Seminal Birthday Well, after a week into this noble enterprise, typing while prostrate on my porch, this summer solstice night, with my son crawling on my lap and we two hidden under a sheet-clad fortress, I am glad to announce that our membership is four persons strong and growing. I encourage you all to come online & post. Farewell.  ¶ 10:08 PM 0 comments

  Oxygen & COPD For those of you who couldn't make it to that recent inservice, I thought I would post a few highlights that I found particularly useful.

• Flowmeters: read the CENTER of the ball; i.e., the ball's horizontal diameter should intersect the tick-marks of the meter.
• If a pt's SpO2 drops or flow rate demands increase beyond previously prescribed parameters, then an MD should be notified, since pathology may underly.
• Nasal cannula on a mouth-breather gives adequate O2, as long as nares are patent, & SpO2 is appropriate.
• Approximate FIO2 levels (q1L=approx. 4% addn'l above RA)
  
• 1 lpm: 24%
• 2 lpm: 28%
• 3 lpm: 32%
• 4 lpm: 36%
• 5 lpm: 40%
• 6 lpm: 44%
• Ventimasks:
• don't cover air entrainment ports on adaptors (too much FIO2)
  
• don't use with humidification (too little FIO2)
• Pursed Lip Breathing:
• insp./exp. ratio of at least 1:2 (the longer exp. = the better O2 exchange)
• Hypoxic Drive Review:
• small % of COPD pts actually respire perforce of Hypoxic Drive
• thus, your patient could benefit from more O2
• If in doubt, get an ABG:
• If CO2 chronically continues to rise (>60mmHg), then consider Hypoxic Driver
• Then, only low PO2 levels (<55-60mmhg)>
• But the actual Hypoxic Drive occurs ONLY in pts who are BOTH hypoxic AND hypercarbic--("the 50/50 club")
• At this point low O2 flows (1-2 lpm) and careful monitoring are recommended.
• Qualifying for home O2: Pulse Oximetry must be done NO SOONER THAN 2 DAYS BEFORE DISCHARGE.

Your Colleague,
Christopher.  ¶ 4:05 PM 0 comments

  Th'Olde Art o'Hart Hearing On Cardiac Auscultation, much pared down

On review it seems that this outline is difficult to read; it was originally a presentation to be supplemented ex tempore. But I publish it anyways, as there are still nuggets and pearls in it and it can begin a thread on this subject. I'll make a few highlights in blue. Further, if you want some websites for heart sounds, see the comment I will post.

