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CS 2015
Block 2 Wrap-upChristian Stricker
Associate Professor for Systems PhysiologyANUMS/JCSMR - ANU
[email protected] http://stricker.jcsmr.anu.edu.au/Wrap_up.pptx
THE AUSTRALIAN NATIONAL UNIVERSITY
CS 2015
CS 2015
Aims
At the end of this lecture students should be able to
• bring together and test a few concepts covered in Block 2
in a single case that spans heart, vascular system, lung
and kidney;
• recognise effective learning via realistic cases rather than
from “textbooks” and notes;
• outline answers for one assessment form, namely
minicase; and
• identify strengths and weaknesses via limited self-
assessment.
CS 2015
Tips for Exam Preparation
• All material is assessable (lectures, PBL sessions, clinical
skill’s days, laboratory (what is not done in prac exam, …),
etc.).
• In MY assessment items I try to concentrate on– concepts (rather than detail): bigger picture;
– application of concepts to “new” or “unexpected” situations (how
physiology is applied…); and
– how different concepts/ideas interact.
• Do not “go over it again”, but try to apply knowledge to
histories (imagination…): what happens if…
CS 2015
Tips for the Exam• Stay cool... and keep confidence!
You can solve it!
• Try and see bigger picture first:– To which “topic area” does it relate (cardio, etc.)?
– What were important concepts in that “area”?
– Try and start with “simple” principles first!
– Do not try to spray answers (I get cranky…)!
• I am not trying to fool you…– but expect something that you may not have seen/heard
before: I try to make exam items so that you should learn
something new.
CS 2015
How This Session Works Best
• Team up with your neighbour.
• Discuss within a minute or two the answer
that each of you would have given.
• Be prepared to solicit your answer to all.– Don’t be shy – others can learn a lot if either a
mistake is made or the correct answer is given.
– A “correct” answer may not exist.
– Nothing goes outside this lecture room...
CS 2015
MinicaseJoe Hockey, a 54 year-old male, is admitted to the Emergency Department
after experiencing chest pain, dizziness and shortness of breath and a
rapidly worsening condition.
• His HR is 120 bpm, regular; BP 100/60 torr; RR 25 bpm; 38.2°C.
Auscultation of
– heart: mild mid-systolic murmur with a clearly split 2nd heart sound.
– lung: basal rales and loud respiratory sounds.
• An emergency ECG is performed.
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ECG on Admission
• Is this ECG normal? Characterise it.– Rhythm?
– Axis in frontal leads?
– Wave abnormalities?
CS 2015
ECG on Admission
• This ECG is abnormal: tachycardia (108 bpm)– Rhythm: Sinus tachycardia; Axis in frontal leads: ~ -60°
– Wave abnormalities: T-wave inversions in V1 - V3, ST elevations in V4 -
V5; QRS complexes > 120 ms (split complex).
CS 2015
MinicaseJoe Hockey, a 54 year-old male, is admitted to the Emergency Department
after experiencing chest pain, dizziness and shortness of breath and a
rapidly worsening condition.
• His HR is 120 bpm, regular; BP 100/60 torr; RR 25 bpm; 38.2°C.
Auscultation of
– heart: mild mid-systolic murmur with a clearly split 2nd heart sound.
– lung: basal rales and loud respiratory sounds.
The emergency ECG confirms sinus tachycardia and shows T-wave
inversions and ST elevations together with bundle block (antero-lateral
infarct ?).
• An emergency chest X-ray is performed.
CS 2015
Chest X-ray
Is it normal? Describe ventricles and pulmonary vessels.
CS 2015
Chest X-ray
CS 2015
MinicaseJoe Hockey, a 54 year-old male, is admitted to the Emergency Department after
experiencing chest pain, dizziness and shortness of breath and a rapidly worsening
condition.
• His HR is 120 bpm, regular; BP 100/60 torr; RR 25 bpm; 38.2°C. Auscultation of
– heart: mild mid-systolic murmur with a clearly split 2nd heart sound.
– lung: basal rales and loud respiratory sounds.
The emergency ECG confirms sinus tachycardia and shows T-wave inversions and
ST elevations together with bundle block (antero-lateral infarct?).
• Chemical pathology results are consistent with myocardial infarction.
• The radiology report states that there are congested pulmonary arteries with
Kerley B lines (consistent with pulmonary oedema) and biventricular
enlargement.
• Why are the vessels in the lower lobes of the lung tissue prominent?
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Chest X-ray
Why are the vessels in the lower lobes of the lung tissue prominent?
CS 2015
Reasons for Prominent Vessels• Perfusion largest in the lower lobes
– reason: positive hydrostatic pressure aids perfusion in
the lower lobes but limits perfusion in the apex.
CS 2015
MinicaseJoe Hockey, a 54 year-old male, is admitted to the Emergency Department after
experiencing chest pain, dizziness and shortness of breath and a rapidly worsening
condition.
• His HR is 120 bpm, regular; BP 100/60 torr; RR 25 bpm; 38.2°C. Auscultation of – heart: mild mid-systolic murmur with a clearly split 2nd heart sound.– lung: basal rales and loud respiratory sounds.
The emergency ECG confirms sinus tachycardia and shows T-wave inversions and ST elevations together with bundle block (antero-lateral infarct?).• Chemical pathology results are consistent with myocardial infarction.• The radiology report states that there are congested pulmonary arteries with
Kerley B lines (consistent with pulmonary oedema) and biventricular enlargement.
