Alterations In OxygenationAlterations In OxygenationCardiac DisruptionsCardiac Disruptions

Cross Section of the HeartCross Section of the Heart

Coronary Arteries & VeinsCoronary Arteries & Veins

Blood Flow Through the HeartBlood Flow Through the Heart

Conduction System of the HeartConduction System of the Heart

I. Overview of alterations in the cardiac systemI. Overview of alterations in the cardiac system

A. Lack of blood supplyA. Lack of blood supply

1. Consequences of decreased flow1. Consequences of decreased flow

Coronary arteries perfuse heart to meet O2 & nutritional needsCoronary arteries perfuse heart to meet O2 & nutritional needs

IschemiaIschemia Stable angina pectorisStable angina pectoris Acute coronary SyndromeAcute coronary Syndrome Myocardial infarctionMyocardial infarction

2. Conditions which cause this2. Conditions which cause this type of cardiac disruption type of cardiac disruption

Can be either: Can be either: increased O2 demand increased O2 demand decreased O2 supplydecreased O2 supply

a) atherosclerosis of the coronary arteries a) atherosclerosis of the coronary arteries

b) thrombus within the coronary arteriesb) thrombus within the coronary arteries

c) vasospasm of the coronary arteriesc) vasospasm of the coronary arteries

d) hypovolemiad) hypovolemia

Occlusion/Collateral CirculationOcclusion/Collateral Circulation

Vessel Occlusion with Collateral CirculationA.Open, functioning coronary arteryB.Partial coronary artery closure with collateral circulation being establishedC.Total coronary artery occlusion with collateral circulation bypassing the occlusion to supply the myocardium

B. Infections of the heartB. Infections of the heart

1. Consequences1. Consequences

Inflammation of the endocardiumInflammation of the endocardium

2. Example of infectious conditions of the heart2. Example of infectious conditions of the heart

a) Infective endocarditisa) Infective endocarditis

a) Infective endocarditisa) Infective endocarditis

Most common causative agents are bacterialMost common causative agents are bacterial Must be:Must be:

endothelial damageendothelial damage microorganisms invade and colonize structures - microorganisms invade and colonize structures -

cause inflammationcause inflammation vegetations - damage valvesvegetations - damage valves interfere with valve function and predispose to interfere with valve function and predispose to

embolus formationembolus formation

Bacterial EndocarditisBacterial Endocarditismitral/bicuspid valve – destructive vegetationsmitral/bicuspid valve – destructive vegetations

C. Immune mediated inflammatory conditionsC. Immune mediated inflammatory conditions

1. Consequences1. Consequences Immune attack on individual’s own tissueImmune attack on individual’s own tissue Can damage many tissues & organs -Can damage many tissues & organs -

including the heart including the heart

2. Example of immune mediated2. Example of immune mediated inflammatory condition inflammatory condition

a) Rheumatic heart diseasea) Rheumatic heart disease Diffuse, inflammatory disease caused by delayed Diffuse, inflammatory disease caused by delayed

immune response to infection by group A beta-immune response to infection by group A beta-hemolytic strephemolytic strep

Antibodies directed against self tissues Antibodies directed against self tissues Acute rheumatic fever is febrile illness - inflammation Acute rheumatic fever is febrile illness - inflammation

of joints, skin, nervous system, heart. Untreated, of joints, skin, nervous system, heart. Untreated, causes scarring & deformity of cardiac structures causes scarring & deformity of cardiac structures rheumatic heart disease (10% occurrence)rheumatic heart disease (10% occurrence) Primary lesion usually is at the mitral/bicuspid valvesPrimary lesion usually is at the mitral/bicuspid valves

Valve DiseaseValve Disease

Disease of the aortic valve as viewed from the aortaA.Stenosis of the valve openingB.An incompetent or regurgitant valve that is unable to close completely

Rheumatic ValvulitisRheumatic ValvulitisChronic rheumatic valvulitis. A view of the mitral valve from the left atrium shows rigid, thickened, and fused leaflets with a narrow orifice, creating the characteristic “fish mouth” appearance of the rheumatic mitral stenosis.

