 NPTE- CARDIOVASCULAR SYSTEM

 METC

 The CV system consists of:

 Heart

 Blood vessel

 Blood

 BLOOD VESSELS

 Blood Vessels

 Blood is carried in a closed system of vessels that begins and ends at the heart

 The three major types of vessels are arteries, capillaries, and veins

 Arteries carry blood away from the heart, veins carry blood toward the heart

 Capillaries contact tissue cells and directly serve cellular needs

 Elastic (Conducting) Arteries

 Muscular (Distributing) Arteries and Arterioles

 Muscular arteries – distal to elastic arteries; deliver blood to body organs

 Arterioles – smallest arteries; lead to capillary beds

 Control flow into capillary beds via vasodilation and constriction

 Arteries

 Influenced by elasticity & extensibility of vessel walls, & by peripheral resistance, amount of
blood in body

 Capillaries

 Capillaries are the smallest blood vessels

 Veins are:

 Formed when venules converge

 Carry deoxygenated blood from the tissues towards the heart (except pulmonary veins)
  Impt. Feature: presence of “valves” to prevent backflow of blood

 Lymphatic System

 Lymphatics (superficial, intermediate, & deep), lymph fluid, lymph tissues and organs (lymph
nodes, tonsils, spleen, thymus, & thoracic duct)

 Lymphatic contraction occurs by:

1. Parasympathetic:, sympathetic, & sensory nerve stimulation

2. Contraction of adjacent muscles

3. Abdominal & thoracic cavity pressure changes during normal breathing

4. Mechanical stimulation of dermal tissues

5. Volume changes within each lymphatic vessel

 Lymphatic System

 Major lymph nodes: submaxillary, cervical, axillary, mesenteric, iliac, inguinal, popliteal, &
cubital

1. Fibrous pericardium- restricts movement of the heart, consists of tough, inelastic irregular
connective tissue

2. Serous pericardium- a thinner delicate membrane forming a double layer around the heart

a. Outer parietal layer- lines the fibrous pericardium

b. Inner visceral layer- epicardium; adheres tightly to the heart

 Surfaces of the HEART

1. Sternocostal (Anterior)- formed mainly by the RA and RV

2. Diaphragmatic (Inferior)- formed mainly by RV & LV

3. Posterior (Base)- formed mainly by the LA

* APEX of the heart- lies at the level of the 5th ICS, 3 ½ inches from the midline of the left clavicle

 Gross Anatomy of the Heart

 4 chambers:

 R & L atria

 R & L ventricles
  4 basic valves:

 tricuspid (R)

 mitral (L)

 semilunars –

 a. Pulmonic-pulmo trunk

 b. aortic- aorta

 VALVES of the HEART

1. A-V Valves

a. Tricuspid valve guards the right A-V orifice; consists of 3 cusps

b. Bicuspid valve  guards the left A-V orifice with only 2 cusps

2. Semilunar valves-

a. Pulmonary valve- guards the pulm. Orifice; consissts of 3 cusps directed upward into the pulm.
Trunk

b. Aortic valve- guards the aortic orifice & with 3 cusps

 WALL of the HEART

1. Epicardium- outer layer compised of mesothelium & delicate connective tissue providing a
slippery texture to the heart’s external surface

2. Myocardium- middlemost layer; cardiac muscle; forms the bulk of the heart responsible for its
pumping action

3. Endocardium- inner layer; consists of a thin layer of endothelium; provides a smooth lining for
the inside of the heart & covers the valves

 Conduction System

 Specialized sections of the myocardium that initiates & regulate the cardiac cycle

1. Sinoatrial (SA) node- located in the wall of the RA near the mouth of the superior vena cava;
pacemaker of the heart

2. Atrioventricular (AV) node- located in the interatrial septum; has a slower rate of conduction

3. Bundle of HIS- divides into left & right bundle branches to supply the left & right ventricles
4. Purkinje fibers- located in the endocardial surface of the heart; rapidly conducts impulse to the apex
of the myocardium & then to the remainder of the ventricular system

 Blood flow through the lungs is the PULMONARY circuit

- Deoxygenated blood from the peripheral system is being sent to the lungs for oxygenation

 The hepato-portal circuit is a subdivision of the systemic that serves the liver

 The Circle of Willis is the systemic circuit at the base of the brain

• Fetal circulation differs from adult

 Systemic Circulation

 The systemic circulation carries oxygenated blood from the LV through the aorta to all parts of
the body (including some lung tissue, but not alveoli) and returns the deoxygenated blood to the
RA.

