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Toni Standley RN ANP MSN Porter Adventist Hospital

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1 Toni Standley RN ANP MSN Porter Adventist Hospital
Cardiac Assessment Toni Standley RN ANP MSN Porter Adventist Hospital

2

3 Cardiovascular Assessment
Obtaining health history Physical exam Assessment of patient’s heart and vascular system

4 Obtaining a Health History
Introduce yourself Chief complaint Cardiac risks Other ailments Personal and family history

5 Chest Pain Assessment another side story
Description Location Duration Radiation Pain scale Intensity

6

7 Chest Pain Assessment cont.
Associated Symptoms Precipitating Factors Alleviating Factors

8

9 BIOSITE SPEAKERS BUREAU
Heart Failure Defined “The situation when the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return.” Heart failure occurs when the heart has progressive changes related to a declining pumping ability and this results in not enough blood to meet the metabolic demands of the body. The classic term “congestive heart failure” doesn’t apply to many patients because systemic and pulmonary congestion aren’t always present. The disturbance of the heart’s pumping function results in HF where fluids accumulate in the blood vessels of organs, causing congestion. Impaired ventricular function can be systolic or diastolic. Systolic: More common in patients due to the contractility of the ventricular muscles becomes less than adequate. The LV can’t adequately contract or squeeze out it’s contents. Acute causes myocardial infarction Gradual causes  cardiomyopathy. Usually caused by ischemic or idiopathic dilated cardiomyopathy. See an increase in preload and decrease in stroke volume. Diastolic: Occurs in up to 40% of HF patients, and occurs when the relaxation, or diastolic function is impaired due to a ventricular filling defect. Usually caused by hypertensive, hypertrophic, or restrictive cardiomyopathy. Ventricular relaxation and filling during diastole are impaired. Pressures in the atria and pulmonary vessels increase to cause pulmonary congestion and stroke volume decreases. Systolic and Diastolic: May see patients with both types, which an extremely low ejection fraction and high pulmonary vascular pressures are seen. Right sided: RV can’t empty or blood backs up into it from the pulmonary circulation, and so insufficient blood is pumped (ineffective right ventricular contractile function). Causes: Chronic obstructive pulmonary disease, left-sided failure, or acute respiratory distress syndrome. Left sided: LV stroke volume is reduced, so blood backs up into the left side of the heart and the pulmonary circulation to increase pulmonary pressures. LV contractile function is impaired. This leads to dyspnea and paroxysmal nocturnal dyspnea due to congestion in lungs from fluid overload. Causes: Hypertension, incompetent or stenotic left-sided heart valves, or ischemia. R and L HF may coexist and either cases results in blood backing up into the systemic circulation to cause liver congestion and peripheral edema. Patients that ambulate you will see edema in the ankles and feet, and bed ridden patients you will see it in the sacral area. E. Braunwald SLIDE SET UPDATE 9

10 Congestive Heart Failure assessment
Weight Gain Difficulty Breathing PND Swelling Medication Compliance Diet/Salt Intake Oxygen Use

11 This is just another pictorial for ventricular remodeling.
11

12 BNP Relationship to NYHA Objective Vs. Subjective Evaluation
BIOSITE SPEAKERS BUREAU BNP Relationship to NYHA Objective Vs. Subjective Evaluation Triage BNP package insert. SLIDE SET UPDATE 12

13 Cardiac Risks a side story
Hypertension Hyperlipidemia Diabetes Smoking Obesity Age Family history

14 MEDICATIONS - A side story
Beta Blockers Aspirin Ace Inhibitors/ ARBS Diuretics Statins Calcium channel blockers Plavix Antiarrythmics/Digoxin

15 PERSONAL AND FAMILY HISTORY - A side story
Married? Children? Occupation? Activities? Living arrangements? Caffeine intake? ETOH intake? Family medical history?

16 Performing a Physical Assessment
Consistent, Methodical Approach Regular Practice Stethoscope with a Bell and Diaphragm Appropriate size blood pressure cuff

17 Performing a Physical Assessment
Consistent, Methodical Approach Vital signs EKG Lab values Previous/recent tests – treadmills, cardiac catherizations, by-pass surgery, previous hospitalizations.

