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Chapter 17: Patient Assessment: Cardiovascular System Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Assessment of Jugular Venous Pressure Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Assessment of Point of Maximal Intensity Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Areas of Auscultation Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Which statement about pulsus paradoxus >10 mm Hg is correct? A. The pulse disappears during expiration and reappears during inspiration. B. The pulse disappears during inspiration and reappears during expiration. C. It is found in a patient with left ventricular failure. D. It is a normal finding caused by breathing. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer B. The pulse disappears during inspiration and reappears during expiration. Rationale: Pulsus paradoxus is an abnormal finding when it is >10 mm Hg, and it is found in patients with COPD or cardiac tamponade. Answer B is the correct definition of pulsus paradoxus. Answers A and D are incorrect. Answer C describes pulsus alternans. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Heart Sounds and Timing in Cardiac Cycle Heart Sound Timing of Cardiac Cycle Mechanism S1 Isovolumetric contraction Closure of mitral, tricuspid valves S2 Isovolumetric relaxation Closure of aortic, pulmonic valves S3 Early ventricular filling Past 35 years of age, seen with ventricular dilation. Systolic heart failure. S4 Atrial contraction Seen with stiff noncompliant ventricle - ventricular hypertrophy Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Where is the left ventricular S4 heard with the bell of a stethoscope? A. Apex B. Lower left sternal border C. Apex with the patient turned slightly to the left side D. Xiphoid Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer A. Apex Rationale: The left ventricular S4 is heard at the apex. The right ventricular S4 is heard at the left sternal border. The summation gallop is heard at the apex with the patient turned slightly to the left side. The right ventricular S3 is heard at the xiphoid or lower portion of the left sternal border. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins ECG Electrode Placement See Figure 17-13. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Dealing With Complications After Cardiac Diagnostic Procedures • Anticipate potential complications. • Keep emergency supplies close by. • Treat the patient first and the monitor/equipment afterwards. • Report and act on changes immediately. • Stay with the patient; call for help as needed. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Which of the following statements made by the client reflects adequate understanding about a thallium stress test? A. I can eat the morning of the test; eating won’t interfere with the test results. B. I can have a caffeinated drink several hours before the test. C. Thallium will not cause renal damage. D. I should take the full dose of my beta-blocker the morning of my test. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer C. Thallium will not cause renal damage. Rationale: Thallium is not nephrotoxic. The client should remain NPO for 4 to 6 hours because digestion would increase the amount of blood to the GI system; this could cause decreased blood supply to the coronary arteries, leading to incorrect results. Caffeine increases the heart rate; the patient would have to exercise for less time to reach the maximum heart rate, and the optimal test results may not be achieved. Beta-blockers should be held the day of the test because they interfere with the patient’s ability to reach exercise potential. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Waveforms of the ECG Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Configurations of the QRS Complex Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Calculating a Corrected QT Interval • Half of preceding R-R interval in seconds • QT interval depends on heart rate • Normal values – Men: not >0.42 seconds – Women: not >0.43 seconds Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Assessing the Rhythm Strip 1. Determine atrial (P-P) and ventricular (R-R) regularity. 2. Determine the atrial (P-P) and ventricular rate (R-R). – If regular, count number of large boxes between 2 consecutive P waves or 2 consecutive QRS complexes and divide by 300. – If irregular, count the number of complexes in 6 seconds and multiply by 10. 3. P waves: present, absent, all look alike or not, ratio of P waves to QRS complexes Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Assessing the Rhythm Strip (cont.) 4. Determine PR interval; normal is 0.12 to 0.20 sec • Does the interval vary? Is there a pattern? 5. Determine the QRS complex; normal is 0.06 to 0.11 sec • Do the complexes look the same? 6. Determine if the ST segment is isoelectric, elevated, or depressed. 7. Determine the corrected QT interval. 8. Is the patient stable or not stable? Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Sinus Rhythms Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Atrial Dysrhythmias Rhythm Etiology Manifestations Management PAC Stress, caffeine, tobacco, alcohol Early complex with P wave present with shorter PR interval No treatment needed PSVT Same as for PAC Often started after a PAC and ends abruptly (150 to 250 bpm) Vagal maneuvers; IV adenosine, cardioversion, or overdrive pacing, if prolonged Atrial flutter Underlying heart disease Sawtooth P waves; 2:1, 3:1, 4:1 (250 to 350 bpm) Consider ventricular response, how long in rhythm, potential for thromboembolism Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Atrial Dysrhythmias (cont.) Rhythm Etiology Manifestations Management Atrial fibrillation Usually underlying heart disease No definable P waves: fibrillatory waves Irregular: irregular pattern No PR interval Consider ventricular response, how long in rhythm, potential for thromboembolism Multifocal atrial tachycardia Severe pulmonary disease Rapid atrial tachycardia with 3 or more different-shaped P waves Treat underlying pulmonary disease and slow ventricular rate Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Junctional Dysrhythmias Rhythm Etiology Manifestations Management PJC Stress, caffeine, tobacco, alcohol, or post-MI Early complex with inverted P wave before, buried within, or after QRS. QRS is usually normal. No treatment needed Junctional rhythm Ischemic damage to SA node, digitalis toxicity, secondary to cardiac meds, hypoxia, hypokalemia P wave may be inverted and before QRS with PR <0.12 sec, or after QRS, or buried in QRS. QRS is normal. Treat underlying cause. Improve cardiac output. Treat if symptomatic with atropine, pacing. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Ventricular Dysrhythmias Rhythm Etiology Manifestations Management PVC Stress, hypokalemia, irritation to heart, heart disease Premature beat No P wave Wide, bizarre QRS with T wave in opposite direction No treatment needed; monitor Ventricular bigeminy Same as for PVC Each sinus beat is followed by PVC Treat any underlying cause Ventricular trigeminy Same as for PVC Two sinus beats are followed by PVC Treat any underlying cause R-on-T phenomenon Cardiac meds, pacemaker firing too close to vulnerable period Treat underlying cause. Treat dysrhythmia. PVC too close to T wave: ventricular repolarization (vulnerable period) - could cause V-fib Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Ventricular Dysrhythmias (cont.) Rhythm Etiology Manifestations Management Ventricular tachycardia MI, irritation to heart, hypokalemia No P wave (usually) Wide bizarre QRS Rate >100 ACLS guidelines Torsades de pointes (QRS polarity changes from positive to negative) Underlying heart disease with prolonged QT, hypothermia, cardiac meds No P wave Magnesium sulfate Wide bizarre IV, isoproterenol, polymorphous QRS overdrive pacing Rate >100 May change to VF or SR Ventricular fibrillation (VF) - coarse or fine MI or other factor that damages the heart Irregular oscillations ACLS guidelines, at baseline emergent No P wave defibrillation No recognizable QRS Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Accelerated Idioventricular Rhythm Rhythm Etiology Manifestations Management Accelerated idioventricular rhythm Acute MI, coronary reperfusion after thrombolytics, digitalis toxicity No P waves Wide bizarre QRS Regular ventricular rate (50 to 100) If because of digitalis toxicity, stop digoxin. If pt is hemodynamically stable, no treatment. If pt is not hemodynamically stable, treat with atropine or atrial pacing. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Heart Blocks Rhythm Etiology Manifestations First degree Drugs or cardiac PR >0.20 sec disease that QRS normal affects AV node No treatment; monitor Mobitz I Wenckebach Drugs or cardiac disease that affects AV node, inferior wall MI, myocarditis Stop med, if cause; no treatment; monitor P waves present Pattern with PR interval progressively lengthens until a QRS is dropped Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Management Heart Blocks (cont.) Rhythm Etiology Manifestations Management Mobitz II Drugs or cardiac disease that affects AV node; acute anterior wall MI Fixed PR interval during AV conduction and nonconducted P wave when block present (2:1, 3:1,4:1) P-P regular May see bundle branch block If pt has symptoms: atropine, pacing If asymptomatic : monitor (could become third degree) Third degree (complete) Cardiac disease that affects AV node P waves present; P-P regular Pacing QRS present; R-R regular No relationship between P and QRS QRS narrow - junctional escape QRS wide - ventricular escape Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Indwelling Arterial Catheter Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Pulmonary Artery Catheter See Figure 17-53. Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Arterial Pressure Waveform Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Normal Pulmonary Artery Waveforms Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Normal Values and Wave Configurations as a Pulmonary Artery Catheter Is Inserted Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nursing Considerations When Assessing Hemodynamic Parameters • Note marking of catheter at insertion site – A black line is 10 cm – A heavy black line is at 50 cm and 110 cm • Maintain consistent leveling, zeroing, and measurement techniques • Perform parameters at end-expiration • Note if it takes less than 1.25 to 1.5 mL of air to wedge • Set alarms and troubleshoot accordingly Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Obtaining Pulmonary Wedge Pressure With Mechanical Ventilation Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Nursing Considerations With Continuous Mixed Venous Monitoring • Enhance O2 delivery – Mechanical ventilator settings at optimum – Positioning and chest physiotherapy – Deep-breathing exercises and coughing – Administer PRBCs • Decrease O2 demand – Use monitor to guide activities Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins