Saturday, June 28, 2008
Wednesday, May 21, 2008
cardiac tips
First you have to know the function of the heart as a
vital organ.Make sure you know the circulation of
blood.from inf and superior vena cava to aorta.The
heart sound will be produced on CLOSURE of valves,that
S1 correspond to closure of Mitral and tricuspid valve
and not Aortic and pulmonic valve which is ur S2.They
both occur during systole or ventricular contraction.
S1 marks the begining of rapid ejection of blood so ur
aorta should be open!It make sense right?S3 sound is
associated with CHF(3 letter) and S4 for MI and
hypertension also known as atrial kick associated with
hypertropied ventricle,both occur on diastole,with S3
produced after S2 and S4 before S1.S1 starts while
blood is pump out so to prevent back flow mitral valve
shld be close,once blood is ejected and volume
decreases mitral valve should open to refill(inc.
PRELOAD) and to create an increase pressure inside the
heart for contraction to be effective (frank starling
law)aorta should be closed(S2).just remember its the
closures of the valves that creates the sound( as in
closing door when ur mad (BANG!!),hard to produce
sound when you open)).Should be remembered coz when
you panic or get nervous you might forget.
Nothing much to know about coronary circulation except
for (R) coronary artery that supplies most(80%) of ur
SAnode(pace maker of the heart) and AV node as injury
can cause a fatal arrhytmia.Coronary arteries fills
during DIASTOLE contrary to other organs that fills
during Systole.Most posterior part of heart is left
atrium and enlargement can cause dysphagia.The apex
beat is located at 5th ICSLMCL,its the most reliable
way to assess heart rate when peripheral pulses are
absent,too weak or unaccesible. Make it a practice to
appreciate abnormal heart sound and for accuracy for
patient with very weak pulses or having
atrial/ventricular fib may present with normal
palpable pulses.Elderly have collapsable artery
(pulse) not good to assess if with heart
condition.Brachial pulse is best for assessment in
kids.
You should know the formula for blood pressure to
understand the diseases esp CHF and effects of meds on
management of hypertension.Remember that BP is the
amount of pressure that the heart should have to pump
the blood and distribute it to circulation.
BP=Cardiac output(CO) x total peripheral
resistances(TPR)
your CO=stroke volume x HR.Your Stroke volume is the
amt of blood inside the heart being pump per
contraction,Your TPR represents the resistance to
blood flow primarilly due to arteries/arterioles which
is your resistance vessels(remember how
atherosclerosis or hardening of ur arteries lead to
hypertension!).Stroke volume is primarirly dependent
on the amount of blood that goes in ur heart ,the
veins which is ur capacitance vessels,and the fluid
both plasma and serum component of blood.It is also
dependent on how strong ur heart contracts(contractile
property of heart loss in CHF).
Now, what are the common meds and how they work?
initial management or meds will include your diuretics
(what makes you pee)this should decrease the preload
or fluid that goes in as CO(same amt with what goes
in)a little of afterload(the load similar to
TPR).Should watch out for fainting or dizziness with
sudden drop of BP.Strong diuretics like
LASIX(furosemide) can even include deafness bec. of
loss of fluid in your circular canal,or loss of
potassium leading to arrythmia and weakness.
2nd line is Beta blockers(those with
OLOL,propranolol(inderal)metoprolol,atenolol,..) will
decrease BP by decreasing HR and force of
contraction(dec. INOTROPIC property).And since its a
beta blocker it should be used with caution in patient
with asthma(treatment for asthma is beta agonist like
albuterol)Should know that Beta 1 is for the heart(u
only have 1 heart) and beta 2 for Lungs(2 lobes)
particularly on ur bronchus.In DM, beta blockers can
masked the effect of TACHYCARDIA as sign of
hypoglycemia,you might think that ur patient have
normal HR but his HR without beta blockers might be
already more than 100.It can also increase blood
glucose level.Use RPE on exercise assessment instead
of HR which is use on most cases.Other relative or
absolute CI is PVD, since it has an effect on smooth
ms lining ur peripheral vessels leading to compromise
blood flow.
So, 3 things to remember:Asthma,DM and PVD.Learn the
rationale so you wont forget!
May include CHF as CI but remember that it can be use
once STABLE not on ACUTE cases (previous and recent
studies shows that like ACEI it can decrease mortality
and morbidity in post MI and CHF including HTN)
Consistent effects of beta blockers is dec. in BP and
HR but for those with sudden drop in BP a compensatory
tachycardia may appear.FYI there are betablockers that
are selective and affect only B1 receptors,relatively
safe for those with previous condition that are CI.
Popular drug like ACE inhibitors(CAPTOPRIL) which
prevent conversion of Angiotensin I to angiotensin II
which is a potent vasoconstrictors(inc. TPR)and
decrease preload like diuretics due to decrease
production of aldosterone(salt production
Na(sodium))Most common side effect is dry COUGH due to
persistent bradykinin production,may be present for
several weeks ,may or may not persist.Replace with
ARB(angiotensin receptor blocker)those with SARTAN ,no
SE of cough.Directly block receptor of Angiotensin
II.Both are not safe for pregnant,teratogenic effect
bec. the fetus need AII for renal development.Renal
protective and prolong life in DM and MI.May increase
level of potassium in combination with
SPIRINOLACTONE(Aldactone)a potassium sparing diuretics
different from other diuretics that dec.level of
potasium, can also lead to arrhytmia.(brady
arrhytmia)remember potassium equals repolarization!
Other not so important meds : vasodilators/calcium
channel blockers-blocks calcium and relaxes arteries
leading to vasodilation,(calcium equals
contraction)some have effect on veins decreasing
preload,more blood remains on the capacitance vessels
not on the heart(nifedipine,hydralazine-can cause drug
induced SLE,verapamil-constipation).
Alpha 1 blockers/antagonist-prevent release of
NE(norepinephrine)-Prazosin(MINIPRESS) known for the
SE of FIRST DOSE EFFECT or sudden drop of BP leading
to syncope.
Alpha II AGONIST(the only adrenergic agonist)Clonidine
(CATAPRESS) facillitates/stimulates reuptake of NE not
to be release in presynaptic terminals.Decrease TPR.SE
includes sudden withdrawal lead to rebound
hypertension.