18 Assessing the Heart pay attention!
Inspection: Overly thin? Obese? Alert? Anxious? Inspect patient’s precordium: Pulsations? Symmetry of Movement? Retractions or Heaves?

19 Assessing the Heart continues…
Palpation with the Heart: Gentle Touch Find Apical Pulse; associated with first heart sound and carotid pulsation Heaves Thrills Fine Vibrations; purring of the cat

20 Assessing the Heart continues…
Percussion Begin Anterior Axillary Line Continue toward Sternum along the 5th Intercostal Space Dullness over Midclavicular Line; left border of the heart Difficult in Obese and Female patients

21 Assessing the Heart continues…
Auscultation Methodical Approach and Lots of Practice Auscultate over the 4 Cardiac Valves Use Bell for Low Pitch Sounds and Diaphragm for High Pitch Sounds Listen with Patient in 3 Positions; on back with HOB, 30 to 45 degrees, sitting up and lying on left side

22 Heart Sounds Anatomy

23 Assessing the Heart continues…
Auscultation continues… Basic Heart Sound S1 Heard at the beginning of Systole Closure of Mitral and Tricuspid Valves

24 Assessing the Heart continues…
Auscultation continues… Basic Heart Sound S1 Heard at the beginning of Systole Closure of Mitral and Tricuspid Valves

25 Assessing the Heart continues…
Auscultation continues… Basic Heart Sound S2 Heard at the End of Systole Closure of Pulmonic and Aortic Valves

26 Assessing the Heart continues…
Auscultation continues… Basic Heart Sound S2 Heard at the End of Systole Closure of Pulmonic and Aortic Valves

27 Assessing the Heart continues…
Auscultation continues… Abnormal Heart Sound S3 ; Ventricular Gallop Rhythm End of Diastole Immediately after S2 Heard Best: over Mitral Area with Bell

28 Assessing the Heart continues…
Auscultation continues… Abnormal Heart Sound S3 ; Ventricular Gallop Rhythm End of Diastole Immediately after S2 Heard Best: over Mitral Area with Bell

29 Assessing the Heart continues…
Auscultation continues… Abnormal Heart Sound S4 ; Summation Gallop Early in Diastole Precedes S1 Heard Best: over Mitral Area with Bell Associated with increased left Atrial Pressure caused by noncompliant LV; Hypertension, Cardiomyopathies and Ischemic Heart Disease

30 Assessing the Heart continues…
Auscultation continues… Abnormal Heart Sound S4 ; Summation Gallop Early in Diastole Precedes S1 Heard Best: over Mitral Area with Bell Associated with increased left Atrial Pressure caused by noncompliant LV; Hypertension, Cardiomyopathies and Ischemic Heart Disease

31 Assessing the Heart continues…
Auscultation continues… Aortic valvular stenosis murmer Heard best at 2nd right interspace Harsh rough quality with a cresendo-decresendo medium Heard best with the Diaphragm Radiates to the Carotid Arteries

32 Assessing the Heart continues…
Auscultation continues… Aortic valvular stenosis murmer Heard best at 2nd right interspace Harsh rough quality with a cresendo-decresendo medium Heard best with the Diaphragm Radiates to the Carotid Arteries

33 Assessing the Heart continues…
Auscultation continues… Mitral Insufficiency or Regurgitation Heard best at the Apex or Mitral Area High Pitched Blowing Quality Murmur Radiates toward the Axilla Heard best with the Diaphragm

34 Assessing the Heart continues…
Auscultation continues… Mitral Insufficiency or Regurgitation Heard best at the Apex or Mitral Area High Pitched Blowing Quality Murmur Radiates toward the Axilla Heard best with the Diaphragm

35 Assessing the Heart continues…
Auscultation continues… Aortic Insufficiency Heard best at the 3rd left Interspace High Pitched Blowing Sound Radiates toward the Sternum Heard best with the Diaphragm

36 Assessing the Heart continues…
Auscultation continues… Aortic Insufficiency Heard best at the 3rd left Interspace High Pitched Blowing Sound Radiates toward the Sternum Heard best with the Diaphragm

37 Assessing the Vascular System
Inspection Similar to cardiac System Inspect the Skin; Lesions, scars, clubbing, and edema of the extremities Inspect the Neck; carotid artery, jugular veins JVD; Patient on back with HOB 30 to 45 degrees

