Assessment of Cardiovascular Function Part 2

JNC Medical Management: ► Achieve and maintain arterial BP at 140/90 mm Hg or lower  130/80 mm Hg for people with DM or CKD Pharmacologic Management: ► Uncomplicated HTN  Diuretics, beta blockers or both à “beta blockers are NOT the first-line” ► Promote adherence  Prescribe simplest treatment schedule  Ideally one pill/day ► Diuretics  Thiazide diuretics  Loop diuretics  Potassium-sparing diuretics  Aldosterone receptor blockers ► Central Alpha-2 Agonists  Reserpine  Methyldopa  Clonidine ► Beta blockers  Atenolol  Metoprolol  Propranolol – also used for someone with migraines (and BP) ► Vasodilators  Hydralazine  Nitroglycerin  Minoxidil ► ACE Inhibitors – concerned w/ hypokalemia and they develop cough down the line  Captopril  Enalapril  Lisinopril ► Angiotensin II Receptor Blockers (ARB)  Losartan  Valsartan ► Calcium Channel Blockers  Diltiazem  Verapamil  Norvasc  Clevidipine ► Direct Renin Inhibitors  Tekturna NURSING PROCESS ► Assessment  Measuring BP (Chart 31-2; p. 866) ► Nursing Diagnosis  Knowledge deficit regarding the relation of the treatment regimen and control of the disease process  Noncompliance with therapeutic regimen related to side effects of prescribed therapy ► Collaborative Problems/Complications  LVH  AMI/Heart failure  CVA/TIA  CKD ► Nursing Interventions  Increasing knowledge  Promoting adherence to therapy  Promoting home and community based care ► Evaluation  Maintains adequate tissue perfusion  Adheres to self-care program  Has no complications Look in the patients eyes –the pt can become blind.. Apical pulse – 5th ICS mid clavicular Retina – look at labs CMP glucose Beta blockers masks hypoglycemia – b/c they function by decreasing the pt HR so sometimes if pt is HTN and diabetic – Beta blockers DROP your HR – but if also someone who’s diabetic getting insulin .. If someone is on a beta blocker and they start becoming diaphoretic check the blood sugar… may be masking HYPOGLYCEMIA! Hypertensive Crisis Classification Hypertensive Emergency ► Clinical dysfunction of target organ ► Extremely elevated BP  HTN of pregnancy  AMI  Dissecting Aortic Aneurysm  Intracranial hemorrhage ► Goal  reduce BP by 20-25% within first hour of treatment (160/100 mm HG) ► IV vasodilators Hypertensive Urgency ► Elevated BP but no evidence of progressive target organ damage ► HA, epistaxis, anxiety ► PO agents with goal of normalizing BP in 24-48 hours CHAPTER 26: DYSHYTHMIAS Unstable Patient? Use “CASH” C-hest pain A-ltered mental status S-hortness of breath or skin color change H-ypotensive -systolic is less than 90 DYSRYTHMIAS  Disorder of the formation or conduction of the electrical impulse within the heart  Irregularity causes disturbances in:  Heart Rate  Heart Rhythm  Both  Causes changes in Hemodynamic effects  Diagnosed by analyzing the electrocardiogram  Named according to site of origin  TX depends on the frequency and severity of the symptoms What is the first sign of decreased CO=decreased LOC then decrease BP If SA node fails then AV node takes over…when they both fail then perkinjes takes over (20-30 bpm) **Electrical Stimulation: Depolarization **Mechanical Stimulation: Systole (contraction) *Electrical Relaxation: Repolarization *Mechanical Relaxation: Diastole “decrease in CO r/t something that is going on with the patient’s heart mechanically, we will see a decrease in the PEDAL PULSES” THE ELECTROCARDIOGRAM (ECG)  EKG/ECG is a graph tracing of the electrical activity of the heart  Not the mechanical activity!  Information obtainable from an EKG rhythm strip analysis:  Heart rate? Yes  Rhythm/regularity? Yes  Impulse conduction time intervals? Yes  Pumping action? No  Blood pressure? No  Cardiac Output? No  What else does the EKG reflect?  