 The aorta is divided into the ascending aorta, the arch of the aorta, and the descending aorta.
Each section gives off arteries that branch to supply the whole body.

 Blood returns to the heart through the systemic veins. All veins of the systemic circulation drain
into the superior or inferior venae cavae or the coronary sinus, which in turn empty into the
right atrium.

 Major Systemic Veins of the Upper Body

 Arteries are usually located in deep and well-protected areas of the body, but veins are usually
easily seen and palpated on the body surface.

 The majority of deep veins parallel the course of the major arteries.

ARTERIES carry oxygenated bld fr the heart

VEINS return deoxygenated bld to the heart

EXCEPTIONS:

 Pulm. Artery – sends deoxygenated bld to lungs fr. RV

 Pulm. Veins – return oxygenated bld. fr. LA after passing from the lungs

 Hepatic portal vein- nutrients fr sm intestine to liver

 Fetal circ- umb vein (O2 bld to fetal heart fr maternal placenta) & umb artery (return deoxyO2
bld to placenta)

 The Hepatic Portal Circuit

  The liver has a dual blood supply:

 R & L hepatic aa

 Portal vein from GIT

 Neurohumoral Influences

Parasympathetic stimulation (cholinergic)

a. Control located in medulla oblongata, cardioinhibitory center

b. Via VAGUS nerve (CN X), cardiac plexus: innervates all myocardium, release Ach

c. Slows rate & force of myocardial contraction: decreases myocardial metabolism

d. Causes coronary artery vasoconstriction

 Sympathetic stimulation (adrenergic)

 Control located in medulla oblongata, cardioacceleratory center

 Via cord segments t1-T4, upper thoracic to superior cervical chain ganglia; innervates all but
ventricular myocardium; releases epinephrine & norepinephrine

 Causes an increase in the rate & force of myocardial contraction & myocardial metabolism

 Sympathetic stimulation (adrenergic)

 Causes coronary artery vasodilation

 The skin & peripheral vasculature receive only postganglionic sympathetic innervation.

 Causes vasoconstriction of cutaneous arteries; sympathetic inhibition must occur to obtain

vasodilation

 Drugs that increase sympathetic functioning are sympathomimetics; drugs that decrease
sympathetic functioning are sympatholytics

 Addt’l Control Mechanisms

Baroreceptors (Pressoreceptors)

 Main mechanisms controlling the heart

a. Located in walls of aortic arch & carotid sinus; via vasomotor center

b. Circulatory reflex: respond to changes in BP

 Increased BP  causes parasympathetic stimulation, decreased rate & force of cardiac
contraction; sympathetic inhibition, decreased peripheral resistance

 Decreased BP  sympathetic stimulation , increased HR, BP, & vasoconstriction of peripheral

blood vessels

 Increased right atrial pressure  causes reflex acceleration of HR

 Chemoreceptors

 Located in carotid body

 Sensitive to changes in blood chemicals: O2, CO2, lactic acid

a. Increased CO2 or decreased O2 or decreased ph  elevated lactic acid  increase HR

b. Increased O2 levels  decrease in HR

 Body temperature

 Increased body temperature  increased HR

 Decreased body temperature  decrease HR

 ION concentrations

 Hyperkalemia: increased conc of K+ ions  decrease rate & force of contraction,  produces
ECG changes (widened PR interval & QRS, tall T waves)

 Hypokalemia: decreased conc of K+ ions produces ECG chnages (flattened T waves, prolonged
PR & QT intervals); arrhythmias  may progress to ventricular fibrillation

 ION concentrations

 Hypercalcemia: increased Ca++ conc  increases heart actions

 Hypocalcemia: decreased Ca++ conc  depresses heart actions

 Peripheral resistance

 Increased peripheral resistance  increases arterial blood volume & pressure

 Decreased PR decreases arterial blood volume & pressure

 Influenced by arterial blood volume: viscosity of blood & diameter of arterioles & capillaries

 CARDIAC OUTPUT
 Blood ejected from the left ventricle / right ventricle into the aorta / pulmonary trunk per
minute

