Altered Perfusion
Perfusion - Forcing blood or other fluid to flow through a vessel and into the vascular bed of
tissue to provide oxygen *affects every system of the body
Requirements for Effective Perfusion
Adequate ventilation and diffusion: ability to breathe in and transport O2
Intact pulmonary circulation: lower part of lung – low surface tension/max blood flow/O2
Perfusion cannot occur without inhalation/diffusion of O2.
O2 enters lungs – crosses alveolar cap junction – pulm circ
∆ requires ventilation (intake of O2), Perfusion (movement of O2).
Ventilation-perfusion ratio (0.8:0.9) indicates that the rate of ventilation is slightly less
than the rate of perfusion
The largest volume of ventilation- perfusion is the lower lungs where they are most easily
inflated due to the low surface tension of the alveoli, which allows ventilation, and
where the perfusion is best due to BP allowing max blood flow (also has gravity
working for it!)
Adequate blood volume and components
Adequate cardiac output: optimal SV, HR, heart rhythm
Intact cardiac control center: needed to regulate HR and force of contractions
Intact receptors: for feedback
Intact parasympathetic and sympathetic nervous systems
Intact cardiac conduction
Intact coronary circulation: maintains perfusion to cardiac structures RCA
Intact systematic circulation
Adequate tissue uptake of oxygen
Types of circulation:
Circulation: effective circulation depends on patency (the condition of not being blocked or obstructed)
of the blood vessels and on the adjustments of the microcirculation to meet the demands of the tissues.
1. Pulmonary- circulation through the lungs provides the ability to transfer O2 from the
environment to the body
includes the right side of the heart and pulmonary arteries/capillaries and veins
pulmonary veins carry oxygenated blood to the left side of the heart
pulmonary artery carries deoxygenated blood to the lungs
Pulmonary circ works at a lower pressure than systemic b/c it moves blood slower
through the lungs for maximal gas exchange
2. Systemic–distributed to body tissues
this system involves all of the arteries and veins except ones in the pulmonary
circulation.
Functions at a higher pressure to work against resistance to get to peripheral tissues
Monitored by the left side of heart (esp. left ventricle which has strongest pumping)
3. Cardiac– this system includes the right coronary artery (RCA), the left coronary artery (LCA)
and the left anterior descending coronary artery (LAD) which perfuse the right and left sides of
the myocardium (muscle) of the heart. Coronary arteries:
1. RCA: supplies blood to the right ventricle
supplies 25-35% of blood to the left ventricle
supplies the SA node
2. LAD: branches off of the LCA
supplies 45-55% of blood to the left ventricle/provides much of the blood flow to the left
ventricle which enables the propulsive force of ejection
known as the “widow-maker” because blockage of this artery is particularly associated
with mortality
3. LCA: main coronary artery
feeds blood to the left side of the heart
Pericardium: outer covering of the heart
holds heart in place/contains receptors that help regulate BP and HR
1 line of defense against infection and inflammation
contains pericardial fluid (lubrication)
Myocardium: thick muscular layer
thickest at left ventricle (works the hardest – systemic circulation)
hypertrophy occurs here as workload increases
Endocardium: inner lining of the heart, continuous layer of endothelium
Cardiac Cycle – one contraction (systole: begins with closure of AV valve, ventricles have greater
pressure and eject blood, lub) and one relaxation (diastole: ventricles relax, pressure greater in
aorta/pulm artery, Aortic/pulm valves close and make the dub)
AV Valves: bicuspid (mitral), tricuspid
Contractions – rely on the passage of ions and electrical impulses from one myocardial cell to another.
These are generated through action potentials. Two major types of action potentials; slow and fast, work
in an organized manner
Phases of action potential:
1. Rapid depolarization: fast Na channels open and the rapid influx of Na into the cell cause it to
become positively charged
2. Early repolarization: fast Na channels close
3. Plateau – slow Na and Ca channels open and Na and Ca slowly enter the cell
4. Rapid repolarization: a regrouping phase in which the cell membrane becomes polarized with a
positive charge on the outside of the cell and a negative charge inside the cell. The cell also
becomes permeable to K and it exits the cell.
