CARDIAC ASSESSMENT, HEART SOUNDS, CARDIAC ENZYME.pptx

Heart is hollow four chamber, muscular pump organ
Pericardium outer layer
Pericardial sac in between parietal and visceral layer ,containing 5-20cc of fluid, protects myocardium
Myocardium makes up the walls of the heart chambers – left ventricle is 5-10 times thicker than right side
Inner endocardium are the cardiac valves and blood vessels.
The intraventricular and intraatrial septa separates the right and left chambers
Atrioventricular valves- tricuspid and mitral valves
Semilunar valves- pulmonic and aortic valves
VASCULATURE
Right coronary artery, left coronary artery, great cardiac veins, anterior cardiac veins, besian veins
Automaticity ( pace maker ability)
Conductivity (Each cell has the ability to conduct impulses to tnext cell)
Contractility (ability to contract)
Irritability (each cell has the ability to contrct on its own)
BP is determined by the cardiac output, the velocity, the resistance of the blood vessels.
Systolic- initial force of contraction of heart
Diastolic-pressure of blood vessels after initial force
Pulse pressure- difference between systolic and diastolic BP
Control of HR, CO, blood vessels and the amount of blood volume
Sympathetic secretes norepinephrine and innervate cardiac plexus and increase rate of SA node
Parasympathetic secretes acetylcholine and innervates cardiac plexus leads to decrease of SA node rate
Both regulates normal heart rate and blood pressure
Prior history collection the nurse should know the data of the patient
Read old charts or summary : previous admission, current and past drugs, reason of admission, social support, allergies, discharge information, chronic medical problems
Ask symptoms of present illness
Maintain a soothing conversation
Don’t rush the patient to answer
Ask the patient to describe illness finally
Record response and can ask more details if necessary
Ask for specific cardiac conditions
Find out any cardiac drugs patient is taking
Assess for any use of alcohol or nicotin
Assess the social factors
Record the findings
INSPECTION
Explain the procedure to the patient
Provide privacy and undress the patient
Sit upright to inspect thorax
Inspect posture and symmetry, color of skin, deformities of bone, the neck, face and eyes
Breathing pattern to be noted
Aware of cyanosis
Central cyanosis -lips mouth and conjunctiva indicates heart disease and poor oxygenation
Peripheral cyanosis- lips, ear lobes, nail buds
PMI (point of maximum intensity): ask to lay on left side and assess skin color of thorax
EYES: Arcus senilis- light gray ring surrounding iris common in older patient. If in younger patient indicate lipid metabolism disorder.
Xanthelasma- yellowish plaques on skin surrounding the eyes ,also in elbow indicate hypercholesterolemia
PALPATION
SKIN: frank edema ,puffiness, pitting edema +1,+2,+3,+4.(feet, ankle, face , sacrum, trunk, abdomen)
BREATHING: lay hands on chest at different location , feel -respiration pattern , rib elevation, precordial pulses
ARTERIES: apical

1. CARDIAC ASSESSMENT, HEART SOUNDS, CARDIAC ENZYME STUDIES, ECG MONITORING, HOLTER MONITORING, STRESS STUDY, ECHOCARDIOGRAM, CORONARY ANGIOGRAPHY PRESENTED BY S A T H E S H W A R I N II YEAR MSC (N)

2. THE HEART Heart is hollow four chamber, muscular pump organ Pericardium outer layer Pericardial sac in between parietal and visceral layer ,containing 5-20cc of fluid, protects myocardium Myocardium makes up the walls of the heart chambers – left ventricle is 5-10 times thicker than right side Inner endocardium are the cardiac valves and blood vessels. The intraventricular and intraatrial septa separates the right and left chambers

3. CONT’D Atrioventricular valves- tricuspid and mitral valves Semilunar valves- pulmonic and aortic valves VASCULATURE R ight coronary artery, left coronary artery, great cardiac veins, anterior cardiac veins, besian veins

4. CONDUCTION SYSTEM

5. ELECTRICAL CONDUCTION PROPERITIES Automaticity ( pace maker ability) Conductivity (Each cell has the ability to conduct impulses to tnext cell) Contractility (ability to contract) Irritability (each cell has the ability to contrct on its own)

6. BLOOD FLOW IN THE HEART

7. BLOOD PRESSURE BP is determined by the cardiac output, the velocity, the resistance of the blood vessels. Systolic- initial force of contraction of heart Diastolic-pressure of blood vessels after initial force Pulse pressure- difference between systolic and diastolic BP

