Exam 1 Flashcards
What key components of CVP management of known?
- normal physiology
- cardiac
- pulmonary
- vacular
What key components of CVP management of applied?
- pathology
- disease progression
- pharmacology
What key components of CVP management of managed?
- primary and secondary prevention
- inpatient and outpatient
What is primary prevention?
directly addressing the disease
What is secondary prevention?
preventing further complications
threat to oxgyen transport =
threat to life
what are three steps of oxygen transport?
- oxgyen delivery
- oxygen consumption
- oxygen extraction ratio
oxygen delivery DO2 =
arterial O2 x cardiac output
VO2 =
(arterial O2 - venous O2) x cardiac outpu
oxygen extraction ratio (OER) =
consumption / delivery
what is the utilization coefficient?
~23% at rest
What may cause VO2 to fall short of demant?
if severe cardiopulmonary dysfunction exists
what kind of biological work requires continuous oxygen supply?
aerobic metabolism
What is DO2 normally based on?
demands of tissues
At rest, DO2 is ______ greater than actual demand
3-4x
What does the 3-4x greater DO2 allow for?
creation of reserve
98% O2 transported in combination with _______________.
hemoglobin
What are determinants of hemoglobin’s affinity for O2?
temperature and oxygen
What 3 structures are involved in oxgyen delivery / gas exchanges?
- lungs
- arteries
- tissue cells
Balance b/n intravascular and _________________ fluid volume is important.
extravascular
If imbalance occurs, what happens?
electrolytes are impacted wich can impact oragn function
What can cause imbalances in the mechanism for delivery?
too much H20
not enougth H2O
too much Na+
not enougth Na+
What impacts delivery of oxygen from outside air to tissues?
- atmospheric air
- air quality
- humidity
How does air quality interfere with repiratory tract filtering?
poor air quality leads to inflammation of alveolar capillary
In dry ENs:
loss of mucus covering, erosion and infection
In alveoli, inspired air saturated w/
water vapor
What are the first 3 steps of oxygens transport?
- inpired oxygen and quality of air
- airways
- lungs & chest wall
What are steps 4-6 of oxygen transport?
- diffusion
- perfusion
- myocardial function
What are steps 7-9 of oxygen transport?
- peripheral circulation
- tisue extraction & utilization of oxygen
- return of partially (de)saturated blood & CO2 to lungs
what are the critical structures included in the airways?
upper respiratory: nasal cavity, pharynx, larynx
lower respiratory: trachea, primary bronchi, lungs
with a relaxed diaphragm: lungs=
chest wall
lungs= elastic force relaxed
chest wall= elastic force relaxed
with inhalation, the diaphragm ______________________________ and the lungs & chest wall __________________.
active muscle contraction
actively expand
* increase in negative pressure, similar to vacuum
during inspiration the external intercostals:
elevate and therefore increase the volume of the pleural cavities
during inspiration the diaphragm:
depresses the inferior wall of the thoracic cavity and, therefore, increase the volume of the cavities
during expiration the internal intercostals:
compress and lower the ribs and therefore decrease the volume of the pleural cavities
during expiration the abdominals:
compress the abdominal cavity which elevates the abdominal organs and passively elevates the diaphragm and, therefore, decreases the volume of the pleural cavities.
diffusion=
transfer of oxygen from alveolar sacs to pulmonary circulation
what 5 principles is diffusion based on:
- surface area of alveolar capillary membrane
- diffusing capacity of alveolar-capillary membrane
- pulmonary capillary blood volume
- ventilation / blood volume
- transit time of blood in alveolar capillary membrane
what does the amount of oxygen that diffuses across alveolar-capillary membrane vary with?
varies directly with size (surface area) and inversely with thickness.
decrease the surface area and increase in thickness –>
decrease in amount of O2 in blood
vent (v) / perf (Q) =
0.8
apical low perfusion =
lung base perfusion increased due to gravity
apical alveoli expand fully =
lung base enlarged vessels compress alveoli
what does optimal function of the heart depend on?
synchronized coupling of electrical conduction and mechanical contraction
cardiac output =
- preload
- force (inotropic effect) & rate of contraction (chronological effect)
- afterload
what are two measures of myocardial impairment?
heart rate
ejection fraction
large vessels =
elastic & connective tissue
medium to small vessels =
more smooth muscle
what do arteriolar regulate blood flow through?
regional vascular beds
hydrostatic = out , oncotic = in
O2 diffusion (__________ content to ____________ content) occurs quickly
high to
low
intravenous at PO2 averages ____mm Hg
23mmHg
Only _____mmHg pressure needed for cell metabolism
3mmHg
OER: amount of O2 extracted at _______ = 23%
rest
rate of O2 extraction regulated by oxygen ___________ (not oxygen availability)
demand
partially desaturated blood and CO2 are removed from:
cells to venous circulation
what are factors that “shake up” O2 transport
normal: activity, position, emotional stress
disease: bed rest, fever, disease itself, inflammation process, medication, fluid imbalance
what is the greatest influence on O2 transport?
Gravity
humans are designed to function:
upright (1G)
60% of body weight is fluid so…:
small shifts in Gravity –> big fluid shifts
restricted activity:
- impacts CO and VO2 with exercise (decrease)
- impacts OER (decrease
- multiple other systems are affected
bed rest also adds the reduction in gravitational forces with physiological impact including:
- change in fluid distribution
- reduced muscle activity
- change in body weight distribution
- aerobic deconditioning and all that impacts with oxygen transport/exchange
Gravity normally keeps fluid in:
body/legs
loss of Gravity allows fluid to shift to:
thorax and head
response to fluid shift –>
reduction in volume
What are examples of general health abnormalities that could be identified during the system assessment?
- weight gain or loss
- fatigue, weakness, malaise
- fever, chills
- sweats, night sweats
What are examples of skin abnormalities that could be identified during the system assessment?
- excessive dryness
- itching (pruritis)
- excessive bruising
- lesion or rash
What are examples of respiratory system abnormalities that could be identified during the system assessment?
- history of lung diseases
- chest pain with breathing
- wheezing or noisy breathing
- shortness of breath (how much activity)
- cough
- sputum (color, amount)
- hemoptysis (bloody sputum)
- medications
What are examples of cardiovascular system abnormalities that could be identified during the system assessment?
- heart or retro sterna pain
- palpations
- cyanosis (blue/purple) –> not enough exertion
- dyspraxia on exertion (amount of exertion)
- Orthoptera (shortness of breath laying down)
- edema
- history of heart murmur, HTN, CAD or anemia
- medications for cardiac disease
What are examples of peripheral vascular system abnormalities that could be identified during the system assessment?
- coldness, ,numbness, tingling of legs
- swelling of legs (time of day and activity)
- discoloration hands or feet
- varicose veins (causes poor venous return)
- intermittent claudication (arteries not pushing blood dismally properly)
- thrombophlebitis (inflammation of veins)
- ulcers
medications
What are examples of hematologic system abnormalities that could be identified during the system assessment?
- bleeding in skin or mucus membranes
- excessive bruising
- lymph node swelling
- blood transfusion and reactions
- medications
What are examples of endocrine system abnormalities that could be identified during the system assessment?
- history of diabetes (medications)
- history of thyroid disease or symptoms (change in skin texture / excessive sweating / extreme thirst / relationship between appetite and weight / nervousness / tremors)
Pale, cyanosis or cold skin are what?
external signs of oxygen transport dysfunction
What is short breath a sign of?
external sign of oxygen transport dysfunction
What is diaphoresis (excessive sweating) a sign of ?
An external sign of oxygen transport dysfunction
What are 4 internal signs of oxygen transport dysfunction?
1) vital signs
2) respiratory patterns
3) hypoxia/ low pulse oximetry
4) poor peripheral circulation
- decreased capillary refill (>3 sec)
pt history –> systems review –> hypothesis –> diagnostic exams and tests –> evaluation –> PT diagnosis –> PT prognosis –> working problem list –> plan of care
pt history –> systems review –> hypothesis –> diagnostic exams and tests –> evaluation –> PT diagnosis –> PT prognosis –> working problem list –> plan of care
List 3 levels of PT interventions:
1) prevention
2) secondary prevention
3) treatment
What is considered prevention?