D. CardiomyopathyD. Cardiomyopathy

Group of diseases that affect myocardium Group of diseases that affect myocardium structure and functionstructure and function

Can be primary or secondary Can be primary or secondary Caused by many thingsCaused by many things

Cardiotoxic agentsCardiotoxic agents HTNHTN Endomyocardial fibrosisEndomyocardial fibrosis Not necessarily related to CADNot necessarily related to CAD

1. Consequences of Cardiomyopathy1. Consequences of Cardiomyopathy

3 different types3 different types Each type has own pathogenesis, clinical Each type has own pathogenesis, clinical

presentation, and treatment protocols presentation, and treatment protocols Regardless of type - often leads to heart Regardless of type - often leads to heart

failure and deathfailure and death

2. Types of Cardiomyopathy2. Types of Cardiomyopathy

a. a. DilatedDilated - most common form. - most common form.

Cardiomegaly w/ventricular dilationCardiomegaly w/ventricular dilation Impaired systolic functionImpaired systolic function Atrial enlargementAtrial enlargement Stasis of blood in LV.Stasis of blood in LV. Heart: globular shape Heart: globular shape

b. b. HypertrophicHypertrophic - 4 main characteristics: - 4 main characteristics:

Massive ventricular hypertrophyMassive ventricular hypertrophy Rapid, forceful contraction of LVRapid, forceful contraction of LV Impaired relaxation Impaired relaxation

as ventricles become noncompliantas ventricles become noncompliant

Obstruction of aortic outflow (not always)Obstruction of aortic outflow (not always) Growth is asymmetricGrowth is asymmetric No dilation of ventriclesNo dilation of ventricles

2. Types of Cardiomyopathy2. Types of Cardiomyopathy

2. Types of Cardiomyopathy2. Types of Cardiomyopathy

cc. . RestrictiveRestrictive - - least frequent. least frequent.

Impairs diastolic filling & stretch.Impairs diastolic filling & stretch.Systolic function remains unaffected.Systolic function remains unaffected.Heart becomes infiltrated by various substances, Heart becomes infiltrated by various substances, resulting in severe fibrosis – can’t stretch.resulting in severe fibrosis – can’t stretch.

(Amyloidosis: protein deposits)(Amyloidosis: protein deposits)

II. Angina PectorisII. Angina Pectoris

A. Definition/descriptionA. Definition/description Pain (angina) in chest (pectoris)Pain (angina) in chest (pectoris) Ischemia related to supply and demandIschemia related to supply and demand Usually transient - about 3 to 5 minutesUsually transient - about 3 to 5 minutes Subsides when precipitating factor relievedSubsides when precipitating factor relieved If blood flow restored, no permanent damageIf blood flow restored, no permanent damage

B. Causes of myocardial ischemia: B. Causes of myocardial ischemia: Supply: decreased O2 supplySupply: decreased O2 supply

Develops if flow of O2 content of coronary Develops if flow of O2 content of coronary blood insufficient to meet metabolic needs blood insufficient to meet metabolic needs of myocardial cells or conditions exist that of myocardial cells or conditions exist that increase hearts O2 demandsincrease hearts O2 demands

Usually caused by atherosclerosis and Usually caused by atherosclerosis and almost always by obstruction of major almost always by obstruction of major coronary artery coronary artery

B. Causes of myocardial ischemiaB. Causes of myocardial ischemia::Demand – increased O2 needDemand – increased O2 need

High systolic BPHigh systolic BP Increased ventricular volumeIncreased ventricular volume Increased thickness of myocardiumIncreased thickness of myocardium Increased HR Increased HR

Angina Pectoris: Risk FactorsAngina Pectoris: Risk Factors

ModifiableModifiableCigarette smokingCigarette smokingHypertensionHypertensionAbnormal lipid profileAbnormal lipid profileObesityObesityHyperglycemiaHyperglycemiaPhysical inactivityPhysical inactivityStressStress

UnmodifiableUnmodifiableAgeAgeSexSexHeredityHeredityRace and ethnicityRace and ethnicity

C. Types of Angina PectorisC. Types of Angina Pectoris

Chronic stable anginaChronic stable angina Unstable anginaUnstable angina

(pre-infarction)(pre-infarction) Printzmetal’s angina Printzmetal’s angina

(variant)(variant) Silent ischemiaSilent ischemia

Types of Coronary Heart DiseaseTypes of Coronary Heart Disease

1. Stable angina1. Stable angina

1. Stable angina1. Stable angina Caused by narrowing & hardening of Caused by narrowing & hardening of

arterial walls – the 4 E’sarterial walls – the 4 E’s ExertionExertion Extremes in temperature – vasoconstrictionExtremes in temperature – vasoconstriction Emotions – SNS stimulationEmotions – SNS stimulation Excessive eating – blood diverted to GI tractExcessive eating – blood diverted to GI tract

