1
Alterations in Blood Flow
•
Vascular resistance
o is primarily regulated by the SNS.
o increased SNS stimulation à increased contraction of the smooth muscles in the
artery/arteriole walls à vasoconstriction.
o less SNS stimulation = less contraction of smooth muscles in the BV walls à vasodilation.
o a certain level of vasomotor tone must be upheld to maintain normal BP
§ A necessary process in order to regulate PVR.
§ blood vessels would dilate without sufficient vasomotor tone.
§ dilated vessels would decrease PVR.
§ even with available blood volume, dilated vessels wouldn't adequately fill the body's
vasculature
§ At any given moment some vessels will be constricted and some will be dilated.
•
Norepinephrine and epinephrine
o released from the adrenal medulla, when stimulated by the SNS
o can also stimulate alpha-1 adrenergic receptors on blood vessels to cause vasoconstriction.
o Epinephrine can also act on beta-2 adrenergic receptors
§ à vasodilation of blood vessels that supply the skeletal muscles and the heart.
•
Local factors that can influence local blood flow.
o increased activity levels of tissues will use resources faster and so will need increased
blood flow to deliver O2 and nutrients and to take away CO2 and metabolic wastes.
o Factors that stimulate local vasodilation and increase blood flow include:
§ a local increase in [CO2]
§ a decrease in pH
§ an increase in temperature
Blood Vessel Pathologies
Aneurysms
• a local dilation of the wall of an artery d/t weakening of that wall.
• Causes
o deterioration of the vessel wall
§ d/t atherosclerosis and arteriosclerosis
o syphilis infections (later stages)
o congenital defects
o trauma
o other infections
•
Hypertension (related to atherosclerosis)
o is a major promotor of aneurysms
o but once the aneurysm is established, an elevated BP will make the
problem much worse
o the increased pressure inside the artery is exerted outward against
the wall, causing the dilated area to expand further.
o periods of high stress can elevate BP and aggravate the problem even further.
§ it may even cause the aneurysm to rupture.
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•
Complications
o Disrupted Flow
§ turbulent (disrupted blood flow) à decreased forward blood flow to tissues (kidneys
and GI) à increased risk of thrombus formation in the arteries à peripheral
thromboembolisms.
o Compression of adjacent tissues
§ Common with aneurysms of the abdominal aorta
§ As the aneurysm expands, it begins impinging on and compressing adjacent arteries
with many negative effects
§ i.e the renal arteries with an abdominal aneurysm à renal failure
§ or the “circle of Willis” (in the brain)
o Rupture
§ can be rapidly fatal.
§ if in the cerebral circulation à fatal/significant strokes.
TWO things that increase the risk of aneurysm formation
o the higher the blood pressure the greater the risk.
o branched blood vessels are more prone to develop aneurysms.
Varicose Veins
• Causes
o a weakness in the vein walls
o defective/incompetent one-way valves.
o most commonly occur in
§ dependent areas of the body (especially lower limbs)
§ areas with little surrounding muscle mass to continue to pump the blood forward
through the veins (the superficial veins of the legs, esophagus, and around the rectum).
o faulty or weak valves
§ allow blood to accumulate over the competent valves à the vessel wall will stretch
and expand.
§ blood accumulation combined with the effects of gravity à increased local HP
• can damage even more valves progressively.
• The elevated HP can then translate back to the capillaries à edema
o Increased distance b/w tissues and their blood supply à ulcerations
o Reduced venous return à decreased CO
• the static and slow blood flow increases the risk of thrombus formation.
• The thrombus will travel to the heart à pulmonary arteries à circulatory
arterioles à PE
• thrombi formed in veins can only cause PE (nothing else)
•
Signs and symptoms
o enlarged, bulging purple-coloured veins (especially if they are superficial)
o an aching sensation
o muscle fatigue
o edema
o The surrounding skin may appear discolored and shiny and may ultimately ulcerate as it
erodes d/t ischemia.
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•
Risk factors
o a genetic/familial predisposition
o trauma
o pregnancy
o thrombophlebitis
•
Factors that can aggravate the condition:
o Pregnancy
§ High levels of progesterone that relaxes smooth muscles.
§ Compression of the vena cava- as the fetus gets bigger.
o workplace situations that involve long periods of standing still
o increasing age
§ d/t a decrease in muscle mass and decreased physical activity
o tight restrictive clothing that impedes venous blood flow.
o Right side HF?
Thrombophlebitis
• the formation of a thrombus (blood clot) in a vein where the vessel walls are inflamed.
• Signs and symptoms (caused by inflammation)
o heat and redness in the local surrounding tissues
o burning, itchiness, aching, and tenderness.
o edema
§ d/t increased venous pressure and upstream pain.
o May have systemic S&S
§ such as leukocytosis and fever.
Phlebothrombosis
• the formation of a thrombus in a vein without the presence of inflammation
• it spontaneously forms d/t stasis of flow
• associated with
o immobility
o CHF
o hypercoagulability (d/t dehydration/hypercalcemia).
• Initially no local S&S (because there is no inflammation).
o Inflammation may develop later in the vein as a result.
• Thrombi that develop this way are less integrated with the inflammation à less firmly attached and
more likely to detach and become emboli.
• From the venous circulation, the clot will circulate through the right side of the heart and enter the
pulmonary circulation, where it is likely to become trapped in smaller pulmonary vessels à
obstruction.
• This can lead to
o Respiratory problems
§ such as pneumonia, pulmonary edema
o Cardiovascular problems
§ such as heart failure.
• Signs and symptoms:
o sudden chest pain and cardiogenic shock.
§ can occur in thrombophlebitis as well, but it is much less common.
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Hemorrhoids
• swollen, dilated veins in the region of the anus or lower rectum.
• common after the age of 50 but also often before that.
• may be internal or external
• can narrow the orifice and be itchy and irritating.
• They can lead to chronic blood loss, significant discomfort and some low risk of infection.
•
Causes
o superficial veins are not well supported by surrounding muscle, can happen d/t:
§ episodes of constipation or straining à increased pressure à swelling of the veins
à inflammation.
§ Pregnancy and labor
§ family history
§ the bathroom habit of occupying the throne a little too long
•
Prevention is usually by
o having a higher fiber diet
o increasing water intake
o increasing exercise to make bowel function more effective.
•
Treatment
o corticosteroid creams
o analgesics
o in some cases surgical removal
o rubber band ligation
o electrical coagulation
o sclerotization.
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Atherosclerosis and Heart Disease
•
Atherosclerosis (can only happen in an artery/arterioles)
o raised fibrofatty plaques (atheromas) in the intimal lining of large and medium-sized blood
vessels.
o is present in almost every human
o plaque formation usually begins in the second decade of life.
o the process is usually asymptomatic until a vessel is ~75% occluded.
§ that’s when the heart can show signs of ischemia (e.g. angina), particularly during
times of physical exertion.
Lipid Metabolism Summary
• lipids cannot readily dissolve in blood plasma à
have to be transported by binding to lipoproteins.
• Lipids absorbed from the GI tract are bound to
chylomicron (lipoprotein) and enter into the lymph.
• The lymph drains into the subclavian veins and
the chylomicron can now circulate around the
body in the blood.
• As the chylomicron passes through adipose
tissue, it releases some of its TGs for storage.
• Once the chylomicron reaches the liver, it is
absorbed and broken down into its components
(TGs, cholesterol, vitamins)
• The liver is responsible for producing cholesterol
for the cells of the body.
o Synthesized cholesterol and cholesterol
absorbed in the chylomicron are
packaged with TG into a Very Low-Density
Lipoprotein (VLDL) and released into the
blood.
o As the VLDL passes through adipose tissue, it releases some of its TG for storage.
o This converts the VLDL into a Low-Density Lipoprotein (LDL).
o LDL can now circulate and deliver cholesterol to the tissues or be taken up by the liver and
recycled.
•
Occasionally, macrophages can consume LDL, which can play a role in the development of
atherosclerosis.
•
The liver also produces a High-Density Lipoprotein (HDL).
o HDL is released into the blood and is responsible for picking up excess cholesterol from the
tissues, and plays a scavenger role.
o The HDL ‘drops off’ cholesterol at the liver and returns it to circulation.
o The cholesterol removed by the HDL is now excreted from the body in the bile.
Atherogenesis: The “Response to Injury Theory”
Although the exact mechanism of atherosclerosis development is not known, it is believed to begin with
endothelial damage and inflammation (response-to-injury theory)
• The intima of an artery can become damaged d/t:
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Mechanical stress (i.e. shear stress)
§ high BP or high blood viscosity
o Oxidative stress
§ certain metabolic processes (áLDL, diabetes, and smoking) result in the generation
of high levels of ROS reactive oxygen species
§ ROS can damage lipids, proteins, DNA, and the intima of coronary arteries.
Damage to the endothelium then:
o induces an inflammatory response
o activates adhesion molecules, growth factors, á Ang II and ACE levels.
Inflammation
o leads to the accumulation of macrophages, which consume LDL and become foam cells
that form the initial fatty streak
Angiotensin II (d/t restricted blood flow to kidneys)
o causes vasoconstriction and reduced NO (Nitric Oxide) vasodilator) levels
o á vascular smooth muscle proliferation
á inflammation, á vasoconstriction, and promotion of
thrombosis.
o promotes cardiac cell growth à can contribute to cardiac
hypertrophy
o
•
•
•
•
•
•
•
•
•
Together, these factors lead to the formation of atherosclerotic
lesions (atheromas)
Atheromas consist of
o foam cells
o proliferating smooth muscle cells
o extracellular lipids
o fibrous tissue
As the lesion grows it:
o occludes the lumen of the vessel
o may form a thrombus à complete occlusion quickly
o weakens the BV wall à decreasing its activity
o may calcify à further rigidity of the BV wall
These factors can lead to aneurysms, rupture, or hemorrhage in the wall
an embolus can break from the thrombus and cause occlusion of other blood vessels, the most
detrimental being cardiac, pulmonary, and cerebral
The stability of plaque may be affected by the amount of lipids in the plaque
o a plaque that contains lots of lipids = unstable and progress faster, since it may attract more
macrophages and platelets.
o A plaque with more fibrous tissue and little lipid will be more stable and less likely to
rupture à decreasing predisposition to thrombosis
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Review of Cardiovascular System Anatomy
•
The heart is a muscular pump which moves blood to the lungs and other tissues of the body
Systemic Circulation
• Supplies the tissues of the body with nutrients and oxygen-rich blood.
