Ryan Johnson Clinical Log –Week 4&5 – September 26/28, 2010

Ryan Johnson
Clinical Log –Week 4&5 – September 26/28, 2010 – CCU
This week I had a 9h shift on Sunday and then a 12h shift on Tuesday. This
will be a double-log. I will outline the conditions of both pts in report format, then
do a complete write-up for one patient. Both patients had similar diagnoses, and
both were 92yo M, but one opted to forego pacemaker implantation (Patient 1) and
one had one placed (Patient 2). Patient 2 will be followed since his course
presented more lessons for learning. The pathophysiology of heart block will be
discussed in great detail and related to both patients. I will also include reports of
what I witnessed, questioned, and performed for all the patients during the course
of both days.
Patient 1 was a very pleasant and talkative 92yo M who was brought to the
ER s/p a fall. He was a resident at the Colonnades, an assisted-living community. He
recently was moved to the SNF side of the campus because of his mild dementia
which had left him prone to falls and unable to direct himself towards the bathroom
at night. His wife, of 71yrs, lived with him in the more-independent side of the
campus up until his transfer 4 months ago.
He is A&Ox1, thin, somewhat undernourished, and in NAD. He was aware
that he was in a hospital, but believed he was in Florida. The details were all correct
according to his previous residence in Florida 5yrs ago, but he had to be reoriented
to his current location. He has documented bradycardic episodes recently and has
fallen two other times in the recent weeks when ambulating with a walker.
Cognitively he is most impaired during the evening (sundowning) and throughout
the day he remains largely lucid but slightly affected and occasionally confused. He
has a Hx of CAD, x3 stent placement (2001) with restenotic complications (2006),
IDDM, dementia, and stomach CA (1982) – in remission.
In the ER he was diagnosed with Second Degree Type I Heart Block
(Wenckebach’s) complicated by BBB. This could likely be contributing to his
diminished LOC when combined with the dementia, and it is the underlying source
of his bradycardia
His wife, daughter, and son-in-law stayed with him in the CCU. The family,
with the patient’s involvement, deliberated during the day and ultimately decided to
forego placement of a pacemaker to control Patient 1’s conduction. For his level of
activity, it was hoped that he would be sustained through drug treatment alone. The
daughter, who wields Power of Attorney for him, deemed the risks too great and the
reward minimal when a more moderate route might suffice.
Patient 1 was given Isoproterenol to address his heart block. This drug
works as a potent nonselective beta-adrenergic agonist. It has the effects of
lowering peripheral vascular resistance, lowering diastolic pressure, and has
positive inotropic effects. By increasing heart function, it is hoped that the body will
remain adequately perfused in spite of the Second Degree Type I Block
My primary patient of focus is Mr. R (Patient 2). He is a 92yo M with a Dx of
bradycardia secondary to Complete heart block. He went into the office of his PCP
in Elkton, VA on 9/27 for a routine visit, whereupon he was found to be bradycardic
with a HR in the 30s. He was sent to the ED, with his daughter driving after he
refused to allow the Rescue Squad to be called (he wanted to drive himself initially).
He was asymptomatic upon arrival in the ED.
He has recently noticed greater cold intolerance and has a hx of chronic
lightheadedness that can occur from time to time spontaneously.
In the ED he was found to have a second-degree AV block Type II and
complete heart block.
PSVT s/p ablation, heart murmur, bradycardia, HTN
-CAD: catheterization in 2003 with EF 54%, 50% proximal LAD, 50%
of microcircumflex, and 40% of proximal R stenosis. Multiple LAD
interventions in the past for recurrent restenosis.
-Aortic aneurysm repair in 1994.
-SVT with successful ablation in 2003 and EP study which showed sick
sinus syndrome (arrhythmias r/t poor conduction of SA presumably
secondary to scar-like tissue damage with age) but no infrahisian
block (below the AV node).
CABG, hernia repair, total hip prelacement (2 on R, one on L), ablation
of melanoma, angioplasty x3.
