cardiac 1

manipulating risk factors to decrease the incidence of disease in a population

process of helping people who already have a disease change lifestyle and behaviour, reducing risk factors for disease progression so it lessens the impact of the disease on the quality of life, morbidity, and mortality

• I - acute period, the initial event, 2-4 weeks in hospital
• II - convalescent or early outpationt (2nd and 3rd month)
• III - late outpatient - much less monitoring than in phase II
• IV - maintenance - solo, in a gym

• I:  inpatient - the event
• II: transitional zone: acute or subacute rehab or homecare
• III: outpatient - pt must fit specific guidelines of disease and treatment to get accepted here
• IV: transitional - pt is still monitored, but no longer on tolemetry
• V: lifetime - gym, changes in ways of life

family history: a 1st degree male relative who suffered or died from CVD when 55 or younger, or a female rel who did when 65 or younger

age - fems greater than 45, men greater than 55

gender - men get it more

• cigarette smoking
• hypertension
• hypercholesterolemia
• impaired fasting glucose
• obesity

SBP - above or equal to 140

DBP - above or equal to 90

• I:    SBP 140-159    DBP 90-99
• II:   SBP 160-179    DBP 100-109
• III:  SBP 180-199    DBP 110-119
• IV:  SBP >200         DBP >120

• SBP - 200
• DBP - 110

diabetics - SBP - 180

• if total is >200, CRF
• if total/HDL <3 = low risk ratio
• if total/HDL 3-5 - averatge risk

if total is 240 pt has almost twice the risk of if it's 200

<130

<100

>60 - meaning it reduces your risk

<40

>150 mg/dl

• less than or equal to 100  - norm
• 110-125  - impaired fasting glucose control
• >125    -  diagnostic for diabetes

mod intensity exercise for 30 min / day most days a week

• at least 10,000 steps/day
• <5000 = sedentary

• <25  - norm
• 25-29.9 - overweight
• 30-34.9 - obese stage I
• 35-39.9 - obese stage II
• 40 and up - obese stage III

pain/discomfort in chest, neck, jaw, arms, or elsewhere that may be due to ischemia

SOB at rest or w mild exertion

dizziness/syncope

orthopnea or paroxysmal nocturnal dyspnea (ask if pt sleeps w multiple pillows or with bed's head area raised)

ankle edema

palpitations or tachycardia

intermittent claudication (cramping pain when walking)

known heart murmur

unusual fatigue or SOB w usual activities

If no systemic disease and no signs/symptoms, then no matter how many CRS, patient's not considered high risk

low risk - no more than 1 CRF (ex: hypertensive, fat, sedentary, high cholesterol)

mod risk - 2 or more CRFs

• high risk - a) systemic disease (diabetes, hypo or hyperthyroidism, kidney disease, etc)       or b) show signs and symptoms
•   

• Low risk - LVEF > 50% (norm is 55)
• functional capacity > 7.5 METS

• Mod risk - LVEF 40-49%
• functional capacity 5-7.5 METS

• High risk - LVEF < 40%
• functional capacity <5 Mets 

CLass A - apparently healthy

Class B - documented, stable cardiovascular disease w low risk for vigorous exercise (so you can do sub max or max testing) but slightly greater than Class A folk

Class C - mod to high risk for cardiac complications during exercise and/or unable to self-regulate activity or to understand recommended activity level (so, should be supervised)

Class D - unstable disease w activity restriction (only physicians should assign exercise)

• low risk - can do both
• mod risk - can do sub, can't do max unless an MD is on site
• high risk - can do either only if an MD is on site

• low risk can do both
• mod risk can do mod, can do mod-high w trained HCP on site
• high can do either w trained HCP on site

hoel between R and L atria in fetus so blood can bypass the lungs

hole from L pulm artery to aorto in fetus to let blood bypass lungs

• oxygenated blood enters via umbilical vein
• half of it bypasses the liver via the ductus venosus
• then it enters the IVC, then the R atrium

this is what becomes of the ductus arteriosus

the name for the foramen ovale if it remains after birth

• adventitia
• external elastic lamina
• tunica media - thickest layer, helps control diameter
• internal elastic lamina - coronary disease/hardening starts here
• tunica intima

veins are similar but with thinner tunica intima, and veins have valves

• L --> left anterior descending (supplies most of L ventricle) and left circumflex
• R --> posterior descending

arteries expand and contract to creat perfusion pressure to help push blood thru

R atrium --> tricuspid valve --> R ventricul --> pulmonic valve --> pulm arteries --> gas exchange --> pulm veins --> L atrium --> mitral/bicuspid valve --> L ventricle --> aortic valve --> systemic + coronary circ