• Oxygenated blood returning from the lungs is pumped from the left ventricle to the aorta and
systemic arteries to the tissues, where gas exchange occurs.
• Deoxygenated blood returns to the right atrium via the inferior and superior vena cava.
Pulmonary Circulation
• Deoxygenated blood is pumped by the right ventricle through the pulmonary arteries
• In the capillaries of the lungs, the blood is oxygenated
• Oxygenated blood returns to the left atrium of the heart through the pulmonary veins
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Cardiac Perfusion
Posterior
Anterior
Left Main
Right Main
Marginal
Circumflex
Circumflex
Left Anterior
Descending
Right Main
Posterior
Descending
•
•
The heart itself receives blood through the coronary arteries, which branch off the aorta
Due to the extreme pressure in the heart during contraction (systole), the heart only receives blood
during relaxation (diastole)
Cardiac Valves
• Changes in pressure determine the flow of blood in the heart and cause the valves to open and
close (a mechanical process).
• Blood moves along a pressure gradient (high to low).
• The valves contribute to the unidirectional flow of blood.
Opening the AV valves (Diastole)
1) Blood returning to the heart travels through the atria and forces the AV valves open
2) The atria contract, forcing additional blood into the ventricles
Closing the AV valves (Ventricular systole)
1) Papillary muscles contract to stabilize the valves
2) The ventricles contract forcing blood against the AV valves
3) AV valves close (first heart sound)
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Opening the Semilunar Valves (Ventricular systole)
• Contraction of the ventricles forces the SL valves open
• Blood rushes into the pulmonary arteries and aorta
Closing the Semilunar Valves (Diastole)
• ventricular relaxation causes intraventricular pressure to fall, and blood flows back from the arteries,
closing the SL valves (second heart sound)
Cardiac Murmur and Valve Disease
• Cardiac murmurs are abnormal sounds created by turbulent blood flow in the heart.
• Murmurs can be caused by pericardial rub, fluid overload, and valve disease.
• Valve disorders occur more frequently on the left side of the heart
o Valve stenosis
o Valve regurgitation
o Aortic stenosis
o Aortic regurgitation
Cardiac Output
• The efficiency of the heart to pump blood is often measured by the cardiac output:
CO = HR X SV
• CO varies with body size and level of activity
• Stroke Volume
o represents the difference between the amount of blood in a ventricle after filling (enddiastolic volume, EDV) and the volume of blood remaining in a ventricle after contraction
(end-systolic volume, ESV)
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o
The main factors affecting stroke volume (SV) are:
1. Preload- filling of the ventricles (venous return)
**á volume à á stretch of cardiac muscle à á strength contraction
(Frank Starling’s Law)
2. Contractility- contractile strength independent of muscle stretch
3. Afterload- the pressure against which the heart must pump
Factors that Affect Preload
• Frank-Starling Mechanism: á venous return stretches the muscle fibers to generate more contractile
force
• too little or excessive preload à â CO
• Note: an extremely fast HR â filling time à â EDV and preload
• á blood volume
o d/t hyperaldosteronism
o á ADH
o Large IV/blood transfusion
• Valve incompetence – doesn’t matter if SL or AV
Factors that Affect Afterload
• Hypertension
• â PVR (atherosclerosis)
• SNS
• Stenosis of the semilunar valves, the heart has to push harder
Cardiac Reserve
• maximum % increase of CO above normal resting levels
• Affected by:
o preload i.e. ventricular filling
o afterload i.e. resistance to ejection of blood from the heart
o contractility
o HR
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Angina, MI, and CHF
Angina Pectoris
• severe chest pain that originates from the heart in response to an inadequate O2 supply to the
myocardial cells compared to demand (ischemia)
• precipitating conditions include
o hyperthyroidism
o hypertension
o á physical activity
o emotional stress
o exposure to cold
• Anginal pain is experienced as recurrent, intermittent, brief episodes of substernal pain
• may radiate to the neck and left arm (referred pain)
• often described as pressure, squeezing, aching, or suffocating
• may manifest as ST segment depression
• if myocardial dysfunction occurs, dyspnea may develop
Stable Angina
• a type of chronic ischemic heart disease
• associated with a stable, fixed obstruction, usually atherosclerotic
• Episodes are precipitated by:
o á physical activity
o emotional stress
o exposure to cold
• Pain is usually short-lived (<5 minutes)
• Pain is relieved with rest (â O2 demand) or administration of nitroglycerin and nitrates
• if pain does not subside within 10 minutes of rest, pain may be due to severe ischemia
Unstable Angina (thrombus à embolism à blockage)
• occurs in individuals with worsening CAD
• atherosclerotic plaque ruptures and stimulates thrombus formation and vasospasm à more
severe, acute ischemia; can progress to MI
• Believed to involve atherosclerotic plaques that contain small amounts of fibrous protein and more
lipid which predisposes them to rupture
• Episodes are unpredictable and occur without exercise, during sleep, or at total rest
• Manifestations
o pain similar to that of stable angina, but it lasts up to 20 minutes, and is not relieved by rest or
nitroglycerin
o If the resulting myocardial ischemia is brief, the ventricular dysfunction is completely
reversible.
o If the ischemia persists for less than 30 minutes, the ventricle may become “stunned” and
have decreased function that can last for weeks
o If blood flow is not restored within 40-60 minutes, infarction ensues, resulting in permanent
myocardial dysfunction
• The risk of MI is greatly increased following unstable angina
• Unstable angina is treated with aspirin and anticoagulants
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Myocardial Infarction (MI)
• is another type of ACS that occurs when ischemia progresses to irreversible damage and necrosis of
the myocardium occurs
• it is the result of prolonged ischemia d/t total obstruction of a coronary artery
• MI differs from unstable angina in that:
o necrosis in MI à release of serum cardiac markers
o in MI
o pain persists after rest or vasodilators
o lasts >20 minutes
o is more severe (“crushing”) and sudden
Myocardial Infarction Development
• Ischemia triggers the switch from aerobic to anaerobic metabolism with inadequate energy
production to maintain normal myocardial function
• Necrotic death of cardiac muscle results from prolonged ischemia (> 60 minutes) and leads to
irreversible dysfunction
• Cardiac muscle death begins at about 1 hour and usually takes up to 12 hours before it is
complete; however, most cell death has occurred within the first 6 hours
• Necrosis begins on the endocardial (inside) surface of the heart and progresses to the pericardial
(outside) surface
• Following a MI there are three zones of tissue damage:
1. Necrotic zone
2. Injured area
o some cells may recover
3. Ischemic zone
o cells will recover if perfusion is restored
Manifestations of MI
1. Chest pain
o that may be similar to anginal pain, may be more severe or “silent”
2. â CO
o from loss of contractile and conductive functions of the necrotic/fibrous area
o ventricular dysfunction
3. Sweating and nausea
o d/t SNS activation
4. Dyspnea, orthopnea, and syncope/presyncope
5. Detection of cardiac serum markers
o enzymes specific to myocardial tissue released from necrotic cells
o CK-MB, LDH-1, Troponin
6. Fever
o d/t release of pyrogens from inflammatory cells
7. Hyperkalemia and acidosis
o d/t necrosis
8. Anxiety
Women vs. Men
• MI’s in women are usually more fatal than in men because:
o symptoms in females are less typical
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•
§ less severe chest pain, often reported as severe heartburn or pain in the breast
o do not seek treatment early in the attack or at all
o onset is later (>65 yrs) when other health conditions may contribute to or complicate
o smaller coronary arteries
Risk factors for MI are the same in females and males as those for atherosclerosis
o e.g. smoking, high LDL, low HDL, African American, obesity, etc.
Heart Failure
• the inability of the heart to pump sufficiently
• may result from
o loss of ability to contract
o impairment to outflow
o or excess work demands
• is the end result of many cardiac disease processes
• HF results in â output (forward effect) and congestion (backup effect)
• á workload of ventricles à hypertrophy and, eventually, failure
• Heart failure can initially involve the left or right ventricle; however, once one ventricle fails, the other
will eventually fail also
• In general, heart failure can result from systolic dysfunction, diastolic dysfunction, or both
o Systolic dysfunction
§ the heart fails to generate enough force to pump blood adequately, resulting in
â contractility and stroke volume.
§ This leads to the “forward” manifestations of heart failure i.e. â CO
o Diastolic dysfunction
§ â ability of the ventricle to fill
§ either d/t
• failure of the myocardium to relax
• increased stiffness of the ventricle
• valvular stenosis.