Social Hx:
Denies ETOH. Denies illicit drug use. Tobacco abuse in distant past
(pipe). Wife (of 70yrs), daughter and granddaughter in room most of
the day. 11 grandchildren and 4 great-grandchildren. Still active,
mows lawn. Retired, used to work at Dupont.
Home Medications
Aspirin tablet 325mg UD #1 PO qAM
-Cardiac prophylaxis (antiplatelet); SE: N/V, gastric ulcers.
Simvastatin tablet 20mg #1 PO qPM
-Statin, stabilizes plaques, lowers cholesterol. SE: HA
Hydrochlorothiazide 12.5mg PO qD
-diuretic, lowers BP and PVR. SE: Hypo-lytes, high blood sugar,
HA, NV, photosensitivity, weight gain
Fish oil 2g PO qD
-supplement. Reduce inflammation, provide fatty acids.
Ibuprofen 400mg qD
-NSAID, anti-inflammatory analgesic – for R knee pain. SE:
photosensitivity, gastric ulcers, IBD
Vit C 500mg qD
-Supplement. Antioxidant. SE: indigestion, diarrhea
Ca 750mg BID
-Supplement. Support bone health. SE: hypercalcemia
Multivitamin #1 tab qD
-nutritional supplement.
Hospital Medications
Heparin INJ 5000U SQ q*H
-VTE prophylaxis.
Hydrochlorothiazide tab 12.5mg PO qAM
- diuretic, lowers BP and PVR. SE: Hypo-lytes, high blood
sugar, HA, NV, photosensitivity, weight gain
Simvastatin tab 20mg PO qHS
-Statin, stabilizes plaques, lowers cholesterol. SE: HA
Vitamins #1 tab PO qAM
-therapeutic with minerals.
Current Status:
A&O x 3, WDWN, 92 yo M NAD.
VS: HR 36; BP 107/48 MAP 73; RR 24; O2 sat 95% RA; temp 36.1
Skin: grossly intact, PWD, IV access 16g in L AC running @ KVO. CABG scar.
Head: Normocephalic, atraumatic. No lesions or signs of abnormality. Wears
Neck: symmetrical, s JVD, s tracheal deviation
Pulses: Present +2 x all 4 extremities, Cap refill < 3s in x 4 extremities
Lungs: CTAB. Respiratory effort unlabored, symmetrical, WNL
Heart: NSR; with murmur, distinct S1- S2 upon
auscultation. NS @ KVO.
Abdomen: rounded, soft and nontender; bowel sounds normoactive.
GI: Independently voiding clear, yellow-colored urine. Good UO +30mL/h
GU: DTV. Dinner last PM in ER. NPO until return from EP lab.
Health Perception/Health Management – Pt has clear drive to overcome
perceptions and expectations about the health status assumed of a 92yo. He
still mows his own lawn, and is remarkably agile – easily moving from bed to
bed with ease. He refused SQ heparin as VTE prophylaxis prior to surgery
because he does not like the effect blood-thinning medications have on his
dizziness. Hopefully, after the surgery his cerebral perfusion will be
enhanced and this will not be an issue. I left before he was schedules for his
first p/o VTE prophylaxis heparin was scheduled, so it remains for the night
nurse to see if he will comply with this measure. Either way, OOB activities
will not be a problem for their prophylactic and recuperative effects.
Nutritional/Metabolic - Pt is tall and lean. Undoubtedly, the malabsorption
attendant with age – his skin is papery and muscle tone is diminished.
Relative to his age, he is remarkably fit, but still adequate nutrition is a
priority for this pt.
Activity/Exercise – Mows the lawn. Hopes to return to fishing soon. Can no
longer fly-fish, but still enjoys other forms of the sport.
Role/Relationship – Role as husband, father, grandfather, and greatgrandfather. Retired. Family close and many members locally available.
Cognitive/Perceptual – Requires bifocals.
Self-Perception/Self Concept – Very committed to being an active and
capable man, regardless of chronological age.