8. AUTONOMIC NERVOUS SYSTEM Control of HR, CO, blood vessels and the amount of blood volume Sympathetic secretes norepinephrine and innervate cardiac plexus and increase rate of SA node Parasympathetic secretes acetylcholine and innervates cardiac plexus leads to decrease of SA node rate Both regulates normal heart rate and blood pressure

9. CARDIAC ASSESSMENT: HISTORY AND CHIEF COMPLAINTS Prior history collection the nurse should know the data of the patient Read old charts or summary : previous admission, current and past drugs, reason of admission, social support, allergies, discharge information, chronic medical problems Ask symptoms of present illness Maintain a soothing conversation Don’t rush the patient to answer Ask the patient to describe illness finally

10. Record response and can ask more details if necessary Ask for specific cardiac conditions Find out any cardiac drugs patient is taking Assess for any use of alcohol or nicotin Assess the social factors Record the findings

11. ASSESSMENT INSPECTION Explain the procedure to the patient Provide privacy and undress the patient Sit upright to inspect thorax Inspect posture and symmetry, color of skin, deformities of bone, the neck, face and eyes Breathing pattern to be noted Aware of cyanosis

12. Central cyanosis -lips mouth and conjunctiva indicates heart disease and poor oxygenation Peripheral cyanosis- lips, ear lobes, nail buds PMI (point of maximum intensity): ask to lay on left side and assess skin color of thorax EYES: Arcus senilis- light gray ring surrounding iris common in older patient. If in younger patient indicate lipid metabolism disorder. Xanthelasma- yellowish plaques on skin surrounding the eyes ,also in elbow indicate hypercholesterolemia

13. PALPATION SKIN: frank edema ,puffiness, pitting edema +1,+2,+3,+4.(feet, ankle, face , sacrum, trunk, abdomen) BREATHING: lay hands on chest at different location , feel -respiration pattern , rib elevation, precordial pulses ARTERIES: apical HR, radial, carotid, brachial, femoral, popliteal, posterior tibialis, dorsalis pedis pulses. Check pulse alternans for radial pulse

14. CAROTID ARTERY: plateau pulse (slow rise, slow collapsed- aortic stenosis), decrease amplitude, bounding pulse (HT, thyrotoxicosis) 0= absent +1= diminished +2= normal +3= full pulse or slight increase +4= bounding pulse

15. CENTRAL VENOUS PRESSURE: ask the patient to sit in bed then lean backward at 45 degree angle, relax for few seconds. Look for internal jugular vein , visible pulsation at the level of sternal notch, Pulsation > 3 cm shows elevation of CVP- indicate right heart failure Normal CVP= 5 to 12 cm H2O , measured by placing a catheter into large vein and attach to manometer Hepato jugular reflex- placing the hand in right upper quadrant of abdomen with firm pressure for one full minute and observe jugular vein. If its pulsation is high then CVP is high

16. CLUBBING OF FINGERS AND TOES: diffuse, bulbous enlargement of the finger and toe tips. Nails appear shiny and curves downward , loss of normal angulations due prolonged hypoxemia JUGULAR VEINS: Venous pulsation feels by gentle pressure Carotid pulse requires firm pressure Venous pulse descends upon inspiration and rises in expiration, usually collapse in sitting position Carotid pulse unaffected

17. Venous pulse

18. HAIR: feel the consistency and texture of hair Very fine hair shafts – hyperthyroidism Very coarse hair shafts- hypothyroidism Both have adverse effect on cardiovascular system

19. PERCUSSION On precordial area of chest percussion-listening for resonant sound indicates normal tissue beneath the fingers Lung tissue- resonant, semi hollow , medium pitched sound will be flat or dull in pitch

20. ASCULTATION “ lub ” and “dub” two major sounds called as S1 and S2 respectively The time between S1 and S2 is shorter than the time between S2 and beginning of next cycle (S1 of the next beat) The time between S1 and S2 corresponds systolic pressure of cardiac cycle Additional heart sounds S3 and S4. S3- early rapid diastolic filling of ventricles. S4 –last heart sound

21. S1- closing of mitral and tricuspid valve S2- closing of aortic and pulmonic valves Physiological or pathological spitting is the valves closed in different timings, one valve closes slightly slower than another valve. To auscultate make the patient relax comfortably, and ascultate the areas

22. Auscultation land marks

23. MURMURS: abnormal heart sound due turbulent or rapid blood flow via heart, greater blood vessels and heart valves. -It is a forward blood flow of constricted valve or dilated chamber -and also backflow of blood in incompetent valve- “rushing” or “swooshing” sound -record timing , characteristics (loudness, intensity, pitch, quality), location and radiation of murmur