§ This leads to the “backup” effects of heart failure i.e. congestion
Etiology of Heart Failure
• Possible causes of heart failure, all of which lead to â CO, include:
1. MI: â muscle/contractile mass
2. tricuspid valve incompetence: â LV preload
3. pulmonary valve stenosis: â LV preload and á RV afterload
4. respiratory disease: á pulmonary resistance d/t damage of lung capillaries à á workload for
RV
5. mitral valve stenosis:â LV preload and á RV afterload
6. aortic valve stenosis: á LV afterload
7. aortic valve incompetence: causes volume overload
8. hypertension: á afterload and workload for LV
9. hyperthyroidism: á metabolic rate and á SNS à á BP, tachycardia and heart failure
10. Pericardial disease: restricts filling
11. Myocarditis: bacterial or viral infection results in loss of contractility
**You are responsible for explaining how each of the above might cause heart failure and â CO**
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Congestive Heart Failure
• CHF is heart failure accompanied by congestion of body tissues with blood
• Initially, impaired heart function is asymptomatic d/t a period of compensatory mechanisms
(compensated heart failure)
• Eventually, these measures fail and/or aggravate the failure à decompensated failure with symptoms
Compensations
1. Frank-Starling Mechanism
increases preload (ventricular end-diastolic volume) à á stretch and contraction force; however,
over-stretching à â contraction force and ischemia ~ á O2 demand à impaired function
2. á SNS
d/t baroreceptor reflex à á HR, á TPR, á contractility; however, á HR à â ventricular filling
and arhythmias , and á TPR à á afterload
3. Renin-Angiotensin Mechanism
activated by â blood flow to kidneys; however, á TPR à á afterload, and angiotensin contributes
to hypertrophy
4. á Endothelin
released from BV endothelial cells; strong vasoconstrictor; however, á TPR à á afterload, and
endothelin contributes to hypertrophy
5. Myocardial Hypertrophy
response to á workload; á # of contractile elements; however, á O2 demand à ischemia, fibrosis,
and impaired function; also, remodeling of ventricle à â chamber size
Etiology of Left-sided CHF
Left ventricular failure can result from:
1) Volume overload
• Occurs with regurgitant mitral or aortic valves
• high-output states
o such as anemia and hyperthyroidism
2) Pressure overload
• Occurs with hypertension and aortic stenosis
3) Loss of muscle mass
• Examples include left ventricular MI and inflammatory diseases like lupus
4) Loss of contractility
• d/t bacterial or viral infection (i.e. Myocarditis)
• d/t certain poisons and toxins
5) Restricted filling
• mitral stenosis and pericardial disease
Manifestations of Left-Sided CHF
• Forward effect: â CO
o Manifestations
§ Fatigue and weakness
§ Dyspnea
§ exercise and cold intolerance
§ cyanosis
o Compensatory manifestations
§ Tacycardia
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o
•
§ Pallor
§ daytime oliguria
§ nocturia
§ polycythemia (an increase in RBC)
Uncompensated manifestations
§ Cyanosis
§ Anorexia
§ Cachexia (muscle mass loss)
Backup effect: pulmonary congestion
o Leads to á capillary pressure and edema; fluid is forced into the alveoli; interferes with gas
exchange à hypoxemia, and predisposes to pneumonia
o Manifested as orthopnea, cough, dyspnea, hemorrhage in the lungs (blood in sputum)
Etiology of Right-sided CHF
often follows left-sided HF as pulmonary congestion impairs flow into the lungs from the RV
Causes (any condition that impairs flow into the lungs) including:
1) Left ventricular failure
• Pulmonary edema increases the afterload on the right ventricle
• i.e. Hypoxic vasoconstriction
2) Loss of muscle mass
• d/t right ventricular or inferior MI
3) Cor pulmonale
• Right ventricle failure occurring secondary to pulmonary disease.
• Impaired ventilation causes pulmonary vasoconstriction that increases afterload and often
results in failure.
• Pulmonary embolism also causes cor pulmonale
4) Tricuspid valve incompetence
5) Pulmonary valve stenosis
6) Congenital defects
• Pulmonary obstructions or shunts can increase the workload on the right ventricle causing it to
eventually fail
Manifestations of Right-Sided CHF
• Forward effect: â CO
o Manifestations (same as LS HF)
§ Fatigue and weakness
§ Dyspnea
§ exercise and cold intolerance
§ cyanosis
•
•
Backup effects
o congestion in systemic circulation à peripheral edema
Manifestations:
o generalized edema
o ascites (collection of fluid in the peritoneal space)
o dependent edema (swelling of the feet and legs)
o Hepatomegaly and splenomegaly
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o
§ fluid accumulation in the liver or spleen causes distention and upper quadrant pain
Elevated jugular venous pressure
§ congestion into the cranium can create CNS symptoms
§ such as headache, visual disturbances, or flushed face
Typical Course and Treatment of CHF
• Digitalis
o This alkaloid produced from foxglove
o increases the amount of Ca++ in the cytosol à increased force of contraction (contractility)
o increases vagal tone à decreases the HR
•
Vasodilators
o ACE inhibitors, CCBs, and a-blockers
o reduce the afterload
o improve ejection fraction (i.e. the percentage of blood ejected during systole)
o decrease HR
•
Diuretics
o Increase urine output
o Prevent fluid overload, edema, and dyspnea.
o ACE inhibitors also produce diuresis by reducing aldosterone production.
Beta 1 blockers
o decrease the epinephrine effects of increasing the secretion of renin
•
Heart Failure in Children
• Congenital heart defects are the most common cause of CHF in children
• Many of the S/S of CHF in children are the same as those seen in adults including
tachycardia, fatigue, effort intolerance, irritability, cough, anorexia, abdominal pain, oliguria, and
hepatomegaly
• Differences:
o dependent edema and ascites are rare
o jugular distention is hard to detect because of their short, chubby necks
o see excessive sweating d/t á SNS
o most common difference is that in children, interstitial edema in the lungs is more common
than alveolar pulmonary edema à impaired ability of the lungs to expand (i.e. â compliance)
and á the work of breathing
§ leads to tachypnea and á respiratory effort
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Heart Failure Treatments
There are two kinds of drug therapies for CHF and other cardiac problems:
1. Drugs that reduce mortality by â the workload on the heart
• ACE inhibitors
o angiotensin-converting enzyme inhibitors
o including Altace (Ramipril), Perindopril, Benazepril, and Enalapril
o â angiotensin activation à block the systemic vasoconstriction effect.
• ARBs
o angiotensin receptor blockers
o including Candesartan, Losartan, and Valsartan
o cause similar effects to ACEIs
o block the receptors for angiotensin on blood vessels
• Beta-blockers
o block Beta-adrenergic receptors à â the effect of epinephrine.
o including Propranolol, Acebutolol, and Metoprolol tartrate
o Beta-1 blockers can â the release of renin and can â cardiac muscle contraction.
• Aldosterone antagonists
o block aldosterone effects à â the absorption of Na+ and water à â blood volume à â BP
o including Aldactone and Inspra.
• Coronary Vasodilators
o including nitroglycerine
o cause coronary arteries to dilate à á blood flow to the myocardium.
2. Drugs that reduce symptoms
• Digitalis (Digoxin)
o a chemical derived from a flowering plant called foxglove.
o á vagal tone à á force of each heart contraction à heart’s pumping action more efficient,
but â HR to â the workload.
• Vasodilators
o including ACEIs, hydralazine, nitroglycerine, CCBs, and alpha-1 blockers
o some cause venous dilation as well as arterial dilation that cause systemic vasodilation
to decrease the afterload on the heart.
• Diuretics
o á urine output à prevent fluid overload problems.
o Blood volume will not increase and the risks of edema and dyspnea are reduced.
o including Lasix, indapamide, and metolazone
• SGLT-2 Inhibitors
o Sodium-glucose cotransporter-2 inhibitors.
o used to control diabetes, but help â BP, â body weight, and help control blood [glucose].
o including Jardiance and Forxiga.
3. The other approaches are primarily about:
• Regular exercise
o to help maintain muscle efficiency so they can work well without requiring a big á in CO.
• Weight loss
• Avoiding cigarettes, alcohol and other stimulants à â demand on the heart.
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The Cardiac Conduction System
Myocardial Cells
• intercalated discs separate one cardiac cell from another
• cardiac cells act as syncytium – meaning they are acting together
• the heart muscles are
o conductors
o contractors
o self excitatory
o autonomous
The Cardiac Cycle
• Cardiac cells are capable of responding to and generating electrical signals (excitable tissue)
o specialized cells generate electrical signals autonomously
o cardiac myocardial cells are electrically connected, allowing electrical signals generated by
specialized cells to spread to neighboring cells
The Cardiac Conduction System
• Cardiac contraction is initiated by a group a
specialized cells called the Sinoatrial (SA) node
• they have the ability to spontaneously depolarize
(autonomously generate APs).
• The SA node is often referred to as the cardiac
‘pacemaker’.
• The electrical signal generated by the SA node then
travels through the interconnected myocardial atrial
cells and reaches the Atrioventricular (AV) node,
where the signal is slightly delayed.
• The signal then travels from the AV node to the
Bundle of His and the Purkinje fibers
• The Purkinje fibers then conduct the signal to the
myocardium of the ventricles, which contract simultaneously
The SA Node and its Action Potential
• The spontaneous depolarization of the SA node is due to the fact that the plasma membrane of the
SA node cells is ‘leaky’ to Na+.
• This prevents the cells of the SA node from ever achieving a true resting state (as soon as they
repolarize, they start depolarizing again)
• The depolarization phase
o slow influx of Na+ to a threshold, then an influx of Ca++
• Repolarization phase
o flow of K+ out of the cell while the Na+ and Ca++ channels close
• At the end of repolarization
o the K+ channels close and slow depolarization begins again
• Only an impulse derived from the SA node will initiate a proper cardiac cycle and stroke volume
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Cardiac Action Potential and the ECG
• When electrodes are placed on the skin, an electrical signal
of the entire heart can be observed. This is called the
Electrocardiogram (ECG)
• The ECG is an important diagnostic tool as it can detect
abnormalities in cardiac conduction, ischemia, infarction,
hypertrophy, and electrolyte abnormalities
Cardiac Dysrhythmias
• Dysrhythmias- alterations in cardiac rhythm
• Arrhythmias imply loss of rhythm.
• Appear as variations in an ECG.
• May indicate alterations in automaticity, excitability, conductivity, or refraction
o May happen due to ischemia and infarction, electrolyte imbalances, drug effects, or defects in
conduction.
• are harmful when they interfere with the heart’s pumping ability.
• Normally, the firing of the SA node is the pacemaker of the heart à P wave on ECG.
• TWO nerves innervate the SA Node:
1. The accelerated nerve (SNS nerve)
• stimulates the SA node to increase the rate of contraction
2. The Vagus nerve (CN X)
• stimulates the SA node to decrease the heart rate
• Normal dysrhythmias include Sinus Bradycardia and Sinus Tachycardia.
o Sinus bradycardia
§ Normal in trained athletes
§ during sleep
§ may occur in acute MI
§ respiratory depression d/t opioids/other drugs.
o Sinus tachycardia
§ Causes
• SNS stimulation by the accelerates nerve
• Seen with exercise or fever
• may occur with CHF, MI, and hyperthyroidism, and certain drugs.