Affected vessels can’t dilate Affected vessels can’t dilate Pain Pain usuallyusually relieved by rest & relieved by rest & nitratesnitrates

2. Variant or Prinzmental’s angina2. Variant or Prinzmental’s angina

Chest pain caused by transmural ischemia of Chest pain caused by transmural ischemia of myocardium myocardium

Occurs unpredictably & almost exclusively at rest Occurs unpredictably & almost exclusively at rest Pain caused by vasospasm of one or more Pain caused by vasospasm of one or more

coronary arteries coronary arteries Pain frequent during rest and at nightPain frequent during rest and at night Rare type of angina, not precipitated by exertion, Rare type of angina, not precipitated by exertion,

etc.etc. Treated with nitrates and Ca++ channel blockersTreated with nitrates and Ca++ channel blockers

3. Unstable angina (Pre-infarction)3. Unstable angina (Pre-infarction)

Angina that is new in onset, occurs at rest, or Angina that is new in onset, occurs at rest, or has a worsening patternhas a worsening pattern

Seldom predictableSeldom predictable Often associated with deterioration of stable Often associated with deterioration of stable

atherosclerotic plaqueatherosclerotic plaque May mean impending infarctionMay mean impending infarction

4. Silent Ischemia4. Silent Ischemia

May only be detected on routine EKGMay only be detected on routine EKG Lack of pain or discomfortLack of pain or discomfort Increases risk of myocardial infarctionIncreases risk of myocardial infarction May precede a sudden & severe MI without May precede a sudden & severe MI without

warningwarning Largely associated with HTNLargely associated with HTN

D. Clinical manifestations & related pathogenesisD. Clinical manifestations & related pathogenesis

Substernal chest discomfortSubsternal chest discomfort May radiate to neck, lower jaw, left arm, left May radiate to neck, lower jaw, left arm, left

shoulder, or backshoulder, or back LT arm most commonLT arm most common But may also radiate to RT armBut may also radiate to RT arm

Often mistaken for indigestionOften mistaken for indigestion May be accompanied by severe apprehension & May be accompanied by severe apprehension &

feeling of impending deathfeeling of impending death

Myocardial cells are viable for 20 minutesMyocardial cells are viable for 20 minutes

Eventually revert to anaerobic metabolism Eventually revert to anaerobic metabolism lactic acid lactic acid pain pain

Locations of Chest Pain During Angina or MILocations of Chest Pain During Angina or MI

Angina Pain AreasAngina Pain Areas

E. Potential medical complicationsE. Potential medical complications

1.1. Myocardial infarctionMyocardial infarction Worst case scenarioWorst case scenario

2.2. Arrhythmias/Arrhythmias/DysDysrhythmiasrhythmias Affects myocardial cell’s sensitivity to nerve Affects myocardial cell’s sensitivity to nerve

impulsesimpulses

Initially, BP rises, then eventually as heart stops pumping Initially, BP rises, then eventually as heart stops pumping effectively & F/F response wears off, CO drops & BP effectively & F/F response wears off, CO drops & BP dropsdrops

Tissue Destruction After MITissue Destruction After MI

Acute MIAcute MI

X-section of ventricles of a man who died a few days after onset of severe chest pain.Transmural infarct & septal regions of the left ventricle.The necrotic/infarcted myocardium is soft, yellowish, and sharply demarcated.