Remember that common cough and cold preparation that
contains phenylephrine,phenylpropanolamine(PPA) can
cause hypertension due to their vasoconstrictive
effect in preventing congestion.TCA
(tricyclicantidepressant)Amitryptylin(ELAVIL),imipramine
(DOFRANIL)- can increase NE,serotonin and dopamine
which is dec. in patient with depression but they also
block alpha adrenergic receptors(leading to
HYPOTENSION) and histamine leading to SEDATION.More
reasons to get depress if you fail to monitor
vitals...
Remember that you have Baroreceptors and
chemoreceptors that regulate your HR and BP.your
Baroreceptors includes ur carotid SINUS and aortic
arch.
Carotid sinus transmits via GLOSSOPHARYNGEAL nerve to
medulla.Your AORTIC arch transmits via VAGUS to
medulla(respond only to increase in BP)vagus as
parasympathetic will dec.HR and BP.Carotid massage
thru increase pressure in carotid will stimulate vagus
leading to dec.HR then BP.Simply stated when you have
increse BP your parasympathetic response will be
activated(dec.BP,contraction and HR) and reverse with
dec.BP as you activate ur symphatetic or as you
decrease stimulation of parasympathetic signals coming
from afferent receptors (CN 9 and 10)take note that 10
or vagus has also an efferent signals coming from
medulla.
REMEMBER that when you examine patency of carotids do
it one at a time not simultaneouslly or patient will
faint.wearing a turtle neck thats to tight may do the
same thing.other reason why stranguation lead to loss
of conciousness.
Remember that your medulla oblongata has
CARDIOINHIBITORY(parasymphatetic via vagus nerve)as
well as CARDIOACCELARATORY center(symphatetic or
adrenergic via T1-T4 releasing NE and Epinephrine).
Chemoreceptors from carotid and aortic BODIES which
responds to dec. in PO2,inc. CO2 and dec.
ph.(acidosis).
In response to cerebral ischemia( more of inc. in CO2
than dec. in O2) ur body will inc. ICP and inc. BP and
HR as sympathetic response but with dec. in HR as O2
level increases.
Some terms to remember:Chronotropic describes property
on inc.
HR(chrono=time)Inotropic(contractility)Dromotropic(pressure).
source: from PTforum
vital organ.Make sure you know the circulation of
blood.from inf and superior vena cava to aorta.The
heart sound will be produced on CLOSURE of valves,that
S1 correspond to closure of Mitral and tricuspid valve
and not Aortic and pulmonic valve which is ur S2.They
both occur during systole or ventricular contraction.
S1 marks the begining of rapid ejection of blood so ur
aorta should be open!It make sense right?S3 sound is
associated with CHF(3 letter) and S4 for MI and
hypertension also known as atrial kick associated with
hypertropied ventricle,both occur on diastole,with S3
produced after S2 and S4 before S1.S1 starts while
blood is pump out so to prevent back flow mitral valve
shld be close,once blood is ejected and volume
decreases mitral valve should open to refill(inc.
PRELOAD) and to create an increase pressure inside the
heart for contraction to be effective (frank starling
law)aorta should be closed(S2).just remember its the
closures of the valves that creates the sound( as in
closing door when ur mad (BANG!!),hard to produce
sound when you open)).Should be remembered coz when
you panic or get nervous you might forget.
Nothing much to know about coronary circulation except
for (R) coronary artery that supplies most(80%) of ur
SAnode(pace maker of the heart) and AV node as injury
can cause a fatal arrhytmia.Coronary arteries fills
during DIASTOLE contrary to other organs that fills
during Systole.Most posterior part of heart is left
atrium and enlargement can cause dysphagia.The apex
beat is located at 5th ICSLMCL,its the most reliable
way to assess heart rate when peripheral pulses are
absent,too weak or unaccesible. Make it a practice to
appreciate abnormal heart sound and for accuracy for
patient with very weak pulses or having
atrial/ventricular fib may present with normal
palpable pulses.Elderly have collapsable artery
(pulse) not good to assess if with heart
condition.Brachial pulse is best for assessment in
kids.
You should know the formula for blood pressure to
understand the diseases esp CHF and effects of meds on
management of hypertension.Remember that BP is the
amount of pressure that the heart should have to pump
the blood and distribute it to circulation.
BP=Cardiac output(CO) x total peripheral
resistances(TPR)
your CO=stroke volume x HR.Your Stroke volume is the
amt of blood inside the heart being pump per
contraction,Your TPR represents the resistance to
blood flow primarilly due to arteries/arterioles which
is your resistance vessels(remember how
atherosclerosis or hardening of ur arteries lead to
hypertension!).Stroke volume is primarirly dependent
on the amount of blood that goes in ur heart ,the
veins which is ur capacitance vessels,and the fluid
both plasma and serum component of blood.It is also
dependent on how strong ur heart contracts(contractile
property of heart loss in CHF).
Now, what are the common meds and how they work?
initial management or meds will include your diuretics
(what makes you pee)this should decrease the preload
or fluid that goes in as CO(same amt with what goes
in)a little of afterload(the load similar to
TPR).Should watch out for fainting or dizziness with
sudden drop of BP.Strong diuretics like
LASIX(furosemide) can even include deafness bec. of
loss of fluid in your circular canal,or loss of
potassium leading to arrythmia and weakness.
2nd line is Beta blockers(those with
OLOL,propranolol(inderal)metoprolol,atenolol,..) will
decrease BP by decreasing HR and force of
contraction(dec. INOTROPIC property).And since its a
beta blocker it should be used with caution in patient
with asthma(treatment for asthma is beta agonist like
albuterol)Should know that Beta 1 is for the heart(u
only have 1 heart) and beta 2 for Lungs(2 lobes)
particularly on ur bronchus.In DM, beta blockers can
masked the effect of TACHYCARDIA as sign of
hypoglycemia,you might think that ur patient have
normal HR but his HR without beta blockers might be
already more than 100.It can also increase blood
glucose level.Use RPE on exercise assessment instead
of HR which is use on most cases.Other relative or
absolute CI is PVD, since it has an effect on smooth
ms lining ur peripheral vessels leading to compromise
blood flow.