 Equal to about 4-5 L/ min

 CO= SV X HR

 Cardiac index: CO divided by body sirface area: normal range is 2.5 to 3.5 L/min

 STROKE VOLUME

 The volume of blood ejected by the ventricle with each contraction

 N= 55-100ml/beat

 Influenced by:

a. Left ventricular end diastolic volume (LVEDV): amt of bld left in the ventricle at the end of
diastole. The greater the diastolic filling (preload) ,the greater the quantity of bld pumped
(Frank-Starling Law)

b. Contractility: ability of the ventricle to contract

c. Afterload: force that the LV must generate during systole to overcome aortic pressure to open
the aortic valve

 Left Ventricular end-diastolic pressure (LVEDP)

 Pressure in the LV during diastole

 N= 5-12 mmHg

 Ejection Fraction

 Percentage of blood emptied fr the ventricle during systole; a clinically useful measure of LV
function

1. EF= SV/ LVEDV

2. Normal EF averages 60-70%; the lower the EF, the more impaired the LV

 Atrial Filling Pressure

 Difference between venous & atrial pressures

 RA filling pressure  decreased during strong ventricular contraction & atrial filling is enhanced

 Diastolic Filling Time

  decreased with increased HR & with heart disease

 Myocardial O2 demand (MVO2)

 Represent energy cost to the myocardium

 Measured clinically by the product of HR and SBP known as the RATE PRESSURE PRODUCE (RPP)

 Increased with activity & with HR &/or BP

 HEART RATE

 The number of heartbeats per minute

 Factors regulating HR:

1. ANS stimulation

2. Hormone regulation (epinephrine, norepinephrine)

3. Ionic concentration differences between ICF & ECF

4. Age, gender, physocal fitness, body temperature

NORMAL HR in Adults: 60-100 bpm

 Normal Heart Sounds

 S1 = “lub” = closure of AV valves

 S2 = “dub” = closure of semilunar valves

 Gallops (N or AbN):

 S3 = ventricular rush

 S4 = atrial rush

 Factors affecting BP

1. Total peripheral resistance

2. Sympathetic nervous system stimulation

3. Renal factors: kidney function

4. Temperature

5. Chemicals
6. diet

 Mean Arterial Blood Pressure (MABP)

 Diastolic BP + 1/3 (Systolic BP- Diastolic BP)

 Systemic Blood Pressure

 Coronary Artery Disease: An atherosclerotic process that narrows the lumina of coronary
arteries, resulting in ischemia to the myocardium; can progress to injury & death

 Atherosclerosis

 Dse of moderate & large arteries; not limited to the coronary arteries

 Thickening of intimal layer of the bv wall from focal accumulation of lipieds, platelets,
monocytes, plaque & other debris

 Risk factors for Atherosclerosis

1. Nonmodifiable risk factors: age, sex, race, family hx of CAD

2. Modifiable risk factors: cigarette smoking, high BP, elevated cholesterol levels & LDL levels,
elevated bld homocystine, obesity, inactivity, stress

3. Contributory disease: diabetes

4. 2 or > risk factors multiplies the risk of CAD

 Clin. Syndromes of CAD: Angina Pectoris

 Substernal chest pain or pressure; may be accomplished by Levine’s sign (px clenches fist over
sternum)

 Represents imbalance in myocardial O2 supply & demand; brought on by:

a. Increased demands on heart: exertion, emotional stress, smoking, extremes of temperature esp
cold, overeating, tachyarrhythmias

b. Vasospasm: symptoms may be present at rest

 Types of Angina

1. STABLE angina: classic exertional angina; occurs ay a predictable rate-pressure product, RPP (HR
X BP), relieved with rest and/or nitroglycerin

2. UNSTABLE angina: preinfarction, crescendo angina): coronary insufficiency with risk for MI or
sudden death; pain is difficult to control; doesn’t occur at predictable RPP
  Main Clin. Syndromes of CAD: MI

 Prolonged ischemic injury & death of an area of the myocardium caused by occlusion of one or
more of the coronary arteries

 Ppting fctors: atherosclerotic heart dse with thrombus formation , coronary vasospasm or
embolism ; cocaine toxicity

 Main Clin. Syndromes of CAD: MI

Zones of Infarction:

1. Central zone:

2. Zone of injury:

3. Zone of ischemia:

 Infarction Sites

1. Trans mural (Q wave infarction)

- Full thickness of myocardium

2. Nontransmural (non Q wave infarctions): subendocardial, subepicardial, intramural infarctions

 Sites of Coronary Artery Occlusion

1. Inferior MI, RV infarction, disturbances of upper conduction system: Right coronary artery

2. Lateral MI, ventricular

ectopy: circumflex artery

3. Anterior MI, disturbances of lower conduction system : left anterior descending artery

 Impaired ventricular functions of MI results in:

1. Decreased stroke volume, cardiac output & ejection fraction

2. Increased end diastolic ventricular pressures

 Heart Failure (HF)/ Cardiac Failure

 Codn wherein the heart is unable to maintain adequate circulation of the bld to meet the
metabolic needs of the body

 Termed as Congestive Heart failure when edema is present

 Heart Failure (HF)/ Cardiac Failure

Etiology:

Results from impairment of left venricular functioning; from coronary artery dse, valvular dse,
congenital heart dse, HPN, or infection

Physiological abnormalities:

Decreased CO, elevated end diastolic pressures (preload); increased HR, impaired ventricular fxn which
may progress to cardiomyopathy

 Left Heart Failure (Forward HF)

 Bld not adequately pumped to the systemic circulation  due to inability of LV to pump ,
increases in ventricular end diastolic pressure & left atrial pressure with:

a. Increased pulmonary artery pressures & pulmonary edema

b. Pulmonary sszx: cough, dyspnea, orthopnea

c. Weakness, fatigue

 Right Heart Failure (Backward HF)

 Bld not adequately returned fr the systemic circulation to the heart  due to failure of RV,
increased pulmonary artery pressure with

a. Peripheral edema: weight gain, venous stasis

b. Nausea, anorexia

 Heart failure

 Compensated HF: symptoms are controlled by medical therapy

 Sympathetic stimulation  tachycardia

 Decreased CO  results in pre-renal failure

 Sudden death

 Medical & Surgical Mgt of CV Disease

 DIET: low salt, low cholestrol, weight reduction

 Medical Therapy: aimed at reducing O2 demand on the heart & increasing coronary blood flow

 ANTIHYPERTENSIVE DRUGS

I. Diuretics
II. Beta-Blockers “-olol”

A. Non selective Beta Blockers

B. Cardioselective Beta Blockers

III. Calcium Channel Blockers

IV. ACE Inhibitors “- PRIL”

V. Angiotensin II Receptor Blockers (ARB)

“ – SARTAN ”

VI. Vasopeptidase Inhibitors

VII. Miscellaneous

 Anti-Hypertensive Drugs

 Control HPN

 Goal: maintain a diastolic pressure < 90 mmHG; decrease afterload, reduce myocardial O2
demand (e.g. Propanolol, reserpine)

 DIURETICS

- Decrease myocardial work (reduce preload & afterload)

- increase the excretion of sodium and water by the kidney

- Different Classes:

Loop Diuretics

ex. Furosemide (Lasix)

Thiazide Diuretics

ex. Hydrochlorothiazide (Esidrix)

Potassium-Sparing Diuretics

ex. Spironolactone (Aldactone)

 Beta-blockers

 Reduce myocardial demand  act to decrease heart rate & contractility; control arrhythmias,
chest pain, reduce BP
  olol

 Nonselective

 Metoprolol (Neobloc)

 Atenolol

 Selective

 Propanolol (Inderal)

 Calcium Channel Blocker

 Inhibit flow of Ca++ ions, Relaxes blood vessels by dilation of coronary arteries; reduces cardiac
workload (HR & contractility), reduce BP, control arrhythmias & chest pain

 Amlodipine (Norvasc)

 Felodipine (Plendil)

 Nicardipine

 Nifedipine (Adalat)

 Verapamil

 Diltiazem (Cardizem, Procardial)

ACE Inhibitors

- angiotensin-converting enzyme inhibitors

- block the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor).