F. ManagementF. ManagementPrimary aim – Reduce myocardial O2 consumptionPrimary aim – Reduce myocardial O2 consumption1. Diagnostic studies1. Diagnostic studies

a. EKG/ECG – Electrocardiographya. EKG/ECG – Electrocardiography May have normal EKG when no pain, so requires May have normal EKG when no pain, so requires

EKG during attackEKG during attack Can indicate which coronary artery is involvedCan indicate which coronary artery is involved Treatment:Treatment:

A. A. B.B. C.C. D. diet & diabetes managementD. diet & diabetes management E. education & exerciseE. education & exercise

b. Serum enzyme level testsb. Serum enzyme level tests

Creatine Kinase (CK)Creatine Kinase (CK) – 3 isoenzymes – 3 isoenzymes CK-MB: present in heart muscleCK-MB: present in heart muscle CK-MM: present in skeletal muscleCK-MM: present in skeletal muscle CK-BB: present in brain tissueCK-BB: present in brain tissue

CK-MB found CK-MB found onlyonly in cardiac cells - rises only in cardiac cells - rises only when damage to cellswhen damage to cells

Always increases in MI:Always increases in MI: Rises 4-6 hours after onsetRises 4-6 hours after onset Peaks at 18-24Peaks at 18-24 Returns to normal in 3-4 days (0-6%) Returns to normal in 3-4 days (0-6%)

TroponinTroponinmyocardial protein released into circulation after injurymyocardial protein released into circulation after injury

Greater specificity: Greater specificity: specific MI indicator specific MI indicator

Rises 2-12 hours Rises 2-12 hours after MIafter MI

Peaks at 24-48 Peaks at 24-48 hourshours

Returns to normal in Returns to normal in 5-14 days (remain 5-14 days (remain elevated for 2 elevated for 2 weeks)weeks)

MyoglobinMyoglobin

O2 carrying protein present in cardiac and O2 carrying protein present in cardiac and skeletal muscleskeletal muscle

Released quickly from infarcted myocardial Released quickly from infarcted myocardial tissuetissue

Not cardiac specificNot cardiac specific Rapidly excreted from urineRapidly excreted from urine

Albumin Colbalt-binding testAlbumin Colbalt-binding test

Measures how much cobalt is bound to Measures how much cobalt is bound to albuminalbumin

Changes in structure of albumin occur with MIChanges in structure of albumin occur with MI Used in conjunction with EKG & troponin testUsed in conjunction with EKG & troponin test

c. Serum lipid level testsc. Serum lipid level tests

Triglycerides Triglycerides

Total Cholesterol Total Cholesterol

Cholesterol fractionationCholesterol fractionation

Not used for MI diagnostic purposes, but reveals if Not used for MI diagnostic purposes, but reveals if high-riskhigh-risk

c. Serum lipid level testsc. Serum lipid level tests C-Reactive Protein (CRP)C-Reactive Protein (CRP)

Appears in blood 6-10 hours after acute Appears in blood 6-10 hours after acute inflammatory process and tissue destructioninflammatory process and tissue destruction

Peaks at 48-72 hours after MIPeaks at 48-72 hours after MI

N High Sensitivity C- Reactive Protein (hs N High Sensitivity C- Reactive Protein (hs CRP) - highly sensitive test for detecting risk CRP) - highly sensitive test for detecting risk of cardiovascular and peripheral vascular of cardiovascular and peripheral vascular diseases. Frequently done with cholesterol diseases. Frequently done with cholesterol screeningscreening

d. Exercise stress testd. Exercise stress test Reveals heart function Reveals heart function

during exerciseduring exercise Attach patient to EKG Attach patient to EKG

& BP cuff& BP cuff Useful to differentiate Useful to differentiate

angina from other angina from other types of chest paintypes of chest pain

Can be done with a scan as wellCan be done with a scan as well Patients who can’t walk may use Patients who can’t walk may use

a bike a bike

e. Nuclear Cardiology Imaginge. Nuclear Cardiology Imaging

Several tests use Several tests use radionuclides to radionuclides to visualize distribution of:visualize distribution of: Blood flowBlood flow Ventricular structuresVentricular structures ““cold spotscold spots”” in infarcted in infarcted

zone – no accumulation zone – no accumulation of radionuclidesof radionuclides

Perfusion or metabolism Perfusion or metabolism of myocardiumof myocardium

f. Coronary angiographyf. Coronary angiography

Diagnostic radiography Diagnostic radiography of heart & blood of heart & blood vessels using vessels using radiopaque contrast radiopaque contrast mediamedia

Used to evaluate Used to evaluate coronary arteries and coronary arteries and collateral circulationcollateral circulation