5. Resting phase PQRSTU Waves: electrical activity imposed by ions on cardiac cells can be measured using ECG/EKG
P = depolarization of atria via SA node
PQ interval = depolarization of AV nodes + bundle fibers
QRS = depolarization of ventricles
T = repolarization of ventricles
U = repolarization of Purkinje fibers
SA Node: pacemaker/ generates rhythmic impulses in atria/stimulated by slow response to NA and Ca
channels opening
AV Node: connects impulses between atria and ventricles/slow to allow atria to empty blood into
ventricle/generates impulses that travel to bundle of His and culminate in Purkinje fibers
Cardiac Output: depends on stroke volume (SV) and heart rate (HR)
CO = SV x HR
average CO is 3.5 – 8.0 L/min (can increase 4x during exercise) Stroke Volume: amount of blood pumped out of one ventricle in a single beat
Heart Rate: number of beats per minute
Major Factors affecting CO:
1. Preload: work imposed on heart just before contraction, depends on adequate venous return
2. Cardiac contractility: the ability of heart to ↑force of contraction without changing diastolic
pressure, affected by Ca.
3. Afterload: amount of pressure in the ventricle toward the end of contraction, increases when
valves are impaired.
4. Heart rate
5. Blood volume
Blood Pressure: pressure or tension of blood in systemic arteries
BP is maintained by:
1. Contraction of left ventricle
2. Peripheral vascular resistance
3. Elasticity of arterial walls
4. Viscosity and volume of blood
*BP is a product of cardiac output and amount of resistance in the arteries
Systolic BP: amount of pressure exerted during contraction of the left ventricle and ejection of blood into
the aorta
affected by SV, HR and resistance
Exercise, smoking and CVD increase it
Diastolic BP: amount of pressure remaining in the aorta during resting phase
Increase in diastolic may mean that the arteries are not allowed to rest between contractions.
Depressions can show lack of resistance in the aorta or backflow of blood
Pulse pressure: difference between systolic and diastolic BP (a narrow pulse pressure indicates a loss of
systolic pressure rather than in increase in diastolic)
MAP: an adequate measure of systemic tissue perfusion is 1/3 pulse pressure + diastolic pressure
Changes in BP occur as a response to:
1. Baroreceptors/chemoreceptors (detect changes in O2, CO2 and pH of blood)
2. RAAS (ANG II works to promote an increase in BP when acting as a vasoconstrictor on arteries
and arterioles)
3. Kidneys (ANG II stimulates the adrenal cortex to increase aldosterone to increase Na/H2O
retention by kidneys to expand BV)
4. Anti-diuretic Hormone (Vasopressin) secreted from posterior pituitary promotes retention of
fluids by acting as a vasoconstrictor (enhances BV)
5. Epinephrine acts to promote BP by stimulating HR and contractility (promotes tension on
vessels) Altered Perfusion- The inability to adequately oxygenate tissues at the capillary level
**most common cause of hypoxia
Cause:
1. Ventilation-perfusion mismatching: most common
Inadequate ventilation in well perfused areas of the lungs (asthma/edema)
Inadequate perfusion in well-ventilated areas of the lungs (embolus)
2. Impaired circulation: lead to inadequate or excessive blood flow to tissues and organs
Injury to vesselsdiabetes (build up of LDL + injury to vessel = inflammation)
Obstruction :
Virchow’s triad: vessel wall damage, excessive clotting, alterations of blood
flow (thrombus formation).
Inadequate blood movement: common sites = bifurcations (regions where vessel
branches), aneurysms (outpouches of weak wall), venous stasis (veins with reduced
return)
Inadequate blood volume
3. Inadequate cardiac output: when heart is unable to successfully eject the necessary
amount of blood to pulmonary/systemic circulation
Changes in blood viscosity (cancerhypercoagulationblood clots)
Impaired ventricular pumping : loss of muscle activity and ability to move blood
forward. Leads to heart failure
Structural heart defects:ASD (opening in L/R atria), VSD (opening in L/R ventricle)
and valve defects such as Stenosis (narrow valves) or Regurgitation (improper valve
closure)
Conductions defects:
cardiac dysrhythmias (problems with SA, AV node or cardiac cells)
fibrillation: problems with ventricle vibrating instead of pumping
heart block: obstruction of cardiac conduction.