Ischemia  Infarction  Electrolyte disturbances  Drug toxicity  Enlarged cardiac chambers  Pericarditis  Enlarged cardiac chambers      P wave: an indication of the atrial function QRS: ventricular depolarization T: repolarization PR: beginning of P wave to QR complex-represents SA node to AV node ST: early ventricular repolarization Normal sinus rhythm = occurs when the electrical impulse starts at a regular rate and rhythm and in the SA node and travels trhough the normal conduction pathway. normal sinus rhythm characteristics** - Ventricular and atrial rate = 60-100 - Ventricular and atrial rhythm = regular - QRS shape and duration = usually normal, but may be regularly abnormal - P wave = normal and consistent shape; always in front of the QRS - PR interval = consistent interval b/w 0.12 and 0.20 seconds - P:QRS ratio = 1:1 P WAVE:  Represents the electrical impulse starting in the SA node and spreading through the atria  Atrial muscle depolarization  <0.11 seconds in length QRS COMPLEX:  Represents ventricular muscle depolarization  1st negative deflection: Q wave  1st positive deflection: R wave  1st negative deflection after the R wave:  S wave  <0.12 seconds in length T WAVE:  Represents ventricular muscle repolarization  Resting phase  Follows the QRS complex PR INTERVAL:  Measured from the beginning of the P wave to the beginning of the QRS complex  Represents time needed for sinus node stimulation, atrial depolarization and conduction through the AV node  0.12-0.20 seconds in length ST SEGMENT:  Represents early ventricular repolarization  Lasts from the end of the QRS complex to the beginning of the T wave  Normally isoelectric  Analyzed above or below the baseline TIME IS MEASURED ON THE HORIZONTAL LINE VOLTAGE IS MEASURED ON THE VERTICAL LINE FIVE STEP APPROACH FOR EKG INTERPRETATION:  Step 1: Heart rate  Step 2: Heart rhythm/regularity  Step 3: P wave  Step 4: PR interval  Step 5: QRS complex  At completion; evaluate the overall appearance (P to P determines atrial rate (not gunna do this) (R to R determines ventricular rhythm) Determining HR from the ECG: - A 1-minute strip contains 300 large boxes and 1500 small boxes - Count the # of small boxes within an RR interval and divide 1500 by that number - Ex. if there are 10 small boxes between the two R waves, the HR is 1500/10 = 150 bpm Sinus Brady When SA creates impulse to AV at a slower rate than normal Less than 60 Usually due to hypoxemia Everything looks normal just more spread apart Causes → basically everything that causes slow HR (Sleeping, Meds, Hypothyroidism, Inc. ICP, etc) Can be result of vagal stimulation from defecation or vomiting In terms of assessment o 1st stimulate pt. o Ask questions, are you dizzy etc S/S o SOB o Decreased LOC o Angina o Hypotension o ST segment changes, PVC’s Medical management o Find cause o Treat symptoms o 0.5 mg Atropine every 3-5 mins (cus it blocks vagal stimulation) → max dose of 3 mg Sinus Tachy SA node creates impulse to AV node at a faster than normal rate HR of 100-160 S/S o Reduces CO cus of decreased filling time o Syncope o Hypotension Caused by: o Things that increase HR o Fever, exercise, hypovolemia, anxiety, stimulants, pain, infection, MI, CHF Medical Management o Abolish cause 1st !