- Blocking this conversion process would cause vasodilation and DECREASES the blood
pressure and the pulmonary vascular resistance at which the heart pumps against

 ACE Inhibitors

captopril (Capoten)

enalapril (Vasotec)

fosinopril (Monopril)

lisinopril (Prinivil, Zestril)

quinapril (Accupril)
ramipril (Altace)

 Angiotensin II Receptor Blockers

 ARBs

 Block the A II Receptors which are potent vasoconstrictors

 “sartan”

 Losartan (Cozaar)

 Telmisartan (Micardis)

 Valsartan (Diovan)

 Vasopeptidase Inhibitors

neural endopeptidase or NEP is an enzyme which regulates blood pressure.

 Inhibition of this enzyme helps decrease blood pressure

Omapatrilat (Vanlev)

 DRUGS FOR CONGESTIVE HEART FAILURE

I. Cardiac Glycosides

digitalis (Lanoxicaps, Lanoxin)

- increase strength of contraction of cardiac muscle contraction

- Decreases HR

- Mainstay tx for CHF (e.g. digoxin)

– are also antiarrhythmic agents

 Digitalis

 has a low therapeutic index  narrow margin between the drug’s therapeutic dose and toxic
dose.

 This, combined with the drug’s long half-life, increases incidence of occurrence of digitalis
toxicity.
Toxicity:

- bradycardia ,irritability,confusion hallucination, diarrhea N/V, appearance of yellow-

green halos around lights.

 DRUGS FOR CONGESTIVE HEART FAILURE

II. Diuretics

- usually combined with cardiac glycosides to prevent digitalis toxicity; these drugs increase the
excretion of sodium and water by the kidney to reduce edema (a common symptom of CHF)

III. ACE Inhibitors

IV. Ca Channel Blockers

 DRUGS FOR CONGESTIVE HEART FAILURE

Miscellaneous Drugs

1. used to increase the contractile strength of the heart and are prescribed for patients who do not
respond to cardiac glycosides and diuretics

inamrinone

milrinone (Primacor)

2. Block the beta1 & beta2 receptors in the heart; these receptors are essentially responsible for an
increase in cardiac activity, therefore, blocking these receptors in the heart would decrease heart rate
and consequently, blood pressure.

Propranolol (Inderal, Inderal LA)

3. Drug blocks both alpha AND beta receptors which will effectively decrease blood pressure

carvedilol (Coreg)

4. Blocks the alpha receptors; this results to dilation of blood vessels only to aid in the decrease in BP

prazosin (Minipress)

5. this drug blocks angiotensin II receptors which helps dilate the blood vessels and decrease the blood
pressure

valsartan(Diovan)

6. A drug class known as the human B-type natriuretic peptides binds the receptors on the blood vessels
and causes them to dilate.
  This drug decreases BP especially in patients with severely decompensated CHF

nesiritide (Natrecor)

 DRUGS FOR ANGINA PECTORIS

Nitrates

- Decrease preload through peripheral vasodilation, reduce myocardial O2 demand, reduce chest
discomfort (angina), may alsodilate coronary arteries, improve coronary blood flow

- The most commonly prescribed nitrate is nitroglycerin.

Isosorbide (Isordil, Imdur)

Routes: sublingual, inhaled, oral, transdermal, topical, IV

Beta Blockers

- “ - OLOL”

Calcium Channel Blockers

“-IPINE”

 DRUGS FOR MI

MI – heart attack; death of some parts of the heart when it loses its blood supply

• Captopril (capoten)

• beta-blockers

 may also be prescribed to reduce the risk of a second heart attack in

patients with previous history of MI

(aspirin, atenolol, propanolol, metoprolol etc)

 DRUGS FOR ARRHYTHMIA

 DRUGS FOR ARRHYTHMIA

• This specific drug treats extremely low cardiac rates by increasing SA node conduction

ATROPINE
* Some drugs may act on the flow of sodium ions from out to in of the cell by decreasing the rate of
exchange of these cations (positively-charged cells); these specifically act on the atrial phase of cardiac
conduction (arrhythmias which are atrial in origin):

clonidine (Catapres, Catapres-TTS-1, Catapres-TTS-2,

Catapres-TTS-3)

dofetilide (Tikosyn)

ibutilide (Corvert)

 DRUGS FOR ARRHYTHMIA

These act on the ventricular conduction phase of arrhythmia:

adenosine (Adenocard)

amiodarone (Cordarone)

bretylium

disopyramide (Norpace, Norpace CR)

lidocaine (Xylocaine HC1 IV for Cardiac Arrhythmias)

mexiletine (Mexitil)

moricizine (Ethmozine)

procainamide (Procanbid, Pronestyl, Pronestyl-SR) also improve CO

propafenone (Rythmol)

tocainide (Tonocard)

