lecture 2 Flashcards
what kind of blood goes of out pulmonary artery?
unoxygenated blood.
what happens when blood goes thru lungs?
picks up O2 and gets rid of CO2.
valve bw the r atrium/ventricle
tricuspid
vavle bw the l atrium/ventricle
mitral valve
thick microvascular basement membrance inc or dec?
inc- narrowed lumen, impaired O2, nutrient, waste xchange
elastin does what?
dec- less stretchy
collagen does what?
inc- scar tissue you want for structure.
dec elasticity of arteries does what?
dec baroreceptor response- less ability to sense changes in BP/HR. inc risk for falling, getting dizzy, passing out.
inc medial fibrosis and intimal thickening does what?
inc arterial tortuosity (twisted vessels, things get stuck there, impairs BF)
inc arterial tortuosity does what?
inc systemic vascular resistance (afterload)- left vent pushing against this pressure, higher the afterload, left vent tires out/hypertrophies
inc afterload does what?
inc systolic BP
inc systolic BP does what?
inc arterial insufficiency
inc vein fibrosis does what?
dilation/stretching
net effect of CV changes
dec tissue/organ perfusion
changes are ____ at rest
insignificant
changes are ____ with stress
significant
VS in elderly
may not see drastic change as a younger person. may have to look at other signs (confusion for pneumonia)
dec pacemaker/conduction tissue does what?
inc irritability
dec coronary artery BF does what?
inc LVH (l vent hypertrophy) and dec efficiency
by age 60 __% less BF to coronary arteries?
35
inc valve rigidity/thickening does what?
inc LVH- l vent pushing against valves that are stiff- dec efficiency
dec # of myocytes does what?
inc lipofuscin, collagen, and fat
lipofuscin
red pigment, indicates breakdown of RBC
collagen
scar tissue. want more stretchy tissue in heart cells
fat
dry tissue, doesnt conduct, can lead to inc irritability
inc lipfuscin, collagen, & fat leads to what?
fibrosis- less contractible heart
fibrosis does what
dec muscle strength/mobility bc heart not able to contract as well
dec muscle strength/ability leads to what
dec compliance & contractility
dec compliance and contractility leads to what?
dec efficiency
net effect of heart changes
dec myocardial efficiency
SA node
fires (pacemaker) and conducts thru atria. goes to the AV node, down bundle of His, into purkinje fibers, contracts l/r ventricles.
elec activity ______
precedes mech activity.
when u have irritation/damage to heart muscle, you ____
have higher risk of irritability of SA node.
if u have CAD, CHF, HTN, cardiomyopathy, elyte disturbance, thyrotoxicosis, cardiac surgery, high alcohol levels, high caffeineâŚ
can irritate heart/SA node and can cause arrythmias.
p wave
electrical stim of atria
AV node stimulated
right before QRS
AV stimulated and putting out beat means what?
thats QRS⌠heart beat, ventricular stimulation
why QRS has up/down figure?
its going down bundle of His and back up again
ST segment
important in MI/ischemia
T wave
ventricular repolarization
S1
right after P wave. bc atria contracts, forces last bit of blood into ventricles, mitral/tricuspid valves close.
âlubâ
S2
ventricles get stimulated, precipitates vent contraction, blood is contracted out into aortic/pulmonic valves and close
âdubâ
S1 happens atâŚ
the beginning of systole
S2 happens atâŚ
the end of systole
systolic murmur
âlub-shhh-dubâ
mostly some kind of valvular problem
clicks
might be from mitral valve prolapse, might be benign
S3
âkentuckyâ
represents CHF, in early diastole,
S4
âtennesseeâ
problem with vent going against very hardened/stiff arteries. Lot of pressure against them. Hear with HTN, in late diastole.
Afib
350-650 bmp
atria quivering. some foci arent getting thru. when it does⌠QRS⌠but dont march out evenly.
in Afib, there is no ___
atrial kick⌠no last little contraction, no last little squeeze of blood into ventricle before mitral/tricuspid valves close.
what happens if no atrial kick?
25% of blood is left in the atria.. it sits there and pools. risk for clotting.
what do you give to when there is inc risk for clotting?
anticoagulants. usually coumadin.. but start with heparin⌠then give coumadin and wait a week to kick in⌠but keep heparin going.
normal valves
open/close nicely. no bld in or out, no leakage.
diseased valves
l vent pumping bld thru valve but valve isnt opening. bld comes back bc not totally closing. stuff regurgitates back. puts more stress on l vent. overtime, gets worn out.
modifiable CVD risk factors:
smoking HTN inc cholesterol inactivity DM obesity inc triglycerides/ LDLs stress
nonmodifiable CVD risk factors:
heredity
age
sex
race
most common 1st sign of CHD in older men
MI
most common 1st sign of CHD in older women
angina
MIs in women are ___
underrecognized
HF definition
heart unable to pump sufficient bld to meet tissue/organ demands; cant pump well enough
HF epidemiology
prevalence doubles/decade.
approx 10% of pts in 80+ have HF; poor prognosis if cause is not identified/fixed bc continues to get worse.
Systolic HF
damaged pump. can be due to CAD, MI, ischemia, cor art blockage, alcoholism, chemo, radiation, viral toxicity, drugs (cocaine/amphetamines)
Diastolic HF
dec stretch/filling. so restricted, cant get as much in there. tend to back up.
effects of diastolic HF
respiratory complaints, pulm congestion, systemic effects
left-sided failure caused by
left vent dysfunction- usually dont have enough pump âfâ. bld isnt able to get pumped out of heart and backs up into lungs.
right-sided failure caused by
bld backing up from right vent into systemic system. so HTN, bld backing up into liver/abd area.
symptoms are left-sided failure
pulm symptoms. edema/fluid in lungs
symptoms of right-sided failure
abd edema, periph edema, inc liver âfâ test, inc JVD, ind fluid in spleen
how does hypothyroidism relate to myocardial failure
everything slows down, HR/BP/endocrine, not able to pump enough bld bc HR so slow to perfuse. means arteries arent getting enough bld as well.
how does anemia relate to volume overload?
dont have enough O2 carrying capacity of bld. Heart has to compensate with inc HR. HR is pumping bld out and gets tired from overpumping to try to get O2 out there since not enough is getting to tissues.
how does thyrotoxicosis relate to volume overload?
too much rubbing of engine/endocrine system. Fast HR/ high BP, all systems overworking. Turning out bld, ventricles pushing out faster & faster. Leads to HF.
what do you assess for CHF pts
pulm edema, fatigue, dyspnea, tachycardia, edema, nocturia, skin changes, behavioral changes, chest pain, wt changes
when treating CHF pts with diuretics, look for:
improvement in lung sounds, is HR down?
what labs can you do for CHF pt
chem panel, ABG/O2 sat, liver studies, CXR, EKG/monitor, echo, BMP
why do liver studies?
shows r sided failure.
CXR shows?
enlargement of heart, fluid in lungs.
echo shows
size of chambers in heart, valves and how well theyre working, ejection fractions, how forcefully ventricles are contracting
BMP shows
hormone released by heart to help inc contractility of heart. there are high levels in pts with CHF
Meds for pts with CHF
O2, morphine, diuretics (lasix), ace inhibitors, digitalis, nitroglycerin
what does morphine do?
helps chest pain, opens up cor arteries & helps them perfuse, relaxes bronchioles, helps them breathe better, dec anxiety
what do diuretics do?
helps bring water out of lungs/body, helps them breathe better.
which combo of meds help mortality rates
ace inhib and diuretics
ace inhibitors do what
help with systolic/diastolic dysfunction. dec morbidity/mortality rates, improves outcome of pt.
digitalis does what?
it is a positive inotrope and inc contractility of heart, dec HR, gives boost to get bld out. makes pts symptoms better but doesnt improve mortality.
what do you watch out for when using digitalis?
cough, can inc k level and cause hyperkalemia.
nitroglycerin does what
dec preload (amt of bld coming into heart), relaxes heart. its a coronary vasodilator and helps open up cor arteries, helps heart get O2 it needs.