Current Labs:
9/27 1700: Na 139; K 4.0; Cl 106; CO2 26; BUN 18; Cr 0.8; Gluc 94
Ca 9.7; GFR(calc) > 60; Mg 2.2; Phos 3.1
Albumin 3.9, T Bili 0.4, Alk Phos 66
ALT 17, AST 23, TP 6.7, Lactic Acid 0.7
PT 16.7 H, PT INR 1.3 H, PTT 28.8
1800: VBG – pH 7.359, pCO2 22.5, O2 sat 31.6, HCO3 29.4, BE 2.9
Hgb 12.7 L, Hct 37 L
9/28 0500: Na 140; K 3.7; Cl 108 H; CO2 24; BUN 17; Cr 0.7; Gluc 88
Mg 2.1; Phos 3.0
TSH 5.83 H, Free T4 0.82
WBC 7.84; RBC 3.72 L; Hgb 11.2 L; Hct 35.0 L; Plt 171
PT 16.9 H, PT INR 1.3 H
Lab Rationale:
The most significant finding from lab work is the abnormal values Patient 2
has for bleeding times. His PT is prolonged but his PTT is not, which suggests that
there is a Vitamin K deficiency or that he has a genetic disorder that makes him
deficient in Factor VII (very rare). Also, he is taking daily ibuprofen for his chronic
knee pain, this could also extent the PT. When looking at the PT INR, which is also
elevated, this is validated as the likely cause.
Another abnormal value is seen in the TSH, which is elevated. Elevated
values of thyroid stimulating hormone suggest that the thyroid is not responding
adequately to the pituitary’s release of this hormone. As a consequence, a feedback
loop leads to an increase in the amount that the pituitary releases. This finding
suggests hypothyroidism, a new diagnosis. The pt received a dose of synthroid inhospital during my shift and will likely be continued on the therapy after discharge.
Leeuwen, A.V., Kranpitz, T., Smith, L. (2006). Davis’ Comprehensive
Handbook of Laboratory and Diagnostic Tests – with Nursing Implications.
F.A. Davis Co.
DIAGNOSIS [Discussed for both Patients 1 & 2]
1. Heart Block: Patient 1 was diagnosed with Second Degree Type I
(Wenckebach’s) Heart Block. However, Patient 2 was diagnosed with
Second Degree Type II and Complete Heart Block.
It is a little confusing to understand the classification system. It is my
understanding that the two classifications (Second Degree and Complete
Heart Block) are mutually exclusive. Things are further complicated
because the Patient 2 also displays episodes of Wenckebach’s, which is a
Second Degree Type I Block. Since I am not a cardiologist, I’ll leave
diagnostics to the pros, but delve into heartblock in general and relate the
science-learned to my patient.
First Degree heartblock is when the PR interval is wider than 0.2s, it
denotes a conduction delay through the AV node. It can be found after
taking certain drugs, with aging and myocardial dysfunction (Urden et al,
2008), and is present in some well-trained athletes (Topol et al, 2007).
Second Degree block looks at the conduction system beneath the AV
node. Here the message to fire does not get passed to the ventricles
effectively, or sometimes not at all. Type I (Wenckebach’s) is when the
conduction is at the level of the AV node. Conduction of the nerve
impulse is progressively delayed by fatigued cardiac nerve cells to the
point that an entire beat is missed and the, now rested, cells have
recovered enough to fire again. Type II is when some beats are dropped
but not in the patterned delay/restart grouping that is evident in
Wenckebach’s (Urden et al, 2008).
Complete (Third Degree) block can rapidly precipitate from Second
Degree Type II. In complete heartblock the distal conduction is entirely
separate from the normal pacemakers. The intrinsic rate of the ventricles
takes over, though it is too slow and unable to compensate so it is a
medical emergency.