Helps determine Helps determine anatomic extent of anatomic extent of CAD CAD

Non-pharmacologic Treatment Non-pharmacologic Treatment EducationEducation

R – RestR – Rest E – ExerciseE – Exercise S – Stop smokingS – Stop smoking C – Count cholesterol & caloriesC – Count cholesterol & calories U – Unwind U – Unwind reduce stress reduce stress E – EducationE – Education

Nitrate TherapyNitrate Therapy First line of defense – First line of defense –

prevention/prophylaxis and treatmentprevention/prophylaxis and treatment Relax smooth muscles in the blood vessel Relax smooth muscles in the blood vessel

wallswalls Improve blood delivery to the heart by Improve blood delivery to the heart by

dilating blood vesselsdilating blood vessels Improve blood delivery to the heart by Improve blood delivery to the heart by

decreasing the workload of the heartdecreasing the workload of the heart Ineffective in sclerosed vessels, effective if Ineffective in sclerosed vessels, effective if

collateral vessels in placecollateral vessels in place

2. Pharmacologic therapy2. Pharmacologic therapy

a. In acute attacksa. In acute attacks

i) Nitroglycerine SLi) Nitroglycerine SL

Actions - increases coronary blood flow by Actions - increases coronary blood flow by dilating coronary arteries & improving dilating coronary arteries & improving collateral flow collateral flow

Destruction by GI tractDestruction by GI tract

Must dissolve sublingually, patient shouldn’t swallow saliva Must dissolve sublingually, patient shouldn’t swallow saliva while dissolvingwhile dissolving

i) Nitroglycerine SLi) Nitroglycerine SL

NI: Give sublingually. Teach patient:NI: Give sublingually. Teach patient: keep tongue stillkeep tongue still keep med with you at all timeskeep med with you at all times very unstable - capped, dark, glass bottlevery unstable - capped, dark, glass bottle inactivated by heat, moisture, air, light, inactivated by heat, moisture, air, light,

time. Should have burning sensationtime. Should have burning sensation Replace every 6monthsReplace every 6months Not fixed dose - patient regulates usageNot fixed dose - patient regulates usage

Nitroglycerine SL - continuedNitroglycerine SL - continued

maximum of 3 tablets in 15 minutes - 5 minutes maximum of 3 tablets in 15 minutes - 5 minutes apartapart

transient side effects – hypotension, headache, transient side effects – hypotension, headache, facial flushingfacial flushing

lie down to prevent fallinglie down to prevent falling carry medic-alert informationcarry medic-alert information journal all attacksjournal all attacks

precipitating factors, duration, pills taken, etc.precipitating factors, duration, pills taken, etc.

b. For chronic anginal prophylaxisb. For chronic anginal prophylaxis

i) Nitroglyercin ointment - topical i) Nitroglyercin ointment - topical

- rotate sites to prevent skin irritation- rotate sites to prevent skin irritation

- remove old patch/paper- remove old patch/paper

- dose may be increased to highest does that - dose may be increased to highest does that doesn’t cause hypotensiondoesn’t cause hypotension

- apply only with measuring applicator- apply only with measuring applicator

- don- don’’t allow contact with your skint allow contact with your skin

DON’T SHAVE an area. This will create small abrasions. Clip hair only.DON’T SHAVE an area. This will create small abrasions. Clip hair only.

ii) Transdermal nitratesii) Transdermal nitrates

Transderm-Nitro, Nitro-Dur, NitrodiscTransderm-Nitro, Nitro-Dur, Nitrodisc apply to hairless siteapply to hairless site remove all previous patchesremove all previous patches apply firm pressure apply firm pressure waterproof - not affected by bathingwaterproof - not affected by bathing do not cut or trim patchesdo not cut or trim patches remove before cardioversion or remove before cardioversion or

defibrillation to prevent burns defibrillation to prevent burns

iii) Long-acting nitratesiii) Long-acting nitrates

Extended release capsulesExtended release capsules Nitrocap T.D., Nitrogly, Nitrolin, NitrospanNitrocap T.D., Nitrogly, Nitrolin, Nitrospan

Extended release tabletsExtended release tablets NitrongNitrong

Taken every 8 to 12 hoursTaken every 8 to 12 hours

iv) SL nitroglycerine prior to activityiv) SL nitroglycerine prior to activity

Can be used to prevent or minimize anginal Can be used to prevent or minimize anginal attacks before stressful eventsattacks before stressful events

Will increase tolerance for exercise & stressWill increase tolerance for exercise & stress Best to take before pain develops Best to take before pain develops

Case StudyCase Study

A 60 year old male was shoveling snow A 60 year old male was shoveling snow after a heavy snowstorm and experienced after a heavy snowstorm and experienced chest pain. He has a history of angina and chest pain. He has a history of angina and has SL nitroglycerin in the house. He has SL nitroglycerin in the house. He keeps it on his windowsill in a clear plastic keeps it on his windowsill in a clear plastic pillbox.pillbox.