HTN
sbp >/= 140; dbp >/=90.
patho of HTN
primary or essential most common= no clear cause; R/T aging changes in periph resistance; ranges from uncomplicated to complicated
secondary HTN
non CV cause . usually caused by kidneys
HTN can lead to what
HF, stroke, periph vascular disease, MI
HTN risk factors
age 60+ DM dyslipidemia positive fam hx male gender postmenopausal smoking target organ disease CV disease Nephropathy PAD Retinopathy CVA/ TIA
MI definition
death of cardiac tissue following reduction/interruption in BF bc blockage of bld/oxygenation to that tissue
epidemiology of MI
35% of elders, 60% of elder hospitalizations R/T to MI
patho of MI
prolonged ischemia -> irreversible hypoxia/cell death; R/T plaque obstruction, hemorrhage into plaque, embolus, coronary spasm, platelet aggregation.
MI on EKG shows
ST elevation
ST depression indicates
ischemia, can lead to infarction. inc risk for arrythmias
what to assess in pts with MI
pain, NV, diaphoresis, fever, feelings of doom, dyspnea, confusion
older pts MI symptoms
more muted, can have classic symptoms but may not. may only be confused so u have to really be clued in. usually have SOB, confusion, fatigue, GI upset.
labs for MI
EKG, chem panel, CBC, cardiac enzymes, troponin, CPK/MB, CXR, echo, INR
why CBC for MI?
see if anemia, bc will dec oxygenation as well. if severe, give transfusion to boost up bld count.
CPK is what
indicator of muscle damage, but doesnt show where damage occured. Has to be broken down in MB bands which are specific to cardiac cells. so if MB elev, means that with CPK elev⌠cardiac muscle damage.
why CXR for MI
to see if enlarged heart, any lung probs
why echo for MI?
show how heart is âfâing. is it stunned? is myocardium not pumping as well? EF?
why INR for MI?
coag factors in body bc if pts arents already anticoagulated, give clot busters to break open clot in bld.
meds for MI
morphine, o2, nitroglycerin, ASA, bblockers, ace inhibitors, digoxin, thrombolytics
what does morphine do for MI
if NTG doesnt control pain. potent vasodilator, reduces workload of heart, helps pt feel less anxious. dec BP/HR. look out for dec respirations
what does nitroglycerin do for MI?
potent vasodilator, reduces workload of heart, dec preload/afterload, can lower BP, if opens cor arteries well enough, can reduce pain of MI
ASA does what for MI
helps stop new clots, breaks up older clots
what does heparin do for MI?
only helps stop new clots from forming but doesnt break up clots already formed.
what do thrombolytics do for MI?
break up clots, use bw 1-6 hours of having chest pain. 30 minutes ideally.
what do Ace inhibitors do for MI?
help prevent ventricular remodeling.
what do bblockers do for MI?
dec HR/BP/contractility. dec myocardial O2 demand. reduce size of infarction
what to watch out for in MI pts when using bblockers?
hypotension, bradycardia
digoxin does what for MI?
inc contractility, squeezes heart, dec HR to help perfuse cor arteries.
dec pulmonary compliance
lungs get stiffer, less elastic recoil, more restriction, ossification of costile cartilages
elders get ___ AP diameter
increased
elders get slightly ___ TLC
smaller
elders get ____ of apices and ____ of lower part of lung
overinflation; underinflation
emphysema
can get air in but hard to get out.