38 Assessing the Vascular System cont.
Palpitation Patient skin; capillary refill, temperature, texture and turgor Arms and Legs; temperature and edema 1 to 4 plus Arterial pulses; carotid, radial, femoral, popliteal, posterior tibial and dorsalis pedis Grade pulses; 1+ (weak) to 4+ (bounding)

39 Assessing the Vascular System cont.
Auscultation Use the Bell Listen over each artery; hum or bruit Assess Upper abdomen for abnormal pulsation; possible abdominal aortic aneurysm Femoral and popliteal pulses; checking for bruit and other abnormal sounds

40 Upon Diagnosis… Assessment: - Angina? - Myocardial Infarction or ACS
- Decompensated CHF - Pericarditis - Atrial Fibrillation or other arrythmias - Valvular Heart disease or endocarditis

41 Upon Diagnosis..

42 In conclusion… Plan: - Telemetry: (LifePak)
- Labs: Troponins, BNP, electrolytes, lipids: - Treadmill tests: Nuclear, stress echo - Echocardiograms: - Cardiac catherization - Medication adjustments - Diet – I/O – Daily weights

43 B-TYPE NATRIURETIC PEPTIDE (BNP)
BIOSITE SPEAKERS BUREAU B-TYPE NATRIURETIC PEPTIDE (BNP) B-Type Natriuretic Peptide (BNP) is a cardiac neurohormone specifically secreted from the cardiac ventricles as a response to: ventricular volume expansion pressure overload resultant increased wall tension1 FDA cleared the first BNP test for use as a diagnostic aid in 2000 BNP or B-type Natriuretic Peptide is part of a family of counter-regulatory hormones to the renin-angiotensin aldosterone system. BNP works by counter-regulating undue ventricular stretch, and this is the stimulus for it’s release into blood. The stretch is caused by blood volume expansion in the ventricle or increased wall tension. This release mechanism suggests that measuring BNP in blood may correlate with patients who are suffering from heart failure. In late 2000, the FDA cleared BNP testing for use as an aid in the diagnosis of heart failure. 1. Burnett JC, J Hypertens 2000 SLIDE SET UPDATE 43

44 BNP Function Found primarily in the cardiac ventricles
BIOSITE SPEAKERS BUREAU BNP Function Found primarily in the cardiac ventricles Is strongly induced during ventricular-wall tension or stretch Potent natriuretic, diuretic, and vasorelaxant peptide Inhibits sympathetic tone, renin- angiotensin axis, and synthesis of vasoconstrictor molecules The natriuretic peptide system and the RAA system oppose each other. When cardiac volume increases and pressure increases in heart failure, the ventricles also release BNP, causing the levels of the peptide to increase in the blood. BNP increases the sodium urinary excretion and increases GFR. It also helps to decrease peripheral vascular resistance and reduces blood pressure. RAAS: renin-angiotensin-aldosterone system SNS: Sympathetic nervous system Listed here are the four common natriuretic peptides. All have a 17-amino acid (AA) ring structure with 11 identical AA’s. This ring structure is essential for receptor binding (granulate cyclase linked receptor). ANP, BNP & CNP affect vascular tone by dilation of the blood vessels. Additionally, ANP & BNP inhibit the release of rennin, aldosterone, and vasopressin (natriuretic activity). In a healthy person, only the atrial myocardium produces ANP and BNP. When the cardiac volume and pressure increase in HF, the ventricles also produce both peptides, causing the levels of ANP & BNP to increase in blood. In asymptomatic patients with LV dysfunction, increases in cardiac volume and pressure activate the ANP to maintain sodium and water balance and to inhibit the RAA system. In severe HF, sodium ions are retained, the RAA system is activated, and the blood levels of both ANP & BNP rise, with BNP surpassing the ANP levels. Atrial Natriuretic Peptide (ANP), is cleaved into the C-terminal piece and it consists of a 28-amino acid hormone produced primarily in the atrium of the heart. ANP is increased with atrial wall tension, reflecting increased intravascular volume. Origin is atria and the stimulus for release is atrial distension. Several hormones (arginine vasopressin, catecholamines) can stimulate ANP secretion. ANP is stored in granules within atrial cardiomyocytes. ANP increases rapidly with exercise. Brain-type Natriuretic Peptide (BNP), The BNP prohormone is cleaved into 2 pieces. The N-terminal portion is called N-terminal proBNP and consists of 76 amino acids. Physiological function of N-terminal proBNP is unknown. The C-terminal portion consists of 32 amino acids and is the physiologically active form of the hormone. The Triage BNP measures the C-terminal. BNP has been found to be a more useful marker for congestive heart failure because the hormone is elevated in patients with CHF. BNP is not stored in granules but is secreted from the ventricles of the heart in response to ventricular stretch and volume overload. C-type Natriuretic Peptide (CNP) is a peptide formed in the endothelium of the heart. Stimulus is endothelial stress for release. CNP has a very low concentration in plasma, and is not elevated in CHF. Though lacking natriuretic activity, CNP dilates blood vessels, helping to lower BP. Urodilatin another member of the natriuretic peptide family is still being identified and characterized. This family of hormonally active peptides have a regulatory role in cardiovascular disease. D-type Natriuretic Peptide (DNP) Is a peptide that has been found to also be present in the green mambo snake’s venom. More research needs to be done on the role of DNP. Maisel et, al Reviews in Cardiovascular Medicine 2003 SLIDE SET UPDATE 44