Changes in peripheral vascular resistance
4. Excessive perfusion demands : inability of heart to meet demands
Excessive demands extreme or prolonged exertion/metabolic alterations such as
hyperthyroidism
Poor perfusion supply
Atherosclerosis:
1. Injury to inner lining of vessel (HTN, smoking, environment
2. LDL filters and gets trapped, becomes oxidized and engulfed by macrophages, producing
foam cells
3. Foam cells accumulate and combine with lipids to make fatty streaks, which become
fibrous plaques
4. Plaques accumulate and get covered by platelets, which continue to expand. General Manifestations:
Variable depending upon source of altered perfusion
Cyanosis, pain, pallor, coolness, edema, shortness of breath, impaired growth,
tachycardia, tachypnea,and fatigue
Hypotension or hypertension
Bleeding (petechiae, purpura, hematoma), bruising (ecchymoses)
Heart murmur
Diagnostic Criteria:
Echocardiography or Doppler ultrasonography
ECG ultrasound of the heart – shows hypertrophy + ejection fraction (+ 55% = normal)
Chest x-ray
Cardiac catheterizationto diameters of LAD, LCA & RCA
Pressure measurements
Stress test
Beta blockers: work by blocking B1 receptors to lower cardiac output
Adrenergic receptors: control vasoconstriction via RAAS
ACE inhibitors: too much blood volume requires a diuretic + 1-2 blockers + ACE inhibitor
Atrial Fibrilation: shows up as a squiggly line on an ECG and heart will not contract properly indicating
inefficient output – get out the paddles
Shocking the heart stops and restarts it at a normal rhythm (can shock 3 times and then each subsequent
shock should be followed by Epinephrine) Hypertension
Pathophysiology: ↑ resistance = peripheral vascular, ↓ vessel diameter= atherosclerosis
A progressive cardiovascular syndrome detected by an elevation in blood pressure and/or
the presence of organ damage due to persistent blood pressure elevations
Primary/ Esstential HTN: (90%-95%) Specific cause is unknown/multifactoral
disease. Often asymptomatic/ when clinical manifestations do present; this indicates
years of undetected HTN
Secondary: due to another cause (kidney/addisons)
↑ BP results in heart attack, weakened blood vessels, ischemia, atropy
Rise in systolic pressure is the #1 predictor of coronary artery disease (CAD)
Promotion of HTN:
1. Sympathetic Nervous System overstimulation (systemic vasoconstriction)
2. RAAS overstimulation (systemic vasoconstriction, Na and H2O retension by kidneys
and increased blood volume)
3. Impaired Na excretion by kidneys (Na and H2o retention and increased blood volume)
Systems Affected
1. CNS: elevated BP overwhelms cerebral blood flow causing intracranial pressure, O2
impairment and decreased brain function
2. Cardiovascular: HTN aids in development of atherosclerosis which contributes to
obstruction in the arteries (pressure in the arterioles can lead to altered function of target
organs especially kidneys, eyes, brain and heart)
Increased strain on the heart (left ventricle is most affected and becomes
hypertrophic)
This impairs venous return and systemic perfusions and leads to pulmonary
edema, myocardial ischemia and peripheral hypoxia
3. Kidneys: prolonged pressure on the kidney arterioles promotes chronic injury and
inflammation which leads to nephrosclerosis (an overgrowth/hardening of tissues)
HTN is perpetuated b/c RAAS is stimulated by reduced blood flow to the
kidneys, ∆ increased renin/ aldosterone
results in poor urinary output, hematuria, and proteinuria
Risk factors:
Family history of hypertension Excessive dietary sodium intake
hypercholestrolemia Smoking (same as diabetes)
Aging Excessive alcohol intake
Diabetes mellit
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