 DRUGS FOR ARRHYTHMIA

Lidocaine (LidoPen Auto-Injector)

 may be auto-injected by cardiac patients to treat their own life-threatening arrhythmia

* To treat both atrial and ventricular arrhythmias:

flecainide (Tambocor)

quinidine (Quinaglute Dura-Tabs, Quinidex Extentabs)  also improves CO

  DRUGS FOR ARRHYTHMIA

Beta-Blockers

- acts by blocking the beta receptors in the heart that give a sympathetic effect (tachycardia).

- Blockage of epinephrine at the beta receptors slows down the arrhythmia of ventricular origin

Calcium Channel Blockers

– prevents the inward movement of calcium ions in the SA node to decrease heart rates

Miscellaneous Drugs

- Cardiac glycosides cause the release of acetylcholine that acts to depress the SA node and slows down
electrical conduction; used to treat atrial fibrillation or atrial flutter.

digoxin (Lanoxicaps, Lanoxin)

- This drug is used to treat ventricular arrhythmias caused by digitalis toxicity.

edetate (Endrate)

 Aspirin

 Decreases platelet aggregation  may prevent MI

 Tranquilizers

 Decrease anxiety, sympathetic effects

 Thrombolytic therapy for MI

 Meds administered to activate body’s fibrinolytic system, dissolve clot, & restore coronary blood
flow (streptokinase, TPA, urokinase)

 DRUGS FOR PERIPHERAL VASCULAR DISEASES

PERIPHERAL VASODILATORS

- increases peripheral blood flow, restoring vascular perfusion in cases such as Buerger’s disease,
Raynaud’s disease, diabetic vascular insufficiency, arteriosclerosis obliterans, etc.

ethaverine (Ethatab / Ethavex)

isoxsuprine (Vasodilan)

papaverine (Pavabid / Vasal)

* Pentoxifylline ( Trental)
  Anti HYPERLIPIDEMIC DRUGS

I. Bile Acid Sequestrants

- some of the cholesterol in bile is reabsorbed back into the bloodstream from the small intestine.

- sequestrant prevent bile acids from being reabsorbed into the blood.

- liver needs cholesterol to make bile so it uses cholest from the bloodstream

- The cholesterol within the bile is then excreted in the feces

cholestyramine (LoCHOLEST, LoCHOLEST Light, Prevalite, Questran, Questran Light)

colesevelam (Welchol)

colestipol hcl (Colestid)

II. HMG - CoA reductase Inhibitors

- HMG-CoA reductase is an enzyme that acts during one of the steps in the production of
cholesterol in the body.

- HMG-CoA reductase inhibitor drugs block this step.

- They also increase the amount of HDL.

- -statin.

- Patients on these drugs are periodically monitored for liver function abnormalities.

atorvastatin (Lipitor) fluvastatin (Lescol, Lescol XL)

lovastatin (Mevacor) pravastatin (Pravachol)

simvastatin (Zocor)

 Other drugs for hyperlipidemia

 Clofibrate

 Fenofibrate

 Gemfibrozil (Lopid)

 Omega-3 fatty acids

 Niacin
 III. Other Drugs

 abciximab (Reopro)- prevent blood clots

 acetazolamide (Diamox)- tx edema of CHF

 cilostazol (Pletal)- vasodilator , tx intermittent claudication

 morphine (Astramorph)-narcotic analgesic , tx dyspnea in pts with severe CHF

 papaverine- peripheral vasodilator , tx bv spasm of coronary arteries & peripheral vas. Disease

 etc.

