cvp cardiac part 2 Flashcards
jugular venous distension is measured with ______, positioned _______, and shows
ruler, 45 degrees laying back, elevated if seen above clavicle which means an increase in volume of the venous system
a normal heart sound is described as “lub-dub” which includes S1 then S2. S1= and S2=
mitral and tricuspid valves close
atrial and pulmonary valves close
what happens during disatole
PV and AV close, TV and MV open for filling (includes atrial kick)
what happens during systole
TV and MV close, ventricle pressure is higher than the aorta causing the pulmonary artery adds pressure on the AV and PV causing them to open
what is the pattern of auscultation of the heart from 1-4
aortic, pulmonic, tricuspid, mitral
all physicians take money
aortic valve is auscultated where
R 2nd intercostal space
pumonic valve is auscultated where
L 2nd intercostal space
tricuspid valve is auscultated where
L 4/5 intercostal space
mitral valve is auscultated where
5th intercostal space, includes point of maximum impulse and is usually heard as the loudest sound
what does mitral regurgitation mean
mitral or tricuspid valve not closing properly
when is mitral regurgitation heard
systole, b/w S1 and S2
when is aortic regurgitation heard
during diastole after S2
when is mitral/tricupsid stenosis heard
during diastole before S1
when is aortic/pulmonic stenosis heard
systole between S1 and S2
what kind of patient would have S3 sound
heart failure
what kind of patient would have S4
LV hypertrophy or long standing HTN
what does S4 cause
late diastole
what does S3 cause
prolong filling
w/ aortic stenosis:
SV ___, afterload ____, preload ____, atrial pressure _____, aortic pulse pressure _____, left atrium
decrease. increase. decrease. increase. decrease. enlarged
w/ aortic regurgitation
____ EDV, _____ EDP, ____ preload _____, mitral regurgitation _____ ,LA blood _____, LA pressure ______, ____ SV
increase. increase. increase. quicker. increase. increase
what is the pnemonic to remember heart murmurs
MRS. ARD. MSD. ASS
SA node rythm ____
AV node rythm ____
bundle of his rythm ____
60-100 bpm
40-60 bpm
20-40 bpm
representation of EKG graph
large box ____
small box ______
normal PR ______
normal QRS _____
0.2 sec
0.04 sec
<0.2
<0.12 or 3 small squares
how can you measure HR on 6 sec strip
10 x # QRS
if only one segment on the EKG is regular how do you identify it
normal except ….
what does fibrillation mean
ventricle not contracting well causing irregular PR interval
early QRS means
premature ventricular/atrial contraction, depends on what else is irregular
what does junctional EKG mean
p wave is not before the QRS
1st degree AV block means
prolong PR, everything else is normal
2nd degree AV block/type 1/wenkelbach
prolong PR that is PROGRESSIVELY lengthening, QRS DROPS
2nd degree AV block type 2
shortened PR that has a suddent QRS DROP
3rd degree AV block type 3
complete block= PR interval not defined, atria and ventricles don’t communicate
p wave
t wave
QRS wave
depoloarization atria
repolarization ventricles
depolarization ventricles and repolarization atria
3 types of SA node rhythms
NSR, sinusbradycardia, sinustachycardia
5 types of atrial dysrythmia
premature atrial contraction, atrial tachycardia, atrial bradycardia, atrial flutter, atrial fibrillation
junction dysrythmis is of what node
AV node
4 types of AV node dysrythmia
premature junctional contractions, junction bradycardia, accelerated junctional rhythm, junctional tachycardia
junctional
___ bradycardia
____ junctional
____accelerated
____ tachycardia
<40
40-60
60-100
>100
5 types of ventricle dysrhtmias
premature ventricular contraction, ventricular fibrillation, ventricular tachycardia, ventricular escape, polymorphic ventricular tachycardia
ventricle
____ bradycardia
____ ventricular rate
____ accelerated
____ tachycardia
<20
20-40
40-100
>100
what parts of the heart are associated with RCA
RA, RV, inferior LV, SA node, AV node
what parts of the heart are associated with LCX
posterior LV, lateral LV
what parts of the heart are associated with LAD
anterior LV, lateral LV, septum
how is ischemia identified on an EKG 12 lead
ST depression (appears as horizontal or downslopping)= NSTEMI if > 0.5mm at J point in 2 or more consecutive leads
what does t wave inversion mean
may be NSTEMI or previous MI
what vascular disease is also atherosclerosis
PAD
what are some risks for a patient with PAD
stroke, MI, thrombosis
what would a patient with PAD usually complain of
intermittent claudation= pain in leg that gets worse w/ exercise and better with rest
what is a medical emergency associated with PAD
critical limb ischemias
what are the 6 p’s of critical limb ischemias
pallor, pain, paresthesia, paralysis, pulselessness, pokilothermia (unable to regulate temperature)
what is a diagnostic imaging PTs can use for PAD
ankle brachial index
what does ankle brachial index mean
ankle BP / arm BP and look at ratio to determine how severe and at risk the patient is
what would indicate a more severe PAD
lower ratio
what does >1.3 of ankle/brachial BP indicate
non-compressible: pulse is unable to obliterate
what BP indicates you shouldn’t do ankle/brachial index b/c BP is too high
250 mmHg