So, 3 things to remember:Asthma,DM and PVD.Learn the
rationale so you wont forget!
May include CHF as CI but remember that it can be use
once STABLE not on ACUTE cases (previous and recent
studies shows that like ACEI it can decrease mortality
and morbidity in post MI and CHF including HTN)
Consistent effects of beta blockers is dec. in BP and
HR but for those with sudden drop in BP a compensatory
tachycardia may appear.FYI there are betablockers that
are selective and affect only B1 receptors,relatively
safe for those with previous condition that are CI.
Popular drug like ACE inhibitors(CAPTOPRIL) which
prevent conversion of Angiotensin I to angiotensin II
which is a potent vasoconstrictors(inc. TPR)and
decrease preload like diuretics due to decrease
production of aldosterone(salt production
Na(sodium))Most common side effect is dry COUGH due to
persistent bradykinin production,may be present for
several weeks ,may or may not persist.Replace with
ARB(angiotensin receptor blocker)those with SARTAN ,no
SE of cough.Directly block receptor of Angiotensin
II.Both are not safe for pregnant,teratogenic effect
bec. the fetus need AII for renal development.Renal
protective and prolong life in DM and MI.May increase
level of potassium in combination with
SPIRINOLACTONE(Aldactone)a potassium sparing diuretics
different from other diuretics that dec.level of
potasium, can also lead to arrhytmia.(brady
arrhytmia)remember potassium equals repolarization!
Other not so important meds : vasodilators/calcium
channel blockers-blocks calcium and relaxes arteries
leading to vasodilation,(calcium equals
contraction)some have effect on veins decreasing
preload,more blood remains on the capacitance vessels
not on the heart(nifedipine,hydralazine-can cause drug
induced SLE,verapamil-constipation).
Alpha 1 blockers/antagonist-prevent release of
NE(norepinephrine)-Prazosin(MINIPRESS) known for the
SE of FIRST DOSE EFFECT or sudden drop of BP leading
to syncope.
Alpha II AGONIST(the only adrenergic agonist)Clonidine
(CATAPRESS) facillitates/stimulates reuptake of NE not
to be release in presynaptic terminals.Decrease TPR.SE
includes sudden withdrawal lead to rebound
hypertension.
Remember that common cough and cold preparation that
contains phenylephrine,phenylpropanolamine(PPA) can
cause hypertension due to their vasoconstrictive
effect in preventing congestion.TCA
(tricyclicantidepressant)Amitryptylin(ELAVIL),imipramine
(DOFRANIL)- can increase NE,serotonin and dopamine
which is dec. in patient with depression but they also
block alpha adrenergic receptors(leading to
HYPOTENSION) and histamine leading to SEDATION.More
reasons to get depress if you fail to monitor
vitals...
Remember that you have Baroreceptors and
chemoreceptors that regulate your HR and BP.your
Baroreceptors includes ur carotid SINUS and aortic
arch.
Carotid sinus transmits via GLOSSOPHARYNGEAL nerve to
medulla.Your AORTIC arch transmits via VAGUS to
medulla(respond only to increase in BP)vagus as
parasympathetic will dec.HR and BP.Carotid massage
thru increase pressure in carotid will stimulate vagus
leading to dec.HR then BP.Simply stated when you have
increse BP your parasympathetic response will be
activated(dec.BP,contraction and HR) and reverse with
dec.BP as you activate ur symphatetic or as you
decrease stimulation of parasympathetic signals coming
from afferent receptors (CN 9 and 10)take note that 10
or vagus has also an efferent signals coming from
medulla.
REMEMBER that when you examine patency of carotids do
it one at a time not simultaneouslly or patient will
faint.wearing a turtle neck thats to tight may do the
same thing.other reason why stranguation lead to loss
of conciousness.
Remember that your medulla oblongata has
CARDIOINHIBITORY(parasymphatetic via vagus nerve)as
well as CARDIOACCELARATORY center(symphatetic or
adrenergic via T1-T4 releasing NE and Epinephrine).
Chemoreceptors from carotid and aortic BODIES which
responds to dec. in PO2,inc. CO2 and dec.
ph.(acidosis).
In response to cerebral ischemia( more of inc. in CO2
than dec. in O2) ur body will inc. ICP and inc. BP and
HR as sympathetic response but with dec. in HR as O2
level increases.
Some terms to remember:Chronotropic describes property
on inc.
HR(chrono=time)Inotropic(contractility)Dromotropic(pressure).