In the case of Patient 2, he had progressed past First Degree Heart
Block and showed bouts of Wenckebach’s Block. My preceptor made an
analogy to passing a ball between the SA node, the AV node and the distal
fibers (Bundle of His and Purkinje fibers). The AV is tired, so while it
might first pass the ball (the electrical stimulus to contract) normally at
first, it becomes progressively more taxed and the PR interval (the time it
holds onto the ball) lengthens. Eventually, it has to sit out a whole pass
and just drops the ball (drops a heartbeat – only a P-wave is seen on the
EKG). After sitting one out though, the AV is rested enough to pass it off
quickly. However it soon tires and the process repeats. The resulting
EKG is a series of PQRSs with increasing PR intervals. Eventually one P
wave occurs and the signal is completely dropped, no QRS follows. Then
it resumes and repeats this pattern. The findings on Patient 2’s EKG were
consistent with Type I (Wenckebach’s) Block when we performed a 12lead.
Looking at Patient 2, he also presented EKG tracings that showed the
pattern of PR extension, followed by an altogether missed beat that is
characteristic of Wenckebach’s. His BBB implication in the AV block is
likely the result of a chronic conduction disease, a diagnosis that almost
always requires a permanent pacemaker (Graettinger, 2009). Learning
this during research for the log makes me question whether the family
was fully informed of the impact the dysrhythmia truly has. I hope that
the likelihood of success with drug treatment is not so low that he will be
back in the hospital soon, in worse shape and the family will be
confronted with the déjà-vu of the decision.
Patient 2’s block has apparently shifted towards Second Degree Type
II and Complete Heart Block, according to his cardiologists. Since an
infrahisian block was ruled-out by an EP study in 2003, it is possible that
this is an infranodal block, involved the bundle of His (Graettinger, 2009).
Conversely, he could have developed an infrahisian block in the
meantime in addition to the infranodal block. Regardless of the type of
distal block, the end-result is that his P-waves were firing at their rate,
while the QRS was firing at it’s own ventricular rate. On his most recent
EKGs the P-waves maintained a repetitive interval at the underlying sinus
rate, but the ventricles fired in response to a QRS at an autonomic rate of
~38-40bpm. Here too, the QRS interval is greatly widened because the
distally-originated impulse is originating downstream so it must travel up
to the AV node then bounce back to the apex and around the ventricles in
order to produce an effective contraction; this longer route implies a
longer QRS (Urden et al, 2008).
The confusing part of Patient 2’s diagnosis is that my preceptor and I
clearly witnessed Secondary Type I (Wenckebach’s), and that he had a
dual-diagnosis of both Secondary Type II and Complete Heart Blocks. In
all that I’ve read the classifications are distinct and exclude each other, a
progression is possible, but I’m unsure whether certain dysrhythmias can
be concurrently transient. I assume this must be true based on this
patient’s EKGs, is it?
A literature review discussing post-operative complications of
pacemaker implantation is found. The risks are real threats to Patient 2,
and reasons why Patient 1 opted-out of having a pacemaker implanted.
1. Potential Complication: Cardiac output decreased r/t to acute perforation
of the atrium and/or ventricle, or failed pacemaker.
2. Potential Complication: Inadequate tissue perfusion r/t venous puncture,
pacemaker failure, cardiac tamponade or pericarditis.
3. Risk for infection r/t implantation procedure, exposure to nosocomial
bacterial threats, and post-surgical site.
4. Risk for Altered Role Performance r/t new reliance on pacemaker,
potentially decreased ability to be involved with previous activities,
confrontation with own mortality and caring for wife and family.
5. Chronic pain AEB c/o R knee being constant hindrance to mobility, use of
ibuprofen, and constant readjusting of leg positioning.
Patient 2 went down to the EP lab for placement of a pacemaker. I was able
to attend the procedure and the fellow, RNs and techs taught me as it went. A
biphasic pacer was implanted, the settings were established and now the pt is
recovering. It is expected that he will remain on the Unit until discharge tomorrow
morning. He is recovering well, awake and alert while chatting with family. His HR
has been brought back into the normal range now, the pacemaker timed to initiate
ventricular contraction according to the sensed p-wave.
