PARTS OF THE HEART BLOOD FLOW LAYERS OF THE HEART a) PERICARDIUM b) MYOCARDIUM c) ENDOCARDIUM PERICARDIUM Outer most layer

r 2 layers of PERICARDIUM a> Parietal pericardium (outer) b> Visceral pericardium (inner) Pericardial space: contains small amount of fluid the pericardial fluid. SUPERIOR AND INFERIOR VENA CAVA (VEINS) UNOXYGENATED BLOOD ENTERS TO RIGHT ATRIUM TRICUSPID RIGHT VENTRICLE PULMONIC VALVE PULMONARY ARTERY LUNGS OXYGENATED BLOOD ENTERS PULMONARY VEINS RIGHT & LEFT LEFT ATRIUM MITRAL VALVE MYOCARDIUM Muscle layer ENDOCARDIUM Inner most layer Has 4 (CHAMBERS) >R&L ATRIUM >R&L VENTRICLES -> Has 4 valves VALVES AV valves: (MITRAL & TRICUSPID) >between ATRIA & VENTRICLES SEMILUNAR valves: >between VENTRICLES going to LARGE BLOOD VESSELS. PULMONIC valves: >RIGHT VENTRICLE to PULMONARY ARTERY AORTIC valve: >LEFT VENTRICLE to AORTA LEFT VENTRICLE AORTIC VALVE AORTA ASCENDING AND DESCENDING

Pericardial effusion: Excessive fluids in the pericardial space due to pericarditis secondary to edema.

VALVE CLOSURE (heart sounds) 1ST H.S: (APEX) closure of A.V valves. 2ND H.S (BASE) closure of semilunar valve Question: Where do each h.s corresponds?? Ans: 1st H.S thru ventricular contraction, pulsation of carotid pulse. 2nd H.S thru ventricular relaxation

EXTRA HEART SOUNDS (S3 & S4) S3- (VENTRICULAR DIASTOLIC GALLOP) >DUE TO RAPID VENTRICULAR FILLING IN EARLY RELAXATION OR DIASTOLIC PERIOD. >NORMAL IN CHILDREN AND YOUNG ADULTS BUT IN 40 AND ABOVE ITS A 1ST SIGN OF CARDIAC HEART FAILURE. >S3 IS HEARD IMMEDIATELY AFTER S2 S4-(ATRIAL DIASTOLIC GALLOP) >OCCURS DURING ATRIAL CONTRACTION IN LATE DIASTOLE. >VIBRATION INSIDE VENTRICLES CAUSES S2 SOUND. >IT IS NOT NORMAL EVEN IN ANY AGE. >USULLY IN HYPERTENSIVE CARDIOVASCULAR DISEASE AND VALVULARBDISORDERS. >S4 SINCE IT IS IN THE LATE DIASTOLE IT IS CLOSER TO S1. PROPERTIES OF HEART MUSCLE a) RHYTHMICITY: normal rate 60-100 bpm b) EXCITABILITY/IRRITABILITY: made of distinct heart muscle (SENSITIUM MUSCLE). ALL OR ONE PRINCIPLE: only 1 muscle is stimulated in your heart muscle, the electrical signal spreads very fast throughout the heart muscle so that THE HEART CONTRACTS AS ONE. c) REFRACTORINESS: refractory/relaxing period. Heart muscle will not respond to any stimuli because the heart needs to relax at some point. Relaxation of the hearT is important.

d) CONDUCTIVITY: (conduction pathways) PACEMAKERS OF THE HEART d.1) SA node: initiates electrical signals @ above the right atrium with intrinsic rate of 60-100 bpm. d.2) AV node: between atria and ventricle. As S.A node fire signal and reaches the A.V node there is a delay of signal when going to PURKINJE FIBERS which causes ventricles to contract. WHY IS IT VERY IMPORTANT?? Because the blood in your atria, when atria contracts it provides what we call ATRIAL TICK additional load of blood from ATRIA goes to the VENTRICLES which is important to cardiac output. IF EXAMPLE: SA node fails to fire signals still AV node can initiate also electrical signals but in a slower rate. Intrinsic rate of 40-60 bpm. So definitely if SA node does not function PATIENT IS BRADYCARDIC. PURKINJE FIBERS AND BUNDLE OF HIS has an intrinsic rate of 40-60 or 20-40 bpm. e) CONTRACTILITY: heart contracts in rhythmic manner. f) AUTOMATICITY: ability of the heart to beat spontaneously and repetitively. g) EXTENSIBILITY/EXPANDABILITY blood enters the heart causes lengthening of muscle fibers to accommodate blood that enters the heart. STARLINGS LAW: The greater the stretch, the greater the force of contraction. >so there is increase in cardiac output.