Questions:Questions:

What type of angina is he experiencing?What type of angina is he experiencing? What should he do to treat this episode?What should he do to treat this episode? After taking the maximum tablets, his pain has After taking the maximum tablets, his pain has

not subsided. What should he do?not subsided. What should he do? What patient teaching is indicated in this What patient teaching is indicated in this

situation?situation?

v) Beta-adrenergic blockersv) Beta-adrenergic blockers

Propanolol (Inderal)Propanolol (Inderal)

Action:Action: Decreases CO and reduces sympathetic Decreases CO and reduces sympathetic

vasoconstrictor tone.vasoconstrictor tone. Decreases renin secretion by kidney.Decreases renin secretion by kidney. Decreases HR, BP, & myocardial Decreases HR, BP, & myocardial

contractility. contractility.

vi) Calcium channel blockersvi) Calcium channel blockers

Action - inhibits transport of calcium into Action - inhibits transport of calcium into myocardial & vascular smooth muscle myocardial & vascular smooth muscle cells, resulting in inhibition of excitation-cells, resulting in inhibition of excitation-contraction coupling & subsequent contraction coupling & subsequent contraction contraction

Nifedipine (Procardia), verapamil (Calan)Nifedipine (Procardia), verapamil (Calan)

Calcium MovementCalcium Movement

Ca2+ channel blocker: mechanism of action

A.During muscle relaxation, K+ inside muscle cell, Ca++ & Na+ outside muscle cell.

A.For muscle contraction to

occur, K+ efflux, Na+ & Ca2+

influx through open membrane channels.

A.When Ca2+ channels are blocked by drug molecules, muscle contraction decreases because Ca2+ can’t move through cell membrane into muscle cell.

vii) Antithrombotic therapy . . .vii) Antithrombotic therapy . . . Aspirin (ASA) Aspirin (ASA)

Action - in low doses, appears to impede Action - in low doses, appears to impede clotting by blocking prostaglandin clotting by blocking prostaglandin synthesis, which prevents formation of synthesis, which prevents formation of platelet-aggregationplatelet-aggregation

81 mg81 mg

(325 mg Rx)(325 mg Rx)

3. Invasive & surgical treatments3. Invasive & surgical treatments

a. Percutaneous transluminal coronary a. Percutaneous transluminal coronary angioplasty (PTCA)angioplasty (PTCA)

Improve blood flow - crack plaque or Improve blood flow - crack plaque or atheroma that has built up & interfering atheroma that has built up & interfering with circulation with circulation

Done more frequently than CABGDone more frequently than CABG

b. Intracoronary stentsb. Intracoronary stents

PTCA with PTCA with intravascular stent intravascular stent over balloonover balloon

When balloon is When balloon is deflated, stent remains deflated, stent remains in artery & holds it in artery & holds it open. Eventually open. Eventually endothelium covers endothelium covers stent & incorporates stent & incorporates into wall into wall

c. Laser angioplastyc. Laser angioplasty

Catheter with small laser introduced into Catheter with small laser introduced into peripheral artery then diseased coronary peripheral artery then diseased coronary arteryartery

Vaporizes plaqueVaporizes plaque

d. Atherectomyd. Atherectomy

Plaque is shaved off Plaque is shaved off using rotational blade using rotational blade

Removes atheromasRemoves atheromas

e. Coronary artery bypass grafting e. Coronary artery bypass grafting (CABG)(CABG)

Blood vessel from another part of body Blood vessel from another part of body (saphenous vein, left internal mammary (saphenous vein, left internal mammary artery) is grafted distal to coronary artery artery) is grafted distal to coronary artery lesion - lesion - ““bypassingbypassing”” obstruction obstruction