His specific pacemaker was a DDDR – it had dual-chamber pacing, sensing,
and has both inhibited and triggered firing. Additionally, the R indicates the
pacemaker adjusts its rate. This type depends on a regular atrial pattern to dictate
the HR (Graetinnger, 2009). For Patient 2, his consistent P-waves were deemed
adequate to support such a type of pacer.
Following discharge, Patient 2 will follow up with his cardiologist, who is also
an attending physician in the CCU. He will be restricted to limited mobility of the L
extremity for 12-14d to ensure that the pacemaker leads are anchored sufficiently.
Risks of this procedure include infections, failure of the sensors to sense or
pace, erosion of the pace generator, thrombosis or dissection of the accessed vessels
for insertion, and/or heart chamber puncture (Ellenbogen et al, 2002). The
deleterious effects of such complications could lead to fluid volume loss through
hemorrhage, pericarditis, pericardial tamponade, or sepsis. Bailey and Wilkoff
(2006) also point out that the pacemaker itself can cause intrinsic complications
related to the settings it is placed on. Some sensors might falsely interpret
vibrations from a car or being rolled in a hospital bed as physical activity and
prompt an increase in HR, for example.
These authors also cited a tendency towards worsening cardiomyopathies
and CHF in patients that are paced from the R ventricle, because of the dysynchrony
between the two ventricles. It will be necessary to monitor Patient 2 for deleterious
effects, as the block in his L ventricle, combined with the dysynchrony, could lead to
electrical remodeling that leads to myocardial remodeling (Bailey and Wilkoff,
Acute perforation of the atrium or ventricle is also a risk, one that might not
be noticed immediately. It could lead to pericardial tamponade and/or pericarditis.
There would also be consequences for blood flow and the concurrent complications
r/t inadequate tissue perfusion and HF (Ellenbogen et al, 2002).
To be on alert for potential complications it will be important to monitor
hemodynamics, lab values, UO, and LOC. Prophylactic abx were also administered
immediately following surgery and two more doses will also be given. Additionally,
if the patient does not refuse, heparin with VTE prophylaxis along with SCDs and
OOB activities will be used to prevent thromboemboli formation.
To address the personal concerns of the patient and family much discharge
teaching has been done and will continue to be provided. Limits in the immediate
recovery stages will be well-understood, and questions will continue to be
addressed. The family will also be alerted for the potential complications and the
signs that would be cause for alarm.
Patient 2 also has chronic knee pain that limits his mobility. He is currently
controlling it with ibuprofen, but he should be informed that light activity helps the
healing process and if the knee pain is preventing him from achieving this, he should
consider seeing a specialist to determine whether the root-cause is arthritis,
orthopedic, or neuromuscular.
Much of the care for these patients - related to analyzing EKGs,
understanding the etiology of these tracings, and the workings of the pacemaker as
a corrective device – were all familiar to me in concept, but the real world
application expanded and solidified my understanding.
The professionalism I witnessed in the EP lab much exceeded that of the cath
lab that I witnessed previously. Everyone, down to the techs, was very aware of the
intricacies of the procedure. In tuning the pacer, the two RNs and two of the techs
got behind the machine to assess the performance. At one point, one of the tech’s
supplemented the fellow’s explanation with even more complexity (I’m assuming
because it sounded really smart).
Pt and family teaching was a priority for the fellow during my shift with
Patient 2, and this was impressive. Also, much heed was given to whether or not a
pacemaker was appropriate for this patient. In the end, due to his high quality of
life, it was clear that an opportunity to maintain high-function was the best tact.
Similarly, this same discussion was addressed during my 9/26 shift with
Patient 1. This was also a 92yo M, but the decision was made to opt-out of
pacemaker implantation. Patient 1 contrasted Patient 2 because he was not entirely
cognitively aware and he had other medical conditions. His activity level was such
that the heart block he presented with was not impeding his ALDs to an extent that
would justify the increased risks the procedure would imply. In this case, choosing
to do-not appeared to be more difficult for the HCPs, notably the medical team.
Nonetheless, what was best for the patient was kept at the forefront.