1. Why learn it?
1. Efficiency - around one minute per pt; with full patient load less than ten extra minutes
2. Vigilance (Early detection) – e.g. Aortic Dissection case (cf. Below @ S2)
3. Taste/Connoisseurship/Aesthetic development of the ear
4. Supremacy over the machine (as good a tool as ECG & XRay)
5. Listening qua listening is an invaluable life skill
6. Nursing Excellence: be no longer a medical minimus!
2. Method of Differentiating Heart Sounds.
1. Normal sounds
1. Ascertain S1 and S2 by one of three methods
1. if rate WNL then use "lub-dub" and longer space as diastole
2. if rate > 80 from base where S2 is louder, inch back to LLSB/Apex
3. or time with PMI pulsation or carotid pulsation (not peripherals)
2. Judge normality or abnormality of S1 & S2, esp. intensity and splitting
1. in S1 intensity is more informative
2. in S2 splitting is more informative (According to Harvey --mimicked by tapping of fingers)
3. Determine Hemodynamic rationale for sound
4. Differentiate etiology of sound
2. Extra Sounds/murmurs/etc.,
1. Ascertain “where & PQRST” of extra sound/murmur/etc., if any
2. Determine Hemodynamic rationale for sound
3. Differentiate etiology of sound
3. Normal Sounds
1. S1 =def. AV valve closure, Semilunar opening, & ejection of blood (to great vessels)
1. Semilunar valves usu. inaudible
2. Loudness, causes of:
1. Thickness of AV leaflets – leaflets like soft/hard cover books falling on hard surfaces
2. Separation of leaflets/valve position –
1. P-R intervals: in heart block, if short, leaves drop from on high; if long, then soft sounds because of time allowed for closure (1 deg. Block/Wenckebach/Rheumatic Fever)
1. NB: Wenckebach & progressive softening of S1
2. 3 deg. AV Block: SB w/ irreg., variable S1
2. AV pressure gradient (mitral stenosis) – separation of leaflets leaves longer distance for valve closure causing increased loudness
3. Rate of Rise in RV/LV pressure – (chiefly contractility affecting)
1. Fast = loud: hyperkinetic hearts (thyrotoxicosis, pregnancy, fever, AV fistulas, PDA, aortic regurgitation)
2. Slow = soft/muffled: CHF
2. S2 -- Said to be “Key to Auscultation of the Heart” (Leatham) & “ranks with electrocardiography and roentgenography as one of the most valuable routine screening test for heart disease.” (Mang. 211)
1. S2 =def. Closing of aortic (A2) and pulmonic (P2) valves (sudden deceleration of blood s/p closure of semilunar valves
1. Best heard @ pulmonic area since P2 can normally only be heard here (esp for splitting)
2. Can tell which is A2 during a split since normally only A2 is audible @ apex
1. If split @ apex then pulmonary hypertension (pathognomic until proven otherwise b/c P2 is abnormally loud); pulmonic hypertension also associated w/:
1. loud and palpable P2 @ pulmonic area
2. Rt sided (LLSB/epigastric) S4
3. pulmonic ejection sound
4. murmur of TV regurgitation
1. Loudness:
1. Increased Pulm./Systemic pressure = loud P2/A2
2. High-output states (e.g., AS defects, VS defects, thyrotoxicosis, aortic regurgitation) = loud
3. Tambour (deriv. French "Drum"
   1. usu. Dilatation of aortic root
   2. if w/ murmur of aortic regurgitation = Harvey’s Sign, as in Marfan syndrome, syphilis, or dissecting aneurysm of ascending aorta (w/ high diastolic pressures)
4. If soft (or even absent) then
1. low CO/low pressures in pulm./syst. circulation
2. reduced mobility of semilunar valves (calcific/sclerotic/stenotic)
2. Physiologic Splitting on inspiration d/t intrathoracic negative pressure gradients & pooling of blood in lungs; (I’ve only heard this w/ athletic habitus)
1. Remember!! Inspiration increases RV volume; Expiration Decreases RV and increases LV volumes
2. Best heard supine (lengthened split); sitting/standing will shorter
4. Pathological Extra Heart Sounds: consider pathological until proven otherwise
1. S3 =def. During rapid, passive filling phase (See Intracardiac pressure) in LV/RV, deceleration in rate of blood flow r/t either increased preload or poor compliance (i.e., poor contractility or low EF), and hence tension on ventricle and AV valve apparatus (usu. reflects ventricular filling pressure of >25mmHg)
1. absent if mitral stenosis, and vice versa (stenosis obstructs the rapid, passive diastolic filling)
2. at the threshold of audibility (40-50 Hz) & intensity changes w/ many variables;
1. high “index of suspicion” is needed in order to prompt aggressive search by maneuvers in pts with HF
2. gingerly allay the bell precisely @ the PMI!! Compress bell for disappearance and diagnosis of sound.
3. if pathologic, usu. lower freq. & gallop lilt
4. first clinical sign of CHF (changing position from sitting to supine may bring out, or with mild exercise as coughing or turning to Lt side or Hand grips)
1. If an S3, may predict excellent response to Digoxin.
2. Consider cardiac patients receiving parenteral fluids, who go into CHF; nurse might Dx situation by hearing this sound.
5. normal, physiologic S3 in kiddies, males<30,>45; may also occur during increased sympathetic tone and increased levels of catecholamines: tachycardia, thyrotoxicosis, anxiety, fever, anemia, pregnancy
2. S4 =def. During late active filling (“presystolic” or during “atrial kick”), increased rate of blood flow to ventricle and tension both on ventricle and AV valve apparatus (may note prominent, or notched P wave on ECG)
1. classically absent in AF & AFl
2. same as w/ S3: gingerly allay the bell @ PMI; if S4 is palpable, then definitely pathologic
3. intensified by maneuvers intensifying intracardiac blood volume and venous return: turn to Lt Lat decubitus position; Valsalva release, exhalation, Hand-Grip, leg raise
4. indicates hypertrophic, thickened, and poorly compliant ventricle
1. b/c of reduced passive diastolic filling, more of an atrial boost responds to fill the deficiency
1. as in HTN (may precede ECG evidence of LV hypertrophy)
2. aortic stenosis, coarctation of the aorta
3. hypertrophic cardiomyopathy
4. CHD (approx 90% of pts with MI)
5. prolonged P-R interval
3. S3/S4 are the substance of the descriptor “gallop”
1. S3 – ventricular gallop mnemonics:
   