 Activity Restriction

 Acute MI, CHF: limited gen to first 24 hrs; or until px is stable for 24 hrs

 Anatomy of the Heart

 Median Sternotomy

 an incision of the chest at the midline, through the sternum.

 provides access to the organs in the mediastinal cavity, particularly the heart.

 most common incision used in open-heart surgery

 Median Sternotomy

 Heart Lung Machine

 Coronary Artery Bypass

 Occlusion of a segment of the coronary artery causes ischemia to a part of the myocardium it
supplies

 CABG

 Surgical circumbention of an obstruction in a coronary artery using an anastomosing graft

(saphenous vein, internal mammary artery)

 Coronary Artery Angioplasty

 PTCA – percutaneous transluminal coronary angioplasty

 Catheter-based therapy performed to relieve coronary artery obstruction

 for patients who cannot tolerate a bypass grafting procedure.

  aid of fluoroscopy ,

cardiac catheterization laboratory

Incision in the femoral or brachial A

 Coronary Artery Angioplasty

 To enlarge the coronary artery,

 Intravascular Stent

 An endoprosthesis (pliable wire mesh) implanted postangioplasty to prevent restenosis &

occlusion in coronary or peripheral arteries

 Transplantation

 Used in end-stage myocardial dse: cardiomyopathy, ischemic heart dse, valvular heart disease

a. Heteroptics – involve leaving the natural heart & piggy-backing the donor heart

b. Orthotopic- removing the diseased heart & replacing it with a donor heart

c. Heart & lung transplantation- involves removing both organs & replacing them with donor organs

d. Major problems post transplantation: rejection, infection, complications of immunosuppressive

therapy

 Ventricular Assistive Devices (VAD)

 Implantable device (accessory pump) that improves tissue perfusion & maintain cardiogenic
circulation

 Used with severely involved px (cardiogenic shock unresponsive to meds, severe ventricular
dysfunction)

 Pacemaker

 Defibrillator

 EKG Basics

The electrocardiogram (EKG) is a representation of the electrical events of the cardiac cycle.

Each event has a distinctive waveform, the study of which can lead to greater insight into a patient’s
cardiac pathophysiology.

 EKG Leads
Leads are electrodes which measure the difference in electrical potential between either:

 EKG Leads

The standard EKG has 12 leads:

 Standard Limb Leads

 Standard Limb Leads

 Augmented Limb Leads

 All Limb Leads

 Precordial Leads

 Summary of Leads

 Arrangement of Leads on the EKG

 Cardiac Depolarization

1. SA NODE initiates Atrial Depolarization = P-wave

2 AV NODE is depolarized; AV nodal delay = 0.10 sec

3. Depolarization is conducted via the Bundle of His

4. Depolarization is conducted further into the ventricles via the Left & Right Bundle Branches

5. Septal Depolarization = Q-wave

6. “Early” Ventricular Depolarization (depolarization of the apex) = R-wave

7. “Late” Ventricular Depolarization (depolarization of the ventricular myocardium) = S-wave

8. Ventricular Repolarization = T-wave

 Vertical Axis = Voltage

 Vertical axis represents voltage on the EKG

 example: obesity, COPD, cardiac tamponade

 Horizontal Axis = Time

 1 small (1 mm) box = 0.04 seconds (40 ms)

 1 large (5 mm) box = 0.20 seconds (200 ms)

  5 large (5 mm) boxes = 1 second (1000 ms)

 15 large (5 mm) boxes = 3 seconds and is marked

on EKG paper

 Approach to EKG Interpretation

 1. Rate

2. Rhythm (includes analysis of intervals)

3. Axis

4. Hypertrophy

5. Ischemia, Injury, or Infarct

 Determining the Heart Rate

 Rule of 300

 10 Second Rule

 Our main objective is to rapidly determine the heart rate from the EKG.

As most EKGs record 10 seconds of rhythm per page, one can simply count the number of beats present
on the EKG and multiply by 6 to get the number of beats per 60 seconds.

This method works well for irregular rhythms.

Determining the Cardiac Rhythm

1. First ALWAYS determine whether the rhythm is Sinus or Non-Sinus (SVT vs. VT)!

2. Determine the Intervals:

a. P-wave duration

b. PR interval
c. QRS interval
d. QT interval

1. Every QRS is preceded by a P-wave

2. P-waves appear normal, that is they are of sinus node origin:

A. Normal Morphology:

1. P-wave duration < 0.12 sec (< 3 boxes)

 2. P-wave height < 2.5 mm

B. Normal Axis – upright P-waves in lead II

 The ECG Tracing: Waves

 P- wave

 Marks the beginning of the cardiac cycle and measures the electrical impulse that
causes atrial depolarization and mechanical contraction