- addresses PA
- addresses CV risk factors
What is considered secondary prevention?
- increase aerobic capacity/ endurance
- improve breathing pattern / ventilation
What is considered treatment?
- airway clearance
- exercise: strength mobility, ADL
Which circulation is the shortest in the body?
Coronary circulation
What structures of body are considered the functional anatomy of the heart?
- sternum
- lungs
- diaphragm
- liver
- colon
- stomach
- heart (left & right ventricles)
What are two membrane coverings of the heart?
- fibrous
- serous (2 layers)
==> pericardial cavity
The heart wall has (___ layers)
3
the __________ pericardium directly touches the heart (myocardium). External to that is the _______________________, which is covered by the ___________________ (which surrounds the _________________________________).
visceral pericardium
pericardial cavity
parietal pericardium fibrous
parietal pericardium serous
the internal anatomy includes the:
chambers and structures
what are two of the primary coronary arteries on the anterior surface of the heart?
- right coronary artery
- circumflex artery
What is a pathological change of the coronary artery?
percutaneous translational coronary angioplasty (PTCA)
Oxygen poor blood come from the _______________ and enters through the inferior and superior ___________________ traveling to the right ______________ then tho the right ___________________ and out to the _______________________. Blood is oxygenated in the capillary beds of the lungs where gas exchange occurs. From there it travels through the ___________________________ to the left __________ to the left ______________________________ out to the body through the _________________________ then the capillary beds of all body tissues where gas exchange occurs.
Oxygen poor blood come from the BODY and enters through the inferior and superior VENAE CAVAE traveling to the right ATRIUM then tho the right VENTRICLE and out to the PULMONARY ARTERIES. Blood is oxygenated in the capillary beds of the lungs where gas exchange occurs. From there it travels through the PULMONARY VEINS to the left ATRIUM to the left VENTRICLES out to the body through the AORTA & BRANCHES then to the capillary beds of all body tissues where gas exchange occurs.
List 3 cardiac muscles:
1) atrial muscle
2) ventricular muscle
3) specialized excitatory and conductive muscle
List 3 structures of micro anatomy of the heart:
1) muscle cells
2) intercalated discs
3) gap junctions (communication pathways)
What are 2 similarities between cardiac and skeletal mechanisms of contraction?
1) striated - myosin/actin mechanism
2) T-tubule mechanism - acting on sacroplasmic reticulum
What are 3 differences between cardiac and skeletal mechanisms of contraction?
1) T-tumble mechanism - direct diffusion of Ca++ (tubules store larger amounts of Ca++)
2) action potential (cardiac muscle “plateau” / plateau results in much longer time of contraction than skeletal mm)
3) strength of contraction (dependent on extracellular Ca++)
The ability of cardiac mm to depolarize and contract is intrinsic and known as:
conduction
What are the components of intrinsic conduction system:
1) sinus node = sinistral/ SA node
2) intermodal pathways
3) AV node
4) AV bundle (bundle branches)
5) Left and right bundle branches of Purkinje fibers
- Smaller diameter muscle fibers
- Almost no contractile muscle fibers
- Connect directly with atrial muscle (mm) fibers
- Cell membranes naturally “leaky” to Na++ and Ca++ ions (therefore, less negative resting membrane potential than other cardiac mm cells)
- Self excitation
All are features of what?
SA node
@ -40mV the __________ are already open.
fast Na++
List the following events in order from first occur in got last:
- K+ permeability accompanied by slow Na+ entry decreases
- Slow depolarization: pacemaker potential
- Fast Ca2+ channels open
- Ca2+ permeability increased
- K+ permeability increase
- Ca2+ permeability decreased
- K+ permeability accompanied by slow Na+ entry decreases
- Ca2+ permeability increased
- Fast Ca2+ channels open
- Ca2+ permeability decreased
- K+ permeability increase
- Slow depolarization: pacemaker potential
during the very early P (PQRST wave) what occurs?
SA node generates impulse: atrial excitation begins
During the p -wave what happens?
impulse delayed at AV node
during the q-way what happens?
impulse passes to heart apex; ventricular excitation begins at the bundle branches
during the QRS segment what is occuring?
ventricular excitation is complete.
Electrical impulses passing through the heart also spread into _____________ and some to the _____________________.
adjacent tissues
surface of the body
the p-wave =
atrial depolarization
QRS complex =
ventricular depolarization
T-wave =
ventricular depolarization
List 5 events that occur from the beginning of one heartbeat to the beginning of the next:
1) chambers and vessel blood volume changes
2) chamber and vessel blood pressures changes
3) electrical activity notes
4) heart sounds occur
5) valves open and close
The cardiac cycle consists of:
- diastole period of relaxation; heart fill in with blood
- systole: contract ration period, heart ejects blood
What is end-diastolic volume (EDV)?
.
What is the definition of end-systolic volume (ESV)?
.
What is the ejection fraction?
fraction of EDV ejected
atrioventricular valves are __________ and aortic and pulmonary valves are ____________ during phase 1. During this phase _____________ filling and _____________ contraction occurs. This happens during mid-to-late ______________.
atrioventricular valves are OPEN and aortic and pulmonary valves are CLOSED during phase 1. During this phase VENTRICULAR filling and ATRIAL contraction occurs. This happens during mid-to-late DIASTOLE.
atrioventricular valves are __________ and aortic and pulmonary valves are ____________ during phase 2b. During this phase ___________________________ occurs. This happens during __________________________ (atria in diastole).
atrioventricular valves are CLOSED and aortic and pulmonary valves are OPEN during phase 2b. During this phase VENTRICULAR EJECTION occurs.This happens during VENTRICULAR SYSTOLE (atria in diastole).
Phase 2a is _________________________. also ventricular systole (atria in diastole)
isovolumetric contraction
During phase 3 _________________________ occurs in early ___________.
Isovolumetric relaxation
early diastole
P wave =
spread of depolarization through atrial tissue followed by contraction
p wave =
increase in atrial pressure
QRS complex : spread of depolarization through ventricular tissue followed by contraction =
ventricular increase pressure
T-wave =
repolarization of the ventricles which represents ventricular relaxation.
The majority of returning venous blood flows directly from _____________ to _______________.
atrium to ventricle
Atrial contraction usually causes an additional ________ ventricle filling, “primer pump”
20%
Atrial function “unnecessary” except during:
vigorous exercise
Atrial pressure changes:
a wave -
c wave -
v wave -
a wave - during atrial contraction
c wave - onset of ventricular con traction
v wave - end of ventricular contraction
Ventricular filling: after systole, A-V valves open due to build up of pressure in ___________________________________________________________________________.
atrial during systole: period of rapid filling of ventricles followed by 2 additional phases
Ventricle as pump = period of __________________, ___________________ and ____________________.
Isovolumetric contraction, ejection, and isovolumetric relaxation.
preload is defined as:
end-diastolic pressure when the ventricle is filled; amount of tension on the muscle when it begins to contract.
Afterload is defined as:
pressure in the artery leading from the ventricle; load against which the muscle exerts its contractile force
Heart and/ or circulation pathology can severely alter:
preload and/or afterload
Chemical energy requirements for cardiac contraction: great dependency / almost exclusive reliance on O2 for energy metabolism (oxidative) compared to ______________________________________________________________________.
skeletal muscle which can utilize anaerobic metabolic sources as well.
Chemical energy requirements for cardiac contraction: energy derived primarily from oxidative metabolism of fatty acids (_________________ of energy source), some lactate, glucose (___________).
70-90%
10-30%
Chemical energy requirements for cardiac contraction: cardiac muscle can also use lactic acid generated by what?
skeletal muscle activity
How is the volume of blood pumped by the heart regulated?