what is the gold standard for dx PAD
angiography
possible pharm tx for PAD
PDE 3 inhibitator, pentoxifyline, xanthine, vasolates, anti-HTN, anti-platelet, cholesterol lowering
surgical tx PAD
stent, angioplasty, thrombectomy, open surgical bypass
what is the typical PT exercise tx for PAD pts: called SET and covered by medicare
30-45 min sessions, 3x/week, 12 weeks total
what instrument should be used for differential diagnosis of vascular disease
ultrasound
what are s/s of venous insufficiency
LE edema, skin changes, discomfort, pitting edema, dilated veins
primary vs secondary venous insufficiency
no precipitating event vs response to previous DVT
what kind of disease is venous insufficiency
progressive. can get worse and develop ulcers and skin changes
3 parts of virchow’s triad- how likely a pt is to develop vascular disease
stasis, hypercoagulability, vessel wall injury
can MRI and CT dx DVT
no, they can’t be used to r/i or r/o
what does AAA mean
vessel diameter > 3cm
what vascular disease may cause LBP and can be confused with MSK pain
aortic dissection
what are the 2 largest lymphatic trunks
r lymph duct and thoracic duct
r lymph: R arm and R side of head
thoracic duct: rest of the body
what is the primary pathway for removing excess fluid in the lung
mediastinal lymph system
what stages of lymphedema are still reversible
0-1
what stages of lymphedema have a + stemmer sign
2-3
what is the most common type of lymphoma
non-hodgkin’s: slow and agressive
what type of swelling is most common in LE of women in a symmetrical pattern found PROXIMALLY
lipedema
what kind of swelling is most commonly found in the extremities and found unilaterally
lymphedema
does primary or secondary lyphedema have an unknown cause
primary. secondary is caused by damage to lymph vessels and nodes
what does a positive stemmer sign mean
when pinching the dorsum of the foot/ hand you’re unable to separate the skin from the bone aka there’s too much fat
examples of PT interverntion for lymphedema
compression, manual lymph drainage, exercise to increase muscle pump activity and facilitate decompression, low impact CV exercise
what is the difference b/w HF and cardiomyopathy
HF= diagnosis
cardiomyopathy= etiology
what causes systolic heart failure
LV is dilated and can’t contract efficiently
what causes diastolic heart failure
LV is stiff and can’t easily relax causing thickening of the LV
how are hormones related to HF
overactive RAAS and sympathetic NS to prevent heart from failing causes diminished natriuretic peptides leading to an imbalance of hormones furthering the decline in heart function
4 physiological causes of cardiorenal syndrome due to overactivation of SNS
vasoconstriction, tachycardia, sodium retension, renin released
RV failure 3 causes
-pHTN or high pressure in the lungs caused by disease or L side HF
-tricuspid pathology or RV dysfunction
-pericardium effusion
why is right side HF systemic symptoms
blood can’t even reach L side since it starts as deoxygenated in the R side
why is left side HF only pulmonic symptoms
blood can’t get through to the lungs themselves
examples of decompensated HF symptoms
hypotension, JVD, altered mental status, weight gain
what is the most common type of cardiomyopathy
ischemic
3 types of non-ischemic cardiomyopathy
dilated LV: most common, caused by virus, postpartum, toxic
restrictive LV: very rare
hypertrophic VALVE: very rare, usually athletes
why is cardiogenic shock a medical emergency
very low BP that may be so severe and cause organ damage
CI <2.2
what is BNP
brain nateruretic peptide: identifies heart STRETCH, if the heart is stretched BNP will be increased
what lab value determines HF that is compensated or decompensated
BNP
what would a CXR and echo of someone w/ HF look like
enlarged heart, wedge pressure >15, abnormal EF
if a heart has mitral regurgitation what would happen to the atria
dilated b/c excess blood
if LV hypertrophy what would likely happen to the pulmonary pressure
increase in pressure
3 types of short term surgical tx for HF
ECMO, IABP, impella
venovenous support is for ______
venoatrial support is for ______
lungs. heart
where is IABP located
proximal descending aorta and commonly inserted in the primary femoral artery
what happens to the IABP during systole _____ and diastole _____
deflated. inflate. the purpose is to assist with diastole inflation
purpose of IABP
decrease afterload and improve CO by filling arteries better and more efficiently
who can be candidate for IABP
acute cardiogenic shock, advanced HF waiting surgery, severe coronary disease
3 indications for lvad
-stage 4 heart failure according to NYHA
-LV EF of <25%
-inotrope dependent
OR
-CI <2.2 not on ionotropes w/ optimal medical management or advanced HF for 2 weeks
3 lvad designations
destination therapy, bridge to transplant, bridge to recovery
LVAD is _____ dependent and _____ sensitive
preload, afterload
4 parameters for LVAD
speed, flow, pulsatility index, power
pulsitality index
native heart’s ability to pump blood and contribute to CO, higher= heart is pulsing on its own, lower= heart isn’t pulsing as much on its own
3 LVAD hemodynamics
native LV contributon, volume status, IV meds
after pt is on LVAD do they get to stop taking meds?
