Cardiovascular Nursing Part I

1. Cardiovascular NursingPart I Welcome to the Heart of Nursing!Welcome to the Heart of Nursing!

2. Located between the lungs Approximately the size of your fist Palpable at 5th intercostal space – known as the PMI= Point of Maximal Impulse Displaced laterally in patients with CHF or Left Ventricular Hypertrophy Located between the lungs Approximately the size of your fist Palpable at 5th intercostal space – known as the PMI= Point of Maximal Impulse Displaced laterally in patients with CHF or Left Ventricular Hypertrophy

3. Chest x-ray showing the position of the heart – white clouded areaChest x-ray showing the position of the heart – white clouded area

4. Structure Composed of 3 histologically distinct tissues Epicardium Myocardium Endocardium Surrounded by fibrous sac Pericardium

5. Endothelial Cell These cells line the endothelium of the blood vessel. Life support tissue, accommodating the vessel to grow and repair The blood supply depends on these cells Function of the cells: Filters Relax and constrict Clotting and inflammation (platelet adhesion) Coagulation Fibrinolysis Pretty important cellThese cells line the endothelium of the blood vessel. Life support tissue, accommodating the vessel to grow and repair The blood supply depends on these cells Function of the cells: Filters Relax and constrict Clotting and inflammation (platelet adhesion) Coagulation Fibrinolysis Pretty important cell

6. Dysfunctional Endothelium inability of arteries and arterioles to dilate fully in response to an appropriate stimulus. Endothelial dysfunction is thought to be a key event in the development of atherosclerosis (Book list 5 other theories Table 33-1) Significant predictor of vascular events including stroke and heart attacks Endothelial dysfunction can result from disease processes, as occurs in septic shock, hypertension, hypercholesterolemia, diabetes as well as from environmental factors, such as from smoking tobacco products Endothelial dysfunction has an increased prevalence in women Endothelial function can be improved significantly by: exercise and improved diet cessation of smoking, loss of weight and treatment of hypertension and hypercholesterolemia inability of arteries and arterioles to dilate fully in response to an appropriate stimulus. Endothelial dysfunction is thought to be a key event in the development of atherosclerosis (Book list 5 other theories Table 33-1) Significant predictor of vascular events including stroke and heart attacks Endothelial dysfunction can result from disease processes, as occurs in septic shock, hypertension, hypercholesterolemia, diabetes as well as from environmental factors, such as from smoking tobacco products Endothelial dysfunction has an increased prevalence in women Endothelial function can be improved significantly by: exercise and improved diet cessation of smoking, loss of weight and treatment of hypertension and hypercholesterolemia

7. The Heart Drives Hgb to the cells Muscle Functions as a pump Mechanical and electrical components Approx. the size of a clinched fist Holds about 500 ml of blood “Beats” to supply O2 rich blood to the body ~100,000 times/day 2,000 gallons of blood/day Through almost 65,000 miles of blood vessels The purpose of the heart is to drive Hemoglobin to the cells. The heart is a muscle that must have effective coordinated contraction to function as a pump. The ion calcium plays an important role in muscle contraction. The more intracellular calcium, the stronger the contraction. The purpose of the heart is to drive Hemoglobin to the cells. The heart is a muscle that must have effective coordinated contraction to function as a pump. The ion calcium plays an important role in muscle contraction. The more intracellular calcium, the stronger the contraction.

8. Anterior viewAnterior view

9. Coronary Arteries The heart has it’s own blood supply known as the coronary Circulation. These coronary arteries are filled during diastole and pump blood to the heart during systole ?Diastolic pressure = ? pressure gradient = ? filling of coronary arteries = ischemia ?could lead to infarction There are four main arteries that we will focus on in this course: RCA: Supplies blood to the R. Atrium, R. Ventricle, bottom of both ventricles, back of septum Also supplies blood to the AV node and the Bundle of His (blockages in the RCA result in conductions problems Right marginal artery Posterior Descending artery Left Main: (“Widow Maker”) Circumflex artery: Supplies L. Atrium, side and back of L. ventricle LAD: Supplies front and bottom of L. Ventricle, and front of the septum Coronary arteries will dilate in response to ?O2 needThe heart has it’s own blood supply known as the coronary Circulation. These coronary arteries are filled during diastole and pump blood to the heart during systole ?Diastolic pressure = ? pressure gradient = ? filling of coronary arteries = ischemia ?could lead to infarction There are four main arteries that we will focus on in this course: RCA: Supplies blood to the R. Atrium, R. Ventricle, bottom of both ventricles, back of septum Also supplies blood to the AV node and the Bundle of His (blockages in the RCA result in conductions problems Right marginal artery Posterior Descending artery Left Main: (“Widow Maker”) Circumflex artery: Supplies L. Atrium, side and back of L. ventricle LAD: Supplies front and bottom of L. Ventricle, and front of the septum Coronary arteries will dilate in response to ?O2 need

10. BLOOD FLOW through the Heart Heart uses 85% of available O2, whereas the brain uses 50% of available O2Heart uses 85% of available O2, whereas the brain uses 50% of available O2

11. The Cardiac Cycle: Refers to complete heart beat Systole = Contraction (pumping) Closure of Tricuspid and Mitral Valves = S1 Heard loudest over Apex (5th ICS) Diastole = Relaxation (filling) Closure of Pulmonic and Aortic Valves = S2 Heard loudest over 2nd ICS (R side) Read slide All four chambers undergo systole and diastole. S1, S2 are best heard with the diaphragm of your stethoscope (high pitched) S3, S4 are best heard with the bell of your stethoscope (low pitched) For extra sounds in the mitral area, pt should lay on left side For extra sounds in the aortic and Pulmonic areas, sit pt. up and lean to the right side. ** Show Animation on Jump Drive** Read slide All four chambers undergo systole and diastole. S1, S2 are best heard with the diaphragm of your stethoscope (high pitched) S3, S4 are best heard with the bell of your stethoscope (low pitched) For extra sounds in the mitral area, pt should lay on left side For extra sounds in the aortic and Pulmonic areas, sit pt. up and lean to the right side. ** Show Animation on Jump Drive**

12. The Cardiac Cycle

13. Cardiac Concepts Cardiac output = amt. of blood pumped in 1 minute CO= SV x HR Stroke Volume = amt. of blood ejected by the LV with each contraction (systole) Ejection Fraction = % of blood ejected from L. Ventricle during systole Preload Volume of blood in any chamber at end of diastole Afterload Amt. of resistance ventricle overcomes to pump Contractility = force of contraction These terms can tell us about the condition of the heart - how well the ventricle is functioning CO = measures how well the heart is working = amount of blood pumped by the ventricle in 1 minute (4-8 L) (systole) Measured using thermodilution, Using dextrose or saline, injected quickly into the PA catheter When CO is ?, then tissue perfusion is compromised EF = this will typically be measured during cardiac cath procedures and reported in the patient’s progress notes Formula: CO=SV x HR Stroke Volume = the volume of blood pumped with each heart beat Stroke volume determined by preload, afterload and contractility Preload: Volume of blood in ventricles at the end of diastole, before the next contraction Afterload: Amount of pressure the left ventricle must use to pump Affected by the size of the ventricleThese terms can tell us about the condition of the heart - how well the ventricle is functioning CO = measures how well the heart is working = amount of blood pumped by the ventricle in 1 minute (4-8 L) (systole) Measured using thermodilution, Using dextrose or saline, injected quickly into the PA catheter When CO is ?, then tissue perfusion is compromised EF = this will typically be measured during cardiac cath procedures and reported in the patient’s progress notes Formula: CO=SV x HR Stroke Volume = the volume of blood pumped with each heart beat Stroke volume determined by preload, afterload and contractility Preload: Volume of blood in ventricles at the end of diastole, before the next contraction Afterload: Amount of pressure the left ventricle must use to pump Affected by the size of the ventricle

14. Cardiac Functioning

15. Hemodynamic Monitoring Measurement Systemic and pulmonary blood pressures Pulmonary Artery Catheter (invasive) Right Atrial Pressure (RA) CVP - R. Ventricle pressure Pulmonary artery pressure PAWP =filling pressure of the LV Cardiac Output -measured using process called Thermodilution Used to monitor patients in shock, Pulmonary edema, post CABG, anytime for complicated cardiac, pulmonary, intravascular problems CVP Central Venous Pressure (invasive) Measures R. ventricular preload Arterial Lines (invasive) Monitors systemic blood pressure * Important to monitor for S&S of Infection at insertion site Hemodynamic monitoring allows the physician to manage critical patients who are hemodynamically unstable Ex: shock Go to next slide to show pictures then come back to this slide and discuss Pulmonary artery catheters – used to be called Swan-Ganz catheters Measures pressures in different chambers of the heart as the catheter is inserted Once inserted gives you systolic and diastolic pressures of the pulmonary artery Inflate balloon between 8-15 seconds (4 resp. cycles) Pulmonary wedge pressure = filling pressure of the LV = (preload) Inflate balloon between 8-15 seconds (4 breaths) Will not cause pulmonary infarction ? pressure readings in CHF & Fluid volume overload ? pressure readings = patient is “dry” Cardiac Output Measured = Dextrose or Saline injected quickly through one port of the Catheter, process called Thermodilution CVP not as sensitive as Swan-Ganz Catheter Only measures right venous pressure (preload) – Right Ventricle Can tell us when there is right ventricular failure, or hypovolemia Arterial lines (A-lines, Art. Lines) Monitor for correct waveform Check site frequently (at least Q1 hour) for Vascular checks If infection is suspected from central line – D/C the line, send the tip to the lab for culture, initiate antibioticsHemodynamic monitoring allows the physician to manage critical patients who are hemodynamically unstable Ex: shock Go to next slide to show pictures then come back to this slide and discuss Pulmonary artery catheters – used to be called Swan-Ganz catheters Measures pressures in different chambers of the heart as the catheter is inserted Once inserted gives you systolic and diastolic pressures of the pulmonary artery Inflate balloon between 8-15 seconds (4 resp. cycles) Pulmonary wedge pressure = filling pressure of the LV = (preload) Inflate balloon between 8-15 seconds (4 breaths) Will not cause pulmonary infarction ? pressure readings in CHF & Fluid volume overload ? pressure readings = patient is “dry” Cardiac Output Measured = Dextrose or Saline injected quickly through one port of the Catheter, process called Thermodilution CVP not as sensitive as Swan-Ganz Catheter Only measures right venous pressure (preload) – Right Ventricle Can tell us when there is right ventricular failure, or hypovolemia Arterial lines (A-lines, Art. Lines) Monitor for correct waveform Check site frequently (at least Q1 hour) for Vascular checks If infection is suspected from central line – D/C the line, send the tip to the lab for culture, initiate antibiotics