24. GALLOPS: S3 and S4 are generally low pitched sounds and are heard best by using bell in the stethoscope. S3 ventricular gallop- sound of blood prematurely rushing into ventricle CLICKS: extra sounds heard in mitral valve prolapse, aortic stenosis, prosthetic heart valve. Opening “snaps” caused by mitral / tricuspid stenosis RUBS: visceral and parietal layer of pericardium rub together due to inflammation in uremic pericarditis, MI, inflammatory condition

25. HEART SOUNDS Systolic murmur- between S1 and S2 Pansystolic or holosystolic murmur- throughout the systolic S1 to S2 phase Diastolic murmur- between S2 and S1 holodiastolic murmur- throughout the systolic S2 to S1 phase Murmurs – early systolic, mid systolic, early diastolic, mid diastolic, late systolic, late diastolic Mitral stenosis – loud S1

26. Bundle branch block- split S1 sound Pulmonic stenosis, ASD – split S2 sound Hypertension – loud S2 sound Chart the basic information – HR, rate , rhythm, intensity, abnormal sounds, location, loudness , pitch

27. CARDIAC ENZYME STUDIES Used since mid 20 th century with MI suspects Troponin is widely used – elevation within 2-3 hours of MI Creatinine kinase – elevation in 6-12 hours Elevation of enzymes interpreted with ECG findings

28. INDICATIONS ACS Routinely following PCI CABG MI

29. TROPONINS T AND I Troponins are protein released from myocytes in irreversible myocardial damage Troponin dependent on infarct size Lower level troponin assay used to know non ST elevated MI Troponin level increases within 3-12 hours from the onset of damage, peak at 24- 48 hours, return to baseline 5-14 days. Normal troponin= 0 and 0.4 ng/ml

30. Troponin should be measured at presentation and again 10-12 hrs from the onset of symptoms Elevated troponin without ACS – CHF, Pulmonary embolism, sepsis, CKD, myocarditis, aortic dissection , often higher after thrombolytic therapy

31. CREATINE KINASE CK MB increases with 3-12 hours, reach peak within 24 hours, return to baseline 48-72 hrs Normal value 22- 198 U/L

32. MYOGLOBIN Found in cardiac and skeletal muscle Released more rapidly than other enzymes i.e. within 2 hours Normal value-= 25-72 ng/ml

33. NATRIURETRIC PEPTIDES ACS shows elevated level B type natriuretic peptide BNP NORMAL < 100 micograms/ ml

34. OTHERS Leucocytosis peaks 2-4 days of MI and returns normal within one week Increased C Reactive Protein CRP . Normal <10 mg/ L ESR values rises within 3 days and elevated for week. Normal 0-22mm/hr

35. FUTURE DEVELOPMENT Heart type fatty acid binding protein Mid regional pro atrial natriuretic peptide ST2 Growth differentiation factor 15 C terminal pro- endothelia 1

36. ECG MONITORING ECG meaning Electro- electricity Cardio- heart Graph- to write

37. It is a trans thoracic interpretation of electrical activity of the heart overtime captured and externally recorded by skin electrodes The device used is ELECTROCARDIOGRAPH

38. INDICATIONS Detect electrolyte imbalance Conduction abnormalities Ischemic heart disease Non cardiac diseases( eg. pulmonary embolism , hypothermia)

39. ECG TIME LINE 1872- Alexander Muirhead - attach wires to patient wrist 1887- Augustus publishes first human ECG, heartbeat projected on photographic plate 1893-Einthoven introduce electrocardiogram 1895- distinguish 5 deflection P,Q,R,S,T 1902- first ECG record on string galvanometer 1912- addresses equilateral triangle formed by standard leads I, II, III called Einthoven’s triangle 1924- Einthoven won Noble prize

40. DEPOLARIZATION During the rise of potential the membrane becomes permeable to sodium ions and potential rise to positive direction. Depolarization is followed by muscle contraction

41. REPOLARIZATION The sodium channel close and there is a rapid diffusion of K ions into exterior, re establishing resting membrane potential. Repolarization is followed by muscle relaxation

42. .

43. U wave

44. RECORDING OF ECG

45. ECG LEAD PLACEMENT

46. .