1. KEN'-tuck-y;
   
2. SLOSH'-ing-in;
   
3. VENT'-ric-le;
   
4. s1---s2-s3
   
2. S4 – atrial gallop mnemonics:
   
1. Ten-ESS'-ee;
   
2. a-STIFF-wall;
   
3. a-TRI'-al;
   
4. s4-s1---s2;
   
3. quadruple rhythm and summation gallop – overlap on rate changes
1. I-can't--keep-up
2. s4-s1---s2-s3
1. in CHF & severe myocardial diseases
2. esp, in pts tacycardic c hypertensive heart failure
3. or in 1st deg. AV block, where prolonged PR interval causes s4 to move backward in diastole
1. Acrostic for the sounds near S2 that may confuse the Auscultator: P-L-O-P-P-S
1. Paradoxical Splitting (A2 is delayed until after P2 on exhalation) – (persistent on standing) LV dysfunction or acute decompensation: (volume/pressure loads on LV [aoritc stenosis, etc]); acute, unstable MI & Conduction defects)
2. Late Systolic Clicks – prolapse and backward ballooning of leaflets
   
3. Opening Snap (diastolic) – high pitched “sail suddenly filling under wind, with ballooning and bellowing and a final snap due to the tight grip of the chordae tendinae”
   1. consider also the opening sound of an atrial myxoma (i.e., a tumor plop) peculiar b/c of its intermittency and cycle to cycle variability of intensity
   1. tumours are pedunculated and attached to the atria by a stalk, and sometimes prolapse through the open valve
   2. pt may also have drops in BP and syncope s/p change in position d/c of transient obstruction of diastolic ventricular flow by the tumor
4. Pericardial Knock sharp, loud, medium to high pitched ventricular filling sound: a peculiar form of the S3 (caveat: if hearing a Gallop, this is more Zebra than Horse) r/t calcific constrictive pericarditis 2nd to old TB processes
5. Pulmonary Hypertension – abnormally intense S2 at the apex (distinguish from relative softening of S1, as in MI)
6. S3 =def. During rapid, passive filling phase in LV/RV, deceleration in rate of blood flow r/t either increased preload or poor compliance
4. Early systolic click (ejection sound) =def. the usu. inaudible component of S1: louder over base; consider indicative of semi-lunar valve or great vessel pathology unless proven otherwise
1. Differentiate origin A2/P2 and note intensity which in stenosis reflects mobility of the valve
1. softening of sounds in fibrosis and disappearance in calcification
2. if seeking P2, and increase in intensity during inspiration is noted then source of click is valvular
1. if intensity is static through inspiration and expiration then think vasculature: pulmonary HTN/dilatation of pulmonary artery.
5. Means-Lerman scratch of hyperthyroidism raspy pulmonic ejection sound with a pulmonic murmur r/t hyperkinetic heart syndrome (also anemia/fever)
6. Pericardial Friction Rub scratching, scraping, leathery, crackling, and oft fleeting on inflammation 2 pericardial layers; one systolic sound (ventricular contraction) and two diastolic sounds (passive and active filling) loudest @ LLSB
1. Dressler’s Syndrome – both pericardial and pleural friction rub.
1. One complication of MI (usu. after 1st 24hrs.) is pericardial effusion and pericarditis, with or without pleurisy; if with then Dressler’s
7. Pleural Friction Rub – holding breath differentiates from pericardium
5. Murmurs =def. occur whenever blood flow becomes turbulent enough to cause auditory vibrations in the cardiac structures (notably concentric narrowing of a vessel or valve, or sudden change in the diameter of a vessel), which causes high pressure gradients and abnormal velocities of blood flow
1. Classification:
1. Most systolic murmurs are benign, i.e., innocent and functional murmurs
1. Most benign murmurs are never more intense than a 3/6 (see below), i.e., never palpable with thrill or thrust
1. further classificaton:
1. ejection – early or mid systole (usually benign ejection through semilunar valves, but may be forward flow across stenotic semilunar valves)
1. regurgitant – holo- or pan-systolic or late systole (will most often extend into and touch S2); if so, probably pathologic (when late may be MV prolapse & papillary muscle disorders; when holosystolic may be MV or TV regurgitation or VSD)
2. Most diastolic are pathological: must ascertain origin, hemodynamic cause, and severity
1. variations by timing:
1. early – aortic or pulmonic regurgitation
1. if aortic and heard at base right, may also hear above Erb’s point Lt 3rd/4th ICS
1. If this is heard in a pt with preexistent diastolic hypertension (i.e., loud, tambour S2), then may be aortic aneurysm or dissection, or both
2. mid – mitral/tricuspid stenosis (low in frq. & rumbling)
3. late – mitral/tricuspid stenosis
1. can bring out with some coughing or maneuvers
4. holo – PDA
1. Continuous murmurs have no pause reflecting cardiac cycling: e.g., to-fro, machine like murmur of Patent Ductus Arteriosus
2. Mangione’s two golden and three silver rules
1. Golden
1. “Always judge murmurs like people–by the company they keep”
1. extra sounds, abnormal pulses, abnormal ECG, abnormal CXR, or any CV symptom
2. Thus, if they’re on our floor, its probably pathologic
2. “A diminished or absent second sound usually indicates a poorly moving and abnormal semilunar valve. . . the hallmark of pathology” & vice versa
2. Silver
1. “All diastolic murmurs are pathologic,” until proven otherwise
2. “All holosystolic or late systolic murmurs are pathologic”
3. “All continuous murmurs are pathologic”
3. Murmur Characteristics: “Where and PQRST” Or The Six S’s
1. P - Pitch Site
2. Q - Quality Single or Multiple
3. R - Radiation Spread (conduction) and these sites
4. S - Severity/intensity Systolic and/or diastolic timing
5. T - Timing Soft/loud, harsh, rumbling (Qual.) Standing, sitting, lying, leaning, (Special Maneuvers) relation to exercise, Valsalva, Respiration, Hand-Grip, Amyl Nitrate (& NTG, etc?)
1. 6. Keep in mind that murmurs on the Rt generally increase w/inspiration, on Lt, decrease
4. Mnemonic for Cause of Systolic Murmur at apex: MACHINE (shipman, 243)
1. Mitral Valve incompetence
2. Anemia: esp., in Pregnancy
3. Coronary thrombosis: papillary muscle involvement with rupture of Chordae tendineae
4. Hypertension with LV enlargement
5. Innocent
6. Narrowing of Aortic Valve (stenosis)
7. Enlarged heart from any cause, e.g. cardiomyopathy
   