source: from PTforum
Friday, May 16, 2008
AMPUTATION
AMPUTATION
-absence of all part of a limb asa a result of surgery,trama,or disease
-aka removal of a limb through the continuity of a bone
-LE-most common cause of amputation is PVD
-UE-most common cause of amptation is trauma
General Classisfication of Amputation:
A.CONGENITALAMPUTATION
-occurs in utero
B.ACQUIRED AMPUTATION
-traumatic
-ischemic-due to PVD
-surgical-done for cosmetic purposes(amputaion secondary to polydactyly)
*can also be classified as:
A.Major-amputation above MCP/MTP
B.Minor-amputation through distal to MCP/MTP
Indications:
1. Vascular accident or disease
-when infection is imminent and wound healing is uncertain
2.Infection
-Most common indication for amputation (i.e.gangrene)
a. Acute-threatens invasion to other parts of the body;endangering life
b. Chronic-source of toxic absorption (i.e. osteomyelitis)
3.Congenital anomaly
-amputation is due to failure of the limb to develop fully
-surgical amputation - is indicated to improve,to form/shape the deformed/deficient limb so that fitting of an artificial limb is possible
4.Trauma
-results in destruction of blood supply or results in extensive destruction where reconstructive is no longer feasible
5.Tumor
-If benign amputationis indicated only if it will result in functional limb
-If malignant,amputation is done to prevent further spread of malignancy
6.Thermal,Chemical or electrical in injury (severe burn inury)
-Injuries from extreme heat /cold (frostbite) can also lead to amputation
SITES OF AMPUTATION:
A.UPPER EXTREMITIY AMPUTATION:
1.Amputation thru the fingers (ray amputation)
3 Basics functions:
a. grasp
b. pinch
c. hook
Thumb
a. imporatntin grasp, vital in pinch
b .40%-50% function loss when thumb is amputated
Index and middle finger
a. most impotant in all 3fucnctions because of their proximity o the thumb
b. srtrogest and most stable
c. 20% index finger and 20% middle finger
Ring and little finger
a. 10% each for ring finger and little finger too
b. provides mobility
c. aids in the combineddexterity of all fingers
2.Amputation about wrist
Advantages:
a. pronation are preserved
b .greater stump adaptability (not as cumbersome/uncomfortable compared to above
the elbow amputation)
c. retains natural wrist flexion and extension if amputation is done thru the carpals
Amputation thru the CARPALS ( midcarpal amputation) with palmar ski
a. easil;y performed since radiocarpal joint is not invaded
b .rounded to smooth contour and covered with palmar skin
c .retains the wrist flexion
Disarticulation of the wrist at the radiocarpal joint
3.Amputation thru the lower third of the forearm
a. poor since the skin is thin and underlying soft tissue are largely tendons and fascia
b. poor since the circulation is not good;the stump is frequently cold,tender and cyanotic
c. secondary skin breakdown is common
d. not adaptable with use of prosthesis(poor muscular padding)
e. NO pronation /supination
4.Amputation at the junction of the middle and lower third of the forearm
a. IDEAL TRANSRADIO-ULNAR STUMP ( functionally and cosmetically)
b. Ideal length:7-8 inches from the tip of the olecranon process to the end of the stump
c. circulation is good in this area
d. full elbow flexion is very possible
5.Amputation above the ideal
a.forearm/elbow flexion may be normal but can be impaired in either its range or
strength
6.Amoputation through the humerus
a.Disarticulation thru the elbow joint
a. at the end of the humero-ulnar and the humero-radial joint
b. retains near normal of the shoulder
b.Transcondylar amputation
a.amputation thru epicondyles(long above the elbow stump)
b. hard to fit with a prosthesis
c.Through the supracondylar region
a.still considered a long above the elbow stump
7.Amputation above the supracondylar region
a. IDEAL TRANSHUMERAL STUMP
b. Ideal length 8 inches from the acromion process to the end of he stump
b. most functional stump
8.Amputation about the shoulder
a. functional prosthesis cannot be worn ( worn only for cosmesis,impractical)
b. 2 possible levels
a. thru the surgical neck of the humerus
b.disarticulation at the scapulohumeral jt
9.Forequarter Amputation (shoulder girdle/interscapulothoracic amputation
a. At the interval between the scapula and the thoracic wall
b. All shoulder functions are obliterated
B. Lower Extremity Amputations
1.Foot amputations
-balance between muscle and bony support is lost
A.Toes
- function in tip-toeing
- amputation results in loss of push-off
Big /great toe
-has supporting role in stance
-fulfills a vital function in gait,principlal wt bearing element in the final
phase of hell-off (adds rhythm and agility)
-when amputated,the loss is felt more during rapid walking and
running
Lesser toes
-principal functions:
1. stabilize the foot by widening the base of support during squatting
and tip-toeing
2.assist the great toe in push-off and heel-off during rapid gait and running
-amputation at the 2nd toe in the proximal phalanx results in hallux valgus deformity
B. Metatarsals
-balance and weight distribution are disturbed in the direct proportion to the extent and location of loss
C. Above metatarsals
-stump is worthless even as support for the prosthesis
2.Amputation thru the metatarsal and ankle joint
a. SYME’S AMPUTATION
-transmalleolar amputation
-designed for weight bearing at the end of the stump
-provides stability for prosthesis,maybe used without prosthesis
b. BOYD’s Amputation
-weight bearing over calcaneous following removal of remaining bones of the foot and
calcaneo-tibial arthrodesis
c. Vasconecelos Amputation
-done if use of an artificial limb is not anticipated
-midtarsal amutation combined with tibiotalar and subtalar arthrodesis and section of the inferior surface of the calcaneous.
d. Pirogoff’s Amputation
-principle of arthrodesis of the tibia to the calcaneous after the latter has been rotated forward and upward 90degrees (anteversion)
-unsuccesful for prosthetic fiiting due to its irregular shape
e. Listfranc’s Amputation
-disarticulation of the foot through the tarsometatarsal joint
-falls into moderate equines deformity
-like the pirogoff’s amputation,unsuccessful for prosthetic use
f. Chopart’s Amputation
-thru the transverse tarsal joint (talonavicular/calcaneocuboid)
-intended for end bearing
-prosthetic fitting not possible
3.Amputation thru the lower leg (IDEAL SHAPE for TRANSTIBIO-FIBULAR :
CYLINDRICAL)
a.thru the lower 3rd of the leg
- unsatisfactory adaptation of the stump to the prosthesis
c. amputation thru the middle third
-IDEAL LENGTH FOR TRANSTIBIO-FIBULAR AMPUTATION
-6 inches (5-7 inches) from the medial tibial plateau/tibial tubercle to the end of the stump
-quadriceps tends to weaken (vastus medialis) since hamstrings tend to pull stump into
flexion
4. Amputation thru the thigh ( IDEAL SHAPE for TRANSFEMORAL AMPUTATION:
CONICAL)
a. Grittie-Stokes amputation
-Similar to syme’s amputation (provides weight bearing and can withstand excessive strain)\
-Utilized sectioned patella fused to the femur at or about the level of the adductor
Tubercle
-osteoplasty which involdves disarticulation of the knee joint,then sawing off the
articular surface of the patella,the patella is approximated to the end of the
femur,created an end bearing stump