47. MAKING ECG REPORTING ECG strip should be correctly labelled with patient data and lead markings, should contain Heart rate Rhythm Various conduction intervals QRS complex, ST segment , T wave Cardiac axis Any abnormal wave

48. HEART RATE CALCULATION

49. Sinus tachycardia HR> 100 b/ mt Sinus bradycardia HR< 60 b/ mt Rhythm controlled by sinus node at a rate of 60-100 b/ mt

50. D isturbance of SA node

51. HR 250-350 b/ mt

52. Rapid and uncordinated ventricular depolarization

53. .

54. ST ELEVATION Acute myocardial infarction Pericarditis Left Ventricular Hypertrophy Left Bundle Branch Block hyperkalemia

55. ST DEPRESSION Ischemic heart disease Hypokalemia

56. Secondary ST segment changes with conduction abnormalities RBBB, LBBB, WPW hypokalemia

57. ABNORMAL ECG FINDINGS Myocardial Ischaemia T inversion, ST depression, U wave inversion Acute Myocardial Infarction Hyperacute T waves, ST elevation, new LBBB, TWI, Q waves Pericarditis ST elevation, PR depression   Pericardial Effusion Sinus tachycardia, low QRS voltage, QRS alternans  

58. Hyperkalaemia Tented T waves, long PR, wide QRS, short QT Hypokalaemia PR prolongation, ST depression, flat T waves, U waves Hypercalcaemia Shortened QT interval, J waves Hypocalcaemia Prolonged QT interval

59. Brugada Syndrome Wolff-Parkinson-White Syndrome Short PR interval, delta wave, wide QRS Congenital Long QT Syndrome Arrhythmogenic Right Ventricular Dysplasia Epsilon waves in V1-V3; localised QRS widening and TWI Catecholaminergic Polymorphic VT Polymorphic VT with alternating QRS morphology Early Repolarisation Syndrome J-point elevation, J-point notching

60. Sodium Channel Blockade QRS widening, ventricular arrhythmias Digoxin Toxicity Scooped ST depression, T wave flattening / inversion Pulmonary Embolism Sinus tachycardia, RBBB, S1 Q3 T3 Acute Stroke ST depression, prolonged QT, T wave inversion Hypothermia Movement artefact, Osborn waves, bradyarrhythmias

61. HOLTER MONITORING The Holter monitor study is a type of  ambulatory electrocardiographic (ECG) monitoring . It is named for Norman J. Holter, the physicist chiefly responsible for its invention in the 1950s. 

62. Holter monitor study is to analyze the  electrical activity of the heart  outside of the clinical setting that is, as a person goes about his or her normal daily activities.

63. When a person has a Holter monitor study, they wear the monitoring device for either 24 or 48 hours, and the  ECG  recorded during this time is subsequently analyzed for any  cardiac arrhythmias  that might have occurred during the monitoring period, as well as for any signs of  cardiac ischemia .

64. PURPOSES if a person is suspected to have an arrhythmia , it is important to diagnose the precise nature of the arrhythmia in order to decide The odds of capturing one of these rare or fleeting arrhythmias while a doctor happens to be recording a standard ECG (which records the heart rhythm for only 12 seconds), is quite small.

65. The Holter monitor was developed to address the problem of diagnosing infrequent or fleeting cardiac arrhythmias. By recording each and every heartbeat that occurs over a prolonged period of time, while a person goes about their activities of daily life

66. WHEN SHOULD DONE Who have transient episodes Syncope Unexplained light headedness palpitations

67. RISK AND CONTRA INDICATION Free of risk, except skin irritation due to electrodes It can used for longer weeks to be implement

68. BEFORE THE TEST 24-48hrs period Patient is not travelling, not doing water activities, not making body sweat Done in outside clinic by technician A comfortable loose clothing should be wear Can eat and drink normally prior to test Bath before the study

69. DURING THE TEST Men should be shaved to remove hairs to attach patch Instruct the patient do’s and don’ts Keep diary with him Normal routine can be followed Note the time he experience symptoms He will return to lab to remove holter

70. AFTER THE PROCEDURE Can meet the doctor within one or two weeks Doctor plan about further treatment

71. INTERPRETATION Many people (most people, in fact) have occasional, benign types of arrhythmias that do not cause any symptoms at all. Seeing such an arrhythmia on the Holter report, without simultaneous symptoms, indicates that this arrhythmia is  not  causing a problem, and (usually) does not require any treatment of further evaluation.

72. On the other hand, when symptoms are well-correlated with a cardiac arrhythmia, that’s an arrhythmia that is causing a problem (at the very least, it is producing symptoms), and that deserves to be addressed.

