bundle branches)=>Action potential defuse wisely through both ventrical(by mean of purkinje fiber).This conductionsys. allow coordinated contraction of the H. chambers.
***When sequence: Very important
_correct: get normal EKG
_seizure up: problem=>life threatening
***2 problems can change the sequences:
_Arteries got clotted/occluded=>damage the area
_Electrical conduction sys. erruption

Front 5

EKG

Back 5

_P=depolariation of atria_beginning firing of SA node
_QRS=depolariation fr. AV node to Ven._Impulse is delayed at AV node to allow time sequence between the end of P wave & begining QRS
_T=repolariation of ventrical_restore to resting potential
_Time interval(interval between the wave reflex)=length of time for the impulse travel fr. 1 area of the heart to another.***deviation fr. these time references, and wave alteration indicate pathology

Front 6

Cardiac output_factors effect(ST:preload, afterload, contractility; HR)

Back 6

_CO=SV*HR= amt. of blood pump by each ventrical per minute.5L/min
_HR: regulate by ANS
_SV:amt blood ejected by ventricular during ventricular contraction.
*Starling Law: greater the fiber stretch=>greater the force of contraction.
*factors effect: preload, afterload, contractility

Front 7

Preload_med

Back 7

_amt blood in ventrical at the end of diastolic before next contraction.It determine the amt of stretch place on myocardial fibers.
*> stetch=>>force of next contraction=>Incr SV while HR constant=>Incr CO. We want CO is constant.=>NOT GOOD=>have to give med to DECR preload.
_Med: Nitroglycerine:
+Decr preload by dilate the vein.
+Decr L. ventrical/diastolic pressure=> decr FDR (funtional diastolic resistance)
+Decr O2 demand.
+Use for Angina(more progress angina, less Nitroglycerine used)
***Administer:
Light sensitivity, renew order q6months
_Sublingual:3 pill, pil last 3 min, 5 min apart( 10/1005/1010)
_Topical(patch):glove on, no touching,take off old patch when appy new one.

Front 8

Afterload_med

Back 8

_pressure in the aorta and peripheral arteries that the left ventrical has to pump against to the blood out=resistance=how much resistance the ventrical has to overcome to get the blood out of the ventrical and to the body
_Effected by: sie of vein, wall tension, arterial BP
_If aterial BP INCR=>INCR the resistance=>Ventricular have to work harder to compensate=>Ventricular hypertropy(Incr cardiac muscle tisse w/o InCR sie of cavity_enlargement of Ven.
_Med to DECR after load, INCR SV, INCR CO.
+ACE inhibitor
+Arresoline
+Hydralaine
+Capoten

**for CHF, HTN

Front 9

Contractility_med

Back 9

_INCR contractility=>Raise SV by incr ventricular emptying
_INC by EP/NEP, dopamine(sympathetic nervous sys.)
_MED: DIGOXIN
*1st USE:INC contractility, SV, CO
*2nd USE(for A.Fib patient: uncontrol=>life threatening_100<P<200:beatting so rapidly): slow conduction fr. AV node, prevent tranmission of every Atrial beat to ventrical.
***DIGOXIN:
_B4 administer, check the apical pulse(<58:hold med, call doc)
_monitor electolyte, esp.K+
_Normal Dig level=????

Front 10

Cardiac reserve

Back 10

_ability to response to (exercise, stress, hypovolemia) by altering CO threefold/fourfold(fight/flight response)
+HR can raise to 180 b/min with out any problem
+regulation of the cadiovascular sys. thru ANS(sympathetic&parasympathetic):
*Sympathetic(stimulation of autonomic sys)Increase HR, impulse of conduction to AV node, force of contraction of atrial &ventricular
*Parasympathetic(indicated by Vegas nerve):DECR HR(action on SV node), Slow conduction thru AV node.

Front 11

Coronary ateries:(CA)
RCA: right coronary arteries
LCX:left circumflex arteries
LAD: left descending ateries

Back 11

_Myocardium has it own blood supply fr. CA.
_IF blood supply by CA interupted:
=> Myocardium (H.muscles): loose abilities to Fnx
=>Effect depend on the sie of area depride of O2
_If blood flow decrease gradually => pt. have chance to develop COLLATERAL CIRCULATION.