BUT THERE IIS LIMITATION!!! (overstretching) which is a common cause of heart failure. Resulting to alteration and can damage the heart muscle which leads to decrease contraction and leads to heart failure.

BLOOD SUPPLY OF THE HEART MUSCLE Provides by the CORONARY ARTERY (right and left C.A) LEFT CORONARY ARTERY: Has circumflex going at the back and LEFT ANTERIOR DESCENDING ARTERY which supplies the very important LEFT VENTRICLE. LEFT MAIN CORONARY ARTERY: Has 3 branches. a) LEFT ANTERIOR DESCENDING which is the most important. b) CIRCUMFLEX which supplies the lateral sides of the left ventricles. c) POSTERIOR DESCENDING which supplies the posterior wall of the left ventricle. RIGHT MAIN CORONARY ARTERY Supplies the RIGHT ATRIUM and RIGHT VENTRICLE as well as the SA node. What happens if there is obstruction in the R.M.C.A?? It can affect the SA node which leads to ARRYTHMIA.

FLOWS AND SUPPLIES O2 TO YOUR MYOCARDIUM. JUST IMAGINE IF YOUR HEART IS BEATING FAST, THE RELAXATION PERIOD IS VERY SHORT AND BLOOD SUPPLY TO MYOCARDIUM IS SMALL.

WHAT WILL PATIENT FEELS IF HEART MUSCLE LACKS BLOOD SUPPLY?? >CHEST PAIN / ANGINA PECTORIS DUE TO LACK OF O2 SUPPLY THAT CUSES THE HEART TO COMPENSATE WHICH IT INCREASES EXERTION.

CORONARY VEINS: Returns blood from the MYOCARDIUM back to the RIGHT ATRIUM.

VERY IMPORTANT THING TO REMEMBER!!!! >BLOOD FLOW IN YOUR CORONARY ARTERY OCCURS DURING DIASTOLE/RELAXATION. BECAUSE DURING VENTRICULAR CONTRACTION CORONARY ARTERIES ARE COMPRESSED SO BLOOD FLOWS THROUGH THE CORONARY ARTERY DURING DIASTOLE, THATS WHY VENTRICULAR RELAXATION IS VERY IMPORTANT BECAUSE THATS THE TIME BLOOD

CARDIAC OUTPUT Vol. of blood ejected from the LEFT VENTRICLE per minute. From the LEFT VENTRICLE going to AORTA per minute. FACTORS AFFECT CARDIAC OUTPUT: >BOTH STROKE VOL. AND H.R an increase in STROKE VOL. or increase in HEART RATE or vise versa = INCREAE IN CARDIAC OUTPUT. IF PATIENT IS BRADYCARDIC 40-50-60 BPM C.O is lesser. Same if heart is not beating strong the stroke vol. is also less leads also to less c.o. STROKE VOLUME Vol. of blood ejected per contraction. FACTORS THAT AFFECT STROKE VOLUME A) PRELOAD THE END DIASTOLIC VOL. >vol. of blood in your ventricles particularly LEFT VENTRICLE @ the end of diastole just before heart will contract. PRELOAD EFFECT An increase in pre load, increases stroke volume and as well as increases cardiac output. FACTORS INCREASING PRELOAD A) HYPERVOLEMIA B) REGURGITATION OF VALVES OVERSTRETCHING OF MYOCARDIUM FIBERS DECREASES THE FORCE OF CONTRACTION AND THEREFORE STROKE VOLUME DECREASES. EXAMPLE: FLUID OVERLOAD INCREASES VENOUS RETURN TO THE HEART INITIALLY IT IS GOOD

