PATHO EXAM 4

respiratory system review

function is to conduct ventilation and gas exchange to supply oxygen to the body

structures and organs involved

- upper & lower respiratory tract

- lungs

- diaphragm

- ciliated epithelial cells

upper respiratory tract: nasal cavity

passage for air

warms air

cilia & hairs defend

upper respiratory tract: oral cavity

passgae for air

upper respiratory tract: pharynx

passage of air from nose --> mouth --> larynx

upper respiratory tract: larynx

passage of air to trachea and vocal cords

upper trachea apart of upt

lower respiratory tract: bronchi

passage of air to left & right lungs

lower trachea apart of lrt

lower respiratory tract: bronchioles

division of bronchi in the lungs

lower respiratory tract: lungs

left and right lungs house tissue for gas exchange

lower respiratory tract: alveoli

tiny air sacs that allow for gas exchange

structures of respiratory system: cilia

mucocillary clearance is a primary defense mechanism to clear airway

cilia move mucus upward to be swallowed or expectorated

cililary function impaired by smoking, alcohol, hypo/hyperthermia, cold air, low humidity, starvation, anesthetic, corticosteroids, noxious gases, the common cold, and increased mucus production

structures of respiratory system: alveoli

main structure conducting gas exchange

- expansion during inhalation to take in oxygen

- deflate during exhalation to expel carbon dioxide

alveolar macrophages phagocytize foreign particles

- can be damaged by smoking

alveoli secrete surfactant

- facilitates gas exchange by lowering surface tension and keeping alveolar sacs open

- type I alveolar cells

- epithelial structural cells

- type II alveolar cells

- produce surfactant

ventilation & gas exchange review: inhalation

diaphragm contracts (flattens) to allow air in

oxygen is passed through alveoli and into capillaries

rbcs absorb oxygen via hemoglobin

ventilation & gas exchange review: exhalation

diaphragm relaxed (returns to dome shape) to force air out of lungs

expelling of carbon dioxide via alveoli

normal spo2

95-100%

normal rr

12 - 20 bpm

diffusion & transport of respiratory gases

alveolar-capillary membrane consists of six barriers

- surfactant

- alveolar membrane

- interstitial fluid

- capillary membrane

- plasma

- rbc membrane

autonomic nervous system

control bronchi & bronchiole smooth muscle

parasympathetic stimulation (rest and digest)

- mediated by acetylcholine via vagus nerve

- constriction of smooth muscle

- slower, deeper breathing

sympathetic stimulation (flight or fight)

- mediated by beta2-adrenergic receptors

- rapid and shallow breathing

- relaxation of the smooth muscle causing small airways to open wide

ans: the respiratory center

located in the pons and medulla oblongata

efferent fibers travel from the brainstem to diaphragm via phrenic nerve to stimulate inspiratory muscles

abrupt cessation of neurostimulation allows for expiration

ans: pneumotaxic center

located in the upper pons

influences rate of respiration

ends inspiration

input from the spinal cord, cortex, and midbrain contributes to smooth pattern of respiration

apneustic center of lower pons influences the pattern of respiration

ans: central chemoreceptors

located in the medullary center

responds to changes in co2 and ph

normal stimulus to breathe is small increase in arterial co2 tension

alveolar ventilation can increase 10-fold with acute rise in paco2

acidosis can increase alveolar ventilation

ans: peripheral chemoreceptors

located in the aortic arch & carotid bodies

respond to decrease in arterial o2

also respond to increases in

- hydrogen ion concentration (decreased ph)

- arterial co2 level (paco2)

what is shock

a life threatening condition where the bodys tissue do not receive enough blood flow, leading to cellular hypoxia and organ dysfunction

- a state of circulatory failure resulting from an imbalance between oxygen supply and demand at the cellular level

- shock is a continuum of events that progresses through multiple stages

- clinical manifestations of shock are defined by shape of compensation

shock: pathophysiology

imbalance between oxygen supply and oxygen demand at the cellular level

common to all types of shock.