Front 12

Collateral Circulation

Back 12

_Some arterial branching exists w/in coronary circulation.
_2 factors:
+present of chronic ischemia
+inherited predisposition to develop new blood vessels.

Front 13

Aging process:
_collagen
_valves
_conduction sys:
_on antianginal drug:
Notes

Back 13

1/Collagen INCR, Elastin DECR=>effect contractility & distensibility(H.Valves not close tight=>regurtiatin=>effect SV, CO)
2/Valves:thicker & stiffer_undergo LIPID accumulation& Calcification, degeneration of valve collagen(esp:aortic & mitral valves)=>valves uncompetence_damage/stenosis=>murmur
3/No. of pacemaker cells in SA node decrease=>SA node dysfnx=>sinus bradycardia
4/Sympathetic Nervous sys. control cardiovascular sys decrease(Decre resp. to Physical and emotional stress(decr resp. to caecholamine & EP) _BLUNTEN resp.; decr Beta-adrenergic receptor=>less sensitive to beta-aderenergic drugs
**Notes:
+Resting HR is not effected by aging
+Apical response to MI (extremely fatigue, weakness, SOB).
+Cardiac rep. to exercise striking decr in cardiac resp(SV, CO, HR decre).CO decr 1%/year).
**If pt. on ANTIANGINAL drugs(Nitroglycerine)cause:
+Hypotention(dilate vein): need to sit 5 min b4 getting up
+Slow HR in pt have degeneration of conduction sys.
+Incr. Risk of TOXICITY (Bcuz kidney & Liver Dysfnx: med accumulate in body longer)
***Envolve pt on Exercise Program: Ince seft-esteem& socialiation=> feeling of moving.

Front 14

Physical assessment

Back 14

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Front 15

Cholesterol

Back 15

THE LOWER THE BETTER(<200)
_HDL:>60
_LDL:<100, AT RISK:<70, AT HIGH RISK:<40
_TRIGLYCERIDE:<150
_CRP (C-REACTIVE PROTEIN):<3,<2, NORMAL=1

Front 16

CARDIAC TESTS AND BENEFITS

Back 16

1/CPK(CK=creatine Kinase):
_3 different enzyme:CPk, Brain, Skeletal.
_If CK INCR=>isoenzyme MB for heart(take 12-24h to peak)
2/Troponin:
_Cardiac DEFINITIVE.They can send pt home if the troponin status is normal regardless the CPK level.
_Can use to Dx MI for up to 1 week after the event
3/C-Reactive protein Test(CRP)( testing for inflamation too)
_INCR CRP => INCR risk for MI
_CRP made in liver and in the wall of coronary artery.
_1 1/2 million ppl in US have MI(leading cause of death_CA:2nd cause od death), 1/2 of these ppl have low LDL=>the inflamatin theory come in.
**This test is not a DEFINITIVE testfor H.Disease compare to CPK and Troponin becuz other things also cause inflammation.EX:
+Pt have chronic disease/infection, smoke/sedentary lifestyle=>CRP =abnormal.
_Normal: CRP < 1mg/L
_Abnormal: CRP >3 mg/L of blood.
_Risk factor: <2
**This is a alert test to potential pro.Can't use this test for DX Heart problem. If rule out every causes elses, it may indicate H. problem.
*Test dose not prevent the Heart disease. it ony help to look for the risk factor!!!
4/ Homocystine:
_Amino Acid(containing Sulfa)
_Break down fr. Amino Acid NETHIONINE( essential amino acid-found in dietary protein)
_High level of Homocystine link to INCR risk of CAD.
_High level of homocystine contribute to artherosclerosis by damaging inner lining of blood vessel, promoting plaque to build up & altering clotting mechanism=>clot occur
_TX: B complex(B6. N12, folic acid)( SE: flushing, uncomfortable)

Front 17

TERMS:
+ASHD
+CAD
+CVHD
+ACS

Back 17

ASHD=athorosclerosis heart disease(AS=atherosclerosis, HD=heart disease)
+CAD=coronary artery disease
+CVHD=Cardiovascular heart disease
+ACS=Acute coronary syndrome
+CHD: coronary heart disease

Front 18

_3 THEORIES:
+DEVELOPMENT OF ATERIOSCLEROSIS.
_INFLAMTION
_HOMOCYSTINE

Back 18

3 theories contribute to predict the potential Heart disease:
1/ Development of artherosclerosis in the vascular sys=>INCR risk of CAD
2/ Inflammation test(CRP) after rule out all causes also alert potential for MI if CRP level INCR
3/ Homocystine theory:INCR level of this acid amine=>INCR potential of CAD, and atherosclerosis.

