Lecture 25: cardiovascular Age-releated changes (has review for pharma as well) Flashcards
Cardinal symptoms of cardiovascular disease: chest, neck or arm pain or discomfort; palpations; dyspnea; syncope (fainting); fatigue; cough’ and cyanosis
Edema and leg pain (claudication) are the most common symptoms of the vascular compoent of cardiovasuclar pathologic conditions
KNOW: R/L heart failreu and when edema is likely present
Angina - know angiona equvilants
* chest pain
Dyspnea
cardiovascular disease, espeically cornary atherosclerosis, is the most common cause of hospitailization and death in the older population in the US
Cardiovascular sidease is likely to be even more of a signfiicant health problem in the future, as it accounts for over 80% of cardiovascular deaths in people 65+
Disease independent changes in the aging heart (happen w/ aging, not because of a specific disease)
* reduction in # of myocytes and cells within the conductive tissue (going to be conductivity issues in the heart)
* The development of cardiac fibrosis
* A reduction in calcium transport across membranes - muscle contraction
* Lower capillary density
* Decreased in the intracellular response to B-adrenergic stimulation (somtimes referred to as blunted b-adrenoceptor responsiveness) -
* Impared autonomic reflex control of the heart rate - slower response to what were doing in our daily life as we age (heart doesnt adapt as quickly)
increased collagen and calcium content - because theres an increase accumulation because its not used properly
* collagen normally present because there is damages - does repeairs.
Atherosclerotic plaque formation happens in the tunica intima
* this fibriosis from the repair causes arteries to become stiffened
This causes increase in systolic BP (cant distand as easily = increase BP)
* happens more due to EX than at rest
* = increase in fatigue of arterial walls
* starts the RAAS system to lower BP
Age releated cardiovasulcar changes
Increased fat
Decreased blood vessel elasticity
* meaning we get increased BP because of decrease desinciability
decreased HR max
* we do this to prescribe EX etc.. meaning we should use RPE scale
Increased resting BP
Increase in cardiac dyshythmias
* name some from clin med 2
Decreased stroke volume
* this is end diastolic volume - end systolic volume
* This tells you the function of the L ventricle
* Decreasibed as ejection fraction - so your ejection fraction decreases - figure out more on this
Decreased cardiac output (normal is 5L)
* volume of blood being pumped by both ventricles of the heart, per unit of time
CO = SV x HR
* normal = 5
* so has Hr increases, SV decreases to maintain CO as close to 5L as possible
The effects of aging on function
The vasculature changes w/ aging as the arterial walls stiffen with age and the aorta becomes dilated and elongated
* possible aneurysm
* can happen in abdomen / thraocic etc…
* Becuase ejction fraction is poor in many older people we wouldnt do surgery as long as anurysm is stable
Calcium deposition and change sin the amount of and loss of elasticity in elastin and collagen most often affect the larger and medium sized vessels
Effects of aging on function
Resting cardiac function (ex: CO, HR etc…) shows what w/ age?
* are changes in functional capcity more appartent during exercise or at rest?
* What happen w/ max HR w/ age?
minimal age releated changes
NOTE: Chnges in functional capacity are more apparent during EX than when at rest
Max HR declines w/ age
* we under dose, because were prescribing off of a lower HR
what happens to BF to the heart w/ coronary artery disease?
reduced BF to the heart
* these are ischemic changes
coroanry artery disease is due to that artheroscloersis
this can lead to a myocardial infarction risk
* we already have plaque formation and reduced BF to an area
we get that angiona because were not getting enough O2 to those tissues
* its a precurser to MI because th tissues are partly blocked but not fully blocked
* We have a full MI when that tissue is fully cut off and we have no O2 getting to that tissue and that area dies
Nitroglycern
* for angina
* subliqual
* review how often they can take it before 911 (I think its 3 but im not 100% sure)
angina scale
Exercise and age-associated changes in the heart
It is commonly accepted that a decline in maximal O2 uptake, heart rate, and reduced max cardiac output w/ aging during exercise, even in older athletes
Exercise can reverse some of the age associated changes in the heart at least partially, supporting the hypothesis that age-releated cardiovascular changes are simply the result of inactivity
Impaired Aerobic Capcity - great diagnosis to include in documentation
* patient cant walk form here to the mailbox, or patient cant be a community ambulator “due to imapred aerobic capcity” - also termed endurance
Causes
* deconditioning
* Age releated physiological changes
* Pathology
we know fo rhte case above we have some decodnitioning / age releated phsyiological changes / pathology because shes been diagnosed w/ hypertension
Cardiac reserve is
The rate at which the heart pumps blood vs its max capcity
Individuals w/ decreased cardiac reserve - she said know these
* Marked need for rest even after mild EX
* Extensive time to recover (15 minutes after climbing stairs to catch breath)
* Shortness of breath / Dyspnea
* Bluish hue to skin, lips, fingertips (indicates not getting enough O2)
* Increase HR with slow or incomplete recovery during rest - something like beta blockers might blunt these responses (so use RPE scale)
* Irregular heart rhythm
* Decrease HR or systolic BP w/ increased workload - this is the opposite of what should be happening. Heart is not worrking correct, as you perform activity your heart rate / BP should icnrease w/ the workload. If there is a decrease of 10+ points on systolic BP that is a real problem
What we would do for our case
Know Hr max equation (220-age) is the easier one to memorize
Know: RPE scale utilized instead of HR when on beta blockers
1Rm guidelness per ACSM
* 60-80% 1RM indicated
Someone who is hypertensive and on medication we aim for what HR?
worked for 6 minutes and needs 15 minute break = way to much, red flag. Thinking reduced cardiac reserve pathology
EX: PT just performed a 6 minute walk test and required a 15 minute break in order to return to baseline - test like question
* This is reduced cardiac reserve
130/80
Females heart are smaller than male hearts and respond differently
* also due to hormonal changes
Women have more mitral valve pathology (espically prolapse) due to structural differences from men
women also much more likel to go into fatal arythmias (ventricular fibrilation)
* Not so worried about atrial fibrillation - this is the most common form of arrythmia
Women also tend to have a higher incidence of bleeding episodes form thrmbolytic agents
* thrombolytic agents are drugs taht break up or dissolve blood clots
Thrombocytosis
sustained and elevated platelet count > 450,000/uL
Thrombocytopenia
decreased in platelet count below 150,000 microL of blood
agents that break up and disolve blood clots
thrombolytics
Arrythmia drug therapys. What are our 4 classes?
Class 1 - sodium channel blockers
Class 2 - beta blockers
Class 3 - potassium channel blockers
Class 4 - calcium channel blockers
NOTE: likely older peopel (espcially older women because they’re more prone to arrythmias) are going to be on some fo these
Single leading cause of death and a signfiicant cause of morbidity among women in the US
* stealth version
Coronary Artery Disease
A stealth form of heart disease called coronary microvascular dysfunction or disease (previously called syndrome X) has been identified in women
* still having the coronary artery on the microvascular level (plaque formation / spasms)
* makes it harder to diagnosises because its hearder to pick up
* Need PET scans for this and unlikely to happen if other testing is normal
Women delay longer than men before seeking help for symptoms of acute MI, referred to as decision delay, further compromising effective treatment and improved outcomes
* because its associated w/ stress/ tradiational family roles (not having time to go out and get checked out)
From above
women w/ CABAG is increasing
* this is litteraly cutting sternum in half to do suergery
* this is where move in the tube comes in (dont let limbs leave the body)
Does coronary microvascular dysfunction show up on angio grams?
* what iamging is needed?
No, needs PEt scan to diagnose it
women w/ this type of heart disease are at increased risk of heart attack, stroke, and reduced quality of life
Hormonal status
Estrogen has been considered to have a cardioprotective benefit for women via a variety of mechanisms. It stimulates the formation of higher density lipoprotein (HDL)
* men produce estrogen in the testies as well
* 3 types of estrogen (were talking about 2, estradiol)
Estradiol acts as a calcium channel blocker to relax arert walls, which helps dilate the arteries, improves blood flow throughout the bran and body, and helps to reduce BP.
* produced in reproductive years, relaxes artery walls
Calcium channel blockers decrease vascular smooth-muscle contraction; decrease myocardial force and rate of contraction (workload) - calcium channel blockers do essentially the same thing as the estradiol
Adverse effects
* Excessive vasodilation leads to swelling in feet and ankles
* Orthostatic hypotension
* Abnormailtiies in heart rate, reflex tachy
* dizziness, HA, and nausea
Does hormonal therapy alter progression of CAD or protect against MI or cornary death
no
More women than men eventually develop hypertension in the US because of their higher numbers and greater longevity
Alc, obesity, and oral contraceptives are important causes of the rise in blood pressure among women
On test again
Hypertension
Pharmacological treatment: Diuretics, meta blockers, vasodilators, ace inhibitors, ang 2 receptor blockers, direct renin inhibitors, calcium cahnnel blockers\
Rehab concern:
* orthostatic hypotension
* weakness/fatigue
* confusion/mood cahnges
* decreased maximal exercise capcity (beta blockers)
* edema and reflex tachycardia (vasodilators)
vasodilators decrease HR but you’re at risk for reflex tacy because body freaks out because its getting to low
know side effects ofr everything above
How do you calculate pulse pressure
what does it predict in older adults
greater than what means you’re in trouble?
Systolic Bp - diastolic BP
Predicts mortality in older adults
> 100 = trouble
each 10 mmHg increase in. PP = increased risk of CV mortality by 20%
normal pulse pressure = 40 (120-80)
Cholesterol concerns for women
low levels of HDL cholesterol are predictive of CAD in women and appear to be a stronger risk factor for women older than 65 years than for men of the same age
HDL is the good one, we want it higher
LDL we want low
Congestive Heart Failure
* Right versus left sided
* Symptoms include LE edema and shortness of breath
* Can be caused as a sequela of any or all the pathologies previously discussed
* Rehab implications: rapid wt gain (edema increases / fluid retintion) after start of exercise routine, marked fatigue or SOB after exercise
* Pharmacological treatment: diuretics, beta blockers, vasodilators, renin-angiotension drugs, positive inotrope drug (digitalis)
PVD (due to PAD)
PAD
atherosclerosis in all arteries (its systemic)
PVD = measured w/ ankel brachial index
* want 0.921
walking program
often leads to hypertension (decerase destensibility)
anti paltelet drugs due to that increased plaque formation
Walking programs for
PAD
want 4/10 pain or less
The ability to move the air in and out of the lungs via a pressure gradient
Ventiliaton
The gas exhcange supplies o2 to the blood and body tissues and removes co2
respiration
Theory of aging
* Cross linkages proteins are throught to be like free radicals
* They link to glucose and then impair protein synthesis throughout the body (explains why it is harder to increase MM when you’re older) - part of aging process
* Cross linked proteins damage cells and tissues = aging
* also explains why diabetes or icnrease glucose in the blood stream affects aging so much
* Theres collagen thats floating around freely in the body (along w/ Ca2+), this combines w/ glucose and impairs protein synthesis - similar to free radicals - happens due to the accumulation of collagen and ca2+ in body as we age - she said dont go super deep here
dimished gas exhange is priamrily due to increased physioligcal dead space - not getting that respiration
* in the upper airway the movment of the cilia slows and becomes less effective in sweeping away mucus and debris
Anatomy of repsiration
Disease process that imapcts the alveolar ducts = emphesemia
What should ventiltaion be as close as possible to? whtas normal
Close to 1
Normal = 0.8
V/Q
* V = airflow
* Q = BF
Gravity, pody pos, and cardiopulmonary dysfunction influence the ratio
PErfusion is greatest in gravity dependent areas
* think lower lobes when sitting
V/Q mismatch leads to dead space and shunt. Expalin both
Dead space - ventilation is in excess of eprfusion (pulmonary embolus)
Shunt - perfusion is in excess of ventilation (alverolar collapse from secretion)
Amount of air under volitional control
Focred vital capcity
* FVC = IRV + TV + ERV
Volume of air that is fordcefully expelled in 1 scond following a full inspiration
* what % in first second
FEV1
75% in first second
all within 3 seconds