BECAUSE IT INCREASES YOUR STROKE VOLUME AND THE HEART TRIES TO COMPENSATE SO INCREASE VENOUS RETURN INCRESE PRELOAD HOWEVER YOUR HEART COMPENSATES BY VENTRICULAR HYPERTROPHY TO ACCOMMODATE GREATER VOLUME. THATS WHY PATIENTS WITH HEART FAILURE SOME OF THEM WILL HAVE CARDIOMEGALY WHICH IS NOT A GOOD SIGN WHICH MEANS THAT YOUR HEAT IS TRYING TO COMPENSATE VENTRICLES ARE OVER WORKED AND LEADS TO POOR CONTRACTION AND EVENTUALLY MAY LEAD TO CARDIAC HEART FAILURE. B) AFTERLOAD The RESISTANCE the LEFT VENTRICLE must overcome to circulate blood into system. FACTORS INCREASING AFTERLOAD A) HYPERTENSION which increases pressure in the systemic circulation. B) VASOCONSTRICTION PATIENTS WITH CHF IS GIVEN ANTIHPN DRUGS. QUESTIONS?? WHICH OF THE FOLLOWING ICREASES PRELOAD AND AFTERLOAD?? FACTORS AFFECTING AFTERLOAD! A) PERIPHERAL VASCULAR RESISTANCE OR B.P B) LEFT VENTRICULAR SIZE if ventricles is dilated more blood is needed left ventricles compensate. C) CHARACTERISTICS OF VALVES PARTICULARLY THE AORTIC VALVE. WHAT PROBLEM IN THE AORTIC VALVE WHICH CAN INCREASE AFTERLOAD?? AORTIC STENOSIS. C) CONTRACTILITY:

The inherent contractile ability of heart muscle. Strength of contraction regardless of blood volume. FACTORS AFFECTING CONTRACTILITY: A)SYMPATHETIC STIMULATION: If STRESS is present it activates the SYMPATHETIC NERVOUS SYSTEM and PALPATATION IS PRESENT DUE TO STRONG MYOCARDIAL CONTRACTION. B) CALCIUM ADMINISTRATION: Promotes contraction of heart muscle. C) EPINEPHRINE: Has same effect with sympathetic nervous system. WHAT DECREASES CONTRACTILITY?? A) HYPOXEMIA lack of o2 supply B) METABOLIC ACIDOSIS REMEMBER: LACK OF O2 SUPPLY DECREASES HEART CONTRACTILITY.

A) BARORECEPTORS: Sensitive in pressure changes, found in the AORTIC ARCH and CAROTID ARTERY. Sensitive also in changes in B.P. >So increase B.P inhibit cardiac activity whereas decrease B.P stimulates cardiac activity. REMEMBER: IF PATIENT IS HYPOTENSIVE MOST LIKELY THE PATIENT IS TACHYCARDIC BECAUSE IT IS THE COMPENSATORY MECHANISM OF THE HEART. HEART RATE OF 120 AND ABOVE IS NOT GOOD. B) CHEMORECEPTORS: Sensitive in change on O2 and CO2 concentration of the blood and P.H. >stimulated when there is decrease in O2 or increase CO2, presence of acidosis and decrease in P.H. C) STRESSRECEPTORS: Found in GREAT VEINS (SUPERIOR VENA CAVA & ATRIA) which are sensitive in BLOOD VOL. changes. REMEMBNER: IF DECRESE B.V IT STIMULATES INCREASE HEART RATE AND PROMOTES VASOCONTRICTION. WHILE INCREASE BLOOD VOLUME IT DECREASES HEART RATE WHICH PROMOTE VASODILATION TO BRING BACK TO NORMAL LEVEL. >ALL OF THESE RECEPTORS SENDS SIGNALS VIA AFFERENT PATHWAYS AND LEADING TO CARDIAC CENTERS OF THE BRAIN WHICH IS IN MEDULLA AND PONS AND THEN IT SENDS SIGNALS VIA EFFERENT PATHWAYS AND WILL EITHER ACTIVATE PARASYMPATHETIC OR SYMPATHETIC.

FACTORS AFFECTING HEART RATE!! A) AUTONOMIC N.V B) BARORECEPTORS CHEMORECEPTORS STRESSRECEPTORS

>These receptors are found in the different parts of the body and the pickup changes in BLOOD VOL, BLOOD PRESSURE and also in ACID BASE so that the heart can respond to any of the changes.