45 Heart Failure Pathophysiology
BIOSITE SPEAKERS BUREAU Heart Failure Pathophysiology Myocardial injury Fall in LV performance Activation of RAAS, SNS, ET, AVP, and others BNP Peripheral vasoconstriction Hemodynamic alterations Myocardial toxicity LV dysfunction begins with some injury to the myocardium and is usually a progressive process, even in the absence of a new identifiable insult to the myocardium. Remodeling, which occurs in association with hemostatic attempts to decrease ventricular wall stress through increasing wall thickness, generally precedes the development of symptoms--by months or even years. The process continues after the appearance of symptoms and may contribute importantly to worsening of symptoms despite treatment. LV function can be evaluated by knowing the ejection fraction (EF) which is the ratio of the SV per beat to the left ventricular end-diastolic volume. The EF normally exceeds 50%, if less, the ventricle is dysfunctional. HF usually begins with LV dysfunction (LV pumps insufficient blood to the systemic circulation). This can cause congestion back through the pulmonary circulation to the right side of the heart. Systolic dysfunction is the failure of the ventricle to eject efficiently with a typical ejection fraction of < 40% & may coexist with diastolic dysfunction. Diastolic dysfunction (preserved systolic function) is due to restricted filling of the ventricle during diastole & is due to decreased compliance of the ventricular myocardium. Normal EF makes diastolic HF difficult to detect. An estimated 35% of the HF population have diastolic dysfunction. Definitions: RAAS – renin angiotensin aldosterone system SNS – sympathetic nervous system ET – endothelin AVP – Arginine vasopressin (hormone causes walls of arteries to constrict) Others – Aldosterone –steroid hormone promotes retention of bicarb & Sodium ions, & water Cytokines – a protein secreted by cells involved in immunity; interferon & interleukins are examples Prostaglandin – hormone-like substance derived from amino acids in response to certain physiologic occurrences, and which generate a certain tissue response, such as vasodilation or decreased glomerular filtration rate. Prostaglandin synthesis by blood vessels counteracts the vasoconstriction associated with HF. Remodeling and progressive worsening of LV function Morbidity and mortality Heart failure symptoms SLIDE SET UPDATE 45

46 BIOSITE SPEAKERS BUREAU
The Natriuretic Peptide System is Overwhelmed in Acute Decompensated Heart Failure ANP BNP Endothelin Aldosterone Angiotensin II Epinephrine Adapted from Burnett JC, J Hypertens 1999 SLIDE SET UPDATE 46

47 Documentation of the Cardiovascular Assessment
AMI COR Measures ACE/ARB contraindicated or for LVSD ASA on arrival or Contraindicated and on Discharge Beta Blocker on Admission and Discharge and if Contraindicated LDL Assessment Lipid Lowering Medication and/or if Contraindicated Smoking Cessation or N/A

48 Documentation of the Cardiovascular Assessment
CHF Core Measures ACE/ARB Contraindicated ACE/ARB if EF <40% Discharge Instruction LVF Smoking Cessation or N/A

49 The End


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