• Hypovolemia and fluid and electrolyte imbalances
§ might be problematic:
§ it requires the heart to work faster à decreased ventricular refill time à decreased
entry to the coronary circulation/compression of the coronary circulation
20
Atrial Dysrhythmias
•
•
•
result from abnormal electrical activity in the atrium
The atrial contribution to ventricular filling is lost, and quite often, the CO decreases
Palpitations and tachycardia are common
Causes of Atrial arrhythmias
• Mitral stenosis
• Ischemia/infarctaion
• cardiac surgery
• hyperthyroidism (T3, T4 increase heart contractility)
• alcohol or caffeine consumption
Examples of Atrial arrhythmias
Premature Atrial Contraction
• may be due to á automaticity in cells other than the SA or
AV node (ectopic foci)
• appears as an abnormal P-wave
• an abnormal conduction pathway and irregular heartbeat
Atrial flutter
• a rapid, regular atrial ectopic tachycardia
• “a bunch of extra P waves”
• usually caused by a large circular reentrant current in the atrium at a
rate of 300 per minute
• this current creates a ‘sawtooth’ pattern on the ECG
• the ventricles contract regularly, but at a á rate (150 b/m) à â CO and
possibly myocardial ischemia and HF
Atrial fibrillation
• occurs in various chronic heart diseases
• d/t multiple uncontrolled depolarizations of the atrium
• atria contract in a continuous, uncoordinated fashion at 350-600 bpm
• the ventricles do not fill or contract properlyà â CO
• may cause syncope or cardiac arrest
The greatest risk for both Atrial flutter and Atrial fibrillation is the stasis of blood in the atrium, which
dramatically increases the risk of cerebral embolism. This can be managed by medications that prevent
likelihood of thrombus formation or even surgery.
Heart Blocks
• occurs when there is a conduction defect in the AV node or bundle branches
• may be normal d/t vagal tone
• may be pathological
• d/t ischemia, infarction, fibrosis, inflammation, surgery, potassium imbalance
21
First-degree AV Block
• delayed conduction through the AV node (~ prolonged PR interval)
• impulses are conducted through to ventricles
• rhythm is regular
• caused by ischemia, MI of AV node, rheumatic fever, myocarditis
Second-degree AV Block
• some impulses from atria are not conducted to ventricles
• some P waves with no corresponding QRS complexes
• localized MI: infarction in His Bundle
• has a poor prognosis d/t fewer ventricular contractions à âCO
• if it becomes very serious, may require a pacemaker
First degree with bundle branch block
Second degree block
Third-degree AV Block (Complete AV Block)
• none of the atrial impulses are conducted to the ventricles
• ventricular contraction still exists
o d/t the self-excitatory attributes of the myocardial cells of the ventricles
o in the absence of a stimulus from the SA nodes, the ventricles will form a ventricular ectopic
pacemaker
• each region is controlled by independent pacemakers à regular but dissociated rates
• ventricular rhythm is slow (~30-40 bpm)
• may arise from impaired conduction at AV node, His Bundle, or Pukinje fibers
• results in drastically âCO with syncope (Stokes-Adams attack), dizziness, episodes or acute heart
failure
• requires permanent pacemaker
Third degree block
Bundle Branch Block
• interruption of conduction through the bundle branches d/t damage to the heart muscle
o the branches normally carry impulses to the myocardium of ventricles
• does not affect the rhythm
• but cells do not contract together à wider QRS complex
• the contraction of the ventricles is not synchronized
• could sometimes show as a prolonged QRS with double peaks as the ventricles contract
• âCO
22
Ventricular Dysrhythmias
•
•
are more serious than those arising in the atria
can directly affect pumping ability of the heart
Premature Ventricular Contraction (PVC)
§ “a few extra contractions” of hyper excitable cells
• caused by ventricular ectopic pacemakers
• often occur secondary to ischemia, infarction, or electrolyte imbalances
• also after consumption of caffeine, stimulants, or alcohol
• characterized by broad, distorted QRS complexes and large T waves followed by a compensatory
pause where ventricles are unable to respond to incoming SA node impulses (are refractionary)
• can progress to serious ventricular arrhythmias in patients with known heart disease.
PVC
Ventricular Tachycardia
• VT and ventricular fibrillation are considered cardiac arrest rhythms since they often do not generate
a cardiac output or palpable pulse
• must be treated immediately with defibrillation and CPR
• caused by reentry secondary to ischemia, infarction, fibrosis, dilated myopathy, and electrolyte
imbalance
• characterized by broad, tall QRS complexes, inverted T waves and a rate of 70-250 bpm
• may progress to VF, especially following an MI
VT
VF
Ventricular Fibrillation
§ “cardiac arrest rhythm”
• occurs with the firing of multiple ectopic foci in ventricles
• ventricles quiver but do not contract à no CO
• results in unconsciousness, absence of pulse, apnea and death
• ECG pattern is grossly distorted with shallow, unidentifiable waves
VF
Asystole
23
Pulseless Electrical Activity
• ECG shows electrical activity, but there is no mechanical ventricular function or pulse
• correctable causes: hypovolemia, hypoxemia, hypothermia, acidosis
• uncorrectable causes: massive infarction, ischemia during resuscitation, pulmonary embolism
• poor prognosis unless corrected
• Asystole- total absence of ventricular electrical activity and contraction (flat line) ~no ventricular
depolarization; poor prognosis
The ST Segment: Ischemia and Infarction
• The ST segment of the ECG represents the repolarization phase of ventricular myocytes.
• The current that creates this segment of the ECG is sensitive to changes in coronary blood flow,
and is therefore used to assess myocardial ischemia and infarction.
ST Segment Depression
• Occurs as a result of myocardial ischemia.
• The exact mechanism for ST segment depression is not known
• it is believed to occur due to a slowed repolarization rate secondary to
decreased cellular ATP or potassium efflux.
ST Segment Elevation
• Occurs during myocardial infarction. ST elevation results from loss of
potassium from the cells (i.e. Hyperrepolarization and decreased resting
membrane potential), and accumulation of intracellular sodium (i.e. Delayed
depolarization).
ST segment Depression
ST Segment Elevation
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Hypertension
•
•
•
•
Arterial blood pressure changes in response to several factors throughout the day.
Adequate measurement may require multiple daily monitoring over an extended period of time.
Hypertension is a chronically elevated BP where SBP is 140 mmHg or higher and DBP is 90 mmHg
or higher
Standards for defining hypertension are being changed as evidence indicates that even lower BP (130
mmHg systolic), if consistent, can lead to vessel damage.
Essential Hypertension
• Hypertension is classified as either essential (primary) or secondary
• Primary hypertension- chronically elevated BP without evidence of other disease, probably related to
á arteriolar vasoconstriction
• It is typically asymptomatic (“silent killer”)
• May have vague, unreliable S/S, including: morning headache, fatigue, malaise, nausea, vomiting
• The most reliable indicator of hypertension is consistently elevated BP under various conditions.
Etiology
• The etiology of essential hypertension is not known, but there are several well-indicated risk factors
Risk Factors
• Family history of HTN (d/t genetics/lifestyle)
• Age
o BP á with age from 50/40 in newborn to 120/80 in adult
• Race
o hypertension is more prevalent, severe, and occurs earlier in those of African descent
• High Salt Intake
• Obesity
• Stress
o physical and emotional
• Cigarette smoking and alcohol
Effects of Hypertension
Uncontrolled hypertension affects
• Kidneys: â blood flow to kidneys à á renin, angiotensin, aldosterone and ADH release which à
further vasoconstriction and á BV
• Arteries: á BP causes damage to arterial walls, predisposing to atherosclerosis, CAD, aneurysm,
rupture, stroke
• Heart: á TPR (á afterload) and blood volume (preload) á workload on the heart à LV hypertrophy
and failure
Secondary Hypertension
• hypertension due to another disease condition including:
o Renal disease
o Renovascular hypertension
o Adrenocorticosteroid hormone disorders
o Pheochromocytoma
o Pregnancy-Induced Hypertension
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Respiratory Review
Quiet Ventilation
Quiet inspiration involves:
1. diaphragm contraction à moving it down à increased thoracic cavity size
2. external intercostal muscle contraction à pulling the ribs up and out à increasing the thoracic
cavity size
• Both these actions will lower the air pressure in the lungs, causing air to move into the lungs via
the patent airways (trachea, bronchi, and bronchioles)
• This takes energy to contract the muscles of inspiration.
Quiet expiration involves relaxing the muscles of inspiration à the diaphragm moves back up, and the
ribs move back down à pressure in the lungs increases à air moves out the airways (from high pressure to
low pressure). No energy is used because muscles just relax.
Forced Ventilation
Forced inspiration involves
1. contracting the muscles of quiet inspiration harder
2. contracting the sternocleidomastoid muscles (accessory muscles) à pull the upper ribs further
up and out.
• This takes much more energy than quiet inspiration.
Forced expiration involves
1. relaxing all the muscles of forced inspiration
2. contraction of the internal intercostals to pull the ribs further down and in
3. contracting the abdominal muscles (your 6–pack) to raise the intra-abdominal pressure à forces
the diaphragm further up
• This will greatly increase the intrathoracic pressure and increase the volume of air expired.
• Note that this takes a lot more muscle contraction and, therefore a lot more energy.
For problems like COPD and asthma
• the individual is forced to do forced ventilation
• takes much more energy and so is exhausting
• it also increases the individual's oxygen requirement à an increased need to ventilate.
Respiratory Insufficiency and Failure
• Will result when there is a significant mismatch of ventilation and perfusion.
• Ventilation is about moving air into and out of the lungs
• perfusion is about the blood flow through pulmonary capillaries.
• Both have to happen in a matched way so that you can maintain a maximum concentration
gradient of CO2 and O2 between the alveoli and the pulmonary capillary blood to optimize the
diffusion rate for these two gases.
• If you have normal perfusion but reduced ventilation (COPD, asthma, respiratory depression…) then
there may be respiratory insufficiency/failure.
• If you have reduced pulmonary perfusion but normal ventilation (right-side heart failure, left-side
heart failure, or a pulmonary embolism), then there may be respiratory failure.
26
Hypercapnia (excess pCO2)
• occurs less easily than hypoxia, so that problems that lead to mild hypoxia do not always lead to
hypercapnia.
• CO2 diffuses much more easily than O2.
• It is more lipid soluble à will often diffuse enough across the respiratory membrane to meet
requirements, even when there is not enough diffusion of O2
• O2 is much less soluble and diffuses more slowly.
• The problem with hypercapnia is that it causes acidosis.
• normally, locally elevated pCO2, which occurs when tissues are very active doing cellular respiration,
will stimulate local vasodilation to increase normal blood flow to meet locally increased needs for
blood perfusion
• if you have systemically increased pCO2, then it may cause widespread vasodilation and reduce
BP.
Respiratory Disorders
•
•
The main function of the respiratory system is gas exchange, which provides body tissues with
adequate O2 for cellular metabolism and removes CO2 (a by-product of metabolism).