net effect of emphysema
less pressure of O2 in system
overall effects of emphysema
dec ventilation/gas xchange
normal PaO2 of 80 yo
70 mmhg
as age, what happens to chemoreceptors
get more blunted, lesser response to low O2 in bld and higher CO2; takes longer for elderly person to respond. less effective breathing control.
dec mucociliary transport
lose ability to brush off foreign agents that come in. more risk of infx/trauma to lung.
why do smokers have chronic bronchitis/infx?
cilia burned off when smokes, less ability to force invading agents out of lungs.
dec effective cough reflex
not able to cough as effectively. when person has stroke/parkinsons, neurogenic innovation in throat ineffective.. higher risk for aspiration pneumonia from food/saliva
dec acute antibody response to extrinsic antigen
not able to respond as much to virus/bact. higher risk for infx/nosocomial.
lose ability to form secretory IgA.. helps neutralize effective viruses.
dec cellular immunity
dec T lymphocytes/macrophages responsible for fighting fungi, intracellular viruses, chronic infectious agents. dec tumor cells- less effective in fighting bacteria, extracellular viruses.
why are elderly less likely to have temp when have pneumonia or other viruses?
might be related to dec in antigen response.. not putting up healthy virulent response.
Pneumonia definition
acute lower resp tract infx & microbial invasion of normally sterile lung tissue (parenchyma)
epidemiology of pneumonia
most common cause of infectious disease-related deaths in elders
patho of pnemonia
infx and inflamm of distal parenchyma w/ influx of PMN leukocytes into alveolar spaces to attack invading agent, edema fluid, RBC breakdown, fibrin, etc.
old-old are ___ more likely to get infx in hospital
2-5x
pneumonia symptoms
can be subtle. cognitive changes, behavioral changes, confusion, may not see inc temp, might not see lab values go up right away.
pts 85+ are __ more likely to die pf pneumonia than young old or old adults
5x
cough up green means
leukocytes fighting infx
cough up rusty color
has RBC/fibrin in it
pneumonia by causative agent:
viral, bacterial (gm+/-), other agent (fungus)
pneumonia by location
lobar, lobular, interstitial
CAP or HAP
pneumonia by other mechanism
aspiration or hematogenous (originates from another site, like UTI)
what to assess for in pts with pneumonia
cough, pain with cough/breathing, fever (might not have), dyspnea, elders may show vague signs or even only confusion
Labs for pneumonia
CXR, CBC, ABG, O2 Sat, C&S (culture&sensitivity), Gm+/-, PFT, bld culture
why CXR for pneumonia
to see fluid in lungs
why CBC for pneumonia
to see inc WBC (bacterial)
to see inc lymphocytes (viral)
why ABG for pneumonia
to see oxygenation status, CO2, hypercapnic?
why C&S for pneumonia?
of sputum to see whats growing. it takes 3 days for result so treat empirically. when results come back, see if theres a better abx
why blood culture for pneumonia?
to see if getting septic. do this before starting ABX bc you wanna catch whatever is causing sepsis withouth it being diminished by ABX
meds for pneumonia
ABX, O2, analgesics, antipyretics, steroids, bronchodilators
what do you wanna give to pneumonia pts?
lots of fluids! wanna keep them hydrated. even in CHF pts.. but be careful. you wanna help pull out toxins, fight infx, water will thin out mucus
how do you wanna position pneumonia pts?
sit them up. encourage them that sitting up will help them get better and that you can give pain meds and pillow.
why do you have to be cautious with diabetic pneumonia pts?
bc with diabetes, there is an inc of sugar in all tissues and bacteria loves sugar. bact can grow.
immune system changes in elderly
dec thymus âfâ
dec in precursor T cells that recognize antigens.
inc in memory T cells
less able to respond to antigens
less response to immunizations
inc immunoglobulins- autoimmune response, more antibodies.
overall net effects of immune system changes
less able to fight infx
higher mortality/morbidity rate as one ages.