PARASYMPATHETIC FIBERS WILL CAUSE IN RELATION WITH VAGUS NERVE?? >POLYNERGIC OR VAGAL RESPONSE. PARASYMPATHETIC NEUROTRANSMITTER is?? ACETYLCHOLINE WHAT IS THE EFFECT OF POLYNERGIC RESPONSE?? >DECREASE ALL and PROMOTES VASODILATION. SYMPATHETIC FIBER IS STIMULATED THE NEUROTRANSMITTER is NOREPINEPHRINE WHICH LEADS TO ADRRENERGIC RESPONSE INCREASE ALL. REMEMBER: VAGAL DECREASES ALL WHILE ADRENERGIC INCREASES ALL SIGNS & SYMPMTOMS OF HEART DISEASES.. A) DYSPNEA: Common cause is LEFT SIDED HEART FAILURE that causes also PULMONARY CONGESTION. REMEMBER: IF LEFT VENTRICLE BEATS SLOW, BLOOD SHUNTS BACK TO THE LUNGS AND LEADS TO ACCUMULATION OF BLOOD OR FLUID IN THE LUNGS WILL CAUSE PULMO. CONGESTION AND PULMO EDEMA. QUESTION! IF PRESENCE OF PULMO. EDEMA WHAT IS THE EFFECT OF GAS EXCHANGE?? >DECREASE GAS EXCHANGE LEADS TO HYPOXEMIA THEN SIGNS OF DYSPNEA IS PRESENT.

TYPES OF DYSPNEA: * EXERTIONAL DYSPNEA An early sign of heart failure. * ORTHOPNEA >ccurs when a person is lying down in SUPINE POSITION >sign of most advanced heart failure. * PAROXYSMAL NOCTURNAL DYSPNEA (PND) >occurs 2-5 hours after the onset of sleep. >also a sign of PULMONARY CONGESTION & LEFT SIDED HEART FAILURE. * CHEYNE STOKES CHARACTERISTIC; Increasing heart rate and depth. FROM SHALLOW TO FAST TO DEEPER & DEEPER THEN SHALLOW TO PERIOD OF APNEA (ABSENCE OF BREATHING). B) CHEST PAIN: 2TYPES B.1) MYOCARDIAL ISCHEMIA (ANGINA PECTORIS). >LACK OF O2 SUPPLY CAUSED BY NARROWING OR OBSTRUCTION OF CORONARY ARTERY DUE TO ATHEROSCLEROSIS. LOCATION AND CHARCTERISTIC >SUBSTERNAL (UNDER THE STERNUM) NOT DIRECTLY OVER THE HEART USUALLY THE PAIN IS IN THE CENTER. -CHEST PAIN -CRUSHING -SQUEEZING -RADIATION TO THE LEFT SIDE (LEFT ARM AND SHOULDER).

B.2) SHARP PRECORDIAL CHEST PAIN. >PAIN IS ABOVE THE HEART LEFT SIDE, DIRECTLY ABOVE OR OVER THE HEART. CHARCTERISTIC: >AGREVIATED BY RESPIRATION >WHEN A PERSON BREATHS DEEPLY THERE IS SEVER PAIN FELT THAT RADIATES ON LEFT ARM AND SHOULDER AND AS WELL AS THE UPPER BACK. >COMMON CAUSE IS?? ACUTE PERICARDITIS. B.3) PALPATATION >FEELING OF POUNDIN OR RACING. COMMON CAUSE: ARRYTHMIAS OR TACHHYARRYTHMIAS >INCREASING THE FORCE OF MYOCARDIAL CONTRACTION. WHAT STIMULATES PALPATATION?? >OVER CONSUMPTION OF COFFEE WHICHN ACTIVATES SYMPATHETIC NERVOUS SYSTEM. > ALSO IT IS CAUSE BY STRESS IT ACTIVATES THE PARASYMPATHETIC NERVOUS SYSTEM. >PREMATURE VENTRICULAR BEATS >HEART FAILURE ESPECIALLY IF (+) CARDIOMEGALY