Bibliography:
See Comments.  ¶ 11:26 AM 3 comments

  From the Desk of J. Rutowski, RN, BSN, CVN I like the idea of a blog site as an informal forum for the nursing staff and would like to help out. As I mentioned before a link to the PEARLS REVIEW site may be helpful and now that we are in the process of reviewing for the Certification exam this may be a good place to link review in formation as well. Thanks for your stick-to-itiveness and ongoing efforts at uniting our staff!

Here is the link to the Pearls review site that I mentioned

http://pearlsreview.com/

I need to get the login info from Lisa Nelson at Mary Dillon’s office. To access it for free as an employee of Sisters you need specific log in codes and I can’t remember them off hand.


Jerry  ¶ 4:19 PM 0 comments

  The Opening Agenda You may remember aways back I circulated a bill with much of the following information on it. Since it has been a great challenge to bring several members of the nursing staff of 4N together at one time, this blog has been created to foster discussions and research bearing on aspects of patient care here at SOCH, esp. on 4N. This is intended as a non-formal meeting place for continuing education and professional comradery. I welcome suggestions regarding the establishment of any guidelines and selection of topics for future discussion. Some topics earlier recommended for discussion were:

1. Basic Cardiac Assessment Review
2. Advanced and Emergent Cardiac Assessment
3. Thoracic and Cardiac Auscultation
4. Clinical Pathways for MI, CHF, Arrhythmias
5. Current Issues in Cardiac Pharmacology
6. Interpretation of Haematology, Chemistry, Labs, etc.
7. Cardiological Genetics
8. The Philosophical Ethics of Nursing: Care and Responsibility
9. The Buisness of Nursing: Management, Staffing, and Salaries
10. Beautification of our environment
11. Maths and Medicine

The possibilites abound. Please leave your contact information (Name/Email) with my email address at christopher.cataldi@gmail.com so that I can begin to draft a members list for this forum, and so you can begin to post your own threads.  ¶ 8:34 AM 1 comments

  How to Post First, you'll need to be invited. This is easy. Email your contact information, i.e., your name and email address, to me at the email I gave you at the bottom of the flyer. When I receive your information, I can invite you. Just follow the instructioins in the email which will be sent to you.  ¶ 8:10 AM 0 comments

  The Pristine Posting This is the first example of the epehemera to be electronically scrawled around the association known as the 4North United Review of Scientific and Educational Supplements, or 4N.U.R.S.E.S., a group established and moderated by Mr. CC, RN, staff nurse at the a Hospital in Buffalo, NY.  ¶ 4:57 PM 0 comments