- hypo perfusion of the tissues

- impaired cellular oxygen utilization

inadequate cellular oxygenation due to:

- decreased cardiac output

- maldistribution of blood flow

- reduced blood oxygen content

pathophysiology across all types: reduced tissue perfusion (hypoperfusion)

all types of shock result in inadequate tissue perfusion, leading to cellular dysfunction and potential organ failure

pathophysiology across all types: compensatory mechanisms

the body activates compensatory mechanisms to maintain perfusion

- the sympathetic nervous system

- release of catecholamines

- activation of the renin-angiotensin-aldosterone system

pathophysiology across all types: hemodynamic changes

tachycardia

hypotension

4 types of shock: hypovolemic

loss of intravascular volume

- trauma

- hemorrhage

- severe dehydration

- burns

4 types of shock: cariogenic

impaired cardiac function (output) despite sufficient vascular volume

- mi

- heart failure

- arrhythmias

- valve dysfunction

4 types of shock: distributive

widespread vasodilation and increased capillary permeability

- anaphylactic

- septic (severe inflammatory response to infection)

- neurogenic (severe loss of vasomotor tone)

4 types of shock: obstructive

impaired blood flow due to physical obstruction in the heart or great vessels

- pe

- cardiac tamponade

- pneumothorax

compensatory mechanisms & stages of shock

1. compensatory

2. progressive (decompensatory)

3. refractory (irreversible)

shock: compensatory stage

the body's initial response to shock, where compensatory mechanisms attempt to maintain tissue perfusion

shock: compensatory stage - sns

increased heart rate and vasoconstricts blood vessels to maintain bp

shock: compensatory stage - renal system

activation of the renin-angiotensin-aldosterone system (raas) leads to sodium and water retention, increased blood volume

shock: compensatory stage - release of adh

promotes water retention by kidneys, helping to increase blood volume

shock: compensatory stage - blood redistribution

blood is diverted to vital organs (brain, heart) at the expense of less critical organs (skin, kidneys)

shock: progressive stage

if shock persists, the body's compensatoru mechanisms begin to fail & organ systems start to experience hypoperfusion and damage

shock: progressive stage - severe hypotension

despite compensatory mechanisms, bp drops significantly

shock: progressive stage - decreased tissue perfusion

organs such as the kidneys and liver begin to suffer from lack of oxygen

shock: progressive stage - anaerobic metabolism

lactic acid builds up due to insufficient oxygen, leading to metabolic acidosis

lack of tap leads to cellular swelling, dysfunction, and death

shock: progressive stage - pulmonary dysfunction

acute respiratory distress syndrome (ards) may develop

shock: progressive stage - cardiac dysfunction

myocardial depression further reduces cardiac output

hypotension & tissue hypoxia

cellular and organ dysfunction result from oxygen free radicals, release of inflammatory cytokines, and activation of the clotting cascade

shock: refractory stage

the final stage of shock where organ damage becomes irreversible, and death is imminent if not treated

- unresponsive to therapeutic interventions

shock: refractory stage - multiple organ dysfunction syndrome (mods)

failure of multiple organ systems (e.g., liver, kidney, lungs)

shock: refractory stage - severe hypoxia & acidosis

cells are unable to maintain function despite intervetnion, & lactic acid accumulation worsens

shock: refractory stage - total circulatory collapse

no effective circulatory volume or pressure to perfuse organs

failure of vasuclar system (unresponsive to compensation)

shock: refractory stage - loss of consciousness

deepening coma and eventual loss of brain function

nursing management of compensatory stages

each stage can be identified through vital signs and clinical assessment

- hemodynamic changes, hr, bp, & rr

- urine output (important indicator of kidney perfusion)

- lactate levels (marker of anaerobic metabolism)

- mental status (alertness vs confusion vs coma)

Early detection

- early identification of shock and intervention is important to prevent progression to later stages

hypovolemic shock: overview

insufficient circulating blood volume (due to blood loss, dehydration, or fluid loss)

hypovolemic shock: clinical manifestations

- depend on the severity of intravascular volume loss

initial stage:

- increased heart rate

- vascular constriction

cardiac output within normal range

- obtaining mean arterial pressure

- average pressure in cardiac cycle

- more accurate indicator or perfusion

- map decreases by 10 mmhg from baseline

hypovolemic shock: treatment

stabilize bp & maintain perfusion

- fluid restriction

- blood transfusions

if bp can't be maintained w/fluids alone

- vasopressor medications

defintive treatment --> addressing the underlying cause

cardiogenic shock: overview

the heart fails to pump effectively, resulting in inadequate blood flow to the tissues

cardiogenic shock: etiology

myocardial infarction

heart failure

arrhythmias

valve dysfunction

cardiogenic shock: pathophysiology

reduced cardiac output due to impaired myocardial contractility

blood backs up into the lungs (pulmonary edema)

decreased tissue perfusion and oxygen delivery

decreased cardiac output and high preload

low co = reduced oxygen delivery to tissues = higher oxygen extraction = low svo2

cardiogenic shock: clinical manifestations

refer back to compensatory stages

- increased heart rate, decreased blood pressure, decreased urine output, decreased ph

cardiogenic shock: treatment

therapy aimed at imrproving co and myocardial oxygen delivery, decreasing workload

- positive inotropic (dopamine), preload-reducing (diuretics), and afterload-reducing agents (beta-blockers)

- must maintain a very tight fluid balance (do not want fluid overload)

- intraortic balloon pump, ventricular assist devices, heart transplantation

obstructive shock: overview

impaired blood flow due to physical obstruction in the heart or great vessels which prevents effective cardiac filling and stroke volume

obstructive shock: etiology

pulmonary embolism

cardiac tamponade

tension pneumothorax

obstructive shock: clinical manifestations

manifests as right-sided failure

also refer to compensatory stages

obstructive shock: treatment

rapid management of underlying obstruction is required to prevent cardiovascular collapse

- example: pericardiocentesis for cardiac tamponade

distributive shock: overview

abnormal distribution of blood flow, resulting in inadequate tissue perfusion despite an adequate circulating blood volume due to widespread vasodilation & increased capillary permeability --> signs of inflammation

- increased capillary permeability --> peripheral pooling of blood

- co inadequate due to reduced preload

anaphylactic shock

severe, life-threatening allergic reaction that leads to systemic vasodilation (hypotension) and increased vascular permeability (edema)

- type I hypersensitivity reaction (IgE mediated)

- triggering allergen exposure --> IgE antibodies formed

- second exposure --> rapid immune response

- IgE antibodies primed on mast cells and recognize antigens --> excessive release of histamine --> systemic effects

anaphylactic shock: causes

antibiotic therapy

allergens

- peanuts & tree nuts

- insect stings

- snake bite

anaphylactic shock: clinical manifestations

urticaria (hives)

bronchoconstriction

stridor

angioedema

wheezing

itching

anaphylactic shock: treatment

maintenance of airway latency, use of epinephrine, bronchodilator, antihistamines, vasopressors, and ivermectin fluids

neurogenic shock: overview

results from loss of sympathetic activation of arteriolar smooth muscles

neurogenic shock: causes

spinal cord injury (lesions of sympathetic nerve fibers)

traumatic brain injury

meningitis

cerebral ischemia

drug overdose

neurogenic shock: treatment

vasopressor & fluids

elevations of the legs

slow position changes

pressure stockings

sepsis/septic shock: overview

sepsis is a systemic exaggerated immune response to a severe infection

- symptoms suggest infection source

- flank pain (kidney)

septic shock is a life threatening condition that arises due to an infection causing widespread inflammatory responses and vasodilation

septic shock: etiology

severe bacterial infections (e.g., pneumonia, utis, bloodstream infections)

fungal or viral infections in some cases

septic shock: pathophysiology

infection triggers the release of pro-inflammatory mediators (cytokines, interleukins)

these mediators cause widespread vasodilation, increased vascular permeability

leads to decreased systemic vascular resistance (svr) and pooling of blood in peripheral tissues, impairing tissue perfusion

organ failure occurs due to inadequate oxygen delivery to tissues

septic shock: pathophys + complications - infectious trigger

septic shock begins with a severe infection, often caused by bacteria, but can be caused by viruses, fungi, or parasites