REMEMBER: DUE TO DECREASE CARDIAC OUTPUT ALSO THE BLOOD GOING TO THE BRAIN DECREASES THEN DECREASE OXYGENATION IN THE BRAIN TISSUES WHICH IT CAN LEAD TO ISCHEMIA. SEEN IN PATIENTS WITH HEART FAILURE. OTHER CAUSES: >HYPOTENSION >HYPOVOLEMIA >ARRYTHMIA (whether slow/fast) FATIGUE: DUE TO DECREASE CARDIAC OUTPUT. POSTURAL or ORTHOSTATIC HYPOTENSION: As blood pressure goes down 15mmhg or the diastole drops to 5mmhg or more! Occurs when?? SUDDEN CHANGE IN POSITION DUE TO THE VEINS ARE DILATED AND IN RELATION ALSO WITH GRAVITATIONAL PULL OF THE BLOOD FROM UPPER TO THE LOWER EXTREMITIES AND SO IT DECREASES CARDIAC OUT PUT AS WELL AS BLOOD GOIN TO THE BRAIN. NECK/JUGULAR VEIN DISTENTION >REPRESENTS PRESSURE IN RIGHT SIDE OF THE HEART IN THE RIGHT ATRIUM. REMEMBER: >IF PRESSURE IS LOW GOING TO THE RIGHT SIDE OF THE HEART NECK VEIN IS NOT ENGORGE, BUT IF PRESSUER IS HIGH NECK VEINS ARE DISTENDED. >DISTENDED NECK VEINS SUGGESTS INCREASE VENOUS

SYNCOPY: (FAINTING) CAUSE in relation with heart disease: >DECREASE OXYGENATION OF THE BRAIN.

PRESSURE AND MOSL LIKELY TO SUGGEST RIGHTSIDED HEART FAILURE. >IF RIGHT SIDE OF THE HEART PUMPS VERY SLOW, BLOOD GUSHES BACK TO THE SYTEMIC VENOUS CIRCULATION THAT IS WHY NECK VEINS ARE DISTENDED. ASSESSING NECK VEIN DISTENTION WHAT POSITION MUST DO?? >IN SUPINE POSITION NECK VEINS ARE NORMALLY DISTENDED BECAUSE LEVEL OF NECK VEIN TO THE RIGHT ATRIUM IS WITHIN LEVEL, BUT WHEN YOU ELEVATE THE HEAD OF THE BED @ 45 DEGREES ANGLE BY GRAVITY VENOUS PRESSURE MUST BE LOW AND NECK VEINS MUST BE FLAT, BUT IF BET IS ELEVATED AND STILL NECK VEINS ARE WELL DISTENDED IT MEANS VENOUS PRESSURE IS HIGH. MURMUR: >Are caused by turbulent blood flow, and vibration of the heart in the great blood vessels. BRUITE sound on AUSCULTATION CAUSE: INCREASE RATE AND VELOCITY OF BLOOD FLOW, BUT MORE OFTEN IT IS CAUSED BY VALVULAR DISORDERS. EITHER VALVULAR REGURGITATION OR VALVULAR STENOSIS. FRICTION/PERICORDIAL FRICTION RUB: CAUSED BY; PERICARDITIS WHICH HAS GRATING OR SCRATCHY SOUND. INDICATION OF GOOD CARDIAC OUTPUT: (SKIN IS WARM) COLD CLAMMY EXTREMITIES: DECREASE CARDIAC OUTPUT

CAUSED BY: COMPENSATORY VASOCONSTRICTION. CYANOSIS: 2 TYPES >CENTRAL CYANOSIS SEEN IN FACE, MOUTH, MUCOUS MEMBRANES, AND TOUNG. >PERIPHERAL CYANOSIS SEEN IN EXTREMITIES, NAILBEDS, EDEMA: Accumulation of fluid, a late sign of HEART FAILURE. WHAT IS AN EARLY SIGN OF VOL. EXCESS?? >SUDDEN WEIGHT GAIN. HOW TO RATE EDEMA?? >(+) PITTING- MILD,MOD,SEV >CAPILLARY REFILL (BRISK OR SLUGGISH) >PRIPHERAL PULSES. PULSE PRESSURE: >THE DIFFERNCE BETWEEN SYSTOLIC AND DIASTOLIC. NORMAL 30 -40 INDICATION OF INCREASE PULSE PRESSURE?? >INCREASE STROKE VOL. AND ICP. INDICATION OF DECREASE PULSE PRESSURE?? >DECREASE STROKE VOL. HYPOVOLEMIA, SHOCK WHICH DECREASES CARDIAC OUTPUT. DIAGNOSTIC TEST: CARDIAC ENZYMES: VERY IMPORTANT, TAKEN IF THERE IS SUSPISION OF M.I. IT INCREASES IF THERE IS M.I.