R side is thinner, and BP is much lower: ~25-30/5-15

a layer of dense connective tissue which forms a skeleton for the heart and provides support for each valve

if it loses its structural integrity you lose recoil of the heart

and it helps slow down electrical flow to give muscle time to contract and relax - it's fibrocartilaginous, and this texture slows the flow

completely encircles the heart and divides the atria from ventricles -- it marks the location of the annulus fibrosus

leaflet valve sperating R atrium from R ventricle

pull tri and bicuspid valves open by pulling on the chordae tendinae which connect the muscle to the valves

SA node --> internodal pathways -->AV node -->bundle of His -->R + L bundle branches -->Purkinje fibres

• parasymp: vagus N. sends fibers over surface of heart and to nodal areas to slow HR and decrease SV
• symp: cervical symp chain and thoracic splanchnic nerves terminate in teh vicinity of SA and AV nodes to increase HR and SV

run along symp pathways .. pain is reffered to arm, shoulder, precordium (part of body over heart and lower chest) and sometimes epigastric region (upper central region of abdomen)

I think this is the same as the anginal pattern (this is unique to each person, but once your anginal pattern is id'ed it'll stay the same for you)

they don't have it, so they don't get reflex tachycardia, so when BP changes the heart can't quickly compensate. SO, they need longer to warm up and cool down in the gym.

they're stretch receptors in the walls of most large arteries

these stretch receptors in the walls of most large arteries are stimmed at pressures between 60 mmHG and 180 mmHG

• 1 - vasodilation vi inhibition of the vasomotor centers of teh medulla
• 2 - decrease the HR and contractility via vagal stim

there's an inherent "leakiness" of the SA node fibers to sodium ions

• most easily depolarized
• has automatic rhythmicity (100bpm)
• electricity goes from here to the AV node via the internodal path

fast sodium channels, slow calcium-sodium channels, potassium channels

-55 to -60 mV

pericardium, epicardium, myocardium, endocardium

it's a leaflet valve btwn R atrium and R ventricle

• R vent and pulmonic trunk
• it's made of cusps which can calcify and then won't open so good

aortic valve - it's a cusp valve

• coronary arteries arise in here, just above cousp of aortic valve, so if there's a narrowing of aortic valve you'll lose perfusion pressure to coronary arteries.
• so, if there's severe aortic stenosis, don't exercise until it's addressed

is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium)

• visceral serous layer and a variable amount of fat
• it's in contact w the serous pericardium

on the annulus fibrosus

a "wringing" type of effect during contraction which reduces the vol. of the chambers during contraction

they don't cross it (the sulcus is between the atrias and ventricles)

the endocardium bc it's on the iner lining of the cardiac chambers, therefore furthest from the coronary arteries which are on the pericardium

• inner lining of cardiac chambers
• in direct contact w blood
• smooth, thin endothelium

• similarly striated
• contain actin and myosin filaments --> cross bridge cycleing results in contraction

• between cardiac myocytes
• they have an electrical resistance 1/400 the resistance of the outer myocyte membrand prmiability = gap junctions, which allow the spread of electrical activity

can beat on their own, so if conducting fibers are damaged, heart can still beat

, search

•  
• The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors located in both atria at the venoatrial junctions.

• (atrial stretch reflext that causes change in HR)
• increase HR from baseline
• decrease HR if heart is beating too fast
• (initiall causes increase, and if maintained causes decrease)

• increase depth and rate of breathing
• get less sensitive w age

• gap junctions
• T-tubules

the sarcopasmic reticulum releases calcium, which binds to the troponin, which results in teh cross-bridge cycling btwn actin and myosin, ...---> myocardial contraction!

• calcium channels close
• calcium is reaccumulated in the sarcoplasmic reticulum
• calcium is also actively removed by specific sodium-calcium pumps in the cell membrane
• ---> end of the myocardial contraction

• turning electrical into mechanical activity
• In cardiac muscle, the method is dependent on a phenomenon called calcium-induced calcium release, which involves the conduction of calcium ions into the cell triggering further release of ions into the cytoplasm (about 75% of calcium present in the cytoplasm during contraction is released from the sarcoplasmic reticulum).

• DBP represents the pressure 2/3 of the time
• with exercise, SBP takes up more time

DBP. The % of time spent in DBP decreases as the HR rises (when HR reaces 180, DBP is just 1/3 of the time), s, the higher the HR, the greater the risk of ischemia