16. Pulmonary-artery catheter Monitor site for signs of infection just like you would any IV or Central Line site If signs of infection occur, line will usually be discontinued. Nursing Responsibility includes sending the end of the catheter to the lab for culture and initiation of antibiotic therapy Monitor site for signs of infection just like you would any IV or Central Line site If signs of infection occur, line will usually be discontinued. Nursing Responsibility includes sending the end of the catheter to the lab for culture and initiation of antibiotic therapy

17. Pulmonary Artery Catheter

18. Preload (Volume) The volume of blood in chamber at the end of diastole, or the degree of myocardial fiber stretch ? Volume/fluid = ? Preload So, preload can be ? by administering fluids ? Volume/fluid = ? Preload Meds used to decrease preload: Diuretics, (Lasix, Bumex) Vasodilators (Natrecor) Nitrates (Nitroglycerin) Morphine So, preload can be ? by diuresis Read slide Preload = as it increases, the force of the following contraction increases = increased SV and CO Greater the preload , the greater the myocardial stretch = greater requirement for oxygen apply oxygen Side Note: Pt. in renal failure with ? preload should get vasodilator instead of diureticRead slide Preload = as it increases, the force of the following contraction increases = increased SV and CO Greater the preload , the greater the myocardial stretch = greater requirement for oxygen apply oxygen Side Note: Pt. in renal failure with ? preload should get vasodilator instead of diuretic

19. Altered Preload Preload can be ?administering fluids Preload can be ?through diuresis Signs and symptoms: Fatigue JVD Edema/weight gain Murmurs CVP - high or low PAWP – high or low Preload affects stoke volume (SV)Preload affects stoke volume (SV)

20. Afterload (Resistance/pressure) The pressure or resistance that the ventricle must overcome to eject blood Resistance of L. Ventricle pumps against systemic arterial pressure, and the size of the ventricle Meds used to decrease afterload “Afterload Reduction”: A - ACE Inhibitors - ARB’s - Alpha Antagonists B - Beta Blockers C - Calcium Channel Blockers ACE Inhibitors - End on “pril”, example Lisinopril ARB’s - Atacand, Diovan, Cozaar Alpha Antagonist - Hydralazine, Clonadine, Cardura,Minipress Beta Blockers - End in “lol”, example Metoprolol Calcium Channel Blockers - Calan, CardizemACE Inhibitors - End on “pril”, example Lisinopril ARB’s - Atacand, Diovan, Cozaar Alpha Antagonist - Hydralazine, Clonadine, Cardura,Minipress Beta Blockers - End in “lol”, example Metoprolol Calcium Channel Blockers - Calan, Cardizem

21. Altered Afterload ?Afterload = ?CO ?Afterload = ?CO Signs and Symptoms: Shortness of Breath/dyspnea Cold, clammy skin Color changes (pallor/cyanosis) Prolonged CRT Decreased peripheral pulses Read slide Afterload affects Stroke Volume (SV)Read slide Afterload affects Stroke Volume (SV)

22. Contractility of the Heart Intracellular calcium causes heart to contract ? contractility=? Preload= ? Stroke Volume causing ventricles to empty Epinephrine & Norephinephrine when released by SNS ? contractility Meds that ? force of contraction are called: Positive Inotropics Digoxin (Lanoxin) Dobutamine (Dobutrex) Dopamine (no brand) Milrinone (Primacor) Epinephrine (brand depends on the route) Occurs because of calcium in the cell We talked in our EKG class that Na+ and K+ were important in the electrical conduction of the heart Well Ca+ is important in the contractility of the heart The more IC Ca the greater the force of contraction Reducing or blocking IC Ca decreases contractility Decreased contractility will lead to Heart Failure Starlings Law: The more fibers are stretched, the greater their force of contraction Cardiac Glycosides: increase contractility, decrease HR, Slow electrical conduction Digoxin – Assess apical pulse, if heart rate <60, check with the M.D. about giving the medication St. John’s Wart can increase levels of Digoxin, causing toxicity When Preload, Afterload, & contractility ? this ? the workload of the heart = ? oxygen demand (patients may need Oxygen support) Drugs decreasing contractility: beta-blockers, calcium channel blockers, alcohol, barbiturates They may still get these drugs because they need them for other reasons, but need to be awareOccurs because of calcium in the cell We talked in our EKG class that Na+ and K+ were important in the electrical conduction of the heart Well Ca+ is important in the contractility of the heart The more IC Ca the greater the force of contraction Reducing or blocking IC Ca decreases contractility Decreased contractility will lead to Heart Failure Starlings Law: The more fibers are stretched, the greater their force of contraction Cardiac Glycosides: increase contractility, decrease HR, Slow electrical conduction Digoxin – Assess apical pulse, if heart rate <60, check with the M.D. about giving the medication St. John’s Wart can increase levels of Digoxin, causing toxicity When Preload, Afterload, & contractility ? this ? the workload of the heart = ? oxygen demand (patients may need Oxygen support) Drugs decreasing contractility: beta-blockers, calcium channel blockers, alcohol, barbiturates They may still get these drugs because they need them for other reasons, but need to be aware

23. Stroke Volume SV – affected by preload, afterload, contractility ? preload, afterload & contractility = ? SV ? SV = ? Workload of the heart = ? Oxygen demand

24. Altered Cardiac Output Related to altered HR/rhythm & SV ? CO may mean ? circulating volume ? CO may mean ? circulating volume ? Cardiac Output can be related to the following: Alteration in ECG rhythm ( like A-fib,) ? heart rate ? B/P ? contractility (like CHF) ?SV S/S of ? CO = Fatigue Lethargy Weakness Dyspnea with exertion ? urine output The body will attempt to reverse a ? CO through the Sympathetic Nervous System – therefore heart rate & B/P may increase initially to compensate S/S of ? CO = Fatigue Lethargy Weakness Dyspnea with exertion ? urine output The body will attempt to reverse a ? CO through the Sympathetic Nervous System – therefore heart rate & B/P may increase initially to compensate

25. Monitoring Cardiac Output Outside of a critical care unit when your patient does not have a PA Catheter, How does the nurse evaluate the patient’s CO??: Parameters include: Heart rhythm Heart Rate Blood Pressure Urinary Output Mental status/LOC Skin Temperature ?Quality of Pulses Anytime you have a change in LOC - always check these 2 things: O2 Level/Sat Glucose LevelAnytime you have a change in LOC - always check these 2 things: O2 Level/Sat Glucose Level

26. The Heart Responds to : Sympathetic System Parasympathetic System Renin/Angiotensin System Baroreceptors and Chemoreceptors The heart respond to all these systems Sympathetic and Parasympathetic systems are part of the Autonomic Nervous System Autonomic system is part of the Peripheral Nervous System Baroreceptors and Chemoreceptors I will mention but will not go into detail, but it is in your bookThe heart respond to all these systems Sympathetic and Parasympathetic systems are part of the Autonomic Nervous System Autonomic system is part of the Peripheral Nervous System Baroreceptors and Chemoreceptors I will mention but will not go into detail, but it is in your book

27. The Sympathetic Nervous System Adrenergic = nerve fiber in the sympathetic system Sympathetic nervous system/Adrenergic system (may be used interchangeably) Chief neurotransmitters or catecholamine's Epinephrine, Norepinephrine, Dopamine Two types of Adrenergic receptor sites: Alpha and Beta Adrenergic system (nerve fiber in the sympathetic system)/Sympathetic Nervous System: One of the two divisions of the Autonomic Nervous System (the other being the parasympathetic nervous system). Sympathetic and Adrenergic may be used interchangeably The neurotransmitters,   L(-)-epinephrine   and  L(-)-norepinephrine, Dopamine are released when the site is stimulated. This causes the “fight or flight syndrome” which:…. speeds the heart = leading to ? B/P contracts blood vessels (vasoconstriction) takes over in 'fight or flight‘ Controls blood vessels There are types of adrenergic receptor sites: Alpha1 , Alpha2 and Beta1, Beta2Adrenergic system (nerve fiber in the sympathetic system)/Sympathetic Nervous System: One of the two divisions of the Autonomic Nervous System (the other being the parasympathetic nervous system). Sympathetic and Adrenergic may be used interchangeably The neurotransmitters,   L(-)-epinephrine   and  L(-)-norepinephrine, Dopamine are released when the site is stimulated. This causes the “fight or flight syndrome” which:…. speeds the heart = leading to ? B/P contracts blood vessels (vasoconstriction) takes over in 'fight or flight‘ Controls blood vessels There are types of adrenergic receptor sites: Alpha1 , Alpha2 and Beta1, Beta2