The respiratory system works in conjunction with the renal system to maintain blood pH and acidbase balance:
CO2 + H2O
lungs
H2CO3
H+ + HCO3-
kidneys
Normal Values
• pH: 7.35-7.45 (reflected in an HCO3- : H2CO3 ratio of 20:1)
• serum HCO3-: 24-31 mmol/L
• serum CO2: 24-29 mmol/L
• Pa CO2: 35-42 mm Hg
• PaO2: 95-100 mm Hg
• arterial O2 saturation (SaO2): 96%-98%
• Base excess or deficit
o is essentially a measurement of HCO3- excess or deficit
o describes the amount of acid or base that must be added to bring the blood pH to 7.4
• O2 saturation (SaO2)
o the degree to which O2 is bound to available sites on hemoglobin, i.e., the oxygenation of the
blood
Respiratory System Review: Anatomy
• Upper Respiratory Tract
o passageways that conduct air between the atmosphere and lungs
o nose, nasal cavity, pharynx, and larynx
• Lower Respiratory Tract
o trachea, bronchi, bronchioles and lungs (alveoli)
• Lungs
o The right lung has 3 lobes
o The left lung has 2 lobes
o lobes are divided into lobules
27
Each lung resides in a pleural cavity and is surrounded by a double-layered pleura
§ The parietal pleura
• attaches the lung to the thoracic wall and diaphragm
§ The visceral pleura
• covers the lung surface
§ layers are separated by a pleural cavity containing pleural fluid
§ fluid creates surface tension
• helps to keep the naturally recoiling lungs inflated
• reduces friction
§ Each lobe has a bronchiole, which brings air to many alveoli
Alveoli
o sac of simple squamous epithelium
o surrounded by capillaries where gas exchange occurs
o The walls of the alveoli, with their fused basement membranes, form the respiratory
membrane across which gas exchange occurs
o
•
Ventilation-Perfusion Coupling
• The ventilation:perfusion ratio (VE/Q)
o reflects the match of airflow through the alveoli to blood flow in the adjacent pulmonary
capillaries
• Gas exchange is most efficient when ventilation matches perfusion
• The pulmonary arterioles will constrict or dilate in order to match ventilation with perfusion
• Mismatch occurs when:
o ventilated alveoli are not well-perfused
o perfused alveoli are not well-ventilated
Respiratory Dysfunction
• Respiratory Failure
o occurs when the lungs fail to adequately oxygenate the blood and prevent CO2 retention
o results from conditions that:
§ impaired ventilation
• disease of the airways and lungs (COPD, Asthma)
§ impaired function of the respiratory center
• drug overdose à hypoventilation
§ cause ventilation-perfusion mismatch
• obstructive or restrictive disease
§ involve chest wall injury/deformities
§ impair diffusion
• edema, pneumonia
§ disrupt blood flow in the lungs
• pulmonary embolus
§ involve respiratory muscle failure
• muscular dystrophy
§ anemia
• can’t transport in blood
§ carbon monoxide
• competes with O2 for binding on RBC
o Is defined by blood gases of:
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§ PO2 < 50 mm Hg (hypoxemia)
§ PCO2 > 50 mm Hg (hypercapnia) and respiratory acidosis
• Respiratory Insufficiency
o A state when blood gases are abnormal but cell function can continue
• Respiratory Arrest
o A cessation of respiratory activity
Hypoxemia
• A condition of reduced arterial [O2]
• Causes
o decreased O2 in air (hypoxia)
o hypoventilation
o impaired diffusion
§ edema
o shunt
o hypoperfusion
§ embolus
o anemia
•
Manifestations
o ~ tissue hypoxia and compensatory mechanisms
o PO2 < 50 mm Hg, â pH
o tachycardia, slight á BP, pale, cool, clammy skin ~ SNS compensation
o hyperventilation ~ low O2 stimulation of peripheral chemoreceptors
o impaired mental function
§ confusion, delirium
o impaired sensory function
§ visual impairment
o Late manifestations
§ stupor and coma
§ bradycardia and â BP
§ cyanosis
•
Compensations
o SNS activity
§ Tachycardia
§ slight á BP
§ pale, cool, clammy skin
o hyperventilation
§ d/t low O2 stimulation of peripheral chemoreceptors
o polycythemia (increased RBC mass)
§ is only beneficial if hypoxemia is not acute or d/t anemia
•
Cyanosis
o a bluish coloration of the skin and mucous membranes
o occurs when large amounts of blood hemoglobin are deoxygenated in the small blood
vessels (5 g or more unsaturated Hb per 100 mL of blood)
1. In anemia
•
29
§ with impaired hemoglobin synthesis (e.g. iron-deficiency anemia), Hb is low, and the Hb
present is oxygenated above 5 g /100 ml à no cyanosis
2. Cyanosis will also not develop in â O2 saturation from carbon monoxide poisoning
because the CO binds to Hb (i.e. the Hb is saturated)
3. Those who are polycythemic may also be cyanotic without being hypoxic
§ d/t áHb
§ blood is more viscous à blood will flow slower à “bluish” appearance without hypoxia
o Bluish coloration of skin is hard to detect in dark-skinned individuals: can be observed in nail
beds or testing blood gas O2 levels
In providing O2 therapy for hypoxia:
o the rate of administration must be closely monitored to prevent oxygen toxicity
o it lead to body disturbances, including lung damage, visual and hearing abnormalities, fatigue
while breathing, anxiety, confusion, twitching, and convulsions.
o Oxidization?
Systemic Hypoxia
• Causes
o inadequate O2 in air (not available)
o decreased perfusion
§ d/t respiratory disease/pulmonary edema
§ causing impaired oxygenation in the lungs
o ischemia
o anemia
§ low concentration of functional hemoglobin or RBCs à â O2 carrying capacity
§ can’t transport in the blood
o generalized edema
• Hypoxia results in
o reduced ATP synthesis à impaired cellular function, membrane integrity, waste removal à
cell swelling, toxification, â pH, loss of enzymes and enzyme function, release of destructive
enzymes à necrosis
• Compensation mechanisms
o A switch to anaerobic metabolism
o á SNS
o á erythropoietin secretion à polycythemia (a long-term response to hypoxia)
• Heart, brain, and kidney cells are most susceptible to hypoxia
o d/t high metabolic rate and O2 requirements
Hypercapnia
• á blood PCO2
• occurs with hypoxia
• Causes
o same as hypoxia
o esp. hypoventilation and ventilation-perfusion mismatch
o á cellular metabolism
o high carbohydrate diet
• central chemoreceptors
o respond to á CO2 by á respiration rate
o become less sensitive overtime
30
•
•
•
peripheral receptors
o control respiration by responding to levels of O2 (hypoxic respiratory drive)
in persons with respiratory disease that cause chronic hypoxia and hypercapnia, administration of
O2 may suppress respiratory drive causing peripheral receptors à â respiration rate à further
hypercapnia
Manifestations
o respiratory acidosis
§ á CO2, â pH, á HCO3- (renal compensation)
o Vasodilation
§ reducsed PVR that lowers BP systemically
§ headache, flushed skin
o suppression of neural function
§ lethargy, drowsiness, disorientation, coma
o air hunger and rapid breathing
Aspiration
• is the passage of food, fluid, or other foreign material into the trachea or lungs
• normally, the cough reflex removes material from the upper tract, and passage into the lower tract is
prevented by the vocal cords and epiglottis
• Complete obstruction of the upper tract inhibits the ability to speak or cough
o life-threatening blockage of the trachea à inadequate oxygenation
• The right lower lung is usually the lodging site of aspirated objects
• Wherever in the tract the object lodges, it obstructs airflow beyond that point
o obstruction of a bronchus à no air delivery and collapse distal to the obstruction (atelectasis)
• Sharp objects and fatty or irritating solids
o cause inflammation à swelling, edema, and bronchoconstriction à block airflow
• Pointed objects
o may form a “bridge” upon which other materials collect à obstruction
• Peanuts and legumes
o may swell and become more firmly lodged
Fluid Aspiration
• Predisposition
o Infants
§ put more objects in their mouths, and move around with them
§ smaller and more elastic airways à lungs can recoil and hold on to foreign objects
§ weak abdominal muscles à harder to cough out objects
o Post-op clients
§ anesthesia depresses cough and swallow reflex; often supine
o Alcohol consumption
§ depresses protective reflexes
o Stroke or other neurological damage
§ depressed cough and swallow reflex
o Lying position
§ absence of gravity to assist in proper swallowing
§ residual fluid in the mouth or pharynx may drip into the trachea
§ more alveoli can be affected
o Elderly
31
§
§
•
•
•
•
•
•
often supine à eat and drink while supine
muscle weakness (abdominal muscles, harder to cough objects out)
Irritating liquids (vomitus, alcohol, milk)
o enter many bronchi à severe inflammation and á secretion à worsen the obstruction and
impair lung expansion
liquid easily passes the epiglottis and vocal cords to enter the lower tract
If the alveoli are affected by inflammation, gas exchange is impaired
o severe inflammation with the accompanying build-up of fluids is called aspiration
pneumonia à predisposes to infection
Respiratory distress syndrome
o Includes extensive breakdown of alveolar and/or capillary membranes
o may develop if inflammation is widespread
Toxic solvents
o may diffuse into the blood and cause systemic damage
Manifestations
o coughing and chocking (incomplete obstruction)
o wheezing ~ liquid aspiration
o dyspnea, tachypnea, tachycardia
o nasal flaring, abnormal chest movements
o hypoxia and cyanosis (if severe/prolonged)
o respiratory and cardiac arrest
§ if larynx or trachea is totally obstructed
Atelectasis
Collapse/incomplete expansion of a lung/portion of a lung à decreased gas exchange and hypoxia
• Causes
o airway obstruction
o compression of the lung
o â surfactant à difficulty expanding the lung
o When the alveoli do not have air, they collapse and shrivel up ~ natural recoil of lung tissue
o Ventilation and perfusion are affected à impaired oxygenation
•
Manifestations:
o â expansion and â breath sounds on the affected side
o tachycardia, tachypnea, dyspnea
o hypoxia, cyanosis
o respiratory distress
Obstructive Atelectasis
• air distal to the obstruction diffuses into the circulation and is not replaced à collapse
• the severity depends on the location of obstruction and the extent of collapse
o if the region is not reinflated quickly à necrosis and permanent damage
• obstruction can result from
o tumors
o mucous
o aspirated objects
32
•
Manifestations
o trachea/mediastinum shifts toward the affected side
o the unaffected lung overinflates
Compression Atelectasis
• Causes
o an external mass (i.e., tumor) that puts pressure on the lung
§ preventing air from reaching that region
o air or fluid in the pleural cavity
§ can compress the lung and separate the pleura à inability of lung to expand
• Manifestations
o trachea/mediastinum shifts toward the UNaffected side
o fever and infection
Asthma
• Characterized by periodic episodes of severe but reversible bronchiole obstruction
o d/t hyperresponsive airways
• Repeated attacks of acute asthma cause irreversible damage à chronic asthma
•
•
•
•
Basic Problems:
o bronchoconstriction
o inflammation of bronchiole mucosa with edema
o excess mucous production
o obstruction to airflow and decreased ventilation of the alveoli
Epidemiology
o most common chronic illness in children <17 y/o
o prevalence rates have increased 102 % between 1980 and 1994
Two Types of Asthma:
o Extrinsic (inflammatory)
o Intrinsic (bronchospastic)
Many individuals suffer from both types
Extrinsic Asthma
• d/t type 1 hypersensitivity to an inhaled allergen/antigen
• antigens bind to increased numbers of antibodies on mast cells in the respiratory mucosa
• onset: usually children; may subside by adolescence
• Early (acute) Response
o immediate bronchoconstriction (within 10 mins of exposure)
§ d/t release of mediators (leukotriens) from activated mast cells that directly
§ these cause bronchoconstriction and stimulation of parasympathetic receptors that
cause reflex bronchiole constriction.