Heart pumps ___________ liters of blood/ minute
4-6 liters
How is the volume of blood pumped by the heart regulated?
Heart may be required to pump ___________ this amount (4-6 liters of blood/ minute) with heavy EX.
4-7 x
How is the volume of blood pumped by the heart regulated?
Blood volume pump is regulated by:
1) intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart.
2) (extrinsic) control of heart rate and strength of heart pumping by the autonomic nervous system
Intrinsic regulation of heart pumping: Frank-starling mechanism
Heart automatically pumps incoming blood, I.e., amount of blood pumped determine primarily by______________________________. As cardiac muscle is stretched with returning blood volume,
by rate of blood flow into heart
approach optima length of actin and myosin fibers for contraction.
Extrinsic regulation of cardiac pump =
- sympathetic nervous system (SNS)
- Norepinephrine released by sympathetic nerve fibers in response to stressors such as fright, anxiety, or exercise; threshold reached more quickly
Norepinephrine released by sympathetic nerve fibers in response to stressors such as fright, anxiety, or exercise; threshold reached more quickly:
- increase cardiac output (CO)
- -> pacemaker fires more rapidly
- -> enhanced mm contractile try
- effects of inhibiting SNS
What are 3 more components of extrinsic regulation of the cardiac pump?
1) parasympathetic nervous system
2) reduces HR when stressors removed
3) Acetylcholine hyper polarizes membranes of cells –> opens K+ channels
- –> PNS fibers in vagus nerves to heart can decrease CO
- —–> primarily affects HR rather than contractile try
parasympathetic NS =
feed, bread, and rest
(constricts pupil, stimulates flow of saliva, slows heartbeat, constricts bronchi, stimulates peristalsis and secretion, stimulates release of bile and contracts bladder).
Sympathetic NS =
fight or flight (dilates pupil, inhibits flow of saliva, accelerates heartbeat, dilates bronchi, inhibits peristalsis and secretion, conversion of glycogen to glucose, secretion of adrenaline and noradrenaline, inhibits bladder contraction)
During the autonomic innervation of the heart the vagus nerve:
sympathetic chain ganglion:
vagus nerve: stimulates SA node and AV nose via parasympathetic fibers
sympathetic chain ganglion: stimulate SA node and AV node via sympathetic fibers
resting conditions include:
- SA node receives impulses from both ________________________________.
- Dominant influence is inhibitory - heart said to exhibit “____________________.”
- “Disconnect” vagaries nerves = HR increases ~____ bpm almost immediately.
- automatic divisions continuously
- “vagal tone”
- 25
normal sinus rhythm =
In a normal sinus rhythm, the electrical impulse originates within the SA node and travels through the AV node. After a brief delay, the impulse travels down the bundle branches.
sick sinus=
resultant in bradycardia (slow heart, often due to problems with SA node)
atrial flutter =
(tachycardia) Upper chambers (atria) of heart beat too fast, making them out of sync with ventricles.
atrial fibrillation =
Atria fibrillate (quiver or twitch quickly). Impulses begin in atria and fight to get through the AV node. (Disorganized electrical pulses causing fast an irregular pattern)
Wolff-Parkinson-white
When there is an extra electrical pathway b/n heart’s atria and ventricle causing tachycardia. (present at birth)
ventricular tachycardia
(cause sudden death) any rhythm faster than 100 (or 120 beats/min), with 3 or more irregular beats in a row, arising distal to bundle of His.
pacemaker =
small device that’s placed in chest or abdomen to help control abnormal heart rhythms. (traditionally inserted into a vein to heart). regulate hearts rate. “new” SA node
Heart pumps ~ 1,9000 gallons of blood through _______________________________ miles of blood vessels each day.
60,000 - 100, 000
there are ____ billion capillaries in the body.
40 billion
the functions of circulation include:
transport of:
- nutrients and O2 to tissues
- waste and CO2 away from tissues
- hormones from one area of body to another
- heat throughout the body
Circulation is primarily influenced by tissue needs by:
dilation or constriction
cardiac output is a response to:
vascular inflow
Arterial pressure generally controlled independently of local tissue flow or ________
cardiac output
circulation is influence by :
- basic physical characteristics of blood
- physical principles affecting the flow of liquids through vessels (fluid dynamics)
key factors of circulation include:
- blood flow
- pressure
- resistance
- control mechanisms mediating these characteristics
What are the 2 circulatory systems?
- pulmonary
2. systemic
List 3 characteristics of arteries:
- transport blood under high pressure
- strong vascular walls
- blood flow is rapid
list 4 characteristics of arterioles:
- final small branches of arterial system
- act as control conduits - blood real ease into capillaries
- strong muscular walls that vasoconstrict/ dilate
- innervates by SNS only
Name 4 characteristics of capillaries:
- exchange site for nutrients, wastes, electro yes, fluid, etc
- walls - VERY thing (unicellular layer of endothelial cells)
- contain small capillary pores
- permeable to small molecular substance, H2O
Name 2 characteristics of venules:
- collects blood from capillaries
2. gradually merge into larger veins
List 5 characteristics of veins:
- transport blood from tissues to heart
- major function: serve as blood reservoir (64% of total blood volume)
- low pressure, thin walled
- contain muscle- can constrict/ dilate
- act as controllable reservoir for extra blood depending on body needs
The distribution of blood volume within the systemic system is:
veins =
arteries =
capillaries =
veins = 64% arteries = 15% capillaries = 5%
The distribution of blood volume within in the pulmonary system is:
total pulmonary =
= 9%
The distribution of blood volume for the total heart =
7%
blow flow is defined as:
the volume of blood flowing through a vessel, an organ, or the entire circulation in a given period (ml/min)
blood pressure is defined as:
the force per unit area exerted on a vessel wall by the contained blood (mmHg)
resistance is defined as:
opposition to flow; amount of friction blood meets when passes through the vessels
In the interrelationship between flow, pressure, and resistance, blood flow is affected by 2 factors:
- pressure gradient
2. vascular resistance (can be caused by PAD)
Ohm’s Law =
calculation of low through a vessel
more resistance -plaque- lower blood flow
Ohm’s law:
F = change in P/ _____
R
F =
blood flow
change in P =
change in pressure b/n 2 ends of vessel
R =
resistance
Normal adult overall blood flow =
~5,000 ml/min = cardiac output
What are the 2 descriptions of blood flow?
- Laminar (smooth, layered-together)
2. Turbulent
Which has less resistance? (laminar or turbulent)
laminar
conductance (ml/sec/mmHg) =
-measure of blood flow through a vessel for a given pressure difference
What is the reciprocal of resistance?
conductance
A small change in vessel diameter causes enormous change in:
conductance
Conductance of a vessel increases in proportion to the _________________________________.
4th power of the diameter
What is Poiseuille’s law?
F = pie (change) P r^4/ 8nl
Poiseuille’s law is related to :
laminar flow
In Poiseuille’s law, diameter plays the greatest role in determining rate of
blood flow
In systemic circulation: 2/3 of resistance to flow is ___________________ resistance
arteriole
Strong mm walls of arteriole so can change ____________________________. Which can increase blood flow up to __________-fold
diameter up to fourfold
256-fold
Viscosity has an inverse relationship to ____________________.
blood flow.
Hematocrit =
% of blood that consists of cells
hematocrit = 40
polycythemia =
many cells in the blood
Who has more hematocrit, males or females??
males
The theory of circulatory function addresses the needs of tissues that tightly controls blood flow; small-tissue specific vessel dilate or constrict locally to control:
flow in addition to change in cardiac output
Cardiac output primarily controlled by:
some of all local tissue flows
In general, arterial pressure is controlled independently of:
local blood flow or cardiac output
MAP =
DBP + (pp/3)
PP (partial pressure) =
SBP - DBP
Mean arterial pressure (MAP) =
pressure that propels blood to tissues
Pulse pressure (pp) =
affected by SV and compliance of “arterial tree”
(arteriosclerosis affects????)
Difference between SBP and DBP. Normally about 1/3 of SBP.