The decision by Patient 1’s family to not accept a pacemaker seemed like the
right decision at the time. The MDs seemed optimistic that medications could
control his block, given his level of activity. It was a little sad to see the reality that
he might not live long enough, or be in good enough overall health to make the
procedure worthwhile, but the family seemed comfortable with the decision. After
seeing a poor prognosis for Type II blocks with BBB from a couple sources, I am
rethinking my outlook.
Now I wonder if Patient 1 will not just be back in the CCU in the near-future
because his illness will be inadequately controlled by medications alone. It is
possible that his general health is worse than I am aware of, perhaps his transfer to
the more attentive side of the Colonnades is reflective of him nearing his end-ofdays.
I am assuming this is the case, because the family was so accepting of the
minimally-invasive option. It appeared right from the beginning that the daughter
had already prepared herself to let her father go soon. It was an interesting
exchange to witness, between her and her father.
Last week I spoke about how one of the nurses who is a consistent leader on
the floor was elevating the practice on the Unit. This past shift he was at it again,
quizzing flashcards with the desk clerk to prepare him for his EMT exam.
Additionally, one of the other RNs on the floor was charge and preparing to
give night report as we approached the end of the shift. Instead of asking my
preceptor for updates on his patients, she intercepted me and had me give report on
the spot. It took me by surprise, and was an anxious moment, but I appreciated that
she challenged me. It also showed that she cared about my development as a nurse
and respected me enough to ask. It did however point out that while I’ve given
report through all my previous rotations, I don’t have a consistent framework to
deliver it – because we were told to adopt the method our first preceptor used and
she wasn’t much of a role model.
Other positive interactions I discussed above, involving the EP lab team and
their cohesiveness and level of expertise.
I am fast approaching my last hours in the CCU, and that disappoints me. It is
definitely my favorite rotation so far. It is the acuity that is so interesting, so I know
that I would be similarly happy in many critical settings. The work-environment in
the CCU is also very conducive to cooperation, and as a learning-environment I am
challenged and supported by the whole staff.
Looking at my experience here thus far, I know that I will need to seek out
such a place to work come graduation. I think critical care fosters collaboration and
recruits the type of people that are progressive and involved in their practice, so I
see myself following that route.
A more specific goal for my final shift is to continue to hone in on one or two
new technologies, procedures, or diagnoses to develop a greater knowledge base. I
also will make sure to thank my preceptor and the other staff on the unit. For their
work, they get a lot of grateful patients and families, and I think that thanks is a big
factor in why it is a positive place to be.
Bailey, S.M., and Wilkoff B.L. (2006). Complications of pacemakers in the elderly. The
American Journal of Geriatric Cardiology. 15(2): 102-107.
Ellenbogen, K. A., Wood, M. A. and Shepard, R. K. (2002). Delayed Complications
Following Pacemaker Implantation. Pacing and Clinical Electrophysiology,
25: 1155–1158.
Graettinger W.F. (2009). Chapter 22. Conduction Disorders and Cardiac Pacing
(Chapter). Crawford MH: CURRENT Diagnosis & Treatment: Cardiology, 3e:
Leeuwen, A.V., Kranpitz, T., Smith, L. (2006). Davis’ Comprehensive Handbook of
Laboratory and Diagnostic Tests – with Nursing Implications. F.A. Davis Co.
Phipps W.J., Marek, J.F., Monahan, F.D., Neighbors, M., & Sands, J.K. (2003). Medicalsurgical nursing health and illness perspectives 7th edition. Mosby, St. Louis,
Topol E.J., Califf R.M., Prystowsky E.N., Thomas J.D., & Thompson P.D. (2007).
Textbook of Cardiovascular Medicine, Third Edition. Lippincott, Williams, &
Wilson. Philadelphia, PA.
Urden, L. D., Stacy, K. M., & Lough, M. E. (2008). Priorities in critical care nursing (5th
ed.), St. Louis: Mosby.
UVa Honor Code: On my honor as a student, I have not given nor
received any unauthorized aid on this assignment.
Ryan Johnson