Front 19

THEORY: THE DEVELOPMENT OF ATERIOSCLEROSIS in vascular sys.
+FATTY STREAKS
+SMOOTH MUSC. CEL PROLIFERATION
+COMPLICATED LESION

Back 19

1/ Fatty streaks:
_lipid fill through smooth musc cells(yellow stringe)=>fiber plaque(begin at 15=>30 y.o.)=>injure endothelial layer(caused by:HTN, high choles., heredity, CO2 poisoning fr. smoke)
2/ Smooth muscle cells proliferation:
_Edothelial injury
_Lipoprotein transport choles. to arterial intima.Lipid damage smooth muscle& thicken the fiber plague=>lesion(Gray, dark white) buid up and is covered by collagen tissue, elastic fibers, smooth cells filled with fat.
_Platelet INCR in large No., arteries is damage=>thrombus(adhere to the wall=>occlude the arteries LUMEN)
3/ Complicated lesion:Most dangerous.
_Plague(cord of lipid material) w/in area of death tissue.Lesion bcome Complex, harden, darken=>necrosis=>totally/partially occulde the arteries.

Front 20

THEORY: INFLAMTION
_GOAL
_Tx:
_TESTING:
_ADV& DISADV:

Back 20

_Direct early steps of atherosclerosis plague
_Goal:
+Stablize the plague , ease inflammation, prevent plague rupture
_Prevention:
+Exercise, lose wt, control HTN, certain meds, DECR LDL...
_Tx:
+Statin=> DECR LDL
+ACE inhibitor=>HTN
+Stop smoking, keep bl. sugar under control, healthy diet
_Testing for inflamtion:C-reactive protein level( CRP)...

Front 21

THEORY: HOMOCYSTINE
_DEF:
_TX:

Back 21

_amino acid(containing sulfa, is produced fr. breaking down amino acid NETHIONINE which found in dietary protein.
+High level of homocystine link to INCR risk of CAD
+High level of homocystin contribute to artherosclerosis in blo. vessel by damaging inner linning,promoting plague buid up , altering clotiing mechanism=>clot occur
_Tx: B Complex( B6, B12, Folic Acid)=>SE: flushing, uncomfortable

Front 22

RISK FACTORS OF CAD:
_MODIFIABLE
_UNMODIFIABLE

Back 22

_risk factor of CAD:INC serum lipid, HTN, Cigarette smoking
_Modifiable:
+INCR serum lipid
+HTN
+Smoking
+Diabetes
+Obesity
+Stress
+Secondary lifestyle
_Unmodifiable:
+Age:
+Gender:
+Heredity
+Race:
**Risk for MI:
_white middle age male
_>60, male=female
_Female are seen w/ CAD earlier bcuz of: stress, smoking, HTN, birth control pills..)
**Family Hx of diabetes have greater risk( even w/ well control). Diabetes manifest CAD earlier equal to M & F

Front 23

LIPID LEVEL A/S CAD

Back 23

_triglyceride: <150
_Lipid to be used in transport need to be soluble in blood by combining w/ Protein( lipoprotein). They are vehicle for fat mobilization and transport.

Front 24

CHOLESTEROL LEVEL A/S CAD:
+LEVELS:
+NUTRITION:
+MED :
TO DECR CHOLESTEROL
+MED TO RESTRICT LIPOPROTEIN, DECR LDL & HISTAMINE

Back 24

_<200; LDL:<100(N), <70(R), <40(HR), HDl:>60
_HDL:
+lipid away from arteries to the liver for metabolism
+Femal & children have greater HDL
+HDL2 protect the arteries
+Exercise: INCR HDL & HDL2
+Low level in Heart attack pt.
_LDL: Contain cholesterol, NEED to DECR level.
_Nutrition: keep wt normal, DECR:saturated fat, R.meat, Salt intake, Alcohol
**Ifcholesterollevel>200, Try healthy diet, retest w/in 3 months. If not DECR, use MED
_Decr Cholesterol: Questran, Colestid
_Restrict lipoprotein, Decr LDL, histamine: Niacin(B Vit.), Atromid, Lopid, Mevacor,Aspirin
** ASA: Antiimflammation, Antiplatelet, Antiaggregate, Antithrombosis.Help decrease prostaglandins(result od inflammation)