TO REMEMBER IN RELATION WITH CARDIAC ENZYME IS THE TIME THE CARDIAC ENZYME LEVEL GOES UP. CKMB: WITHIN 6-8 HRS IT INCREASES. : RETURN TO NORMAL 2-3 DAYS. :USED AS AN EARLY DIAGNOSIS OF M.I. LDH: 24-48 HOURS TIME OF ELEVATION AFTER M.I. MYOGLOBIN: IT RISES 1 HR, AFTER CELL DEATH. > SEEN ALSO IN SKELETAL MUSCLE >it is used for early detection of myocardial injury?? >TROPONIN-I AND CKMB ERY TROPONIN: LEVEL RISES WITHIN 3 HRS AND VERY SENSITIVE AND IT IS ONLY FOUND IN THE HEART MUSCLE.. AND PERSIST EVEN 4DAYS AFTER THE ATTACT. ELECTROLYTES POTASSIUM: VERY IMPORTANT >IT CAN AFFECT HEART MUSCLE, PARTICULARLY PATIENTS RECEIVING DIURETICS IN WHICH IT CAUSES HYPOKALEMIA EFFECTS OF HYPOKALEMIA: >CARDIAC IRRITABILITY >INCREASES THE RISK OF DIGITALES TOXICITY WATCH OUT SPECIALLY WHEN RECEIVING BOTH DIGITALES AND DIURETIC(LASIX AND FUROSEMIDE) HYPERKALEMIA ALSO CAUSES VENTRICULOAR IRRITABILITY, SEVERE LEVELS OF HYPERKALEMIA CAN CAUSE CARDIAC ARREST. HOW TO ADMINISTER K?? >I.V ENCORPORATION

CALCIUM: IT IS IMPORTANT FOR BLOOD CLOTTING WHICH IS THE CLOTTING NUMBER 4. >IMPORTANT ALSO FOR NEUROMASCULAR ACTIVITY AND MUSCLE CONTRACTION. >BOTH HYPO AND HYPERCALCEMIA CAN CAUSE DYSRETHMIA. SODIUM; MOST OFTEN AFFECT FLUID BALANCE HYPONATREMIA: MAY INDICATE FLUID EXCESS BECAUSE INCREASE H2O CAN DILUTE PRESENCE OF Na HYPERNATREMIA: MAY INDICATE FLUID DEFICEIT BECAUSE DECREASE H2O ----INCREASES SODIUM. BLOOD COAGULATION: >IMPORTANT FOR PATIENTS WHO ARE RECEIVING ANTICOAGULANTS. PROTHROMBIN TIME: USED TO MONITOR ORAL ANTICOAGULANTS LIKE (WARFARIN AND COMADINE). APTT: MORE SENSITIVE AND USED TO MONITOR WARFARIN. LIPIDS: SERUMLIPIDS: IMPORTANT TO ASSESS RISK FOR CORONARY ARTERY DISEASE OR RISK FOR ATHEROSCLEROSIS. PREPARATION FOR PATIENT: >FASTING FOR 12 HOURS. LIPOPROTEINS: VLDL: MAY ASSOCIATE WITH ATHEROSCLEROSIS WITH HIGH LEVELS OF TRIGLYCERIES THAT IS COMPOSED OF FATTY ACIDS.

LDL: COMOSED OF 50% CHOLESTEROL. >HIGHLY CORROLATED WITH CAD BECAUSE IT TRANSPORTS CHOLESTEROL IN THE TISSUE AND CAN BE DEPOSITE IN TO THE BLOOD VESSELS. HDL: A GOOD CHOLESTEROL BECAUSE IT CONTAINS SMALL AMOUNT OF CHOLESTEROL AND LIPIDS MOSTLY MADE OF PROTEIN AND IT TRANSPORTS CHOLESTEROL AWAY FROM THE TISSUES AND SENDS BACK TO THE LIVER FOR EXCRETION. NORMAL LEVEL: 35-85 >LDL SHOULD BE LOW >HDL SHOULD BE HIGH :it is to protect you from CAD EKG ECG PQRST P-WAVE: CORRESPONDS TO ATRIAL CONTRACTION OR DEPOLARIZATION P-R INTERVAL: CONDUCTION FROM THE ATRIA TO THE VENTRICLES. VENTRICULAR DEPOLARIZATION .SEEN IN QRS COMPLEX MOST IMPORTANT IS LOOKING @ THE S,T SEGMENTS IN WHICH IT CORRESPONDS TO REPOLARIZATION THAT INDICATES ISCHEMIA OR INFARCTION. T-WAVE: CORRESPONDS TO VENTRICULAR REPOLARIZATION INVERTION OF T-WAVE: INDICATES ISCHEMIA/INFARCTION 2D ECHO: TO ASSESS FOR VALVULAR DEFORMITIES OR