 QRS- Complex

 Measures the impulse that causes ventricular depolarization

○ Q-wave- may or may not be evident on the ECG

○ R-wave- first upward deflection following P wave

○ S-wave- the first downward deflection following the R-wave

 T- wave

 Marks ventricular repolarization that ends the cardiac cycle

 Intervals and Segments

 P-R interval-

 Time interval for impulse to go from the SA to the AV node

 normal 0.12-0.20 secs

 QRS Interval

 Time interval for impulse to go from AV node to stimulate Purkinjie fibers

 Less than 0.12 secs

 QT Interval

 Time interval from beginning of depolarization to the end of repolarization

 Should not exceed ½ the length of the R-R

 ST segment

 end of the S to the beginning of the T

 The ECG Tracing

  ECG Changes : Ischemia

 T-wave inversion ( flipped T)

 ST segment depression

 T wave flattening

 Biphasic T-waves

 ECG Changes: Injury

 ST segment elevation of greater than 1mm in at least 2 contiguous leads

 Heightened or peaked T waves

 Directly related to portions of myocardium rendered electrically inactive

 ECG Changes: Infarct

 Significant Q-wave where none previously existed

 No Q-wave in Subendocardial infarcts

 Criteria

 Depth of Q wave should be 25% the height of the R wave

 Width of Q wave is 0.04 secs

 Diminished height of the R wave

 EKG Intervals

1. P-wave < 0.110 sec (approximately 3 small boxes)

2. PR interval = beginning of the P-wave to the

beginning of QRS. Normal = 0.120 – 0.200 sec

3. QRS interval = from the first deflection to return to the baseline. Normal < 0.120 sec

4. QT interval = beginning of the QRS to the END of the T-wave. Normal < 0.450 sec

 The QRS Axis

The QRS axis represents the net overall direction of the heart’s electrical activity.

Abnormalities of axis can hint at:

 Ventricular enlargement

Conduction blocks (i.e. hemiblocks)

 The Quadrant Approach

1. Examine the QRS complex in leads I and aVF to determine if they are predominantly positive or
predominantly negative. The combination should place the axis into one of the 4 quadrants below.

2. In the event that LAD is present, examine lead II to determine if this deviation is pathologic. If the
QRS in II is predominantly positive, the LAD is non-pathologic (in other words, the axis is normal). If it is
predominantly negative, it is pathologic.

 Finally: EKG Axis for Dummies!

 Lead I = left thumb and aVF = right thumb

 If both I & aVF are up = Normal Axis

 If I is up but aVF is down = LAD

 If I is down but aVF is up = RAD

 If both I & aVF are down = Extreme RAD

 ST Elevation and non-ST Elevation MIs

 Left Ventricular Hypertrophy

 Bundle Branch Blocks

 ST Elevation and non-ST Elevation MIs

There are two distinct patterns of ECG change depending if the infarction is:

 ST Elevation Infarction

ST depression, peaked T-waves, then T-wave inversion

 ST Elevation Infarction

A. Normal ECG prior to MI

B. Ischemia from coronary artery occlusion results in ST depression (not shown) and peaked T-waves

C. Infarction from ongoing ischemia results in marked ST elevation

D/E. Ongoing infarction with appearance of pathologic Q-waves and T-wave inversion

F. Fibrosis (months later) with persistent Q- waves, but normal ST segment and T- waves
  ST Elevation Infarction

Look at the inferior leads (II, III, aVF).

 Non-ST Elevation Infarction

Now what do you see in the inferior leads?

 Non-ST Elevation Infarction

ST depression & T-wave inversion

 Non-ST Elevation Infarction

Note the ST depression and T-wave inversion in leads V2-V6.

 Left Ventricular Hypertrophy

Compare these two 12-lead ECGs. What stands out as different with the second one?

 Specific criteria exists to diagnose LVH using a 12-lead ECG.

 For example:

○ The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm.

With Bundle Branch Blocks you will see two changes on the ECG.

1. QRS complex widens (> 0.12 sec).

2. QRS morphology changes (varies depending on ECG lead, and if it is a right vs. left
bundle branch block).

 What causes BBBs?

 Coronary artery disease

 Thickened, stiffened or weakened heart muscle (cardiomyopathy)

 Infection (myocarditis) of the heart muscle

 Hypertension

 Scar tissue after heart surgery

 Congenital abnormality