Front 25

HYPERTENTION:
1/ PRIMARY HTN
2/ SECONDARY HTN

Back 25

**HTN:
_Sustain(140/90), desire(120/80).
_Affect atherosclerosis:shearing stress causing denuding of endothelial lining.
_May contribute to Stroke, Renal failure(A/s with, Not cause).
_Silent KILLER( bcuz:NO SYMPTOMS)
1/ Primary HTN:
_95% all cases.
_Exactly cause:UNKNOWN
_INCR CO & SDR (systemic vascular resistance)
_Gerotology: prevalent elderly >60 y.o. given following reasons:
+Loss tissue elasticity, INC collegen
+Stiffnessof myocardium
+INC peripheral resistance
+Decr renal Fnx
+Elderly on Antihypertentive drug may DECR/ALTER absorption of drug=>Slenic blood flow=>TOXIITY
+Postural HTN bcuz of Meds/ Vol depleted=>dehydration=>DECR BP.=>MD start fr. LOWER dose .
1/ Secondary HTN:
_5%, other process kick in cause HTN: Rena dis., head injury, sleep apnea, pregnancy, DM, Lupus, certain meds, Birth control pill.
_If symptom occur, they fr secondary cause=>effect on the target organ damage.
+S/s:fatigue, DECR activity tolerance, diziness, palpitation, angina
+Target organs:CAD, L. Ventricular hypertropy, CVD, PVD, renal insufficiency, Retinopathy.

Front 26

TREATMENT FOR HTN:
1/Life style modification
2/Na+, Alcohol restriction
3/Loose wt.
4/Physical active
5/HTN MEDICATION:
_ACTION:
_GOAL:
_CATEGORIES(abcd & n)
+Adrenergic inhibitor & Angiotensin inhibitor
+Beta blocker
+Calcium channel blocker
+Diuretic
+Nicotine
***NOTES:

Back 26

1/Life style modification
2/Na+(DASH diet), Alcohol restriction
3/Loose wt.: >30 % BMI=>consider obese. Obese not lead to HTN, but HTN present 60% obese ppl.Motality of CAD high in obesity ppl
4/Physical active:30 min, 3 X per wk, >30-50 beats/min
5/HTN MEDICATION:
_ACTION:DECR SVR & BP
_GOAL:drop BP<135/85(young), elderly <140/90
_CATEGORIES(abcd & n)
+Adrenergic inhibitor :
*Vasodilator, Decr SVR, BP
*Don't abruptly STOP=>rehab HTN
+Angiotensin inhibitor(ACE inhibitor)
*NIGHT best
+Beta blocker:
*DAY best
*DECR myocardial contractility,HR, SVR, BP=>O2 demand
*SE: bradycardia, Hypotension, wheezing, GI, Wt.gain, depression
+Calcium channel blocker
*Systemic/ coronary vasodilation, DECR SVR, myocardial contractility
*Potentiate the action of Digoxin=>monitor Dig level
+Diuretic
*DAY/NIGHT
*Inhibit NaCl reabsorption(INCR Na+, Cl-)
*DECR SVR, BP moderatly w/in 2-4 wks

+Nicotine:
*Cause Catecholamine release
*INCR HR, BP, cardiac work load
*Peripheral vasoconstriction, greater myocardial, O2 consumption, contain cusenic & benzine
***NOTES
_Start at lowest dose, least expensive, least SE
_Tx w/in 2 months. If BP not decr, add 2nd med or change med.

Front 27

_DIFFERENT RANGE OF BP:

Back 27

_OPTIMAL:<120/<80
_NORMAL:<130/<85
_HIGH NORMAL:130-139/85-89
_HTN Stage I:140-159/90-99
_HTN stage II:160-179/100-109
_HTN stage III:>=180/>=110

Front 28

Stress:Type ABCD personality

Back 28

_A: anal, control, eady get mad, perfect, agenda
_B: easy going, does not get mad
_C:combination
_D:???