OTHER STRUCTURAL DEFORMITIES. UTZ of the heart: ASSESSING THE SIZE OF VENTRICLES, ATRIA, AND THE FLOW OF BLOOD INSIDE THE HEART TO CHECK FOR STENOSIS OR REGURGITATION. ALTER MONITORING: ECG DONE OVER 24 HRS BY USING PORTABLE ECG MONITOR TO ASSESS THE RHYTHM OF THE HEART FOR A LONG PERIOD OF TIME EVEN IN SLEEPING IT RECORDS THE ELECTRICAL ACTYIVITY OF THE HEART. STRESS TEST OR EXERCISE ELECTRIC CARDIOGRAM: >ECG AND OTHER V/S ARE TAKEN WHILE PERFORMING EXERCISE USING TREDMILL/STATIONARY BIKE. VERY IMPORTANT IN CHECKING THE CORONARY ARTERY IS TO CHECK WHETHER IT CAN PROVIDE ADEQUATE AMOUNT OF O2 WHILE PERFORMING AN ACTIVITY. IMPORTANT HEALTH TEACHINGS FOR STRESS TEST: >LIGHT MEAL BEFORE THE TEST >NO COFFEE OR CAFFEINATED FOOD, SMOKING, ALCOHOL >NO STRANUOUS ACTIVITIES >WEAR COMFORTABLE CLOTHING. AFTER THE STRESS TEST: ALLOW PATIENT TO RELAX UNTIL VITAL SIGNS RETURN TO BASE-LINE. ANGIOGRAPHY: >FOR BY PASS SURGERY CHECKING. >INVOLVES INJECTION OF DYE TO THE ARTERIES THEN X-RAY IS TAKEN AFTER.

>USED FOR PATIENTS WITH M.I >CATHETER IS INSERTED IN THE RIGHT BRACHIAL OR FEMORAL ARTERY MOST OFTEN IN THE FEMORAL UNTIL IT REACHES THE CORONARY ARTERY. FOR PREPARATION: >CONSENT >NPO >ASSESS FOR ALLERGY AFTER THE PROCEDURE: >CHECK FOR BLEEDING >ASSESS DISTAL EXTREMITIESS FOR BLOOD CLOTS >PLACE PATIENTS IN BED REST 6-8 HOURS >DONT MOVE EXTREMITIES >I.V FLUIDS TO PROMOTE DYE REMOVAL. CARDIAC CATHETERIZATION: RIGHT CATH: INSERTED IN VEIN >FROM VEIN TO RIGHT SIDE OF HEART. LEFT CATH: INSERTED IN ARTERY >FROM ARTERY TO LEFT SIDE OF THE HEART. HEMODYNAMIC MONITORING: CENTRAL VENOUS PRESSURE (CVP): >IT MEASURES THE PRESSURE PARTICULARLY THE BLOOD VOLUME ENTERING @ RIGHT SIDE OF THE HEART. NORMAL(CVP): >H20 IS USED FOR MEASURING 4-10 CM WATER. >WATER MANOMETER IS USED. >CVP CATH IS INSERTED IN A VEIN. >CVP READING: TURN THE STOP CUFF GOING TO THE CATHETER AND IF

WHERE THE FLUID STABILIZES THAT IS YOUR CVP READING. >0 POINT OF MANOMETER IS @ THE 4TH ICS MIDAXILLARY LINE. >INCREASE CVP MORE THAN 10 IS AN INDICATION OF RIGHT SIDED HEART FAILURE. >DECREASE CVP INDICATES HYPOVOLEMIC SHOCK. PULMONARY ARTERY PRESSURE: >REQUIRES USE OF SPECIAL CATHETER THE SWAN GANZ CATH. >MEASURES LEFT HEART PRESSURE IN THE PULMONARY ARTERY. >INCREASE IN PAP INDICATES LEFT VENTRICULAR HYPERTROPHY OR LEFT SIDED H.F OR