MIDCABG – newer procedure; limited useMIDCABG – newer procedure; limited use

Coronary Artery RevascularizationCoronary Artery Revascularization

4. Prehospital emergency care 4. Prehospital emergency care of chest pain (from AHA) of chest pain (from AHA)

For person with unknown CHD:For person with unknown CHD: recognize symptoms - chest pain, recognize symptoms - chest pain,

sweating, nausea, SOB, weaknesssweating, nausea, SOB, weakness stop activity and sit or lie downstop activity and sit or lie down if pain persists for 5 minutes or more, if pain persists for 5 minutes or more,

activate the EMS activate the EMS

4.4. Prehospital emergency care Prehospital emergency care of chest pain (From AHA)of chest pain (From AHA)

For person with known CHD:For person with known CHD: recognize symptoms - chest pain, recognize symptoms - chest pain,

sweating, nausea, SOB, weaknesssweating, nausea, SOB, weakness stop activity - sit or lie downstop activity - sit or lie down place one NTG tablet under tongue. place one NTG tablet under tongue.

Repeat at 5 minute intervals up to 3 times Repeat at 5 minute intervals up to 3 times if symptoms persist, activate the EMS if symptoms persist, activate the EMS

III. Congestive Heart FailureIII. Congestive Heart Failure

A. DefinitionA. Definition

Abnormal condition Abnormal condition involving impaired involving impaired cardiac pumping cardiac pumping

Associated with Associated with numerous types of numerous types of heart disease - esp. heart disease - esp. long-standing HTN long-standing HTN and CADand CAD

Characterized by:Characterized by:

ventricular ventricular dysfunctiondysfunction

reduced exercise reduced exercise tolerancetolerance

diminished quality of diminished quality of lifelife

shortened life shortened life expectancyexpectancy

Can be:Can be:

Systolic Failure Systolic Failure Results from inability of heart to pump Results from inability of heart to pump

blood. Caused by:blood. Caused by: impaired contractile functionimpaired contractile function increased afterloadincreased afterload CardiomyopathyCardiomyopathy mechanical abnormalitiesmechanical abnormalities

Decreased CODecreased CO

Can be: Can be:

Diastolic FailureDiastolic Failure Impaired ability of ventricles to fillImpaired ability of ventricles to fill Results in decreased stroke volumeResults in decreased stroke volume Decreased CODecreased CO

Mixed systolic and diastolic failureMixed systolic and diastolic failure

B. Compensatory MechanismsB. Compensatory Mechanisms

Overloaded heart tries to compensate to Overloaded heart tries to compensate to maintain adequate COmaintain adequate CO

1. Ventricular dilation 1. Ventricular dilation Chambers enlarge when pressure Chambers enlarge when pressure

elevated over timeelevated over time Muscle fibers stretch and increase Muscle fibers stretch and increase

contractile forcecontractile force

2. Ventricular hypertrophy2. Ventricular hypertrophy

Heart hypertrophies in response to Heart hypertrophies in response to overworkoverwork

Will lead to increased COWill lead to increased CO

3.3. Sympathetic nervous systemSympathetic nervous systemactivationactivation

Inadequate stroke volume and CO caused Inadequate stroke volume and CO caused sympathetic nerve activationsympathetic nerve activation

Results in increased HR, myocardial Results in increased HR, myocardial contractility, and peripheral vascular contractility, and peripheral vascular constrictionconstriction

Initially increase in HR and contractility Initially increase in HR and contractility improve CO, but detrimental over timeimprove CO, but detrimental over time

4. Neurohormonal responses4. Neurohormonal responses

Decrease blood flow to kidneys causes Decrease blood flow to kidneys causes release of reninrelease of renin

Renin caused conversion of angiotension I Renin caused conversion of angiotension I to II – which caused adrenal cortex to to II – which caused adrenal cortex to release aldosterone (increased sodium release aldosterone (increased sodium retention & ↑ peripheral vasoconstrictionretention & ↑ peripheral vasoconstriction

Posterior pituitary secretes ADH – ↑ water Posterior pituitary secretes ADH – ↑ water reabsorption in renal tubelsreabsorption in renal tubels