28. Sinus Tachycardia Note differences in P waves Can occur when the sympathetic nervous system is stimulated, producing an increased heart rateCan occur when the sympathetic nervous system is stimulated, producing an increased heart rate

29. Parasympathetic Nervous System Parasympathetic Nervous System Acetylcholine - Neurotransmitter Source of Vagal Response if stimulated Vagus nerve when stimulated, releases Acetylcholine causing heart to contract while chambers are empty (after systole) Cholinergic = means the release of Acetylcholine. Cholinergic System/ Parasympathetic nervous system :The system of nerve cells that uses acetylcholine as its neurotransmitter Neurotransmitter is the chemical that carries information across the synapse Acetylcholine decreases HR, slows conduction through the AV node, Leads to ?B/P This is the cause of the vagal response if the vagus nerve is stimulated. Vagus nerve = Cranial Nerve X When it is inhibited the heart rate will increase. Vagal Response Causes heart to contract forcefully while chambers relatively empty, Reduces sympathetic activity and stimulates parasympathetic activity, resulting in bradycardia and vasodilation, followed by fainting. Typical S&S: pt states I don’t feel well, pale, clammy, dropping heart rate, may see eyes roll back like fainting – May see this in post recovery of cardiac cath when they return with sheaths in placeCholinergic = means the release of Acetylcholine. Cholinergic System/ Parasympathetic nervous system :The system of nerve cells that uses acetylcholine as its neurotransmitter Neurotransmitter is the chemical that carries information across the synapse Acetylcholine decreases HR, slows conduction through the AV node, Leads to ?B/P This is the cause of the vagal response if the vagus nerve is stimulated. Vagus nerve = Cranial Nerve X When it is inhibited the heart rate will increase. Vagal Response Causes heart to contract forcefully while chambers relatively empty, Reduces sympathetic activity and stimulates parasympathetic activity, resulting in bradycardia and vasodilation, followed by fainting. Typical S&S: pt states I don’t feel well, pale, clammy, dropping heart rate, may see eyes roll back like fainting – May see this in post recovery of cardiac cath when they return with sheaths in place

30. Sinus Bradycardia Rhythm you would see when the parasympathetic system is in controlRhythm you would see when the parasympathetic system is in control

31. Other Controls of the Heart Baroreceptors: Located in Aortic Arch & Carotid Sinus Triggers enhancement of Parasympathetic Nervous System Chemoreceptor's: Located in the Aortic Arch and Carotid Artery Responds to changes in O2 CO2 and pH of blood Increases activity Baroreceptors Located in: Aortic Arch, and Carotid Sinus (where the internal carotid artery originates) Sensitive to stretch or pressure When receptors are stimulated info sent to the brainstem Causes temporary inhibition of the sympathetic system, and enhancement of the parasympathetic system (decrease heart rate, peripheral vasodilation Chemoreceptor's: Located in Aortic arch and carotid artery When stimulated, they stimulate the brainstem to increase cardiac activity.Baroreceptors Located in: Aortic Arch, and Carotid Sinus (where the internal carotid artery originates) Sensitive to stretch or pressure When receptors are stimulated info sent to the brainstem Causes temporary inhibition of the sympathetic system, and enhancement of the parasympathetic system (decrease heart rate, peripheral vasodilation Chemoreceptor's: Located in Aortic arch and carotid artery When stimulated, they stimulate the brainstem to increase cardiac activity.

32. Renin/Angiotensin/Aldosterone System Renin – enzyme/hormone = kidney ? Angiotensinogen = liver ? Angiotensin I ? ACE ? Angiotensin II ? Aldosterone = adrenal glands ? Increased water reabsorbed = ? Blood Pressure Renin/Angiotensin System: Renin: enzyme/hormone synthesized and secreted by the kidney Regulates blood pressure, blood flow, glomecular filtration What affects release of renin???: drop in b/p, drop in sodium delivered to the kidney Once secreted, joins with Angiotensinogen (secreted by the liver) to form Angiotensin I, ACE (Angiotensin Converting Enzyme) – from the lung is released, Which converts I into Angiotensin II (Powerful Vasoconstrictor) Aldosterone is then secreted by the Adrenal Glands Aldosterone: causes increase of reabsorption of Na+ which increases water reabsorbed, which increases b/p Remember “Water follows Sodium” This system can be activated in response to an injury Renin/Angiotensin System: Renin: enzyme/hormone synthesized and secreted by the kidney Regulates blood pressure, blood flow, glomecular filtration What affects release of renin???: drop in b/p, drop in sodium delivered to the kidney Once secreted, joins with Angiotensinogen (secreted by the liver) to form Angiotensin I, ACE (Angiotensin Converting Enzyme) – from the lung is released, Which converts I into Angiotensin II (Powerful Vasoconstrictor) Aldosterone is then secreted by the Adrenal Glands Aldosterone: causes increase of reabsorption of Na+ which increases water reabsorbed, which increases b/p Remember “Water follows Sodium” This system can be activated in response to an injury

33. Common medications affecting Renin-Aldosterone system ACE inhibitors All the “prils” Angiotensin II receptor blockers End in “Sartan” Atacand (Candesartan) Diovan (Valsartan) Cozaar (Loesartan) Review Table 32-8 –Excellent guide for drug categories and associated drugsReview Table 32-8 –Excellent guide for drug categories and associated drugs

34. Review Three main systems that affect the: Heart and Blood Pressure: Adrenergic/sympathetic Cholinergic/parasympathetic Renal-Angiotensin/Aldosterone If you know the actions of these systems you will understand cardiac meds by knowing their classification. Ex: If you know what the Sympathetic system does, then you will know what the mechanism of action is for Adrenergic AntagonistIf you know the actions of these systems you will understand cardiac meds by knowing their classification. Ex: If you know what the Sympathetic system does, then you will know what the mechanism of action is for Adrenergic Antagonist

35. Chapters 31 & 35 (6th Edition) Chapters 32 & 36 (7th Edition)Chapters 31 & 35 (6th Edition) Chapters 32 & 36 (7th Edition)

36. Symptoms = Cardiovascular Problems Fatigue Fluid Retention Irregular Heart Beat Dyspnea Pain Tenderness in Calf or leg Leg Pain Syncope Changes in sensory or motor function Table 32-2 Read slide Refer to Table 31-3 and Table 31-5 excellent resources Intermittent Claudication = Leg pain with increased activity/walkingRead slide Refer to Table 31-3 and Table 31-5 excellent resources Intermittent Claudication = Leg pain with increased activity/walking

37. Health HistorySubjective History of symptoms Hx chest pain, SOB, anemia Activity, sleeping, breathing, falls, dizziness, passing out Smoking , alcohol other substances Congenital heart anomalies, HTN, DVT, claudication, varicosities, edema, cyanosis, melena Hx syncopal episodes, CVA, TIA’s or previous MI DIABETES MELLITUS Medications: Including OTC and herbals Surgery or other treatments Table 32-4 Information we need to obtain from our patients through the interview process. Information we need to obtain from our patients through the interview process.

38. Medication History Tricyclic antidepressants – Arrhythmias Oral Contraceptives – Thrombophlebitis Lithium – Arrhythmias Corticosteroids – Na+ and Fluid retention Theophylline – Tachycardia & Arrhythmias Illegal Drugs – Tachycardia and Arrhythmias Digoxin – Toxicity Common medications that cause cardiovascular problems.Common medications that cause cardiovascular problems.

39. Assessing Cardiac StatusObjective Vital Signs - BP supine, sitting, standing, Rt and Left arm, correct cuff size Auscultation of lungs and heart: extra heart sounds, abnormal heart sounds Inspect for pallor, cyanosis, edema, JVD, CRT, Homan’s Sign Palpation of pulses, quality and regularity Review Table 32.5 for complete listing Read slide B/P – a normal reduction of up to 15mm Hg, systolic, upon standing is normal B/P taken in the lower extremities will typically be 10 mm Hg higher than in the upper extremities S3 and S4 are extra heart sounds Venous distention should be evaluated gradually from supine to 30-45 degrees – continue to elevate and examine for continued distention.Read slide B/P – a normal reduction of up to 15mm Hg, systolic, upon standing is normal B/P taken in the lower extremities will typically be 10 mm Hg higher than in the upper extremities S3 and S4 are extra heart sounds Venous distention should be evaluated gradually from supine to 30-45 degrees – continue to elevate and examine for continued distention.

40. Cardiac Changes associated with aging Myocardial Hypertrophy ?B-Adrenergic receptors ?Responsiveness to Adrenergic Agonists ?CO, ?HR in response to stress Stiffening of arterial vessel walls ? B/P, widened pulse pressure Diminished pedal pulses Review Table 32-1 May have only 10% of pacemaker cells in SA node This increases likeliness of SA node dysfunction (decreased rate – bradycardia) Decrease in beta adrenergic receptors causes decrease response to physical and emotional stress. ? in B/P due to loss of elasticity of blood vessels. May have only 10% of pacemaker cells in SA node This increases likeliness of SA node dysfunction (decreased rate – bradycardia) Decrease in beta adrenergic receptors causes decrease response to physical and emotional stress. ? in B/P due to loss of elasticity of blood vessels.