73. The doctor may also discuss with the other results shown on the Holter monitor report, including the maximum, minimum, and average heart rate, the total number of  premature atrial complexes (PACs)  and  premature ventricular complexes (PVCs)  that the person may have had, and any episodes of possible ischemia.

74. If a person is having a Holter study to look for silent ischemia, finding strong signs of ischemia on the test will likely lead either to further testing (perhaps with a nuclear stress test or a cardiac catheterization), or to a change in your anti-ischemia therapy.

75. STRESS TEST An exercise stress test is used to determine how well the individual heart responds during times when it’s working its hardest. During the test, the person will be asked to exercise typically on a treadmill while he hooked up to an  electrocardiogram (EKG)  machine. This allow s the doctor to monitor the individual heart rate. The exercise stress test is also referred to as an exercise test or treadmill test.

76. PURPOSE Determine person heart receives enough oxygen Order for people experiencing chest pain Determine the level of health To know the risk of heart disease

77. RISK RARE RISK Chest pain Collapsing Fainting Heart attack Irregular HR

78. PREPERATION Perform history collection and physical examination Assess for stiff joints Check blood sugar Wear loose dress NPO three hours before procedure Stop certain drugs Report any chest pains

79. DURING PROCEDURE Attached to EKG machine Start off walking slowly Watch for difficulties POST PROCEDURE Give water and make patient rest If results reveal arrhythmias plan for cardiologist consultation

80. ECHO Echocardiography is a test that uses sound waves to produce live images of the heart. The image is an echocardiogram. This test allows the doctor to monitor how the heart and its valves are functioning. The images can help them spot: blood clots in the heart fluid in the sac around the heart problems with the aorta, which is the main artery connected to the heart

81. USES To inspect heart valves , chambers Check hearts ability to pump

82. TYPES Transthoracic ECHO Transesophageal ECHO Stress ECHO Three dimensional ECHO Fetal ECHO

83. RISKS Very safe TRANSTHORACIC-discomfort of leads TRANSESOPHAGEAL- esophageal scrap Medication and exercise increases HR

84. PREPERATION TRANSESOPHAGEAL- 3hrs NPO STRESS ECHO- loose cloth

85. AFTER ECHO If any abnormalities found out , patient refers to cardiologist for further treatment

86. CORONARY ANGIOGRAPHY Coronary Angiography is a procedure that uses a special dye [contrast material ] and x- rays to see how contrast material filled blood flows through the coronary arteries of the heart.

87. IMPORTANCE Coronary angiography is the gold standard for the evaluation of coronary artery disease. It can be used to identify the exact location and severity of coronary artery disease.

88. INDICATIONS Acute MI Unstable Angina Chronic stable angina Abnormal stress test Ventricular arrythmias

89. Left ventricular dysfunction Valvular heart disease Pre operative coronary assessment Periodic follow up after cardiac transplantation

90. CONTRA INDICATIONS Coagulopathy Active bleeding Malignant hypertension Acute or chronic renal failure Electrolyte imbalance

91. Fever Active systemic infection Transient ischemic attack

92. BEFORE PROCEDURE Explain procedure and get consent Record vital signs Blood tests- BUN, Cr, PT,PTT,INR, Blood glucose level ECG must take Skin preparation IV access Remove ornaments Check puncture site for allergy and also pulsation

93. EQUIPMENTS Sterile gowns and gloves Sterile towels or drapes Gauze Syringes for heparin, lidocaine, saline flush

94. Skin preparation solution Needles, scissors, hemostasis Catheters and wires Medications-fentanyl, heparin, lidocaine, contrast

95. ACCESS SITES Femoral artery Radial artery Brachial artery

96. PROCEDURE Done with cardiac catheterization Will give mild sedation Patient lies on X ray table, may be tilted Xray cameras move around Electrodes on chest monitor HR A small amount hair is shaved at access site A small incision is made for easy insertion of catheter

97. Dye is injected through the catheter- patient feels flushing and warmth As dye moves through can visualize blockages Based on report plan for further treatment The total procedure take an hour to complete

98. RISKS Heart attack Stroke Injury to the catheterized artery Irregular heart rhythms (arrhythmias) Allergic reactions to the dye or medications used during the procedure Kidney damage Excessive bleeding Infection

99. POST PROCEDURE Remove the sheath. Tight dressing should be done. Continous monitoring of vital signs, saturation. Check for any bleeding, hematoma. Check the pedal pulse. Instruct to avoid flexing or hyperextending the affected extremityfor 12- 24 hours. Unless contraindicated encourage oral fluids.