o released mediators (histamine, kinins, PGs) also cause edema and á mucous secretion
•
Late Response
o develops 4-8 hours after exposure
o may last days or weeks
33
o
involves inflammation
§ inflammatory mediators are released from mast cells, macrophages, and epithelial
cells à prolonged bronchoconstriction, epithelial injury and edema, reduced
clearance of secretions, and á responsiveness to intrinsic factors
Intrinsic Asthma
• hyperexcitable smooth muscle reaction
• acute attacks occur from triggers other than allergens
o infections
o cold exposure
o exercise
o dehydration
o stress
o cigarette smoke
o aspirin
o chemicals (perfumes, deodorants)
• onset: usually in adults
• features similar responses to extrinsic
o Include early/acute response followed by late response
Asthma Manifestations & Complications
• During an asthmatic attack the airways become narrowed d/t
o Bronchoconstriction
o Edema
o Mucous plugs
• Obstruction can be partial or complete:
o Partial
§ obstruction interferes with expiration à air trapping past the obstruction
§ causes hyperinflation of the lungs
§ residual volume á, inspiratory reserve capacity â à more energy required for breathing
§ involves use of accessory muscles to maintain ventilation and gas exchange
o
Complete or prolonged
§ results from mucous plugs that completely block airflow à atelectasis, (VE/Q)
mismatch, hypoxemia and hypercapnia
§ á workload on RV ~ hypoxemia and hyperinflation à pulmonary hypertension
§ hypoxia and cyanosis
Status Asthmaticus
• Manifestations
o Mild attack
§ chest tightness
§ á respiration rate
§ prolonged expiration
§ mild wheezing or cough
o
Severe attack
§ use of accessory muscles
34
§
§
§
§
§
o
•
distant breath sounds
loud wheezing
fatigue
severe dyspnea
labored speaking
Prolonged attack
§ Will cause respiratory failure
§ inaudible breath sounds
§ diminished wheezing
§ ineffective cough
§ cyanosis
§ respiratory acidosis
Status Asthmaticus
o Severe and prolonged asthma that is unresponsive to treatment
o may become fatal
§ d/t severe hypoxia and acidosis à cardiac arrhythmias and CNS depression
o impaired perception of dyspnea may prevent the pt. from seeking medical attention
35
Respiratory Pathology
Respiratory Failure and Respiratory insufficiency
We can classify respiratory failure into FOUR main categories based on cause:
1. Pulmonary Obstructive Causes
• in some way or another, the airways are blocked or narrowed à airflow is restricted
• this can be anywhere in the airway system.
• Some examples:
o asthma
§ edema and bronchoconstriction narrow the bronchi and bronchioles.
o cystic fibrosis (CF)
§ thick and sticky mucous obstructs the airways
o tumors
§ that impinge on the airways
o aspiration
§ where solids of liquids block the airways
2. Pulmonary Restrictive Causes
• where the lungs are not as compliant (lungs cannot expand and recoil as effectively)
• the body can’t achieve as big pressure changes to promote ventilation.
• Some examples:
o Emphysema
§ the lungs lose elasticity, as alveolar walls are destroyed
o pulmonary edema or pneumonia
§ will restrict the expansion and contraction of alveoli
o asbestosis or fibrosis of the lungs
§ d/t exposure to asbestos fibers
o atelectasis (lung collapse)
§ i.e. impaired surfactant production
• common in premature newborns
§ or in Adult Respiratory Distress Syndrome
• can be d/t toxic fumes inhalation in a fire
o pneumothorax
§ leading to lung collapse
* Note that both Pulmonary Obstructive and Pulmonary Restrictive causes will all reduce Ventilation
3. Cardiovascular Causes
• These causes all involve reduced perfusion of the lungs.
o Pulmonary Embolism (PE)
§ blocking blood flow through the pulmonary circulation
o Heart Failure (HF)
§ either LS causing pulmonary hypertension or RS causing decreased pulmonary
blood flow
o Myocardial Infarction (MI)
§ causes a decreased cardiac output
o Vascular Diseases
§ such as microangiopathy
36
4. Non-Pulmonary / Non-Cardiovascular
• Most of these causes involve restricted ventilation d/t
o a loss of neural control over respiration
o or a musculoskeletal problem
• Some examples:
o Damage to the RCC
§ in the medulla or pons
o General CNS depression, such as with
§ elevated ICP
§ drug-induced respiratory depression
§ hypoxia and severe acidosis
§ exposure to toxins
o Spinal cord injuries
§ especially to the phrenic nerve (formed from cervical spinal nerves) that controls
the diaphragm
o hypokalemia (↓K+)
§ causing respiratory muscle weakness
o postural problems that restrict breathing
§ such as scoliosis or kyphosis
o neuromuscular diseases
§ such as Guillain-Barre syndrome, Muscular Dystrophy
A Ventilation-Perfusion Mismatch
• disrupts the optimization of the concentration gradients for O2 or CO2, a mechanism necessary for
efficient diffusion that allows for adequate gas exchange.
• Causes
o adequate ventilation with inadequate perfusion
o inadequate ventilation but adequate perfusion
• Two significant outcomes of any of the above could lead to
o Hypoxia (inadequate O2 to meet needs)
o Hypercapnia (excessive pCO2)
• Many of the causes of hypoxia may not as rapidly lead to hypercapnia; however, because CO2
dissolves faster in plasma and is much more lipid soluble, it can much more easily diffuse across the
respiratory membranes for exchange.
• The most likely way for hypercapnia to develop is with reduced ventilation.
Hypoxia/Hypoxemia
• Causes
o Hypoventilation that can happen d/t:
§ problems with the MSK structures of breathing and the nerves that control them
§ problems with the RCC in the medulla/pons
§ airway obstruction
§ and restrictive problems.
o impaired perfusions d/t problems with the CV system, such as HF or PE.
o mismatches of ventilation/perfusion
o unavailability of oxygen
§ at a higher atmosphere (up high in the mountains where the atmosphere is less dense)
§ or if in a sealed space where the O2 is being used up
37
Inadequate Oxygen transport
§ anemia
§ not enough RBCs in circulation d/t excess destruction or inadequate production
§ or the level of hemoglobin level in the RBCs is too low d/t iron or B12 deficiency
Manifestations
o TWO early obvious changes:
§ reduced function of the CNS
§ reduced skeletal muscle function
o all tissues will slow in their metabolism and functions (reduced growth and repair).
Compensatory manifestations
o an SNS response
o attempts at increasing ventilation
o pulmonary vasoconstriction
o increased HR
o Longer term compensations:
o increased erythropoietin secretion by the kidneys to increase RBC production in the
bone marrow
o cardiac hypertrophy
o the growth of new blood vessels in the periphery to increase local blood flow.
o
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O2 Saturation
• Normally, one way to determine whether there is adequate O2 available to tissues is to measure the
level of O2 saturation (the % of the total hemoglobin that is bound to (saturated with) oxygen.
• The normal range for O2 saturation in arterial blood is 95-100%.
<95% usually requires supplementary oxygen.
• Note that even venous blood returning from the tissues still typically has an O2 sat of 70%
• Though we typically think of O2 as a good thing - that is only true if we have it at the right levels
i.e. the levels that we have evolved with.
• Oxygen is a highly reactive element
o It can damage many biomolecules and tissues at higher levels.
o Exposure to higher levels of oxygen for too long may lead to s/s of damage from oxygen
toxicity.
§ For example, 60% O2 for >36 hours or 100% O2 for >6 hours
o Damage could include
§ alveolar wall damage à fibrosisà acute respiratory distress syndrome (ARDS) à
atelectasis (lung collapse)
§ when premature newborns are given too much O2, they may damage their lens and
lose vision irreversibly (retrolental fibroplasia).
•
Cyanosis
• Is another common sign of hypoxia
• involves a bluish coloration of the skin and mucosa d/t a color change in the hemoglobin
pigment when it becomes deoxygenated.
• oxyhemoglobin is red
• deoxyhemoglobin is bluish-purple.
• This can happen when there is inadequate gas exchange in the lungs (ventilation/perfusion
mismatch)
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However cyanosis does not always indicate hypoxia accurately.
Two exceptions are
1. With a very slow circulation
o such as when blood viscosity is increased with polycythemia
o or when there is peripheral vasoconstriction when exposed to cold air
o In these cases, there is still plenty of O2 to meet tissue needs, but the level of
deoxyhemoglobin is rising.
2. With anemia
o Individuals may be severely hypoxic but not show cyanosis
o Happens because the hemoglobin level is so low so the coloration of deoxyhemoglobin
does undetected.
Hypercapnia
• involves elevated levels of CO2 in extracellular fluids
• will result whenever CO2 production > elimination.
• CO2 is produced as a product of cellular respiration (whenever metabolism is increased, CO2 levels
will increase).
• CO2 is eliminated in gas exchange between luminary capillary blood and the alveolar air.