C. Types of CHFC. Types of CHF

1.1. Left-sided heart failureLeft-sided heart failure

a. Pathogenesisa. Pathogenesis Left ventricle fails - unable to pump Left ventricle fails - unable to pump

adequate blood coming to it from lungs adequate blood coming to it from lungs Increases pressure in pulmonary Increases pressure in pulmonary

circulation - causes fluid to be forced into circulation - causes fluid to be forced into pulmonary tissuespulmonary tissues

Left-Sided Heart FailureLeft-Sided Heart Failure

2. Right-sided failure 2. Right-sided failure

a. Pathogenesisa. Pathogenesis

Venous congestion in systemic circulation Venous congestion in systemic circulation results in:results in:

peripheral edemaperipheral edema hepatomegalyhepatomegaly splenomegalysplenomegaly vascular congestion of GI tractvascular congestion of GI tract jugular venous distentionjugular venous distention

Right-Sided Heart FailureRight-Sided Heart Failure

3. Clinical manifestations3. Clinical manifestations

a. Fluid retention and a. Fluid retention and edemaedema

EdemaEdema

NocturiaNocturia

b. Respiratory manifestationsb. Respiratory manifestations

Pulmonary edemaPulmonary edema

DyspneaDyspnea OrthopneaOrthopnea

Paroxysmal nocturnal dyspneaParoxysmal nocturnal dyspnea CoughCough

c.c. Fatigue & limited exercise toleranceFatigue & limited exercise tolerance

FatigueFatigue

TachycardiaTachycardia

Anxiety and Anxiety and restlessnessrestlessness

d. Cachexiad. Cachexia

Weight lossWeight loss

MalnutritionMalnutrition

e. Cyanosise. Cyanosis

Skin changesSkin changes

4. Complications4. Complications

a.a. Pleural effusionsPleural effusions

b.b. ArrhythmiasArrhythmias

c.c. Left ventricular thrombusLeft ventricular thrombus

d. Hepatomegalyd. Hepatomegaly

E. ManagementE. Management

1. Diagnostic studies1. Diagnostic studies

a. CXRa. CXR

b. EKGb. EKG

c. Echocardiogramc. Echocardiogram

d. Radionuclide angiographyd. Radionuclide angiography

e. Labse. Labs

Normal EKGNormal EKG

2. Pharmacologic Therapy2. Pharmacologic Therapy

a. ACE inhibitors (Angiotension Convertinga. ACE inhibitors (Angiotension ConvertingVasotecVasotec

Prevents production of Angiotension II by Prevents production of Angiotension II by blocking itblocking it’’s conversion to the active form - s conversion to the active form - results in systemic vasodilation results in systemic vasodilation

Decreases preload & afterload in patients Decreases preload & afterload in patients with CHF with CHF

Angiotensin ConversionAngiotensin Conversion

b. Inotropicsb. Inotropics

DigoxinDigoxin

Increases force of myocardial contraction, Increases force of myocardial contraction, decreases conduction through SA and AV decreases conduction through SA and AV nodes, slows heart rate and increases nodes, slows heart rate and increases diastolic filing timediastolic filing time

Increases CO, slows heart rateIncreases CO, slows heart rate

NI - Take AP for one minute. Hold & notify NI - Take AP for one minute. Hold & notify MD if below 60MD if below 60

c. Diureticsc. Diuretics

Promotes excretion of edema fluid and helps Promotes excretion of edema fluid and helps sustain cardiac output and tissue perfusion sustain cardiac output and tissue perfusion by reducing preloadby reducing preload

Review notes on Thiazides, loop diuretics, Review notes on Thiazides, loop diuretics, and K+ sparing diureticsand K+ sparing diuretics

d. Vasodilator drugsd. Vasodilator drugs

NitratesNitrates Reduces circulating volume by decreasing Reduces circulating volume by decreasing

preload and also increases coronary preload and also increases coronary artery circulation by dilating coronary artery circulation by dilating coronary arteries arteries

e. Beta adrenergic blockerse. Beta adrenergic blockers

Becoming more important in management Becoming more important in management of CHF of CHF

Block sympathetic nervous systemBlock sympathetic nervous system’’s s negative effects on the failing heart - such negative effects on the failing heart - such as increased heart rateas increased heart rate

3. Supportive3. Supportive

a.a. Supplemental oxygenSupplemental oxygen

b.b. RestRest

c.c. Daily weightsDaily weights

c.c. Sodium restricted dietSodium restricted diet