b. Ischial bearing amputation
-IDEAL TRANSFEMORAL AMPUTATION
_Ideal length:10-12 inches from the greater rochanter to the ned of the stump
-utilizes the power of adductur muscles
-iliopsoas (hip flexors) and gluteus medius (abductors) unaffected
-Gluetus maximus (hip extensors) and adductor magnus reduced in volume and power
5. Amputation thru the thigh above the ideal level
-the shorter the stump, the greater the difficulty in maintaining and activating the
prosthesis
-greater tendency for contractures
-when te stump is only 3-4 below ischial tuberosity and adductor tendon insertion,it is
it is impossible to retain the stump within the socket of the prosthesis
6.Amputaton about the hip
-amputation thru the trochanters,femoral neck and hip disarticulation
-needs to be fitted with a tilt table type of prosthesis
7.Hindquarter Amputation
-done only in cases where there is a malignant tumor
-removal of the pelvis by disarticulation of the symphysis pubis and section of the
posterior portion of the ilium near the SI jt (together with the severance of the soft
tissues connecting the trunk with the extremities)
8.Hemicorporectomy
-removal of the entire lower extremity through the last 2 lumbar vertebrae (L4-L5)
sacrum,coccyx,half of the pelvis
-Involves the creational of an artificial bladder and rectum
LEVELS OF AMPUTATION:
A.UE
-if unilateral
percentage from Normal
a.Transhumeral ---------------Classification
0=shoulder disarticulation
0-30 =humeral neck
30-50 =short transhumeral stump
50-90= long transhumeral stump,
elbow disarticulation
b.transradio-ulnar
-absence of all part of a limb asa a result of surgery,trama,or disease
-aka removal of a limb through the continuity of a bone
-LE-most common cause of amputation is PVD
-UE-most common cause of amptation is trauma
General Classisfication of Amputation:
A.CONGENITALAMPUTATION
-occurs in utero
B.ACQUIRED AMPUTATION
-traumatic
-ischemic-due to PVD
-surgical-done for cosmetic purposes(amputaion secondary to polydactyly)
*can also be classified as:
A.Major-amputation above MCP/MTP
B.Minor-amputation through distal to MCP/MTP
Indications:
1. Vascular accident or disease
-when infection is imminent and wound healing is uncertain
2.Infection
-Most common indication for amputation (i.e.gangrene)
a. Acute-threatens invasion to other parts of the body;endangering life
b. Chronic-source of toxic absorption (i.e. osteomyelitis)
3.Congenital anomaly
-amputation is due to failure of the limb to develop fully
-surgical amputation - is indicated to improve,to form/shape the deformed/deficient limb so that fitting of an artificial limb is possible
4.Trauma
-results in destruction of blood supply or results in extensive destruction where reconstructive is no longer feasible
5.Tumor
-If benign amputationis indicated only if it will result in functional limb
-If malignant,amputation is done to prevent further spread of malignancy
6.Thermal,Chemical or electrical in injury (severe burn inury)
-Injuries from extreme heat /cold (frostbite) can also lead to amputation
SITES OF AMPUTATION:
A.UPPER EXTREMITIY AMPUTATION:
1.Amputation thru the fingers (ray amputation)
3 Basics functions:
a. grasp
b. pinch
c. hook
Thumb
a. imporatntin grasp, vital in pinch
b .40%-50% function loss when thumb is amputated
Index and middle finger
a. most impotant in all 3fucnctions because of their proximity o the thumb
b. srtrogest and most stable
c. 20% index finger and 20% middle finger
Ring and little finger
a. 10% each for ring finger and little finger too
b. provides mobility
c. aids in the combineddexterity of all fingers
2.Amputation about wrist
Advantages:
a. pronation are preserved
b .greater stump adaptability (not as cumbersome/uncomfortable compared to above
the elbow amputation)
c. retains natural wrist flexion and extension if amputation is done thru the carpals
Amputation thru the CARPALS ( midcarpal amputation) with palmar ski
a. easil;y performed since radiocarpal joint is not invaded
b .rounded to smooth contour and covered with palmar skin
c .retains the wrist flexion
Disarticulation of the wrist at the radiocarpal joint
3.Amputation thru the lower third of the forearm
a. poor since the skin is thin and underlying soft tissue are largely tendons and fascia
b. poor since the circulation is not good;the stump is frequently cold,tender and cyanotic
c. secondary skin breakdown is common
d. not adaptable with use of prosthesis(poor muscular padding)
e. NO pronation /supination
4.Amputation at the junction of the middle and lower third of the forearm
a. IDEAL TRANSRADIO-ULNAR STUMP ( functionally and cosmetically)
b. Ideal length:7-8 inches from the tip of the olecranon process to the end of the stump
c. circulation is good in this area
d. full elbow flexion is very possible
5.Amputation above the ideal
a.forearm/elbow flexion may be normal but can be impaired in either its range or
strength
6.Amoputation through the humerus
a.Disarticulation thru the elbow joint
a. at the end of the humero-ulnar and the humero-radial joint
b. retains near normal of the shoulder
b.Transcondylar amputation
a.amputation thru epicondyles(long above the elbow stump)
b. hard to fit with a prosthesis
c.Through the supracondylar region
a.still considered a long above the elbow stump
7.Amputation above the supracondylar region
a. IDEAL TRANSHUMERAL STUMP
b. Ideal length 8 inches from the acromion process to the end of he stump
b. most functional stump
8.Amputation about the shoulder
a. functional prosthesis cannot be worn ( worn only for cosmesis,impractical)
b. 2 possible levels
a. thru the surgical neck of the humerus
b.disarticulation at the scapulohumeral jt
9.Forequarter Amputation (shoulder girdle/interscapulothoracic amputation
a. At the interval between the scapula and the thoracic wall
b. All shoulder functions are obliterated
B. Lower Extremity Amputations
1.Foot amputations
-balance between muscle and bony support is lost
A.Toes
- function in tip-toeing
- amputation results in loss of push-off
Big /great toe
-has supporting role in stance
-fulfills a vital function in gait,principlal wt bearing element in the final
phase of hell-off (adds rhythm and agility)
-when amputated,the loss is felt more during rapid walking and
running
Lesser toes
-principal functions:
1. stabilize the foot by widening the base of support during squatting
and tip-toeing
2.assist the great toe in push-off and heel-off during rapid gait and running
-amputation at the 2nd toe in the proximal phalanx results in hallux valgus deformity
B. Metatarsals
-balance and weight distribution are disturbed in the direct proportion to the extent and location of loss
C. Above metatarsals
-stump is worthless even as support for the prosthesis
2.Amputation thru the metatarsal and ankle joint
a. SYME’S AMPUTATION
-transmalleolar amputation
-designed for weight bearing at the end of the stump
-provides stability for prosthesis,maybe used without prosthesis
b. BOYD’s Amputation
-weight bearing over calcaneous following removal of remaining bones of the foot and
calcaneo-tibial arthrodesis
c. Vasconecelos Amputation
-done if use of an artificial limb is not anticipated
-midtarsal amutation combined with tibiotalar and subtalar arthrodesis and section of the inferior surface of the calcaneous.