• Normally, breathing regulation is based on CO2 blood levels
o detected by chemoreceptors in the aorta and carotid arteries à send impulses to the RCC in
the medulla, which controls the rate and depth of breathing.
• However, with severely compromised ventilation (like with COPD) PaCO2 levels will be so high that
it is no longer useful as a signal to stimulate breathing.
o there will be a switch over to using PaO2 as the basis for control
o using chemoreceptors sensitive to O2 à hypoxic drive.
o Becomes problematic when they are given supplemental oxygen.
o This increased O2 now satisfies the chemoreceptors, so there is no stimulus to breath, and
CO2 levels will rise to much higher levels.
•
The TWO main negative effects of hypercapnia are:
1. CO2 combines with water to produce carbonic acid which will dissociate to release H+.
§ The increase in [H+] will lower the pH à acidosis
§ has a lot of negative effects, including CNS depression.
2. increased levels of CO2 will stimulate widespread vasodilation.
§ Systemically, this can lead to a decrease in BP
§ Locally, it may cause cerebral blood vessels to vasodilate à severe headaches and
a rise in ICP.
Chronic Obstructive Pulmonary Disease (COPD)
• refers to a group of respiratory disorders that involve the chronic, irreversible, and progressive
degeneration of respiratory tissue and obstruction of the airways.
• Including chronic bronchitis, emphysema, and chronic asthma.
• COPD ultimately places the individual at
o risk of respiratory failure
o risk of right-sided CHF.
Chronic Bronchitis (Blue Bloaters)
• usually develops as a result of long-term exposure to respiratory irritants
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•
•
o such as cigarette smoke or some industrial pollutants
most common in middle or older adults, though, depending on when exposure problems began.
TWO changes occur in the bronchi and decrease the capacity to ventilate the lungs, leading to
hypoxia, cyanosis, and edema (“blue bloater”).
o inflammation and edema of the mucosa à fibrosis and increased airway wall thickness à
a narrowed lumen.
o The mucous glands undergo hypertrophy and increase the secretion of thick, sticky
mucous.
Ultimately, the quality of life is greatly diminished as the effort at ventilation precludes normal
communication and most forms of physical activity and even makes eating very difficult à an overall
decline in health with pulmonary hypertension associated with cor pulmonale.
Emphysema (Pink Puffers)
This disorder involves the:
• breakdown of the alveolar walls
• breakdown of elastic connective tissue
Effects
• Decreased surface area à decreased gas exchange
• Decreased elastic stretch and recoil à deceased compliance
• NO elastic recoil à even harder to breathe à SUPER barrel-chested (hyperinflated)
• changing clusters of distinct small alveolar sacs into large singular air spaces that are permanently
hyperinflated but which present a much-reduced surface area over which gases can be exchanged
between the blood and the air.
Causes
• There are two major causes of emphysema
1. cigarette smoke or other air pollutants
o direct destruction of the tissue
o by stimulating WBCs (neutrophils) to enter the tissue and release proteolytic enzymes,
thus destroying elastic connective tissue.
2. An inherited (recessive) genetic deficiency
o of alpha 1-antitrypsin, a protease enzyme that works to prevent or block the effects of
protease enzymes such as elastase that are produced by WBCs.
limited production à more rapid elastase effect à increasd breakdown of connective tissue
o This inherited deficiency is the usual cause for the rare form of emphysema that develops in
younger individuals (ie. < 40).
•
The tissue damage of emphysema usually involves the breakdown of the alveolar walls
o either in the distal alveoli or in the bronchiolar area.
o leads to:
§ decreased surface area
§ decreased pulmonary capillaries for gaseous exchange
§ decreased elastic recoil of the lungs for EXpiration.
o The loss of structural integrity of the walls can also lead to partial collapse and the
development of "blebs" or local lesions.
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Effects
• air trapping associated with reduced expiration à hyperinflated lungs à the development of a
"barrel chest" (increased anterior-posterior diameter).
• the diaphragm appears flattened
o d/t the increased downward pressure by the hyperinflated lungs.
• loss of both perfusion and ventilation with a severe sense of dyspnea.
o Much more effort is required in ventilation (especially EXpiration) to maintain blood gases at
nearly normal levels (accessory muscle use).
§ This is exhausting but ventilation and perfusion may be initially kept matched.
§ For this reason, these individuals are sometimes referred to as "pink puffers".
§ to try to prevent lung collapse (during EXpiration):
• forward leaning position
• pursed his lips (to slow air outflow and help maintain internal airway pressure).
• increased pulmonary infections
o d/t decreased mucous clearance from airways.
• weight loss
o d/t difficulty with eating associated with dyspnea
o as well as increased energy expenditure with increased ventilatory effort.
• Chronic hypoxia will lead to
o severe exercise intolerance
o polycythemia.
Complications of COPD
• COPD tends to be relentlessly progressive, with the damage being irreversible.
• Often, the different disorders overlap, with one leading to the development of the other.
• Cigarette smoking is by far and away the most significant cause of COPD.
• One of the most noticeable aspects is the accumulation of mucous in the airways.
o Cilia are damaged à reduced sweeping action towards the pharynx
à mucous accumulates.
o Loss of elastic recoil with the loss of strength and exhaustion of respiratory muscles
à decreased mucous clearance.
o Dehydration d/t increased ventilatory effort
à even thicker and stickier mucous.
o The accumulated mucous can lead to
§ further narrowing and obstruction of the airways
§ and an increased risk of pulmonary infection.
• Chronic hypoxia from the COPD leads to a variety of tissue changes including:
o an overall decrease in tissue functioning
o exercise intolerance
o polycythemia.
o Local tissues may respond with
§ neovascularization
§ and changes such as clubbing of fingers.
• Progressively, COPD will lead to greater levels of respiratory insufficiency, making daily activities
increasingly difficult until, finally, respiratory failure develops when gaseous exchange levels drop
too low.
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•
Cor Pulmonale
o occurs when pulmonary hypertension develops d/t pulmonary changes in COPD.
o This HTN increases the afterload on the right ventricle, which responds by gradually
increasing its muscle mass (hypertrophy).
o At the same time, the kidneys respond to the decreased O2 delivery and stimulate
polycythemia à increasing blood viscosity and aggravating pulmonary hypertension.
o Finally, the workload becomes too much for the right ventricle and it fails.
**It isn’t normally the COPD that kills you. It’s usually pneumonia**
Pneumonia
an acute inflammation of the lungs resulting from a microbial infection.
• The most common sources of infection are:
o the inhalation of infectious aerosols (small suspended droplets)
o the aspiration of infected secretions from the oropharynx.
• Sometimes pneumonia may also develop s/t systemic infections spread to the lungs via the blood.
• Pneumonia-causing organisms can include:
o Streptococcus pneumoniae (most common cause)
o other bacteria such as Hemophilus influenzae and aureus
o viruses (e.g., influenza virus and adenovirus)
o fungi such as Candida albicans and Pneumocystis carinii
o other microorganisms such as Mycoplasma and Chlamydia.
•
The risk of pneumonia is increased where there is:
a. Respiratory compromise
• CF or Chronic Bronchitis (especially with mucous accumulation).
b. Immunological compromise
• AIDS or other immunodeficiency disorders
• antirejection drug use post-transplant
• other underlying health problems that reduce immunity (diabetes/Cushing's disease)
• postoperative or immobile individuals
• The very young and the elderly also are more susceptible because of generally lower
levels of immunological effectiveness.
c. Cardiovascular disorders
• such as CHF
Pneumonia can be classified according to the anatomical involvement.
• Lobar pneumonia involves most of one lobe
• lobular or bronchopneumonia has a more patchy distribution involving areas around the bronchi.
We also distinguish forms of pneumonia in terms of source (community/hospital acquired).
Community-Acquired Bacterial Pneumonia
• The most common cause of this form is the bacterium Streptococcus pheumoniae (or
pneumococcus)
• most commonly in the elderly and the chronically ill
• it can occur in otherwise healthy younger adults as a primary illness.
• it usually develops as lobar pneumonia.
• The pathophysiology involves
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o congestion of the infected lobe
o vascular engorgement of the alveolar blood vessels
o inflammation of the alveolar walls
o the production of an exudate.
Blood cells such as WBCs and RBCs and blood proteins such as fibrin enter the exudates, forming a
consolidation or solid mass.
Typically, this irritates and is coughed up as sticky, purulent, rusty-colored sputum
It is a common cause of death
o often as a result of respiratory failure or cardiac failure
o results from the increased afterload on the right ventricle in combination with increased
demand (with fever) and hypoxia.
Vaccines are available to prevent pneumococcal pneumonia.
Manifestations
• Characteristic Signs and Symptoms
o rusty sputum
o sudden onset
o initial rales sounds followed by loss of breath sounds in the affected lobe as the mass
consolidates
o high fever and chills
o difficulty breathing (dyspnea), which is often accompanied by pleuritic pain.
•
Respiratory acidosis
o d/t reduced gaseous exchange, leading to elevated blood PaCO2 levels.
o further exacerbated by the fever, which increases tissue metabolism
§ leading to greater CO2 production in combination with increased anaerobic
respiration as hypoxia develops d/t decreased gaseous exchange.
§ The dehydration that accompanies the fever also contributes.
o Exudate accumulation acts as a barrier to diffusion along with the edema and fibrous
exudates that dilute surfactant in the alveoli, ultimately reducing gaseous exchange.
•
Pleuritic pain
o occurs when the pleura adjacent to the infected area becomes inflamed
§ d/t irritation from the rough fibrous exudates.
o Typically, pain occurs during INspiration.
•
Pleurisy
o refers to the infection extending to the pleura over the infected areas (the visceral pleura).
•
Pleural effusion
o involves the accumulation of inflammatory exudates in the pleural cavity (between the
visceral and parietal pleura).
o Fluids can shift into this space d/t the increased permeabilities with inflammation.
Empyema
o refers to the accumulation of purulent exudates (pus) around the lungs.
o This usually has to be drained.
•
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Bronchopneumonia or lobular pneumonia
• caused by a variety of different bacteria and possibly a mix of other microorganisms.
• involves a patchy distribution in several lobules in both lungs
o especially in dependent areas.
• It is most common in the very young or the very old and usually involves
o yellow or greenish mucopurulent sputum
o moderate fever
o rales sounds.
• It is usually self-limiting and causes no permanent lung damage.