MAP and PP decrease with:
increasing distance from heart
Mean pressure ~0mmHg at:
venae CAVAE
mean pressure at capillaries =
~17mmHg
mean pressure of pulmonary circulation =
~16mmHg
What is the difference b/n MAP and Mean pressure?
???
What are 3 effects of pressure on blood flow?
- increases force on blood flowing through vessels
- distends vessel
- what are the effects of vessel distension
Distension linty: veins ____ arteries
veins > arteries
Compliance = capacitance =
total quantity of blood that can be stored in a given portion of the circulation for each mmHg pressure rise
compliance = distensibility X :
volume
Central venous pressure =
right atrial pressure ~0mmHg
venous pressure influences on ____________________
R atrial pressure
venous pressure increase or decrease in _______________
R atrial pressure (potential pathology)
What is the gravitational effect of venous pressure:
- quiet stance
- movement “venous pump”
Where are blood reservoirs located?
veins spleen liver heart lungs (>60% blood usually in veins)
Different tissues have different _____________ needs over time.
metabolic
blood flow/ 100 g of tissue
Regulated to provide the necessary level of blood flow to provide needs –>
no “extra”
What are the 2 phases of local blood control?
1) acute
2) long-term
Describe the acute phase of local blood control:
fast adjustment of arteriole so, metarterioles, and pulmonary sphincter a (i.e. small vessels)
Describe the long-term phase of local blood control:
adjustment over days/ weeks/ months to control blood blow to tissue
Increase blood flow leads to _________________ O2 saturation.
decreased arterial O2 saturation
What is the vasodilator theory?
-Vasodilator substance released from local tissue
List examples of vasodilator theory:
adenosine CO2 Adenosine phosphate compounds histamine potassium ions H+
Describe the oxygen lack theory (aka nutrient lack theory)
- pre capillary sphincter a
- metarteriole sphincter
- other ‘lack of substances’ may facilitate vasodilation
Dilating “upstream” arteries, larger arteries “upstream” from local tissue control respond to effects of ________________________
“downstream regulation”
Drag on “upstream” endothelium of vessel walls by rapid increased flow allows release substance that can _______________________ the “upstream” vessels
vasodilate
Endothelium- derived relaxing factor (EDRF) made primarily of________________. Reduces the resistance to _______ in upstream arteries
nitric oxide (NO) BF
What are 2 other mechanisms affecting local blood flow:
- reactive hypermedia
2. active hyperemia
What is auto regulation of BF?
concept that after increase in BF to a tissue due to increase in arterial pressure, BF returns to near normal levels
- tissues have varying abilities to autoregulate
What are the 2 theories of autoregulate on?
- metabolic
2. myogenic
Long-term mechanisms:
provide _______________________
affects _____________________
Deficiency of nutrients/O2 release of ____________________
vascularization “built” for ______________________.
- provides more complete regulation
- affects tissue vascularization
- deficiency of nutrients / O2 - resistance of angiogenic factors
- vascularization “built” for maximum need
What are 2 factors of humoral control?
- vasoconstriction
2. vasodilators
Name 4 vasoconstrictors:
- norepinephrine/ epinephrine
- angiotensin II
- vasopressin
- endothelium
Name 2 vasodilators:
- Bradykinin
2. histamine
What are the 3 primary atherosclerotic diseases?
- coronary disease
2 cerebrovascular disease - peripheral arterial disease
What demographic has the highest reported % of deaths due to heart disease?
Whites (% of deaths = 25.1%) African Americans (24.5%) Asians or Pacific Islanders (23.2%) Hispanics (20.8%) American Indians or Alaska Natives (18%)
About 2,150 Americans die each day from cardiovascular diseases, one every _________ seconds
40
Cardiovascular diseases claim more lives than:
all forms of cancer combined
Heart disease is the ______ cause of death in the world and the leading cause of death in the US, killing over 375,000 Americans a year.
no. 1
List 6 cardiovascular risk factors:
- cigarette smoking
- abnormal lipids (apo B)
- hypertension
- diabetes
- abdominal obesity
- psychosocial stress
What are 3 cardio protective factors?
- fruit/veggies
- Ex
- moderate alcohol
What factors contribute most to CV risk?
abnormal lipids (Apo A & B ratio) AND smoking
What is the least life-threatening acute coronary syndrome?
unstable angina
non-St elevation MI =
NSTEMI
- fatty material is deposited in vessel wall
ST-elevation MI =
STEMI = full occlusion ; no blood is getting through
What is atherosclerosis?
- one type of ARTERIOsclerosis
- A progressive process affecting large and middle sized arteries
What are the consequences associated with atherosclerosis?
- narrow size (smaller diameter) of artery
- blockage
- stiffness (less reactivity)
- TURBULENT flow
What are the 3 layers of the arterial wall?
- tunica intima
- tunica adventitia
- tunica media
Tunica intima =
endothelium that lines the lumen of the vessels
tunica adventitia =
collagen fibers
tunica media =
smooth muscle cells and elastic fibers
The initial injury of atherosclerosis involves:
- excess levels of low-density lipoproteins LDL in blood penetrate blood vessels and become trapped
- LDL oxidizes, releasing anions (oxidative stress)
In atherosclerosis, endothelial dysfunction causes:
oxidative stress
- chemical & adhesion factors attract monocytes & platlets
What is the normal function of smooth muscle?
- smooth muscle emigration from media to intimal. Macrophage activation
- macrophages and smooth muscle cells engulf lipids
- smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid.
* DEVELOP A CAP THAT WILL KEEP THEM (?) somewhat stable
What are foam cells?
lipid enhanced macrophages
smooth muscle cells engulf foam cells, & lipids –>
fatty streak
fibrous cap over:
fatty streak
2 types of caps
What are two types of plaque?
stable and unstable
what is stable plaque?
has a thick calcified cap and a smaller fatty core. It is the primary cause of hardened and narrowed arteries (atherosclerosis)
What is unstable plaque?
has a thin calcified cap covering a larger fatty core. Is more likely to rupture which can trigger a heart attack or stroke.
Which is more likely to rupture, stable or unstable plaque?
unstable
An embolism is an example of what type of plaque?
unstable
What is coronary artery disease?
atherosclerosis of coronary vessels alters myocardial perfusion
When does myocardial perfusion occur?
during periods of muscle relaxation (diastole)
What is ischemic heart disease?
imbalance of myocardial supply & demand. (heart is not getting O2 that it needs)
What influences supply?
- coronary blood flow O2
- carrying capacity of blood
What influences demand?
- increased with HR
- increased contractile state (activity, fright)
- increased systolic tension (HTN, cold)
The right coronary artery is:
inferior
The left anterior descending is:
anteroseptal
The left anterior descending (distal):
anterioapical
circumflex is:
anterolateral
The right coronary artery is:
posterior
What are 5 clinical conditions:
- chronic stable angina
- unstable angina
- myocardial infarction
- cardiac muscle dysfunction
- sudden cardiac death
What are possible areas of radiating pain?
neck, jaw, upper abdomen, shoulders and arms
What are cardiac dysfunction symptoms for males:
- crushing pain
- “elephant on chest”
- nausea
- left arm pain
- jaw pain
What are cardiac dysfunction symptoms for females:
- nausea / vominting
- fatigue
- anxiety
- mid back tightness
- discomfort
Which is predictable, stable or unstable angina?
stable angina
Stable angina is:
substernal ches pain radiating to elbow.
including crushing /pressure
What is associated with SOB, nausea, and diaphoresis (cold sweating)
stable angina
What relieves stable angina: (2 things)
- rest
2. nitroglycerin
Stable angina occurs at a ________________ level of activity.
predictable
In stabile angina, myocardial O2 consumption =
rate of pressure-product
Rate pressure product =
(HR x SBP)
- how hard the heart is working
What is important to remember about unstable angina?
need to stop!!