d. Pirogoff’s Amputation
-principle of arthrodesis of the tibia to the calcaneous after the latter has been rotated forward and upward 90degrees (anteversion)
-unsuccesful for prosthetic fiiting due to its irregular shape
e. Listfranc’s Amputation
-disarticulation of the foot through the tarsometatarsal joint
-falls into moderate equines deformity
-like the pirogoff’s amputation,unsuccessful for prosthetic use
f. Chopart’s Amputation
-thru the transverse tarsal joint (talonavicular/calcaneocuboid)
-intended for end bearing
-prosthetic fitting not possible
3.Amputation thru the lower leg (IDEAL SHAPE for TRANSTIBIO-FIBULAR :
CYLINDRICAL)
a.thru the lower 3rd of the leg
- unsatisfactory adaptation of the stump to the prosthesis
c. amputation thru the middle third
-IDEAL LENGTH FOR TRANSTIBIO-FIBULAR AMPUTATION
-6 inches (5-7 inches) from the medial tibial plateau/tibial tubercle to the end of the stump
-quadriceps tends to weaken (vastus medialis) since hamstrings tend to pull stump into
flexion
4. Amputation thru the thigh ( IDEAL SHAPE for TRANSFEMORAL AMPUTATION:
CONICAL)
a. Grittie-Stokes amputation
-Similar to syme’s amputation (provides weight bearing and can withstand excessive strain)\
-Utilized sectioned patella fused to the femur at or about the level of the adductor
Tubercle
-osteoplasty which involdves disarticulation of the knee joint,then sawing off the
articular surface of the patella,the patella is approximated to the end of the
femur,created an end bearing stump
b. Ischial bearing amputation
-IDEAL TRANSFEMORAL AMPUTATION
_Ideal length:10-12 inches from the greater rochanter to the ned of the stump
-utilizes the power of adductur muscles
-iliopsoas (hip flexors) and gluteus medius (abductors) unaffected
-Gluetus maximus (hip extensors) and adductor magnus reduced in volume and power
5. Amputation thru the thigh above the ideal level
-the shorter the stump, the greater the difficulty in maintaining and activating the
prosthesis
-greater tendency for contractures
-when te stump is only 3-4 below ischial tuberosity and adductor tendon insertion,it is
it is impossible to retain the stump within the socket of the prosthesis
6.Amputaton about the hip
-amputation thru the trochanters,femoral neck and hip disarticulation
-needs to be fitted with a tilt table type of prosthesis
7.Hindquarter Amputation
-done only in cases where there is a malignant tumor
-removal of the pelvis by disarticulation of the symphysis pubis and section of the
posterior portion of the ilium near the SI jt (together with the severance of the soft
tissues connecting the trunk with the extremities)
8.Hemicorporectomy
-removal of the entire lower extremity through the last 2 lumbar vertebrae (L4-L5)
sacrum,coccyx,half of the pelvis
-Involves the creational of an artificial bladder and rectum
LEVELS OF AMPUTATION:
A.UE
-if unilateral
percentage from Normal
a.Transhumeral ---------------Classification
0=shoulder disarticulation
0-30 =humeral neck
30-50 =short transhumeral stump
50-90= long transhumeral stump,
elbow disarticulation
b.transradio-ulnar
ECG lecture of PTMD
ELECTROCARDIOGRAM
Normal Sinus Rhythm
• Each P wave is followed by a QRS
• P wave rate is 60 bpm
Rate < 60 = sinus bradycardia
Rate > 60 = sinus tachycardia
P wave – atrial depolarization
PR segment – conduction delay through AV node
- normally <200 msec / 0.12 – 0.20 sec
QRS complex – ventricular depolarization
- normally <120 msec / .08 - .12 sec
QT interval – mechanical contraction of the ventricles
T wave – ventricular repolarization
Atrial repolarization is masked by QRS complex
ST segment – isoelectric, ventricles depolarized
U wave – caused by hypokalemia
ANALYZING THE ECG
1. RATE
The first step is to determine the RATE, which can be eyeballed by the following technique. Locate the QRS (the big spike) complex that is closest to a dark vertical line. Then count either forward or backwards to the next QRS complex. For each dark vertical line you pass, select the next number off the mnemonic "300-150-100-75-60-50" to estimate the rate in beats per minute (BPM).
In other words if you pass 2 lines before the next QRS, the heart rate (HR) would be less than 150. Remember that this is merely an estimate
2. RHYTHM
- determine if its sinus or an ectopic rhythm
- If there is a P wave before each QRS and the P is in the same direction as the QRS, the rhythm can be said to be sinus.
3. AXIS
normal axis- I (+) and AVF (+)
- I (+) and left axis deviationAVF (-)
right axis deviation- I (-) and AVF (+)
- extreme right axis deviationI (-) and AVF (-)
*LEADS (important for MI)
• V1 V2 -- anterior note: sometimes V1 V2 V3 V4 (anterior)
• V3 V4 --septal
• V5-V6, I, aVL -- lateral
• II, III, aVF – inferior
4. HYPERTROPHY
Right Atrial Hypertrophy
o P wave in lead II taller than 2.5mm (2.5 small squares)
Left Atrial Hypertrophy
-P wave duration > 0.12s in frontal plane (usually lead II)
-Notched P wave in limb leads with the inter-peak duration > 0.04s
Right Ventricular Hypertrophy
-Reversal of precordial pattern
-Tall R in V1 and V2
-Deep S in V5 and V6
-Normal QRS duration
Left Ventricular Hypertrophy
-S in V1 or V2) + (R in V5 or V6) >35 mm (over age 35)
CONDUCTION ABNORMALITIES
ATRIO-VENTRICULAR (AV) BLOCKS
RHYTHM ABNORMALITIES
SUPRAVENTRICULAR TACHYARRHYTHMIAS
1. Sinus Tachycardia
- Ventricular rate >100 bpm
-Normal P waves before every QRS
2. Paroxysmal Atrial Tachycardia (PAT)
-Rapid ectopic pacemaker in atrium (not sinus node)
-Rate > 100 bpm
-P wave with unusual axis before each normal QRS
3. Atrial Flutter
-A characteristic 'sawtooth' or 'picket-fence' waveform of an intra-atrial re-entry circuit usually at about 300 bpm.