• Overall, how could you describe the patient’s presentation?• What could cause a sudden increase in left atrial pressure?• How could your suspicion be substantiated?
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Reasons for Left Atrial Pressure↑ • Cardiovascular shock (insufficient perfusion of vital
organs).– Tachycardia, low mean arterial pressure, and clinical signs
(dizziness)
• Insufficient LV output (compared to RV function):– Myocardial damage → contractility↓ → CO↓
– Valvular damage: mitral regurgitation (as a consequence of
myocardial damage) → CO↓• Mid-systolic murmur with splitting of 2nd heart sound.
• Echocardiography– What can be seen in the following documentation?
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Reasons for Left Atrial Pressure↑
• Ruptured and free floating papillary muscle
causing acute mitral regurgitation.
• Why is 2nd heart sound “clearly split”?
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Splitting of 2nd Heart Sound
• RV volume overload causes prolongation of contraction
(load↑): pulmonary valve closure delayed.
• Due to regurgitation, LV ejection phase is reduced: aortic
valve closure earlier.
• How would the LV P-V loop look like?
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P-V Loop in Mitral Regurgitation• Isovolumetric phases gone
due to regurgitation.
• Psys↓.
• Large SV (“virtual”).
• How are the following
haemodynamic parameters
affected?– Right atrial pressure (PRA).
– PMSF (mean systemic filling
pressure).
– Venous return (VR).
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Haemodynamic Consequences• PRA↑ due to volume overload (endsystolic volume↑ in RV
due to higher pulmonary pressure: Tricuspid closes at
higher pressure).
• PMSF↑: for the main reason that PRA↑ (pooling).
– But baroreflex activity↑, Rsys↑ (tachycardia) → PMSF↓.
• Venous return↓ because– PRA↑ and
– venoconstriction due to baroreflex (Rven↑).
• How could you rationally improve the haemodynamic
condition this patient is in?
CS 2015
Rational Therapy• Mitral valve replacement
• Until then– treat pulmonary oedema.
• Diuretics
• O2 donation (see later…)
– improve CO: Lower systemic resistance (Rsys).
• Theoretically: – α-blockers (certainly not β-blockers…)
– ACE inhibitors (if fast enough?)
– etc.
• What were his most likely blood gas values (O2 and CO2)
on admission?
• Would it help to give this patient O2? Explain.
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Respiratory Side• With CO↓, blood gas values altered - increased diffusional
distance in lung: O2 more than CO2.
– CO2↑ (driver for tachypnoea – CO2 retention).
– O2↓ (because CO↓ and diffusion distance↑ - peripheral extraction↑).
• O2 therapy helps because driving force for diffusion can be
elevated: PAO2↑
– predicted to lower pulmonary resistance (might be a mild effect):
alveolo-vascular effect.
• As compared to normal, how would pulmonary oedema
affect residual volume, vital capacity, FEV1 and lung
compliance?
CS 2015
Lung Volumes• Residual volume↓ because some of it will be filled with
plasma filtrate.
• Vital capacity↓ because some of it will be filled with
plasma filtrate (contributes to ).
• CL↑ due to watery solute in alveoli.
• FEV1↑ because CO2↑ in bronchioli (alveolo-bronchiolar
effect): bronchiolar smooth muscle tension↓.
• What is this patient’s GFR and the renal Na+
reabsorption rate?
• What is the amount of ADH secreted?
• What is the osmolality of secreted urine?
CS 2015
GFR, Na+ Reabsorption, ADH• Due to sympathetic activity↑ → GFR↓ (afferent vessel
constriction): effectively a volume contraction response
as effective renal perfusion↓.
• Na+ reabsorption in proximal tubule↑ as a consequence
of sympathetic activity↑.
• Due to volume constriction, ADH↑: also helps to increase
blood pressure.
• Osmolality likely high, at best 1200 mOsm (ADH action).
• What is the state of the renin-angiotensin-aldosterone
system? What is K+ excretion state?
CS 2015
RAA System & K+
• Due to volume contraction, renin is secreted resulting in
angiotensin II production (also increases blood pressure).
As a result aldosterone is activated; however, it is unlikely
that the aldosterone effect has taken effect yet (takes a
day or more…).
• K+ is likely normal or sightly elevated (due to small K+ shift
as a consequence of acute respiratory acidosis).
CS 2015
MinicaseJoe Hockey, a 54 year-old male, is admitted to Emergency Department after
experiencing chest pain, dizziness and shortness of breath and a rapidly worsening
condition.
His HR is 120 bpm, regular; BP 100/60 torr; RR 25 bpm; 38.2°C. Auscultation of
heart: mild mid-systolic murmur with a clearly split 2nd heart sound. Auscultation of
lung: basal rales and loud respiratory sounds.
The emergency ECG confirms sinus tachycardia and shows T-wave inversions and
ST elevations together with bundle block (antero-lateral infarct?).
The radiology report states that there are congested pulmonary arteries with Kerley
B lines (pulmonary oedema?) and biventricular enlargement.
Chemical pathology results are consistent with myocardial infarction.
After emergency angiography, the patient was transferred to surgery for mitral valve
replacement and multiple bypasses. He subsequently recovered well.
CS 2015
Go and Invent Other Cases
It is simple - just take a case or so from
one of your clinical skill days…
Try and explain all findings - even
“normal” ones…
CS 2015
That’s it folks…