Unstable angina is considered:
presence of angina in absence of increased demand
Unstable angina includes the 4 following situations:
- angina at rest
- angina that occurs at lower lower level of EX compared to usual
- angina different than normal pattern
- BP decreases with same amount of activity
Myocardial infarction =
decreased (lower) O2 supply / increased (higher) O2 demand
myocardial infarction results in:
death of myocardial tissue and thus abnormal myocardial function
tissue death = resulting in scar tissue –>
change in EKG @ Q wave
What wave of the EKG is changed due to myocardial tissue death?
Q wave
Rise of cardiobiomarkers >99th percentile and evidence of one of the following signs of ischemia =
myocardial infarction
Discomfort > 20 minutes, EKG changes, development of pathologic Q waves are signs of :
myocardial infarction
Imaging evidence of loss of viable myocardium may be a result of:
myocardial infarction
What is a biomarker of myocardio infarction?
Troponin increase (3-4hrs) (peak 18 hr)
The more EKG leads with MI changes –>
the worse prognosis
EKG changes associated with MI include:
ST elevation
Q waves
What are 3 explanations for ST segment depression?
- injured cell partially depolarized prior to stimulation
- ischemic cells have leaky cell membranes
- creates flow directed toward electrode, shifts baseline upward
If ST segment is lower than baseline & whole wave-from is shifted:
STEMI
Do necrotic muscles generate electrical force?
NO, necrotic muscle does not generate electrical forces - Q wave results from absence of electrical force
The __________ often provides permanent ECG evidence of previous MI in multiple leads
Q wave
Name 2 classifications for NSTEMI:
- subendocardial
2. NSTEMI
Name 2 classifications of STEMI:
- Q wave
2. transmural (existing or occurring across the entire wall of an organ or blood vessel
What are 2 recommendations for EX testing for Diagnosing CAD?
- not recommended for asymptomatic individuals with low CV risk (
What 4 variables does EX treating for CAD evaluate:
- hemodynamic response (HR & BP)
- EKG waveforms
- Limiting signs & symptoms
- gas exchange or ventilatory responses (VO2 max)
What are 5 EX test responses that suggest myocardial ischemia?
- ST segment depression >1mm
- ST segment elevation in leads with previous MI (Q wave)
- Multifocal PVCs or runs of V-tach
- Peak EX HR > 2 SD below age predicted HR (not on beta blockers)
- exertional hypotension (SBP drops > 10 mmHg)
Nuclear imaging is _______ sensitive in detecting early CAD
90%
What are 3 methods for managing a cardiac event?
- control risk factors
- control symptoms
- revascularization
How do you control symptoms?
nitroglycerin
How do you revascularize?
- PCI (precutaneous coronary intervention)
2. CABG (coronary artery bypass graft)
What are the implications for physical therapists?
- prevention
- recognize S& S of ischemic disease to refer correctly
- red flags, angina, nitroglycerin
- all chest pain needs to be evaluated before PT
- counsel patients on risk factor management including taking BP initial visit
- cardiac rehabilitation
What are 4 characteristics of peripheral artery disease?
- decreased blood flow to legs
- claudication pain (angina in legs)
- Higher risk of MI & stroke
- smoking and diabetes increase risk of PAD
What are the 4 steps of ankle-brachial index?
- doppler ultrasound amplifies the sound of aterial blood flow
- pressure recorded in the brachial artery of the arm
- sound of arterial blood flow located in ankle
- pressure recorded in arteries of the ankle after each arterial flow is located
What are the main risk factors for PAD?
smoking & diabetes
What are 4 signs of intermittent claudication?
- achy, cramping feeling in the legs
- occurs w/ walking/exercise
- decreases with rest
- onset of pain is predictable
What is claudication?
a condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries.
elastic arteries:
need to stretch and recoil with each heartbeat (recoil helps maintain pressure)
Muscular arteries:
adjust diameter for blood pressure control; some regulate blood flow to parts of the body
arterioles:
control flow to tissues
capillaries:
serve tissues; local control determines how much blood the tissue recieves
venules:
collect blood from the capillaries
veins:
collect blood from the venules
Tour of the blood vessels: Heart–> elastic arteries–> ___________________–> arterioles–> _____________–> venules –> ___________________.
Heart–> elastic arteries–> MUSCULAR ARTERIES–> arterioles–> CAPILLARIES–> venules –> VEINS.
What system controls blood flow?
autonomic nervous system
Nervous regulation is more _______ in effect
global
How does the autonomic nervous system regulate a more global effect?
- redistributes blood to different areas of body prn
- affects heart rate
- can rapidly change arterial blood pressure
What is the primary nervous system that influencing the regulation of circulation?
SNS
What system assists in regulation of heart function?
PSNS
In SNS distribution, sympathetic vasomotor nerves leave the spinal cord through thoracic and 1st 1 or 2 __________________________.
lumbar spinal nerves
From the lumbar spinal nerves the sympathetic vasomotor nerves pass into the:
sympathetic chain
From the sympathetic change the vasomotor nerves continue to either / or:
sympathetic nerves
spinal nerves
SNS innervates all vessels EXCEPT:
capillaries, precapillary sphincters, metarterioles (in most cases)
Innervation of small arteries and arterioles allows:
stimulation to vasoconstrict
Increase vasoconstriction –> increased contraction –>
increased heart rate
sympathetic nerves–>
heart & other organs
spinal nerves –>
vessels & arterioles
Capillarlies already controlled by:
- lack of O2
2. vasodialator
What is most rapid controlled?
arteries and arterioles
Additionally, vasoconstriction leads to:
- reduced flow to region
- more resistance through vessel
- more movement
Vasoconstriction in large veins:
increase cardiac return
SNS stimulation to veins increases the volume because of:
vasoconstriction
How does it affect the peripheral circulatory system?
The blood pushed back to the heart, the heart will respond to increased stretch (Frank Starling), contracting harder to get blood pushed to periphery
What does the frank starling law state:
hat the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant.
What happens with blood loss due to trauma, etc
- Reflexes elicited from aortic bodies and carotid sinus
- stimulates sympathetic nerve impulses to the veins
- -> results in reduction in reservoir, almost normal circulation up to 20% blood loss
What is circulatory shock?
condition in which blood vessels are inadequately filled & blood can’t circulate normally
What are 3 types of circulatory shock?
- hypovolemic shock
- vascular shock
- cardiogenic shock
Describe hypovolemic shock:
low blood volume
- due to major hemorrhaging, vomiting, diarrhea, and extensive burns.
Describe vascular shock:
Occurs due to vasodilatation or drugs
- anaphylactic shock
- ->allergic reaction
- —>histamine (vasodilator)
- Septicemias
What is septicemias:
massive bacterial infection, goes through blood
Bacteria are vasodilators
-gone systemically through body
Cardiogenic shock is what?
the heart has stopped working
“pump failure”
Sympathetic nerves carry ____________ vasoconstrictor fibers and ________ vasodilator fibers.
MANY vasoconstrictor
few vasodilator
What are 3 characteristics of vasoconstrictor fibers?
- distributed to all segments of circulation
- largest distribution to kidneys, intestines, spleen and skin (fight or flight)
- Less distributed to skeletal mm and brain
Where are cardioregulatory and vasomotor centers located?
in the medulla oblongata
The vasomotor center includes what 3 areas?
- vasoconstrictor area
- vasodilator area
- sensory area
Glossopharyngeal nerve and vagus never provide input to :
vasomotor center in brainstem
Get information from heart to center. But when we pick up something in vessel (baroreceptors), send info down about needing change. Then?
get response through SNS and makes change.
receptors in cardiac inhibitory center:
decrease HR
receptor in cardiac accelerator center:
increase HR, stroke volume
What are the 2 functions of the sympathetic vasoconstrictor tone?
- maintains normal vasomotor tone
2. contributes to maintenance of BP
What happens if we loose normal vasoconstrictor tone control?
arteries, arterioles dilate (not capillaries)
Neurons in vasoconstrictor area secrete:
norepinephrine
The secretion of norepinephrine causes excitation of:
SNS vasoconstrictor fibers
SNS transmits signal through the spinal cord and peripheral sympathetic nerves to:
(almost all) blood vessels of body
keeping them slightly contracted (smooth muscles & arteries)
Neuronal fibers int eh vasodilator area project up toward the vasoconstrictor area and ________________ vasoconstrictor area.