41. ECG RhythmsOf Gerontological patients

42. Geriatric Assesment Findings Irregular cardiac rhythms can result from: ? amplitude of QRS complex Lengthening PR, QRS, QT intervals ? SA Node cells Fibrosis of Conduction System

43. Sick Sinus Syndrome Sick Sinus Syndrome may be due to many causes: Loss of SA node cells can lead to Sick Sinus Syndrome SA node not working properly A type of bradycardia Can also have alternating patterns of bradycardia and tachycardia Symptoms also vary from none to palpitations and dizziness Requires permanent pacemaker insertion May have many manifestations on the ECG A type of Bradycardia SA Node not working properly Alternating pattern of Bradycardia and Tachycardia Can have many causes Symptoms also vary from none to palpitations, dizziness TX = Typically pacemakerSick Sinus Syndrome may be due to many causes: Loss of SA node cells can lead to Sick Sinus Syndrome SA node not working properly A type of bradycardia Can also have alternating patterns of bradycardia and tachycardia Symptoms also vary from none to palpitations and dizziness Requires permanent pacemaker insertion May have many manifestations on the ECG A type of Bradycardia SA Node not working properly Alternating pattern of Bradycardia and Tachycardia Can have many causes Symptoms also vary from none to palpitations, dizziness TX = Typically pacemaker

44. Atrial flutter

45. Atrial fibrillation

46. Wenckebach PR interval increases with each beat till QRS is dropped, then repeats pattern 2nd degree block Also called Mobitz I or Type I In Class Exercise: Chapter 36 case study = ECG (A.Fib, syncope) – virtual CD = syncope (Projector)PR interval increases with each beat till QRS is dropped, then repeats pattern 2nd degree block Also called Mobitz I or Type I In Class Exercise: Chapter 36 case study = ECG (A.Fib, syncope) – virtual CD = syncope (Projector)

47. Assessment of the chest and major vessels Inspection; Thorax Palpation; Thrills, abnormal pulsation over the chest = valve disorders or aneurysm Abnormal pulsation over the abdomen = aneurysm Auscultation; Bruits, Heart sounds, Murmurs * Auscultate apical heart rate & palpate radial pulse simultaneously Difference between the two = pulse deficit = possible arrhythmias Bruit over the chest or carotid arteries would not be an normal finding Bruit over the chest or carotid arteries would not be an normal finding

48. Areas of Auscultation Aortic: 2nd ICS right sternal border Pulmonic: 2nd ICS left sternal border Tricuspid: 4th or 5th ICS left sternal border Mitral: 5th ICS MCL Read slide Chapter 32 – video clip (Instructor jump drive or WebCT link) JUMP DRIVE Inspection & Palpation – Cardiac Ausculatory landmarks Auscultation – Cardiac w/ diaphragm Auscultation – Cardiac w/ bellRead slide Chapter 32 – video clip (Instructor jump drive or WebCT link) JUMP DRIVE Inspection & Palpation – Cardiac Ausculatory landmarks Auscultation – Cardiac w/ diaphragm Auscultation – Cardiac w/ bell

49. Auscultation points

50. Auscultation Points

51. Physical Assessment Inspection; color, symmetry, presence of obvious heaves Auscultation; S1, S2, murmurs graded 6-point scale, clicks, friction rub, bruits Extra Heart Sounds (S3, S4) are not an expected finding in adults – use bell of stethoscope Table 32-5 description of sounds Document: timing, location, pitch, position, characteristics Palpation; heaves, thrills, abnormal pulsations, record PMI location, Percussion; heart borders assessing for hypertrophy Auscultation: S1 heard loudest over Mitral valve (5th intercostal space MCL) – Closure of Tricuspid and Mitral Valves S2 heard loudest over aortic and Pulmonic valve (2nd IC space to the right of the sternal border) – Closure of the Aortic and Pulmonic Valves Extra Sounds (S3 & S4 heard best with the bell) An S3 typically heard in children, and third trimester pregnancy due to increased volume, or any condition w/ increased volume from valve disease or heart failure, mitral regurgitation Immediately follows S2 – heard as “Kentucky” S4 – athletes, CAD HTN, aortic and Pulmonic stenosis – heard as “Tennessee” These extra sounds are heard best with the bell of your stethoscope because of their low pitch Sitting and leaning forward accentuates extra sounds over the 2nd ICS’s (Aortic and Pulmonic) Laying on left side accentuates extra sounds over the mitral area Murmurs – Graded on a Roman numeral scale I-VI Clicks – heard with mechanical valves Friction rub – sounds like a rub (Pericarditis, complication following CABG) Bruits – Humming sound caused by a narrowing or bulging of vessel wall Heaves – Sustained lifts of the chest wall in the precordial area Thrills – Feel a rush of blood (ex. AV shunt) PMI – Point of maximal impulse – pulsation of the apex of heart, record based on ICS, and Midclavicular line- if to the left = cardiac hypertrophy Chapter 32 – Audio Clips Diastolic Murmur Systolic Murmur S4 Audio CD = S3 & S4 Auscultation: S1 heard loudest over Mitral valve (5th intercostal space MCL) – Closure of Tricuspid and Mitral Valves S2 heard loudest over aortic and Pulmonic valve (2nd IC space to the right of the sternal border) – Closure of the Aortic and Pulmonic Valves Extra Sounds (S3 & S4 heard best with the bell) An S3 typically heard in children, and third trimester pregnancy due to increased volume, or any condition w/ increased volume from valve disease or heart failure, mitral regurgitation Immediately follows S2 – heard as “Kentucky” S4 – athletes, CAD HTN, aortic and Pulmonic stenosis – heard as “Tennessee” These extra sounds are heard best with the bell of your stethoscope because of their low pitch Sitting and leaning forward accentuates extra sounds over the 2nd ICS’s (Aortic and Pulmonic) Laying on left side accentuates extra sounds over the mitral area Murmurs – Graded on a Roman numeral scale I-VI Clicks – heard with mechanical valves Friction rub – sounds like a rub (Pericarditis, complication following CABG) Bruits – Humming sound caused by a narrowing or bulging of vessel wall Heaves – Sustained lifts of the chest wall in the precordial area Thrills – Feel a rush of blood (ex. AV shunt) PMI – Point of maximal impulse – pulsation of the apex of heart, record based on ICS, and Midclavicular line- if to the left = cardiac hypertrophy Chapter 32 – Audio Clips Diastolic Murmur Systolic Murmur S4 Audio CD = S3 & S4

52. Treating Cardiac Problems Speed up HR Slow down HR Control Ectopy Introduce pacemaker Permanent, Temporary, AICD Administer electric shock Defibrillation Cardioversion Do nothing Possible treatment optionsPossible treatment options

54. Cardiac Medications Adrenergics – (Agonists & Antagonists) Anticholinergics Nitrates Anticoagulants Anti-Platelets Low-Molecular Weight Heparin Cardiac Glycosides Antiarrhythmics: Class IA, IB,IC, II, II, IV and misc. Beta Blockers Calcium Channel Blockers ACE Inhibitors Antilipemics Morphine Now with an understanding of the systems cardiac medications effect We will discuss specific medications from the following classes: Adrenergics, Anticholinergics, cardiac glycosides, antiarrhythmics, and Antianginals. By now some of this will be a review Important to understand two terms when discussing medications Expected outcomes – what we expect the medication to do (ex. ? heart rate, ? B/P) Patient effectiveness – how the patient responds to the drugh therapy (ex. ? chest pain, ? SOB, ? in ADL’s etc) Keep this in mind when taking your exams (hint, hint)Now with an understanding of the systems cardiac medications effect We will discuss specific medications from the following classes: Adrenergics, Anticholinergics, cardiac glycosides, antiarrhythmics, and Antianginals. By now some of this will be a review Important to understand two terms when discussing medications Expected outcomes – what we expect the medication to do (ex. ? heart rate, ? B/P) Patient effectiveness – how the patient responds to the drugh therapy (ex. ? chest pain, ? SOB, ? in ADL’s etc) Keep this in mind when taking your exams (hint, hint)

55. Agonists Work together Enhances Some medications work to enhance the sympathetic nervous systemSome medications work to enhance the sympathetic nervous system

56. Adrenergic Agonists Medications that enhance the SNS: Causing ? B/P, ? HR Dobutamine Dopamine Epinephrine Some Broncho-dilators Albuterol Are Friends! Work in conjunction to enhance the effects of the adrenergic system Read Slide Effect = Vasoconstriction & increased venous return = ? in B/P & ? HR Knowing this, what happens to preload? - Increased Are Friends! Work in conjunction to enhance the effects of the adrenergic system Read Slide Effect = Vasoconstriction & increased venous return = ? in B/P & ? HR Knowing this, what happens to preload? - Increased

57. Adrenergics Epinephrine Powerful stimulant Used in Emergency Situations Given IV, SQ, or by Inhalation Epinephrine is a powerful stimulant of the adrenergic system. Produces vasoconstriction, increased blood pressure, heart stimulation, and bronchodilation. It is used to treat anaphylaxis, acute asthma attacks restore cardiac rhythm during cardiac arrest. It has a very short half life and may be given in successive doses. In cardiac emergencies epinephrine is given in 1mg. Doses q 3-5 minutes.Epinephrine is a powerful stimulant of the adrenergic system. Produces vasoconstriction, increased blood pressure, heart stimulation, and bronchodilation. It is used to treat anaphylaxis, acute asthma attacks restore cardiac rhythm during cardiac arrest. It has a very short half life and may be given in successive doses. In cardiac emergencies epinephrine is given in 1mg. Doses q 3-5 minutes.