Nosocomial Pneumonia
• acquired during hospitalization.
o tend to occur 48 hours or more after hospitalization
• They are usually caused by gram-negative enteric aerobe bacteria
o such as Klebsiella pneumonia, Escherichia coli, Enterobacter, and Pseudomonas aeruginosa
• can also be caused by the gram-positive bacteria Staphylococcus aureus, which is ubiquitous in
the hospital environment.
• They tend to cause extensive damage to lung tissue
o can lead to abscesses, emphysema, and relatively high levels of mortality (up to 50 %).
• a result of oropharyngeal (or gastric) colonization.
• Aspiration becomes more common
o d/t NGTs, drug effects that cause reduced gag reflexes, and altered consciousness.
• Drugs that reduce gastric pH also increase gastric colonization.
• Individuals are usually compromised by underlying illness and therapeutic interventions
o such as mechanical ventilation, drugs, surgery, endotracheal intubation...
• We have also managed to select for widespread antibiotic resistance in many of the common
nosocomial infectious agents, making them even harder to control.
• Often, the symptoms include
o yellowish or green-colored sputum
o significant consolidation (seen on a chest x-ray).
Viral Pneumonias
• most caused by influenza virus (type A & type B)
o other viral types can be involved, including adenoviruses, parainfluenza virus and varicella.
• Typically, viral pneumonia is mild and self-limiting
o with cold-like symptoms
o accompanied by mild fever, muscle aches, headache, and a dry, unproductive cough.
o Sometimes, however, they can do greater damage and may even cause death directly or
predispose to bacterial infection.
• Viral infections are the most common cause of pneumonia in children but only account for about 10%
of adult pneumonia.
• The highest risk of mortality developing d/t influenza virus infections are for:
o adults >65
o adults or children with chronic health problems
§ such as CVS
§ pulmonary disorders (CF, asthma…)
§ metabolic disorders (diabetes).
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health care workers
§ especially those working with high risk patients (a higher risk of transmission).
Individuals in these groups should be vaccinated to reduce the risk to them, but actually, vaccination
of all school-age children would be the most effective way to prevent a flu outbreak in the general
population.
o
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Primary Atypical Pneumonia
• is caused by Mycoplasma.
• These are very small bacteria-like organisms that, however, have no cell wall and are obligate
intracellular parasites.
• Typically, they colonize the pharynx and bronchi
• in about 10% of cases, they can invade deeper lung tissue.
• occurs most commonly in young adults, especially in schools and military barracks.
• The S/S are similar to viral pneumonia with a dry cough, muscle aches, fatigue, fever, and the
potential to predispose to bacterial infections.
• They can be treated successfully with some antibiotics.
Tuberculosis
• This disease is caused by Mycobacterium tuberculosis, which initially develops as a lung infection
in most cases but can later affect many different body tissues.
• In the primary infection stage
o the pathogen is usually acquired through direct contact with infected droplets.
o it then enters the lungs, where it provokes macrophages to attempt to engulf it and initiate
an inflammatory response.
o it resists destruction and becomes surrounded by macrophages and lymphocytes forming
a granulomatous mass known as a tubercle.
o as it develops
§ the inside of the mass becomes necrotic, caseous, or cheeselike at the center
§ but with live bacteria still present.
o Ultimately, these tubercles are walled off by fibrous connective tissue and become calcified.
o The individual may be relatively unaffected by these clusters of tubercles (referred to as
Ghon complexes) in the lungs and lymph tissue.
•
often the only evidence of their presence is
o an image of these calcified structures on a chest x-ray
o a positive sputum culture of M. tuberculosis
o a positive skin test (a few weeks after the initial infection)
§ as the result of a Type IV hypersensitivity reaction to the Mycobacterium.
§ The positive skin test involves the formation of a large raised, reddish, and hardened
area in response to exposure to proteins from the TB microorganism.
•
The main problem with TB is that (secondary infection stage)
o if the infected individual at some point becomes immunocompromised
§ with severe stress, another illness, malnutrition, or d/t drugs use that lowers resistance…
o the individual may then develop a secondary infection.
o this can cause the bacterium to break out of the tubercles and spread widely throughout the
lungs but also enter the blood stream to virtually any other tissues in the body.
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In the lungs we see cavitation (formation of big empty spaces) and hemoptysis.
At this point,
o the respiratory function is greatly compromised,
o the individual becomes infective to others via infected sputum.
o elsewhere in the body, the bacterium destroys tissues such as kidneys, liver, and bones
o can lead to large-scale organ damage.
o if untreated it is typically fatal.
Vaccines have been highly effective at controlling this disease
but it is still quite common in many parts of the world where vaccination levels are insufficient to
prevent epidemics.
TB is especially common in populations with
o high levels of poverty
o overcrowding
o inadequate access to health care.
In Canada, it is mainly found within the
o aboriginal community (d/t woeful mismanagement by the federal government )
o in the homeless
o in some recent immigrant communities.
TB is a reportable communicable disease and rapid and effective treatment is required involving a
long course of multiple different antibiotics (varies depending on the antibiotic resistance of the
strains involved).
Unfortunately the affected populations are not always positive about the long course of treatment and
the supervision that is typically required during treatment.
Also, unfortunately, we have become a little too lax about surveillance for this disease, and the
Mycobacterium has developed resistance to many of the previously most effective drugs.
Trauma
• Rib Fractures
o are commonly associated with
§ Falls (workplace or domestic injuries involving ladders)
§ Recreational sports.
§ Car accidents
o they may interfere with the normal changes in chest size necessary for ventilation.
o tend to be painful and, of course, can’t really be immobilized for repair.
•
Flail Chest
o a result of
§ fracturing multiple ribs (>3) in several locations
§ or fracturing the sternum and several consecutive ribs
§ enough to interfere with the normal breathing movements – the broken segment
tends to “float” free of the constraints of the rest of the ribs.
o This will lead to the opposite or paradoxical movement of the broken segment.
§ During INnspiration
• the ribs usually move up and out to lower the pressure in the thoracic cavity
• in the case of the flail chest, the broken section of the ribs moves INwards,
pulled in by the lowered pressure in the chest.
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•
this prevents full expansion of the lungs and may even compress adjacent
areas, forcing air out instead of in.
• Some of this air being forced out will even be drawn into the other lung, further
reducing the efficiency of gaseous exchange.
§ During EXpiration
• the ribs usually move down and in to raise the pressure and move air out.
• in this case, though, the broken segment will be pushed OUTward by the
pressure à reducing the pressure difference à expiration is less effective
• this can also cause some of the air being expired by the normal lung to be
drawn into the lower pressure of the affected lung.
o Clearly, the above will lead to
§ a reduced inspiratory volume
§ reduced vital capacity
§ a decrease in gaseous exchange
à ultimately leading to hypoxia.
o If the flail chest segment is large enough
§ the resulting pressure differences between the affected and unaffected lung may lead
to a shifting of the trachea and mediastinum to one side.
§ During INspiration
• as the pressure is lowered more on the normal side
• the mediastinum will shift towards that side (to the unaffected side)
§ On EXpiration
• the higher pressure on the normal side will shift the mediastinum over
toward the other side (to the affected side).
• this shifting and the pressure changes can:
o interfere with venous return to the heart and reduce cardiac output.
o If the rib fracture leads to a broken rib bone puncturing the pleura it may lead to atelectasis.
Pneumothorax
• the introduction of air to the pleural cavity between the visceral and parietal pleura.
• this disrupts the surface tension between the two wet membranes
• can allow partial or complete collapse of the affected lung.
Closed Pneumothorax
• When air enters the pleural cavity through an opening from the lung airways.
Causes
• Primary Pneumothorax
o when the bleb or tear occurs idiopathically (cause unknown)
§ often occurs in tall adolescent or young adult males
§ associated with an episode of rapid growth.
• Secondary Pneumothorax
o can occur spontaneously
§ when an air-filled blister or bleb (associated with emphysema, asthma, or CF)
ruptures
o or when a tumor causes an erosion
§ that makes an opening for air from the lung spaces to enter the pleural cavity.
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Manifestations
• The affected lung collapses
• the mediastinum shifts towards the affected side
• the other lung tends to expand further.
• dyspnea
• elevated RR and elevated HR.
• pleural pain
• asymmetrical chest movements
o as the affected side lags during inspiration.
• Usually no breath sounds are heard on the affected side.
• Hypoxemia can result from the reduction in gas exchange.
Open Pneumothorax
• the introduction of air enters the pleural cavity through an opening in the chest wall.
• a result of penetrating injury with trauma (knife wounds or car accidents involving penetrating debris
or fractured ribs) or surgery.
• As air enters the pleural cavity, the cavity pressure increases and causes immediate atelectasis.
• During INspiration
o more air enters the pleural cavity
o causing the pressure on the affected side to be greater
o pushing the mediastinum toward the unaffected side
o and the expansion of the unaffected side is now limited.
• During EXpiration
o air is forced out of the pleural cavity
o the mediastinum shifts back towards the affected side.
o This mediastinal movement back and forth is referred to as mediastinal flutter and it
interferes with:
§ ventilation à reduced ventilation à hypoxemia
§ and with venous return à reducing cardiac output.
•
though in milder cases of open pneumothorax and in primary closed pneumothorax:
pulmonary vasoconstriction in the affected lung will increase blood flow to the unaffected lung
leading to normal O2 saturation within a day or so.
•
With an open pneumothorax, there will often be a sucking sound if the chest wound is large.
o This is the sound of air rushing into and out of the pleural cavity with chest movements.
o This usually indicates a larger wound with a greater impact on respiratory and cardiovascular
function.
Tension Pneumothorax
• occurs when there is an open wound or a closed pneumothorax
• the wound edges form a flap that acts as a one-way valve
o allowing air into the pleural cavity BUT not letting it back out again
o i.e. the increasing pressure causes the valve-like flap to close.
• causes the pressure on the affected side to continue to rise
• ultimately compressing
o the other lung
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o and the mediastinal veins (vena cava), as the mediastinum is shifted over dramatically.
This can rapidly become life-threatening
o as severe hypoxia, cyanosis, and, finally, respiratory failure develops.
Compression of the vena cava may cause
o bulging and distension of the neck veins
o a major decrease in cardiac output, leading to shock.
There will be no breath sounds from the affected side.
This situation requires immediate emergency treatment
o involving widening of the opening or removing the tissue flaps to create an open
pneumothorax that lets air out of the pleural cavity during EXpiration.