INHIBIT
By turning off vasoconstriction, we get ___________________. From vasodilator activation
vasodialation
Sensory nerve impulses received from circulatory system via:
vagus & glossopharyngeal nerves
Sensory are output helps control which areas?
vasoconstrictors and vasodilators
The adrenal medulla receives SNS stimulation simultaneously with:
blood vessels
The result of the adrenal medulla stimulation is:
medullae secrete norepinephrine and epinephrine into blood system
What does the secretion of norepinephrine and epinephrine into the blood system cause?
vasoconstriction
Epinephrine occasionally causes what?
vasodilation in some tissues
What does a bleed in the adrenal medulla lead to?
disruption of control of BP
The cardiac center is adjacent to:
part of the vasomotor center
The cardiac center adjusts rate and force of heart contraction to meet?
the needs of the body.
The cardiac center includes which other sub-center?
- cardioacceleratior center
2. cardioinhibitory center
Vasoconstriction:
sympathetic NS
Cardioacceleratory center acts through which fiber type?
sympathetic
Cardioinhibitory center acts through which fiber type?
parasympathetic
Sympathetic fibers regulates:
speed / rate of contraction & force
Parasympathetic fibers regulate:
HR
Parasympathetic fibers run through / as:
vagus nerve
cardiovascular center =
cardiac center + vasomotor center
Stimulation of vasomotor center under normal conditions also stimulate ______________________. Therefore, controlling heart function and vascular function simultaneously. Which leads to:
cardiac centers
- increased vasoconstriction w/ increase HR
- vasodilation w/ decreased HR (PNS_)
BP regulation =
rapid control of arterial pressure by nervous system
Which is the nervous systems most rapid response?
control of BP
The nervous center can increase the BP within:
seconds
A 2-fold increase in BP within ________________________
5-10 seconds
ex. 120 to 240 mmHg
A decrease in BP to 1/2 normal can occur in __________ seconds
10-40 seconds
Increase in arterial pressure occurs from simultaneous stimulation of _______________________ and _____________________.
vasoconstrictor and cardioaccelerator
Reciprocal inhibition of PNS vagal signals to the:
heart
What are 3 major changes that result from an increase in arterial pressure:
- most arterioles constrict
- veins and other large vessels constrict
- SNS stimulation of heart
Mechanisms that can increase blood flow during exercise:
???
How is normal arterial pressure maintained?
by subconscious reflex systems in place to monitor and maintain normal arterial BP
Baroreceptors are neural receptors in the ____________ sinuses, aortic arch and walls of nearly every large ____________ in the _______ and thorax.
carotid
artery
neck
Baroreceptors are pressure sensitive: so they respond to _________ or _______________ in vessel walls.
stretch or
lack of stretch
Baroreceptors stretch sends rapid impulses to the ________________ center and ___________________ center.
vasomotor center and
cardiac center
Baroreceptors decline in MAP initiates reflex vasoconstriction and increases ___________________.
CO - BP rises
See slide 24 on baroreceptors
See slide 24 on baroreceptors
Which part of the diagram (slide 24) occurs when you rise from a seated position?
???
Protect circulation agains acute changes in BP:
“pressure buffer system”
What reflexes protect circulation against acute changes in BP?
carotid sinus reflex
aortic reflex
As part of baroreceptor function is variation in BP minimized?
yes, variation in BP is minimized
Baroreceptor function becomes ineffective with ___________________________________.
Prolonged pressure changes - adapt
Baroreceptors will “reset” at ______ set point with prolonged pressure change, which limits their ______________________ to perceived higher pressure
higher
long-term response
Is there another system for long-term BP regulation?
???
Chemoreceptors respond to changes in ______. CO2 and ______.
O2, CO2, and H+
Chemoreceptors are located in __________________ bodies and ________________ bodies.
carotid bodies and aortic bodies
Chemoreceptors stimulate nerve fibers traveling to the _____________ center.
vasomotor
Chemoreceptors are important at low arterial pressures (
decrease in O2 –> decrease ____________ ;blood / gas
decrease pressure
What are consider mechanisms of action for chemoreceptors?
- in contact w/ arterial blood
- senses low O2 or high levels of CO2 or H+ that results with a drop in arterial pressure
- initiates reflexive vaso/venoconstriction
Arterial reflexes within walls of atria:
respond to change in pressure
low-pressure receptors (stretch receptors) =
minimize arterial pressure changes
bainbridge reflex (stretch receptors) =
with increase arterial pressure, will get an increase in HR and strength of contraction to prevent blood from “backing up” into system.
Damage to atria can reduce effective response to _____________.
pressure changes
When does the CNS ischemic response occur?
when blood flow to vasomotor center severely decreased - compromises nutritional access = cerebral ischemia.
When blood flow to vasomotor center severely decreased:
get strong reaction of vasoconstrictor and cardioaccelerator centers.
Large rise in systemic arterial pressure is due to?
higher levels of CO2
CNS Ischemic response can raise the MAP to ~250 mmHg for up to ___________
10 minutes.
What is the most powerful activator of SNS vasoconstrictor system?
CNS ischemic response
Massive decrease in BP –>
decrease in cerebral blood flow
decrease in cerebral blood flow –>
increase in PCO2 and increase in H+
increase in PCO2 and increase in H+ –>
activation of VMC
activation of VMC –>
increased sympathetic (action)
increased sympathetic (action) –>
increased HR & Increased TR
increased HR & Increased TR –>
restores BP
From the brain, decrease in BP activates cardiac centers in medulla leading to:
increase in sympathetic center activity & decreased parasympathetic activity
increase in sympathetic center activity –>
- increased contractility of cardiac muscle
- increased epinephrine in blood
- increased HR
decreased parasympathetic activity –>
increased HR
increased contractility of cardiac muscle –>
decreased ESV
decreased ESV –>
increased stroke volume (SV)
increased stroke volume –>
increased cardiac output (CO = SV x HR)
increased HR –>
increased cardiac output (CO = SV x HR)
increased epinephrine in blood –>
increased HR
Increased activity of respiratory pump (ventral body cavity pressure) ; Increased activity of muscular pump (skeletal muscles ) leads to
increased venous return
increased venous return —>
increased EDV
increased EDV –>
increased stroke volume (SV)
Why might precapillary sphincters open?
?
How is circulation controlled in relation to tissue?
?
How are the heart and circulation controlled to provide needed blood flow and arterial pressure?
?
How is blood volume controlled to regulate blood flow?
?
How many gallons of blood pass through the 2 kidneys every day?
~ 50 gallons
How many quarts of urine are produced from the 50 gallons of blood that pass through the kidneys every day?
~1.3 gallons
The kidney is about the size of a:
computer mouse
What is one important function of the kidneys?
maintaining BP
The rapidly acting arterial pressure control mechanism of the SNS:
effect on total peripheral vascular resistance and capacitance and cardiac pump.
Based on maintaing a balance between intake and output of body fluid, overall regulation of kidney excretion of ________ and __________.
H2O
Na+
Increase in extracellular fluid results in:
increased blood volume and arterial pressure
Normal body response of kidneys:
kidneys excrete excess extracellular fluid and returns the pressure to normal.
The normal body response of kidneys reverses if:
there is a reduced blood volume.
What is pressure diuresis?
renal output of water
Pressure natriuresis is:
renal output of salt
increase blood volume –>
increase blood pressure
decrease in blood volume –>
decrease in blood pressure
Excess salt intake = increase H2O retention –>
increase MAP
Excess salt intake =
increase H2O retention
A urinary volume output of about 1 and an arterial pressure mmHg of about 100 is were the volume x pressure relation dramatically:
increases
over long-term, water and salt intake must equal:
output
2 determinants of long-term arterial pressure =
- location of renal output curve (shift?)