58. Adrenergic -Dobutamine Stimulates Beta I receptors ? Contractility of the heart ? CO, little effect on HR Short term management of CHF ? Afterload IV Infusion Only. (mcg/kg/min) Can cause HTN or hypotension, tachyarrhythmia's and PVC’s Monitor B/P, HR, EKG Rhythm Read SlideRead Slide

59. Adrenergic - Dopamine Small Doses – (Renal Dose 2-5 mcg/kg/min) – Renal vasodilation, Effect = ?urine output New Research as published in Nursing Journal 2007 states this is not as effective as once thought Larger Doses – Cardiac Stimulation ?B/P, ?CO Renal Vasoconstriction w/ doses >10mcg/kg/min IV drip titrated (mcg/kg/min) Can cause arrhythmias and hypertension Monitor blood pressure, heart rate, pulse pressure, ECG, PCWP, Monitor urine output continuously Small doses (Renal dose – causes renal vasodilation, increase urine output) ?GFR & ?Creatinine Levels Not titrated, Given IV at a set rate, may see this on Med-surg floors Larger doses cause cardiac stimulation as well as renal vasodilation except in high doses >10mcg/kg/min Results in increased cardiac output, b/p, renal blood flow (except in high doses) Ordered as IV drip and dosed in mcg/kg/min, typically titrated Dopamine stimulates all the alpha and beta receptors differently at different dosage levels. When given in low doses it will improve perfusion to vital organs and is given this way commonly to improve renal perfusion. In high doses it is given to produce vasoconstriction and improve blood pressure during shock or resuscitation. It is given by continuous IV infusion only and may be titrated to maintain blood pressure. Small doses (Renal dose – causes renal vasodilation, increase urine output) ?GFR & ?Creatinine Levels Not titrated, Given IV at a set rate, may see this on Med-surg floors Larger doses cause cardiac stimulation as well as renal vasodilation except in high doses >10mcg/kg/min Results in increased cardiac output, b/p, renal blood flow (except in high doses) Ordered as IV drip and dosed in mcg/kg/min, typically titrated Dopamine stimulates all the alpha and beta receptors differently at different dosage levels. When given in low doses it will improve perfusion to vital organs and is given this way commonly to improve renal perfusion. In high doses it is given to produce vasoconstriction and improve blood pressure during shock or resuscitation. It is given by continuous IV infusion only and may be titrated to maintain blood pressure.

60. Calc. For Dopamine and Dobutamine Infusions These drugs are ordered mcg/kg/min Equation: DO- mcg ordered x pt wt. Kg x 60 OH- drug concentration = IV infusion rate (ml/hr) Example- Order: Dopamine to run at 5mcg/kg/min Pharmacy sends Dopamine 200mg in 250 ml of NS Pt’s weight = 132 lbs. What will you set your pump at 1st = Calculate pts’ weight in kg. = 132/2.2 = 60kg 2nd = Figure out your drug concentration so your med amts. are the same! (Remember Apples to Apples) 200mg = 200,000 mcg (move 3 decimal places)/250 ml = 800mcg/ml Now you are ready to plug in your numbers into the formula 5mcgX60kgX60min. = 18,000 18,000 800mcg = 22.5 ml/hr. Always lock the IV pump when patients are on calculated drips!1st = Calculate pts’ weight in kg. = 132/2.2 = 60kg 2nd = Figure out your drug concentration so your med amts. are the same! (Remember Apples to Apples) 200mg = 200,000 mcg (move 3 decimal places)/250 ml = 800mcg/ml Now you are ready to plug in your numbers into the formula 5mcgX60kgX60min. = 18,000 18,000 800mcg = 22.5 ml/hr. Always lock the IV pump when patients are on calculated drips!

61. Dopamine Infiltration Very Serious Severe vasoconstriction Tissue necrosis will result if not treated right away Antidote: Phentolamine (Regitine) Alpha1 adrenergic blocker Onset =Immediate Given SubQ Must observe IV site frequently If infiltrated dopamine can cause extreme vasoconstriction in the soft tissues. Results in tissue necrosis if it is not reversed with the alpha Adrenergic Blocker/ Antagonist, Phentolamine (Regitine) Regitine will reverse vasoconstriction caused by norephinephrine or dopamine Onset is immediate, peaks in 2 minutes Watch for hypotension (vasodilator) If infiltrated dopamine can cause extreme vasoconstriction in the soft tissues. Results in tissue necrosis if it is not reversed with the alpha Adrenergic Blocker/ Antagonist, Phentolamine (Regitine) Regitine will reverse vasoconstriction caused by norephinephrine or dopamine Onset is immediate, peaks in 2 minutes Watch for hypotension (vasodilator)

62. Antagonists Work Against Block the effects of either: Sympathetic Nervous System ParaSympathetic Nervous System Work against the system Blocks the release of the neurotransmitters In the SNS the neurotransmitters are: Epinephrine, Norepinephrine, dopamine In the Para SNS the neurotransmitters are: AcetylcholineWork against the system Blocks the release of the neurotransmitters In the SNS the neurotransmitters are: Epinephrine, Norepinephrine, dopamine In the Para SNS the neurotransmitters are: Acetylcholine

63. Adrenergic Antagonists Meds affecting this system: Adrenergic Inhibitors/Antagonists Central-acting Peripheral-acting Alpha Blockers Beta Blockers – end in LOL Alpha and Beta Blockers Adrenergic Inhibitor/Antagonists means: Works against has the opposite effect Blocks effects of SNS Effect = ?HR, ?B/P See Table 32-8 Beta Blockers Action Why do we give them What types of patients Common side effects Adrenergic Inhibitor/Antagonists means: Works against has the opposite effect Blocks effects of SNS Effect = ?HR, ?B/P See Table 32-8 Beta Blockers Action Why do we give them What types of patients Common side effects

64. Beta Blockers Medications ending in “lol” ( like metoprolol) Compete for adrenergic neruotransmitters Epinephrine, Norepinephrine, Dopamine Expected results: ?HR, ? B/P, Reduction of workload of the heart Side Effects: nightmares, depression, bronchospasms, erectile dysfunction, hypoglycemia in diabetics Measuring effectiveness: Reduction in angina, reduction of symptoms associated with ADL’s ? CO ? Renin Secretions ? CO ? Renin Secretions

65. Adrenergic System Receptorsand their Effects As we talk about Beta Blockers and their mechanism of action, Beta-Blockers work on cells in the body based on specific receptor functions. Receptors are found in all cells Adrenergic receptors are associated with cells tied to the Sympathetic Nervous System These Adrenergic Receptors are broken down into alpha and beta receptors according to their response to adrenergic activity or their response to blocking agents (like Beta Blockers) Different receptors are configured differently These receptors can recognize and bind with molecules that are introduced to the cell like drugs Read slide Alpha1 – in blood vessels found primarily in the skin and GI Alpha2 - Beta1 – found primarily in the heart Inoptropic = increases contractility Beta2 – Found primarily in the lungs Beta3 – Found primarily in adipose tissueAs we talk about Beta Blockers and their mechanism of action, Beta-Blockers work on cells in the body based on specific receptor functions. Receptors are found in all cells Adrenergic receptors are associated with cells tied to the Sympathetic Nervous System These Adrenergic Receptors are broken down into alpha and beta receptors according to their response to adrenergic activity or their response to blocking agents (like Beta Blockers) Different receptors are configured differently These receptors can recognize and bind with molecules that are introduced to the cell like drugs Read slide Alpha1 – in blood vessels found primarily in the skin and GI Alpha2 - Beta1 – found primarily in the heart Inoptropic = increases contractility Beta2 – Found primarily in the lungs Beta3 – Found primarily in adipose tissue

66. Adrenergic meds are often non-discriminating May affect either receptor Non-discriminating or non-selective beta-blockers cause bronchoconstriction as well as a ? in HR, ?contractility Never give a nonselective beta-blocker to a patient with pulmonary diseaseNon-discriminating or non-selective beta-blockers cause bronchoconstriction as well as a ? in HR, ?contractility Never give a nonselective beta-blocker to a patient with pulmonary disease

67. Cholinergic Antagonists(Also referred to as Anti-cholenergic) Atropine Scopolamine Some Parkinson’s drugs Drugs that block acetylcholine Effect will be: increase heart rate, decreased salivationDrugs that block acetylcholine Effect will be: increase heart rate, decreased salivation

68. Anticholinergics Atropine Blocks Cholinergic System Increases Heart Rate Indications; symptomatic Bradycardia, heart block Atropine is used to treat symptomatic bradycardia or reduced heart rate. A reduced heart rate can reduce cardiac output and therefore leading to ? blood pressure resulting in dizziness, syncopy, and inadequate perfusion to vital organs.Atropine is used to treat symptomatic bradycardia or reduced heart rate. A reduced heart rate can reduce cardiac output and therefore leading to ? blood pressure resulting in dizziness, syncopy, and inadequate perfusion to vital organs.

69. ACE Inhibitors “Prils” (like Lisinopril) Remember the Renin/Aldosterone System: Renin – enzyme/hormone = kidney Angiotensinogen = liver Angiotensin I ACE Inhibitors Block from here: Angiotensin II Aldosterone = adrenal glands Increased water reabsorbed Increased Blood Pressure Blocks the conversion of Angiotensin I to the vasoconstrictor Angiotensin II that occurs in the lungsBlocks the conversion of Angiotensin I to the vasoconstrictor Angiotensin II that occurs in the lungs

70. ACE Inhibitors (cont’d) Drug of Choice in Tx. Of CHF Expected Results: ? B/P in hypertensive patients ? Afterload in CHF patients Side Effects: Dry, Hacking Cough, Hypotension, Hyperkalemia (monitor potassium), Renal insufficiency in high doses (monitor creatinine) Therapeutic Results: improves EF (Ejection Fraction), ? activity tolerance Drug of choice in treatment of CHF patients ACE Inhibitors - are good for people with normal kidney function Good for Diabetics - it will protect the kidneys But if patient has early Renal Insufciency - the ACE Inhibitor will ? the insuffciencey Drug of choice in treatment of CHF patients ACE Inhibitors - are good for people with normal kidney function Good for Diabetics - it will protect the kidneys But if patient has early Renal Insufciency - the ACE Inhibitor will ? the insuffciencey

71. Cardiac Glycosides Digoxin Increases Intracellular Calcium Positive Inoptropic effect ? Contractility Negative Chronotropic effect ? Heart Rate Indications; Treatment of CHF, Tachyarrhythmias (PAT, atrial fibrillation, atrial flutter) Loading dose may be required Drugs causing hypokalemia, such as: Thiazide Diuretics, Corticosteroids, Laxatives, Quinidine. Can increase risk for toxicity Digoxin effects electrical conduction properties of cardiac cells, decreasing the rate increases intracellular calcium, increasing contractility. Don’t give if apical heart rate <60, cal the MD Inotropic –? cardiac contractility Negative Chronotropic effect = ?HR Because Digoxin increases the force of contraction it is often given in congestive heart failure. It also decreases conduction This reduces the HR and helps to counteract atrial fibrillation commonly seen in CHF. Digoxin effects electrical conduction properties of cardiac cells, decreasing the rate increases intracellular calcium, increasing contractility. Don’t give if apical heart rate <60, cal the MD Inotropic –? cardiac contractility Negative Chronotropic effect = ?HR Because Digoxin increases the force of contraction it is often given in congestive heart failure. It also decreases conduction This reduces the HR and helps to counteract atrial fibrillation commonly seen in CHF.

72. Cardiac Glycosides:Mechanism of Action Increase myocardial contractility Change electrical conduction properties of the heart Decrease rate of electrical conduction Prolong the refractory period Area between SA node and AV node Result: reduced heart rate and improved cardiac efficiency

73. Cardiac Glycosides:Adverse Effects Digoxin (Lanoxin) Very narrow therapeutic window Drug levels must be monitored Electrolyte levels must be monitored

74. Cardiac Glycosides Digoxin Levels 0.5-2.0 Monitor for: 1. ?Potassium, 2.?Magnesium, and 3. ?Calcium levels Is the patient on Lasix (Furosemide) or other loop diuretic? Can easily lead to Toxicity: Many drugs interfere with Digoxin; Reglan, Rifampin, Phenytoin, antacids, antibiotics It is monitored by serum drug level. Digoxin has a narrow therapeutic range of 0.5-2.0. Because hypokalemia, hypomagnesaemia, and hypercalcemia may cause an increased susceptibility to Digoxin toxicity these electrolytes should also be monitored. St. John’s Wart can also lead to Dig Toxicity It is monitored by serum drug level. Digoxin has a narrow therapeutic range of 0.5-2.0. Because hypokalemia, hypomagnesaemia, and hypercalcemia may cause an increased susceptibility to Digoxin toxicity these electrolytes should also be monitored. St. John’s Wart can also lead to Dig Toxicity

75. Patients At Risk for Dig Toxicity Diuretics Beta blockers Calcium preparations Amiodarone (Cordarone) Cardizem (Diltiazem) Erythromycin, omeprazole Verapamil, Quinidine Read slide Diuretics= produce low potassium Beta Blockers = effect is ?HR Calcium preparations = increase circulating calcium Ask for Dig level if you haven’t seen one in a whileRead slide Diuretics= produce low potassium Beta Blockers = effect is ?HR Calcium preparations = increase circulating calcium Ask for Dig level if you haven’t seen one in a while

76. S/S of Dig. Toxicity N/V Anorexia Visual disturbances “yellow” vision Headaches Fatigue/Maliase Arrhythmias (PVC’s, A-fib, 1st degree block) Bradycardia Treatment for Dig Toxicity: Dig Immune Fab or Digibind Read SlideRead Slide

77. ST Segment Depression - Dig. toxicity

78. Antiarrhythmics Divided into 4 classes (I,IA,IB,IC,II,III,IV) Classified based on effect of the conduction system Plus a “Miscellaneous” class Goal = ? symptoms, ?Hemodynamic stability Read slide Classified by their effects on cardiac conduction tissue Class I = Na+ Blocking Class II = Beta Blockers Class III – Potassium Blockers Class IV – Calcium Channel BlockersRead slide Classified by their effects on cardiac conduction tissue Class I = Na+ Blocking Class II = Beta Blockers Class III – Potassium Blockers Class IV – Calcium Channel Blockers

79. Most Common Antiarrhythmics Lidocaine - PVC’s Monitor for signs of confusion Onset & Peak Immediate Amiodarone (Cordarone) Onset = 2hr., peak = 3-7 hr. Half-life = 13-107 days Diltiazem (Cardizem) Ca+ Channel Blocker IV = onset 2-5 min, peak = 2-4 hr. Half life = 3.5 -7 hours Verapamil (Calan) Ca+ Channel Blocker Procardia (nifedipine) Digoxin The drug of choice is based on the conduction problem and physician preference. With Lidocaine, monitor patient for signs of toxicity (disorientation/confusion) Amiodarone causes anorexia, pts. C/O “funny taste” Megase may be ordered to increase appetite, however causes prolonged QT Interval Marinal (Marijuana derivative) ? appetite, but does not hurt the heartThe drug of choice is based on the conduction problem and physician preference. With Lidocaine, monitor patient for signs of toxicity (disorientation/confusion) Amiodarone causes anorexia, pts. C/O “funny taste” Megase may be ordered to increase appetite, however causes prolonged QT Interval Marinal (Marijuana derivative) ? appetite, but does not hurt the heart

80. Antiarrhythmics “Miscellaneous” Class Adenosine (Adenocard) Slows Conduction through AV node Treats PSVT Given Rapid IVP, can cause pronounced flushing and transient arrhythmias or asystole for a few seconds Digoxin, and atropine in this class also Adenosine or Adenocard slows conduction through the AV node usually produces a few seconds of asystole when administered. Used to treat symptomatic supraventricular tachycardia. It has a half-life of 10 seconds and must be given fast IV push to be effective. It is given when calcium channel blockers are not effective or if they are contraindicated. Adenosine or Adenocard slows conduction through the AV node usually produces a few seconds of asystole when administered. Used to treat symptomatic supraventricular tachycardia. It has a half-life of 10 seconds and must be given fast IV push to be effective. It is given when calcium channel blockers are not effective or if they are contraindicated.

81. Nursing Implications Monitor for therapeutic response Decreased BP in hypertensive patients Decreased edema Decreased fatigue Regular pulse rate Pulse rate without major irregularities Improved regularity of rhythm Improved cardiac output

82. Various Drugs Anticoagulants Inhibit the action or formation of clotting factors Prevent clot formation Antiplatelet drugs Inhibit platelet aggregation Prevent platelet plugs Thrombolytic drugs Lyse (break down) existing clots Antilipemics

83. Anticoagulants Have no direct effect on a blood clot that is already formed Used prophylactically to prevent Clot formation (thrombus) An embolus (dislodged clot)

84. Anticoagulants:Mechanism of Action All ultimately prevent clot formation heparin Low-molecular-weight heparins warfarin (Coumadin)

85. Anticoagulants: Indications Used to prevent clot formation in certain settings where clot formation is likely Myocardial infarction Unstable angina Atrial fibrillation Indwelling devices, such as mechanical heart valves Major orthopedic surgery

86. Antiplatelet Drugs Prevent platelet adhesion Aspirin - (now considered an Anti Thrombetic) Dipyridamole (Persantine) Clopidogrel (Plavix) and ticlopidine (Ticlid) ADP inhibitors Tirofiban (Aggrastat), eptifibatide (Integrilin) New class, GP IIb/IIIa inhibitors

87. Thrombolytic Drugs Drugs that break down, or lyse, preformed clots Patient selection is required Bleeding is a complication IV therapy – Bolus or drip Critical monitoring of patient Monitor for re-perfusion How do we assess our patient to know if the drug is working (meaning the patient is re-perfused)???? Answer – For Cardiovascular Reperfusion = Assess your patients chest pain level - Drug is working and tissue is being re-perfused if the patient’s chest pain is decreasing and/or is eliminatedHow do we assess our patient to know if the drug is working (meaning the patient is re-perfused)???? Answer – For Cardiovascular Reperfusion = Assess your patients chest pain level - Drug is working and tissue is being re-perfused if the patient’s chest pain is decreasing and/or is eliminated

88. Thrombolytic Drugs (cont’d) streptokinase (Streptase) – older drug anistreplase (Eminase) alteplase (t-PA, Activase) – newer drug reteplase (Retavase) tenecteplase (TNKase) drotrecogin alfa (Xigris)