‼ o Cardioversion (either with med or shock) o Beta blockers/ Ca channel blockers, Lopressor o Increased fluid/ Na Atrial Flutter “saw tooth” Conduction problem in the atrium, rapid atrial depolarization Creates atrial rate between 250-400 bpm and ventricular rate of 75-150 bpm o HR>100 “uncontrolled” o HR > 150 “rapid ventricular rate” Not all atrial impulses are conducted to ventricle bc of therapeutic block (would cause v-fib if not blocked) P wave looks like saw toothed (F waves) Usually occurs in patients o COPD o Hypoxia o MI o Pulomary HTN o Valvular disease o Thrytoxicosis o Following open heart sx Manifestations o Chest pain o Dyspnea o Hypotension o Diaphoresis Management o Unstable  Cardioversion o Stable  Vagal manuvers  Adenosine → causes sympathetic block(pushed rapidly, if HR doesn’t go down give larger dose)  Beta blockers, Ca Channel blockers, Digitalis, Cardizam  Antithrombotic  Ablation is long term tx Atrial Fibrillation Rapid, disorganized, uncoordinated atrial muscle Ventricular rate 120-200 bpm Reduced diastole filling time reduces coronary artery perfusion leading to ischemia Causes o Any heart related process o Electrolyte imbalance o S/p heart surgery o ETOH o Excessive caffeine o Rheumatic o Valve disease very common Clinical Manifestations: o Palpitations o Fatigue o Malaise o SOB o Exercise intolerance o Chest pain o Pulmonary Causes loss of AV synchrony (atria and ventricles contract at diff times) → palpitations Pulse deficit → numeric difference between apical and radial Stagnant blood → at risk or for thrombi Management o Determine stability CASH alerted mental status, shortness of breath, o If stable:  Adenosine, Digoxin, Ca blockers, Beta blockers, Amioderone o If unstable  Cardioversion must be initiated within 48 hours to avoid blood clots  Avoid cardioversion if more than 48 hours because pt. needs Coumadin at this point. Must be on Coumadin for 3-4 weeks before cardioversion → so they don’t have a stroke.  If no evidence of thrombus heparin drip before cardioversion Premature atrial complex (PAC) Premature atrial complex (before its fully repolarized) Disoriented p wave (may be hidden in QRS) Usually seen with sinus Tachy Causes o Caffeine o ETOH o Nicotine o Anxiety o Hypokalemia o Hypervolemia (stretches atria) o Atrial ischemia, injury, or infarction Clinical manifestations → my heart skipped a beat Management o Reduce stress o Eliminate stimulates Premature Ventricular Complexes (PVCs) It’s the same as PAC but this one eventually be life threatening Causes: o Can occur in healthy patients (intake of caffeine, alcohol, nicotine) o Cardiac ischemia or infarction o Digitalis toxicity o Hypoxia o Acidosis o Electrolyte imbalance AV Nodal Reentry Tachycardia (SVT) Impulse that is conducted to an area in the AV node that causes impulse to be rerouted back into area over and over again @ very fast rate (SA node lost control) Paroxysmal Ventricular rate 120-200 bpm Causes any stimulants o Caffeine o Nicotine o Hypoxemia o Stress o CAD o Cardiomyopathy Clinical manifestation o Reduced cardiac output symptoms o If p waves are not seen → called SVT o If p waves seen → ventricular tachycardia Medical management o Vagal maneuvers 1s  Gag reflex  Breath holding o Adenosine o Cardioversion o Ablation NURSING MANAGEMENT:  Acquire Health history  Presence of coexisting conditions  Indications of previous occurrence  Assessment:  Indicators of cardiac output  Oxygenation  Changes in level of consciousness.  Physical assessment includes:  Rate and rhythm of apical and peripheral pulses  Assess heart sounds  Blood pressure and pulse pressure  Signs of fluid retention  Continuous ECG monitoring  Administration of medications and assessment of medication effects  Provide education to patient regarding dysrhythmias  Provide support to decrease anxiety  Obtain consent for adjunct therapy (cardioversion, pacemakers)   It is IMPERATIVE, AT ALL TIMES, to observe and treat the patient based on his or her clinical presentation regardless of the rhythm being observed on the EKG monitor. Ask yourself: “How is this rhythm clinically significant to my patient?”