2. level of intake line
Arterial pressure =
CO x TPR
If increase TPR =
- get acute rise in arterial pressure
However, normal kidney function will respond by returning arterial pressure to:
the pressure level of the equilibrium point.
** why? goal is to maintain equilibrium
Increased extracellular fluid volume –>
increases blood volume
increases blood volume –>
increased mean circulatory filling pressure
increased mean circulatory filling pressure –>
increased venous return
increased venous return –>
increased CO
increased CO –>
increased arterial pressure
In regards to CO, what are 2 mechanisms to increase arterial pressure?
- direct effect
2. indirecte effect
What is a direct effect?
increased CO increases pressure
What is indirect effect?
autoregulation
Effect of increased NA+ greater than effect of what?
increased H2O
Why is an increased Na+ a greater effect compared to increased H2O?
pure H2O excreted equally quick as injected
** salt can stick around longer
The amount of salt accumulation in the body is:
the main determinant of extracellular fluid volume
What is the MAP value in chronic hypertension?
> 110mmHg
With dialysis, what happens if patient’s body fluid level is not kept at a normal level?
???
What is the first mechanism of the kidneys?
control of arterial pressure
What is the second system of the kidneys?
renin-angiotensin
renin = protein release by kidneys
Renin =
hormone that acts as an enzyme; releases when arterial pressure drops - i.e., when renal perfusion is inadequate
What helps raise arterial pressure?
renin
Can renin be a life-saving system in circulatory shock?
Yes!
Is renin a strong vasoconstrictor?
NO!
Decreased arterial pressure –>
renin (kidney)
renin (kidney) –> acts on:
renin substrate
renin substrate –> results in :
angiotensin I
angiotensin I –> transforms into
angiotensin II
what is a powerful vasoconstrictor?
angiotensin II
angiotensin II –>
- retention (salt/H2O)
- vasoconstriction (of blood vessels)
- inactivation
- retention (salt/H2O) and
2. vasoconstriction (of blood vessels) lead to
increased arterial pressure
The direct effect of angiotension is that kidneys:
retain salt and water
The indirect effect of angiotension is that kidneys:
causes adrenal glands to secrete aldosterone which increases salt/water reabsorption by kidneys
What does the renin-angiotension and salt regulation allow the body deal with?
widely varying Na+ intake and maintain normal BP
increased salt intake –>
increased extracellular volume
increased extracellular volume –>
increased arterial pressure
increased arterial pressure –>
decreased renin and angiotension
decreased renin and angiotension –>
decreased renal retention of Na+ and H2O
decreased renal retention of Na+ and H2O –>
return of extracellular volume almost to normal
return of extracellular volume almost to normal –>
return of arterial pressure almost to normal
primary (or essential) hypertension =
“silent killer”
What is the cause of primary hypertension?
cause unknown.
i.e. not secondary to a known cause
There is an influence of weight gain and ______________________ on hypertension.
Sedentary lifestyle
What are 3 changes to HTN associated with weight gain and obesity?
- increased CO
- SNS activity increased
- Angiotensin II/ Aldosterone levels increased
Significant increase in angiotensin II / Aldosterone ; b/c increase SNS –>
increase in Renin
What do we see an increase in SNS activity with obesity?
possible from Leptin
All new fat tissues need more O2; increase demand –>
increase HTN
What are treatment options for HTN?
- lifestyle modifications (diet & ex)
- pharmacological (vasodilator drugs & natriuretic or diuretic drugs)
Rapid (w/in) seconds control of arterial pressure are based on:
- baroreceptor feedback
- CNS ischemic response
- Chemoreceptor reflex
Semi-rapid (minutes/hours) control of arterial pressure are based on:
- renin-angiotensis vasoconstrictor mechanism
2. fluid shift through capillary walls
Long-term (hours/days/months/ years) control of arterial pressure are based on:
- Renin-body fluid system
2. can involve aldosterone
hemorrhage, excessive sweating inflammation –>
- decreased blood volume, decreased blood pressure
- Blood pH and O2 level decreased, blood CO2 level increased
Crisis stressors (ex, physical or emotional trauma, increased body temperature) –>
Blood pH and O2 level decreased, blood CO2 level increased
Blood pH and O2 level decreased, blood CO2 level increased –> (short term)
chemoreceptors to brain
Decreased blood volume, decreased blood pressure–> (long term)
renal activity
Decreased blood volume, decreased blood pressure –> (short term)
Baroreceptors to brain
Renal activity –>
Conservation of Na+ and water
Decreased release of ANP –>
Conservation of Na+ and water
Conservation of Na+ and water –>
increased blood volume
Increased blood volume –>
Increased venous return
Increased activity of muscular pump and respiratory pump –>
Increased venous return
Increased venous return –>
increased stroke volume
In the brain, reflex activation of vasomotor and cardiac acceleratory centers –> (short term)
increased stroke volume
Increased stroke volume –>
Increased cardiac output
Increased heart rate –>
Increased cardiac output
In the brain, reflex activation of vasomotor and cardiac acceleratory centers –> (short term)
Increased heart rate
Increased cardiac output –>
Increased mean systemic arterial blood pressure
In the brain, reflex activation of vasomotor and cardiac acceleratory centers –>
Decreased diameter of blood vessels
Increased body size, obesity –>
increased blood vessel length
Increased blood vessel length –>
Increased peripheral resistance
Increased peripheral resistance –>
Increased mean systemic arterial blood pressure
Decreased diameter of blood vessels –>
Increased peripheral resistance
Bloodborne chemicals (NE, epinephrine, antidiuretic hormone, [ADH], angiotensin II) generated by renin release by kidneys, endothelin (secreted by endothelial cells); reduced release of NO by endothelial cells –>
Decreased diameter of blood vessels
Dehydration, high hematocrit –>
Increased blood viscosity
Increased blood viscosity –>
Increased peripheral resistance
What is heart failure?
a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood
Name 3 cardinal manifestations:
- dyspnea
- fatigue
- flulid retention
Which is preferred, heart failure or congestive heart failure?
heart failure
What are 3 clinical manifestations of HF?
- marked decrease in EX tolerance
- decline in functional status
- decrease in quality of life (QOL)
How common is HF?
affects 5.1 million americans
550,000 new cases are diagnosed annually
How much money is spent on HR?
It is the mostly costly cardiovascular illness in the United states, with total treatment costs estimated at $32BILLION.
Compared to $132 million for lung cancer research (400,000 americans)
What is the prognosis of HF?
1 in 9 deaths list HF as contributing cause
~50% of those diagnosed with HF die within 5 years
Why are 4 categories for etiologies of HR?
- intrinsic cardiac disease
- myocardial damage
- excess work load
- other
Intrinsic cardiac disease:
CHD (congenital heart disease), CM (cardiomyoathy), valve disease
Excess work load:
HTN, aortic stenosis (narrowing), pulmonary HTN
Myocardial damage:
post MI or s/p chemotherapy radiation, drugs
Other (etiologies of HF):
family history of chronic alcohol abuse anabolic steroid - long-term use
Cardiomyopathy:
the heart muscle loses its ability to pump effectively. The heart becomes larger as it tries to compensate for its weakened condition
One of pathophysiology of HF is abnormal SV. Abnormal SV is due to:
- impaired contractility
- increased after load
- impaired ventricular filling
Ejection fraction (LVEF) =
fatigue extremely quickly (basic ADLs become exhausting)
what is a normal ejection fraction?
55-75%
What is the normal amount of blood moved in 1 min?
4-8 L/min
left ventricular enddiastolic pressure (LVEDP), and left ventricular enddiastolic volume (LVEDV):
amount of blood right before it contracts, right before diastole
exercise stress test:
EKG measuring, determine someones response to exercise.
What are 5 measurements of HF?