89. Thrombolytic Drugs: Indications Acute MI – most beneficial w/in 1st hour Can be administered up to 6 hours Goal in AMI = Stop the infarction Ideally = 1st hour Must = within first 6 hours DVT Occlusion of shunts or catheters Pulmonary embolus Acute ischemic stroke Table 33-14

90. Antilipemics Drugs used to lower lipid levels

91. Antilipemics HMG-CoA reductase inhibitors (HMGs, or statins) Bile acid sequestrants Niacin (nicotinic acid) Fibric acid derivatives Cholesterol absorption inhibitor Combination of these drugs Table 34-6

92. Antilipemics: HMG-CoA Reductase Inhibitors (HMGs, or statins) Most potent LDL reducers lovastatin (Mevacor) pravastatin (Pravachol) simvastatin (Zocor) atorvastatin (Lipitor) fluvastatin (Lescol) Lower the rate of cholesterol production First-line drug therapy for hypercholesterolemia New studies show:has anti-inflammatory effect on the endothelium

93. HMG-CoA Reductase Inhibitors (cont’d) Adverse effects Mild, transient GI disturbances Rash Headache Myopathy (muscle pain), possibly leading to a more serious condition = Rhabdomyolsis Important to ask about muscle pain/tenderness Monitor for elevations in: liver enzymes CK levels Interferes with absorption of: Digoxin Thiazide Diuretics Beta BlockersInterferes with absorption of: Digoxin Thiazide Diuretics Beta Blockers

94. Bile Acid Sequestrants Also called bile acid–binding resins and ion-exchange resins cholestyramine (Questran) colestipol hydrochloride (Colestid) colesevelam (Welchol)

95. Bile Acid Sequestrants (cont’d) Mechanism of action Prevent resorption of bile acids from small intestine Bile acids are necessary for absorption of cholesterol May be used along with statins Should be taken by itself – can interfere with other drugs Side Effects: GI, gritty taste

96. Niacin (Nicotinic Acid) Vitamin B3 Lipid-lowering properties require much higher doses than when used as a vitamin Effective, inexpensive, often used in combination with other lipid-lowering drugs

97. Niacin (Nicotinic Acid) (cont’d) Adverse effects Flushing (due to histamine release) Expected Side Effect Pruritus GI distress

98. Fibric Acid Derivatives Also known as fibrates gemfibrozil (Lopid) fenofibrate (Tricor) Effect: Reduces Triglycerides ?HDL Side Effects: Mild GI Enhance anticoagulants

99. Cholesterol Absorption Inhibitor ezetimibe (Zetia) Inhibits absorption of cholesterol and related sterols from the small intestine Results in reduced total cholesterol, LDL, triglyceride levels Also increases HDL levels Works well when taken with a statin drug Natural Lipid Lowering Agents – pg. 796 Mild GI upset Natural Agents Niacin Garlic (hypoglycemic effect in larger amounts) Can enhance anticoagulants-coumadin Omega 3 fatty acids Milk Thistle Fiber Plant Sterols (nutsm soybeans, seeds) Soy CO Q10Mild GI upset Natural Agents Niacin Garlic (hypoglycemic effect in larger amounts) Can enhance anticoagulants-coumadin Omega 3 fatty acids Milk Thistle Fiber Plant Sterols (nutsm soybeans, seeds) Soy CO Q10

100. Laboratory Testing CBC BMP CK TROPONIN PT, INR PTT/APTT BNP BUN, Creatinine Table 32-7 K Magnesium Cholesterol Triglycerides Sed rate Sed Rate Rate of which RBC settle and descend in plasma or saline. RBC tend to stack up, increases weight and causes them to descend quickly Can be a non-specific test Chronic infection, inflammation, collagen or vascular diseases Increased with MI but normal with anginaSed Rate Rate of which RBC settle and descend in plasma or saline. RBC tend to stack up, increases weight and causes them to descend quickly Can be a non-specific test Chronic infection, inflammation, collagen or vascular diseases Increased with MI but normal with angina

101. Creatine Kinase CK: Enzymes specific to cells of brain, myocardial, and skeletal muscle CK-MM CK-BB CK-MB CK-MB index Ratio of CK-MB to total CK More definitive for diagnosing an MI If CK-MB and the Index are both elevated= highly suggestive of an MI Enzymes characteristic of tissue injury Elevated 6 hrs post MI; peaks at 18 hrs CK enzymes are broken into: CK-MM – skeletal muscle CK-BB- brain and nervous system CK-MB –myocardial tissue CK-MB Index Ratio of CK-MB to total CK Elevated CK & index >2.5 = MI High CK-MB indicates infarction already occurred, thereforeThrombolytics probably not appropriate Enzymes characteristic of tissue injury Elevated 6 hrs post MI; peaks at 18 hrs CK enzymes are broken into: CK-MM – skeletal muscle CK-BB- brain and nervous system CK-MB –myocardial tissue CK-MB Index Ratio of CK-MB to total CK Elevated CK & index >2.5 = MI High CK-MB indicates infarction already occurred, thereforeThrombolytics probably not appropriate

102. TROPONIN Troponin protein released with injury of myocardial cells Two types I & T Troponin I (begins to rise as early as 1 hour post pain) _ Lewis textbook <0.4 normal baseline (Lewis) These values vary greatly depending on the reference you use and laboratory equipment. Become elevated sooner and remain elevated longer than CK-MB Also exist in skeletal and cardiac tissue Troponin T & Troponin I only present in cardiac tissueBecome elevated sooner and remain elevated longer than CK-MB Also exist in skeletal and cardiac tissue Troponin T & Troponin I only present in cardiac tissue

103. Cardiac Enzyme Chart These lab results are never used to diagnose cardiac disease independently Lab results in conjunction with patient S&S and an EKG are used to confirm cardiac infarction These lab results are never used to diagnose cardiac disease independently Lab results in conjunction with patient S&S and an EKG are used to confirm cardiac infarction

104. Lipid Testing Cholesterol Goals: Total Cholesterol 140 - <200=Good HDL (Good) <35=low Not Good >60=Great LDL (Bad) Keep < 160 Triglycerides 40-190 = Good Factors effecting test High/Low Density Lipoproteins Must fast 12-14 hours, otherwise the meal they just ate will affect resultsHigh/Low Density Lipoproteins Must fast 12-14 hours, otherwise the meal they just ate will affect results

105. Lipo Protein Testing New Lipid testing Enzyme promotes vascular inflammation ? levels (Lp-PLA) associated with CAD Called the PLAC Test Sometimes LDL levels are OK but Lp-PLA2 ? in MI patients May be ordered in conjunction with cholesterol and triglycerides Sometimes LDL levels are OK but Lp-PLA2 ? in MI patients May be ordered in conjunction with cholesterol and triglycerides

106. Prothrombin Time (PT) Normal value: 10-14 seconds Prothrombin is a protein produced by the liver and is used in the clotting of blood Used to monitor clotting and Coumadin therapy An INR (International Normalized Ratio) is based on the PT. Measures clotting ability of fibrinogen and prothrombin When these clotting factors are decreased, the PT is prolonged Reported in seconds High PT means blood is thinner Reported along with a control value Not all labs reported results the same, now use INR in conjunction with PT PT and INR usually reported togetherMeasures clotting ability of fibrinogen and prothrombin When these clotting factors are decreased, the PT is prolonged Reported in seconds High PT means blood is thinner Reported along with a control value Not all labs reported results the same, now use INR in conjunction with PT PT and INR usually reported together

107. International Normalized Ratio (INR) This is the ratio of a patient’s PT to normalized PT. The results can be consistently replicated from one lab to the next. Normal INR = 1 Most anticoagulation ( chronic A-Fib) INR=2-3 Valvular replacement or cardiovascular prosthesis, DVT therapy: INR=3-4

108. PTT/APTT (Activated Partial Thromboplastin Time) Normal APTT: 30--45 seconds Used to monitor Heparin therapy Values should be 1.5-2 times normal for anticoagulation

109. B type Natriuretic Peptide (BNP) <100pg/ml = Normal Brain Natriuretic Peptide (Cardiac) Increases in CHF Related to reduction in Na= ions, the body’s attempt to control fluid overload in the lungs BNP = Brain Natriuretic peptide Misnomer, highest level does not exist in the brain, but in cardiac ventricular muscle These peptides oppose the renin-angiotensin system. BNP are secreted when there is a stretch in the atrial or ventricular muscles Corresponds to left ventricular pressure Very good for diagnosing CHF If BNP level is elevated, the SOB is caused by CHF If BNP is normal, SOB is pulmonary BNP can be elevated with acute MI, and prolonged systemic HTN BNP <100 pg/ml BNP = Brain Natriuretic peptide Misnomer, highest level does not exist in the brain, but in cardiac ventricular muscle These peptides oppose the renin-angiotensin system. BNP are secreted when there is a stretch in the atrial or ventricular muscles Corresponds to left ventricular pressure Very good for diagnosing CHF If BNP level is elevated, the SOB is caused by CHF If BNP is normal, SOB is pulmonary BNP can be elevated with acute MI, and prolonged systemic HTN BNP <100 pg/ml