no, they must continue taking meds to keep their immune system and body functioning properly
orthotopic heart transplant (OHT) requirements
<70 yo, end stage heart disease, signficiant risk mortality, no active infection, no cancer, no organ impairment, BMI <35, abstain from alcohol and tobacco, medical and financial support
methylprednusolone
glucocorticoid, anti-inflammatory by reversing capillary permeability, used in IV after surgery, SE: acne, adrenal suppression, fluid retention (all hormone related)
prednisone
PO, anti-inflammatory, SE: anaphylaxis, bradycardia, moon face
what happens with OHT hemodynamics
no parasympathetic or sympathetic input so pts will have an increase in resting HR and rely on catecholamines to increase HR during activity
rejection of transplant symptoms and why are they important
usually similar to HF symptoms so pts may not be as quick to report them to us: fatigue, edema, irregular heartbeat, decreased activity tolerance
goals of HF meds
either increase contractility to decrease HR OR decrease afterload to reach euvolemia (neutral volume)
group of guideline directed medical therapy drugs
ACEI/ARB, beta blocker, aldosterone antagonists, nitrates
how does ACEI treat HF
decrease afterload, decrease preload, increase CO by dilating vessels
how does beta blocker treat HF
only used for stable HF b/c blocks SNS system to decrease ionotropy and increase preload
how does aldosterone antagonist treat HF
very common K+ sparing drug which prevent arrythmias. PT related: risk for hypotension, dehydration, hyperkalemia
how do nitrates treat HF
dilate vessels to decrease afterload and increase SV b/c allows heart to function better
NY classes of HF class 3 compared to class 4
3= symptoms only during activity and not at rest
4= symptoms at rest and during activity
what are loop diuretics good for HF tx
decrease edema (symptom relief), causes vessel walls to become less dilated since there’s less fluid there, also increases risk for dehydration
why would vasopressors be used to treat HF
they do vasoconstriction so are good for tx of cardiac arrest, septic shock, hypotension
alpha receptor
beta 1 receptor
beta 2 receptor
significant vasoconstrictor
heart: some vasoconstriction
lungs: vasodilation
doses of epinephrine differences in reaction
beta= lower dose = dilates= decrease BP
alpha= higher dose= constrict= increase BP
norepinephrine
most commonly used vasopressor= increase systemic vascular resistance, increase BP
why is vasopressin given exogenously
with septic shock vasopressin stores are depleted by 96 hours
dopamine doses
low= vasodilation
medium= increase HR and ionotrophy
high= vasoconstriction
what does iontrope do
assist with contractility
when would iontrope be given
end stage HF, cardiogenic shock, CI < 2.2
primacor
positive ionotrope, vasodilator, decreases afterload, increases SV
dobutrex
catecholamine. vasodilates. increases contractility
other drugs that can be used as iontrope
digoxin, epinephrine low, dopamine medium dose
what’s a CI for 6MWT
unstable angina recently
high risk 6 MWT
<200 m predictive of hospitalization or mortality COPD
<300 m predictive HF
if a patient is on O2 can they titrate their own
yes, they can
SPBB
for 3 physical performance tests designed to capture limitations in lower extremity functioning that relate to gait, balance, strength
what is considered an angina equivalent
dizziness
SPBB results mean
<9 considered frail
helpful for screening LVAD pts to see how frail they are
FITT components
frequency, intensity, time, type
mod intensity
vigorous intensity
exercise
50-70% HRR
75-90% HRR
MET =
metabolic equivalent (energy cost at rest)
borg RPE scale
6-20
cardiac rehab purposes
improve aerobic condition, decrease risk disease, decrease symptoms, improve knowledge and self management of disease, decrease hospitalization
3 types of cardiac rehab
inpatient, supervised, unsupervised
phase 2 cardiac rehab
supporting physician is immediately available, only specific diagnoses are allowed: acute MI, stable angina, valve replacement, stable chronic HF, heart/lung transplant
who prescribes exercise in cardiac rehab
physician
stable chronic heart failure def
LVEF <35% or NYHA class 2+, not hospitalization in past 6 weeks
difference in billing cardiac rehab
whether or not EKG monitoring was used continuously
most commonly used outcome measure cardiac rehab
RPE
easiest and non-invasive way to diagnose CHD
echo
cyanotic CHD
acyanotic CHD
right to left shunting, s/s hypoxia, SPO2 is low
left to right shunting, s/s heart failure
most common CHD
ventricular septal defect, can lead to pHTN and RV failure
7 symptoms of cyanotic CHD
tetralogy of fallot, transposition of the great vessels/arteries, tricuspid atresia, truncus anteriosus, total anomalous pulmonary venous return, pulmonary atresia, hypoplastic LH syndrome
most common cyanotic defect
tertralogy of fallot
tetralogy of fallot examples
squatting, cyanosis, clubbing, syncope