- ejection fraction
- CO
- LVEDV or LVEDP
- Echocardiogram
- Exercise stress test
When preload is abnormal in pts with HF, heart can’t fully contract –> increased:
volume in ventricles
When HF, the _________________ is lower in comparison to normal functioning at the same end-diastolic pressure (preload).
stroke volume
too much fluid –> increased pressure –>
plasma leakage
In a non-failing heart, the LVEDP is around 10mmHg with a stroke volume of about 80mL. A failing heart in comparison has a LVEDP at about 25mmHg with a SV of about 40mL. What is the effect of medication on LVEDP and SV?
- diuretic reduces preload (15mmHg , 40mL)
- vasodilator reduces afterlaod (18mmHg, 60mL)
- beta-agonist increases inotropy (20mmHg, 70mL)
Afterload =
resistance encountered by left ventricle when tries to eject blood (systole)
In normal heart afterload _________ with EX.
increases
With HF, afterload increased with:
increase in arterial vasomotor tone
Increased afterload causes increased:
decreased:
increased: myocardial oxygen consumption (pumping against resistance) &
decreased: stroke volume
In normal heart, increased afterload _______________ effect on SV. In HF, small increases in atferload can have ________ effects on SV.
little
big
Higher afterload –>
worse SV
What are 3 main types of prime examples of what can happen in HF:
- dilated
- restrictive
- hypertrophic
Heart with dilated cardiomyopathy =
increase in preload
muscle fibers have stretched heart chamber enlarges
heart with restrictive cardiomyopathy =
reduced preload
ventricle walls stiffen and lose flexibility
Is it possible to get R-sided HF from having L-sided HF?
yes
Systolic dysfunction:
- loss of contractility
- dilated ventricle
- increased LVEDV
- lead to decreased EF
diastolic dysfunction:
-impaired filling due to hypertrophy or decreased filling
-results from HTN or aortic stenosis
(**trouble getting blood into heart)
Decreased ejection fraction is a sign of what?
cardiac dysfunction
Normal systole (contraction) = EF 0.55 / Systole immediately after HF = EF
0.25
In dilated cardiomyopathy, LVEDP is ______ (think volume), force of muscle contraction is __________ and we get ________________.
increased
low (decreased)
Systolic (loss of contractility, larger dilated ventricle)
In hypertrophic cardiomyopathy, LVEDP is ______, force of muscle contraction is __________ and we get _________.
decreased LVEDP
varies (initially high)
diastolic (impaired filling)
Name 3 causes of right sided heart failure:
- increased pulmonary resistance
- increased afterload - pulmonary HTN or valve stenosis
- Low preload or poor pump
Name 4 causes of right sided heart failure:
- impaired contractility
- increased afterload
- loss of myocardial tissue
- low preload
What are 4 symptoms of right sided heart failure:
- weight gain
- peripheral edema
- hepatomegaly (abnormal enlargement of liver)
- jugular venous distention
What are 6 symptoms of left heart failure:
- dyspnea
- orthopnea
- paroxysmal nocturnal dyspnea
- S3 heart sound
- excessive weight gain (>2lbs /day)
- decreased EX tolerance
Why is dyspnea a symptom of left sided heart failure?
b/c blood is backing up into lungs, caused belabored breathing
What is orthopnea?
trouble breathing while laying down
What is S3 heart sound?
abnormal sound associated w/ HF (normal in kids)
With left sided heart failure what sound is heard during auscultation?
crackles / rales
Describe the pulmonary edema associated with left sided heart failure?
- when pulmonary venous pressure > 20mmHg, fluid into lungs (increased hydrostatic pressure)
- decreased pulmnary compliance = increased work of breathing
The neurohormonal compensatory mechanism of decreased cardiac output leads to:
- sympathetic stimulation
- stimulate ADH (anti-diuretic) & increase vascular volume
- renin - angiotensin
Decreased cardiac output –> Sympathetic stimulation leads to:
increase HR, increase contractility, and vasoconstriction.
Decreased cardiac output –> Renin-angiotensin, leading to:
vasoconstriction and increase in BP
The PURPOSE of compensatory adaptations in HF is to maintain_____________________ and _________ that adequately perfuses the brain and the heart.
CO
arterial pressure
The MAGNITUDE of the compensatory adaptations eventually leads to maladaptive processes which lead to a:
decompensated state or end-stage HF
List 5 compensatory mechanisms:
- increase in MAP
- Moderate fluid retention
- increase LVEDP
- Decreased strok volume (decreased EF)
- Decreased contractility
“In compensated HF, symptoms are ______, and many overt features of fluid retention and pulmonary oedema are _____. Decompensated HF referst to a ___________, which may be present either as an acute episode of pulmonary oedema or as _______ and _______, a reduction in EX tolerance and increasing ________________ on exertion.”
“In compensated HF, symptoms are STABLE, and many overt features of fluid retention and pulmonary oedema are ABSENT. Decompensated HF refers to a DETERIORATION, which may be present either as an acute episode of pulmonary oedema or as LETHARGY and MALAISE, a reduction in EX tolerance and increasing BREATHLESSNESS on exertion.”
Which one (compensated or decompensated) can you work with as a PT?
Compensated
What is B-type natriuretic peptide (BNP)?
-Endogenous neurohormones that maintain normal fluid status and promote normal cardiac function.
BNP is secreted by ______ ventricle in response to volume expansion & pressure overload - “myocardial stretch”
left
What is the purpsoe of BNP?
Counter-regulation of renin-angiotensin - aldosterone system (RAAS)
What does BNP encourage?
encourages vasodilation, diuresis while inhibiting the RAAS.
BNP >______pg/ml is diagnostic for CHF (sens 82%, spec 93%).
> 100pg/ml
Class I HF:
No limitation of PA
Class II HF:
Slight limitation of activity - OK at rest
-Dyspnea & fatigue w/ “ordinary” PA
Class III HF:
OK at rest
-symptoms of HF with less than “ordinary” activity
Class IV HF:
Symptoms present @ rest
How do you control HF?
correct the underlying cause
Controlling HF, preload:
control salt and water retention (low sodium diet, diuretics)
Controlling HF, Improve contractility (cardiac muscle performance):
B-Blockers, inotropic meds (change force of heart contraction), pacemaker or decrease workload
Controlling HF, afterload:
reduce peripheral resistance (lower BP)
What medications are included in the “triple drug cocktail”?
- ACE inhibitor
- Diuretics
- Beta-blockers
What do ACE inhibitors do?
decrease afterload
What do diuretics do?
decrease volume
What do Beta-Blockers do?
Limit sympathetic stimulation to heart, hold heart rate down
What agents increase cardiac muscle contraction?
Digitalis (Glycosides)
How do digitalis (glycosides) work?
- inhibit NA/K pump, increase intracellular Ca++
- Increases cardiac outpu
- Low therapeutic window
- Signs of digitalis toxicity (N/V, headache, confusion, arrhythmias, sinus bradycardia)
(** recently fallen out of favor)
Name 2 other treatments to adjust cardiac muscle contraction?
- ventricular assist
2. heart transplant
Most clinical measures of cardiac function correlate ______ with clinical severity of HF
poorly
EX intolerance in CHF depends on 3 variables:
- Disease
- Level of inactivity
- Other
Measurements of EX capacity in HF include:
- peak oxygen uptake
2. anaerobic threshold
Peak VO2
6 MWT predicts?
VO2
For the 6 MWT, 40% who walke
Acute CARDIAC responses to EX in pts w/ HF = progressive _______ in cardiac output, stroke volume, and HR reserve capacity. EX tolerance is limited by reduced __________________________.
decrease
CO during EX.
Acute CIRCULATORY responses to EX in pts w/ HF: muscle blood flow is ________ during an acute bout of EX in pts with HF.
Not entirely due to a reduction in _____________ or ________________. Change in the distribution of _____________ during EX.
- reduced
- CO or local vascular impairment
- blood flow
Acute SKELETAL MUSCLE METABOLIC responses to EX in pts w/ HF: higher _______ levels at submaximal workloads. Slower on-and-off _________ w/ Ex
lactate
kinetics