110. Other Labs BUN ( may be decreased in CHF), Creatinine interpreted in conjuction with BUN (10/1 approx) Serum Potassium <3.5 or >5.0 critical values Serum Magnesium 1.3-2.1 CRP C Reactive Protein CRP= Dx: Abnormal protein produced by the liver during an acute inflammatory process Positive test indicates the presence of inflammatory disease but not the cause May be diagnostic of: bacterial infectious disease Inflammatory diseases Will be elevated when CK-MB levels are elevated Peaks occur 1-3 days later CRP= Dx: Abnormal protein produced by the liver during an acute inflammatory process Positive test indicates the presence of inflammatory disease but not the cause May be diagnostic of: bacterial infectious disease Inflammatory diseases Will be elevated when CK-MB levels are elevated Peaks occur 1-3 days later

111. Other Diagnostics Re CXR ECG Holter Monitor Stress Test Echocardiogram TEE Cardiac Catheterization EPS Refer to Table 32-7 (7th ed) Review this for complete understanding of diagnostics Refer to Table 32-7 (7th ed) Review this for complete understanding of diagnostics

112. CHEST X-RAY (CXR) A CXR can be used to assess the size, shape, and position of the heart. Calcification of great vessels Pericardial effusion Placement of central lines Pleural effusion, CHF Wonderful, all around good diagnostic tool Obtain CXR to confirm placement prior to using a central line whether it is a PA catheter or a triple-lumenWonderful, all around good diagnostic tool Obtain CXR to confirm placement prior to using a central line whether it is a PA catheter or a triple-lumen

113. CXR showing a pericardial effusion Pericardial effusion = fluid that accumulates between the visceral and parietal pericardium (the two layers of the pericardial sac CXR showing a pericardial effusion Pericardial effusion = fluid that accumulates between the visceral and parietal pericardium (the two layers of the pericardial sac

114. Electrocardiogram (EKG/ECG) Noninvasive, painless Telemetry or 12 lead Can identify arrhythmias Different leads can assist in detection of location of MI

115. Holter Monitor 24 hour to 30 day monitoring of EKG Inform patient to keep a daily diary of activity and/or chest pain Do not shower or remove monitor

116. Stress Test Goal=_________________ Exercise or Pharmacologic Adenosine, Dobutamine, Persantine With or without Nuclear Imaging using Radioisotopes: Thallium, Cardiolite, Myoview Consent Typically NPO Check about administration of cardiac meds and caffeine Monitor for chest pain & ECG changes – may indicate ischemia ST Segment Depression Goal = Exercise to peak HR (220-age) or peak tolerance. Terminated for significant ?? in B/P, severe chest discomfort, or ECG changes Most hospitalized patients no longer walk on the treadmill Medications given to simulate exercise, heart response evaluated A nuclear scan involves the use of a tracer uptake that helps differentiate normal muscle (which receives more of the tracer) from the reduced uptake demonstrated by muscle that is supplied by a narrowed coronary artery. In other words, areas of the heart that have adequate blood flow quickly picks up the tracer material. In contrast, muscle with reduced blood flow pick up the tracer slowly or not at all. Analysis of the images of the heart (taken by a scanning camera) can help identify the location, severity and extent of reduced blood flow to the heart (Abdulla, 2006). Typically requires several scans of the patient’s heart to be done. Check policy regarding no caffeine for 12 hours, beta blocker meds, nitrates (nitro paste) May need to be held to keep from altering results of the test APA Reference: Abdulla, A. (2006). Isotope stress test. Retrieved January 12, 2007 from www.Heartsite.com/html/isotope_stress.html Goal = Exercise to peak HR (220-age) or peak tolerance. Terminated for significant ?? in B/P, severe chest discomfort, or ECG changes Most hospitalized patients no longer walk on the treadmill Medications given to simulate exercise, heart response evaluated A nuclear scan involves the use of a tracer uptake that helps differentiate normal muscle (which receives more of the tracer) from the reduced uptake demonstrated by muscle that is supplied by a narrowed coronary artery. In other words, areas of the heart that have adequate blood flow quickly picks up the tracer material. In contrast, muscle with reduced blood flow pick up the tracer slowly or not at all. Analysis of the images of the heart (taken by a scanning camera) can help identify the location, severity and extent of reduced blood flow to the heart (Abdulla, 2006). Typically requires several scans of the patient’s heart to be done. Check policy regarding no caffeine for 12 hours, beta blocker meds, nitrates (nitro paste) May need to be held to keep from altering results of the test APA Reference: Abdulla, A. (2006). Isotope stress test. Retrieved January 12, 2007 from www.Heartsite.com/html/isotope_stress.html

117. Echocardiography Noninvasive Painless Used to assess structure of heart, especially valves

118. Echocardiography

119. Trans-esophageal Echocardiography (TEE) Patient usually NPO Consent required Transducer placed in esophagus to assess structure of heart Assess post procedure: Gag reflex Possible complications: Esophageal perforation, Vaso-vagal response, arrhythmias, Hypoxia Evaluates heart size, wall motion, valve abnormalities More precise than the echoEvaluates heart size, wall motion, valve abnormalities More precise than the echo

120. TEE

121. Cardiac Catheterization Angiography of coronary arteries http://www.heartsite.com/html/cardiac_cath.htmlows blockages Shows actual footage of procedure Should know if patient has good renal function prior to administration of dye Look at BUN and Creatnine, depending on levels depends on how cardiologist will proceed. May use minimal amount of dye Change fluid concentrationShould know if patient has good renal function prior to administration of dye Look at BUN and Creatnine, depending on levels depends on how cardiologist will proceed. May use minimal amount of dye Change fluid concentration

122. Cardiac Catheterization Invasive procedure Diagnostic or Interventional Right or Left Heart Cath Measures intracardiac pressures and oxygen levels Dye is injected – causes a “flush” feeling Chambers, vessels and blood flow Are visualized Diagnostic – evaluate only, no intervention is done Cardiologists are credentialed to perform either diagnostic only or interventional This may be why, a patient has two cardiac caths within a few days If during the diagnostic portion it is determined that the patient needs a stent, it can only be performed by cardiologist who is credentialed and in a facility that offers Open Heart Surgery as a back up This should be eliminated with Vero and Martin getting Open Heart Interventional – PTCA/Stent Left heart cath – most common Catheter inserted in the femoral artery (typically the right side) Brachial artery can also be used Catheter is advanced through the aorta, left atrium and into the left ventricle Right heart cath Catheter inserted in the femoral vein (typically right side) Advanced into the Vena Cava, right atrium and right ventricle & PAWP Assess for allergies to dye, shellfish, patient will probably be given benedryl and solumedrol prior to and possibly after the procedureDiagnostic – evaluate only, no intervention is done Cardiologists are credentialed to perform either diagnostic only or interventional This may be why, a patient has two cardiac caths within a few days If during the diagnostic portion it is determined that the patient needs a stent, it can only be performed by cardiologist who is credentialed and in a facility that offers Open Heart Surgery as a back up This should be eliminated with Vero and Martin getting Open Heart Interventional – PTCA/Stent Left heart cath – most common Catheter inserted in the femoral artery (typically the right side) Brachial artery can also be used Catheter is advanced through the aorta, left atrium and into the left ventricle Right heart cath Catheter inserted in the femoral vein (typically right side) Advanced into the Vena Cava, right atrium and right ventricle & PAWP Assess for allergies to dye, shellfish, patient will probably be given benedryl and solumedrol prior to and possibly after the procedure

123. Cardiac Catheterization ( Pre cath) Consent Usually NPO after Midnight Check for allergy to iodine Preprocedure checklist and meds Plavix, ASA, Coumadin, Heparin Check re: holding or D/C prior to test Prep patient if ordered VS , Assess pedal pulses and document Check BUN & Creatnine Levels renal insufficiency or failure R/T: Dye Mucomyst given PO prior to & after procedure Check hospital/ MD policy regarding meds that need to be held prior to procedure Diagnostic of cardiovascular disease 2 Types Diagnostic Interventional (PTCA/Stent) Percutaneous Transluminal Coronary Angioplasty (previously just called angioplasty) Also can determine Ejection Fraction = % of blood ejected from the L. Ventricle during systole Normal = 60%-70% Versus Stroke Volume = amount of blood ejected by L. Ventricle at each heart beat (systole + diastole) Versus Cardiac Output = amount of blood ejected from the ventricle in 1 minuteCheck hospital/ MD policy regarding meds that need to be held prior to procedure Diagnostic of cardiovascular disease 2 Types Diagnostic Interventional (PTCA/Stent) Percutaneous Transluminal Coronary Angioplasty (previously just called angioplasty) Also can determine Ejection Fraction = % of blood ejected from the L. Ventricle during systole Normal = 60%-70% Versus Stroke Volume = amount of blood ejected by L. Ventricle at each heart beat (systole + diastole) Versus Cardiac Output = amount of blood ejected from the ventricle in 1 minute

124. Post Cardiac Cath Bed Rest Monitor Vital Signs closely Monitor groin (or site) for bleeding and hematoma Might have a sandbag in place Monitor pedal pulse, color and temperature of leg Assess for arrhythmia's or S/S of clots = pulmonary embolus MI Stroke Acute PAD in affected leg Watch for site infections from closure devises (teach patients S&S of infection) Medication required post procedure and daily - Plavix - Platelet Aggregation Inhibitor ASA – Anti Thrombetic Watch for site infections from closure devises (teach patients S&S of infection) Medication required post procedure and daily - Plavix - Platelet Aggregation Inhibitor ASA – Anti Thrombetic

125. Electrophysiology Study (EPS) Electrodes placed inside the heart chambers Evaluates : SA node, AV node, Ventricular function Used to determine the source of arrhythmias Pts. w/ Hx of V Tach, or symptomatic SVT