4. Atrial Fibrillation
- Wavy baseline without discernible P waves
- Variable and irregular QRS response
- The rhythm is irregularly irregular
5. Premature Ventricular Contraction
o Ectopic beats arise from ventricular foci
o Common and often benign
o It is usually asymptomatic, but may cause palpitations
o Causese include hypoxia, electrolyte abnormalities, hyperthyroidism
o ECG tracings revealed early, wide QRS complexes that are not preceded by a P wave.
o PVCs are followed by a compensatory pause
o No treatment if asymptomatic. If symptomatic, give B-Blockers or other antiarrhythmics. Treat the underlying causes
6. Ventricular Tachycardia
o Associated with CAD and MI
o Three or more consecutive PVCs
o Wide QRS complexes in a regular and rapid rhythm
o AV dissociation
7. Ventricular Fibrillation
o A completely erratic rhythm with no identifiable waves.
o Treat with immediate electrical cardioversion and ACLS protocol
Normal Sinus Rhythm
• Each P wave is followed by a QRS
• P wave rate is 60 bpm
Rate < 60 = sinus bradycardia
Rate > 60 = sinus tachycardia
P wave – atrial depolarization
PR segment – conduction delay through AV node
- normally <200 msec / 0.12 – 0.20 sec
QRS complex – ventricular depolarization
- normally <120 msec / .08 - .12 sec
QT interval – mechanical contraction of the ventricles
T wave – ventricular repolarization
Atrial repolarization is masked by QRS complex
ST segment – isoelectric, ventricles depolarized
U wave – caused by hypokalemia
ANALYZING THE ECG
1. RATE
The first step is to determine the RATE, which can be eyeballed by the following technique. Locate the QRS (the big spike) complex that is closest to a dark vertical line. Then count either forward or backwards to the next QRS complex. For each dark vertical line you pass, select the next number off the mnemonic "300-150-100-75-60-50" to estimate the rate in beats per minute (BPM).
In other words if you pass 2 lines before the next QRS, the heart rate (HR) would be less than 150. Remember that this is merely an estimate
2. RHYTHM
- determine if its sinus or an ectopic rhythm
- If there is a P wave before each QRS and the P is in the same direction as the QRS, the rhythm can be said to be sinus.
3. AXIS
normal axis- I (+) and AVF (+)
- I (+) and left axis deviationAVF (-)
right axis deviation- I (-) and AVF (+)
- extreme right axis deviationI (-) and AVF (-)
*LEADS (important for MI)
• V1 V2 -- anterior note: sometimes V1 V2 V3 V4 (anterior)
• V3 V4 --septal
• V5-V6, I, aVL -- lateral
• II, III, aVF – inferior
4. HYPERTROPHY
Right Atrial Hypertrophy
o P wave in lead II taller than 2.5mm (2.5 small squares)
Left Atrial Hypertrophy
-P wave duration > 0.12s in frontal plane (usually lead II)
-Notched P wave in limb leads with the inter-peak duration > 0.04s
Right Ventricular Hypertrophy
-Reversal of precordial pattern
-Tall R in V1 and V2
-Deep S in V5 and V6
-Normal QRS duration
Left Ventricular Hypertrophy
-S in V1 or V2) + (R in V5 or V6) >35 mm (over age 35)
CONDUCTION ABNORMALITIES
ATRIO-VENTRICULAR (AV) BLOCKS
RHYTHM ABNORMALITIES
SUPRAVENTRICULAR TACHYARRHYTHMIAS
1. Sinus Tachycardia
- Ventricular rate >100 bpm
-Normal P waves before every QRS
2. Paroxysmal Atrial Tachycardia (PAT)
-Rapid ectopic pacemaker in atrium (not sinus node)
-Rate > 100 bpm
-P wave with unusual axis before each normal QRS
3. Atrial Flutter
-A characteristic 'sawtooth' or 'picket-fence' waveform of an intra-atrial re-entry circuit usually at about 300 bpm.
4. Atrial Fibrillation
- Wavy baseline without discernible P waves
- Variable and irregular QRS response
- The rhythm is irregularly irregular
5. Premature Ventricular Contraction
o Ectopic beats arise from ventricular foci
o Common and often benign
o It is usually asymptomatic, but may cause palpitations
o Causese include hypoxia, electrolyte abnormalities, hyperthyroidism
o ECG tracings revealed early, wide QRS complexes that are not preceded by a P wave.
o PVCs are followed by a compensatory pause
o No treatment if asymptomatic. If symptomatic, give B-Blockers or other antiarrhythmics. Treat the underlying causes
6. Ventricular Tachycardia
o Associated with CAD and MI
o Three or more consecutive PVCs
o Wide QRS complexes in a regular and rapid rhythm
o AV dissociation
7. Ventricular Fibrillation
o A completely erratic rhythm with no identifiable waves.
o Treat with immediate electrical cardioversion and ACLS protocol
CTSIB
Static balance, the Clinical Test of Sensory Interaction for Balance (CTSIB)
The Clinical Test for Sensory Interaction of Balance (CTSIB) is a more complex sensory strategy balance test. It is administered by:
1) manipulating the support surface (ie, firm vs foam),
2) visual conditions (ie, eyes open, eyes closed), and
3) vestibular system (sway reference by using a dome or computerized sway platform ), while an individual is asked to maintain their standing balance.
The CTSIB test helps determine which sensory system (visual, somatosensory, or vestibular) the person relies on to maintain balance.
The Clinical Test of Sensory Interaction and Balance is a timed test (normal is 30 seconds) that was developed for systematically testing the influence of visual, vestibular, and somatosensory input on standing balance.[2] This test is inexpensive, requires minimal equipment, and is currently in use by some clinicians. Conditions 1, 2, and 3 involve standing on the floor with eyes open, eyes closed, and wearing a visual-conflict dome. The dome provides a sensory conflict by depriving the subject of peripheral vision and introducing a sway-referenced image. Use of the conflict dome results in a discrepancy between vestibular input stimulated by postural sway and visual flow.[1] Thus, conditions 2 and 3 should examine different aspects of sensory organization of visual information that may require different postural adjustments.[3] That is, condition 2 examines how well subjects maintain balance in the absence of any vision, and condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.
Conditions 4, 5, and 6 involve standing on foam and repeating the visual conditions described for conditions 1 through 3. For each condition, the length of time the subject can maintain standing and the amount of body sway that occurs are assessed.
1: eyes open and firm surface, ( all 3 sensory systems are available here, vision, somatosensory and the vestibular system, normal standing time is at least 30 sec)
2: eyes closed and firm surface, (2 sensory system are available here, somatosensory/vestibular. You take away the vision; patients who are dependent on vision become unsteady here. That is, condition 2 examines how well subjects maintain balance in the absence of vision)
3: eyes open, visual conflict (dome) and firm surface ( All three systems are available, but you have a conflict between eyes and vestibular information, patients who are dependent on vision are unsteady here; condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.)
X
4: eyes open and unstable surface (foam) ( if patients are dependent on surface/somatosensory inputs, they are unsteady in this position, and number 5 and 6; i.e . all positions on foam/unsteady surface; vision and vestibular system are available)
5: eyes closed and unstable surface ( you have taken away vision and the reliance on the surface/somatosensory system; patients with vision dependency due to somatosensory or vestibular loss are unsteady here)
6: eyes open, visual conflict and unstable surface ( visual conflict can create a problem for patients depending on their vision for balance, patients with somatosensory or vestibular loss are unsteady here)
X
In Summary:
• Patients dependent on vision become unstable in conditions 2,3, 5 & 6 where we either close the eyes, or have a conflict between vision and the vestibular system
• Patients dependent on surface/somatosensory inputs become unstable in conditions 4,5 & 6 because we stand the patient on a soft surface ( foam)
• Patients with vestibular loss become unstable in conditions 5 &6 because they can’t rely on vision or surface/ somatosensory function
• Patients with sensory selection problems become unstable in conditions 3-6.
Treatment: Treatments may involve the manipulation of sensory input while performing a task. This may be done for any of the three systems responsible for providing sensory feedback. For example, to encourage use of vestibular input, visual and somatosensory information may be challenged. Visual input is challenged by taking it away (e.g., eyes closed) or by destabilization (e.g., involving head and eye movements in the task). Unstable surfaces (e.g., rocker board or rough terrain) or compliant surfaces(e.g., foam) help to challenge somatosensory input. Vestibular input may be manipulated by changing the position of the vestibular organ (e.g., neck extension or repeated head movements).
The Clinical Test for Sensory Interaction of Balance (CTSIB) is a more complex sensory strategy balance test. It is administered by:
1) manipulating the support surface (ie, firm vs foam),
2) visual conditions (ie, eyes open, eyes closed), and
3) vestibular system (sway reference by using a dome or computerized sway platform ), while an individual is asked to maintain their standing balance.
The CTSIB test helps determine which sensory system (visual, somatosensory, or vestibular) the person relies on to maintain balance.
The Clinical Test of Sensory Interaction and Balance is a timed test (normal is 30 seconds) that was developed for systematically testing the influence of visual, vestibular, and somatosensory input on standing balance.[2] This test is inexpensive, requires minimal equipment, and is currently in use by some clinicians. Conditions 1, 2, and 3 involve standing on the floor with eyes open, eyes closed, and wearing a visual-conflict dome. The dome provides a sensory conflict by depriving the subject of peripheral vision and introducing a sway-referenced image. Use of the conflict dome results in a discrepancy between vestibular input stimulated by postural sway and visual flow.[1] Thus, conditions 2 and 3 should examine different aspects of sensory organization of visual information that may require different postural adjustments.[3] That is, condition 2 examines how well subjects maintain balance in the absence of any vision, and condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.
Conditions 4, 5, and 6 involve standing on foam and repeating the visual conditions described for conditions 1 through 3. For each condition, the length of time the subject can maintain standing and the amount of body sway that occurs are assessed.
1: eyes open and firm surface, ( all 3 sensory systems are available here, vision, somatosensory and the vestibular system, normal standing time is at least 30 sec)
2: eyes closed and firm surface, (2 sensory system are available here, somatosensory/vestibular. You take away the vision; patients who are dependent on vision become unsteady here. That is, condition 2 examines how well subjects maintain balance in the absence of vision)
3: eyes open, visual conflict (dome) and firm surface ( All three systems are available, but you have a conflict between eyes and vestibular information, patients who are dependent on vision are unsteady here; condition 3 examines how well subjects maintain balance when vision is present but that information conflicts with vestibular information.)
X
4: eyes open and unstable surface (foam) ( if patients are dependent on surface/somatosensory inputs, they are unsteady in this position, and number 5 and 6; i.e . all positions on foam/unsteady surface; vision and vestibular system are available)
5: eyes closed and unstable surface ( you have taken away vision and the reliance on the surface/somatosensory system; patients with vision dependency due to somatosensory or vestibular loss are unsteady here)
6: eyes open, visual conflict and unstable surface ( visual conflict can create a problem for patients depending on their vision for balance, patients with somatosensory or vestibular loss are unsteady here)
X
In Summary:
• Patients dependent on vision become unstable in conditions 2,3, 5 & 6 where we either close the eyes, or have a conflict between vision and the vestibular system
• Patients dependent on surface/somatosensory inputs become unstable in conditions 4,5 & 6 because we stand the patient on a soft surface ( foam)
• Patients with vestibular loss become unstable in conditions 5 &6 because they can’t rely on vision or surface/ somatosensory function
• Patients with sensory selection problems become unstable in conditions 3-6.
Treatment: Treatments may involve the manipulation of sensory input while performing a task. This may be done for any of the three systems responsible for providing sensory feedback. For example, to encourage use of vestibular input, visual and somatosensory information may be challenged. Visual input is challenged by taking it away (e.g., eyes closed) or by destabilization (e.g., involving head and eye movements in the task). Unstable surfaces (e.g., rocker board or rough terrain) or compliant surfaces(e.g., foam) help to challenge somatosensory input. Vestibular input may be manipulated by changing the position of the vestibular organ (e.g., neck extension or repeated head movements).
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