- gram-negative bacteria: endotoxins in bacterial cell walls stimulate massive immune system activation

septic shock: pathophys + complications - immune response activation

the immune system responds to the infection by releasing pro-inflammatory cytokines (interleukin-I (IL-I) and tumor necrosis factor alpha (TNF-alpha))m initiating a systemic inflammatory response

septic shock: pathophys + complications - vasodilation & increased cap permeability

pro-inflammatory cytokines cause widespread vasodilation, reducing systemic vascular resistance, and leading to low bp

septic shock: pathophys + complications - microvascular dysfunction

micro thrombi formation in small blood vessels, along with impaired endothelial function, contributes to microvascular dysfunction

septic shock: pathophys + complications - disseminated intravascular coagulation (dic)

the inflammatory response can activate the coagulation system, leading to dic

- dic results in a complex interplay of clot formation and consumption of clotting factors, contributing to both bleeding and thrombotic complications

septic shock: clinical manifestations

sepsis leads to septic shock if:

- systolic blood pressure is below 90 mmhg or has fallen 40 mmhg below baseline or if lactate level is elevated (serum lactate level > 2 mmol/L

only type of shock with warm and flushed skin

mottled skin is a sign of extreme hypoxemia and hypoperfusion

- if you see this, you need to something about it stat

septic shock: management & treatment

therapy aimed at restoring intravascular volume, increasing oxygen delivery to tissues, and reversing organ dysfunction

administration of fluids & drugs to improve cardiac and vascular performance to improve distribution of blood flow

find the source and control it, once initial resuscitation is completed

acute respiratory distress syndrome (ards): overview

most associated with septic shock

development of refractory hypoxemia, decreased pulmonary compliance, and radiographic evidence of noncardiogenic pulmonary edema

- the primary cause of death in ards = multiple organ failure, not severe hypoxemia

ards: pathophysiology - lung injury

when shock occurs, organs don't get enough oxygen, which can damage the lungs and make it harder for oxygen to get into the bloodstream

ards: pathophysiology - fluid build-up

in ards, the lungs fill with fluid, which reduces the ability of oxygen to pass from the air sacs into the blood leading to breathing problems

ards: pathophysiology - severe breathing trouble

as ards worsens, patients may require mechanicla ventilation (a breathing machine) to help them breathe since their lungs cannot do it on their own

disseminated intravascular coagulation (dic): overview

usually occurs in septic shock

immune activation of the clotting cascade

dic: pathophysiology - abnormal clotting

dic occurs when the body's clotting system is activated inappropriately, causing tiny blood clots to form throughout the body, often after shock

dic: pathophysiology - bleeding & clotting

while small clots form in the blood vessels, they use up clotting factors, leading to increased bleeding in other parts of the body --> gums, skin

dic: pathophysiology - organ damage

the widespread clots can block blood flow to organs, leading to organ damage and failure, which is common in severe shock

dic: diagnostics

platelet count and fibrinogen levels are low, fibrin degradation products (d-dimer) are elevated

acute kidney injury

reduced blood flow to the kidneys

- in shock, the body's bp drops, and there is not enough blood flow to the kidneys, which can lead to damage

impaired kidney function

- with less blood reaching the kidneys, they can't filter waste properly, causing the buildup of waste & fluids in the body

potential kidney damage

- if shock persists w/o treatment, the kidneys may be permanently harmed, leading to acute kidney injury that may require dialysis

multiple organ dysfunction syndrome(mods): overview

mods is life threatening and often result in death if the underlying shock isn't reversed or managed effectively

- 2 or more systems are failing

most common causes: sepsis & septic shock

- intiated by immune mechanisms that are overactive and destructive

mods: pathophys - widespread inflammatory response

cytokines affect endothelium, recruit neutrophils, and activate inflammation in vascular beds leading to tissue destruction and organ dysfunction systemically

mods: pathophys - multiple organ failure

when shock is severe and untreated, it leads to the failure of several organs like the kidneys, liver, and heart due to lack of blood flow & oxygen

mods: pathophys - cascading damage

as one organ fails, it worsens the function of other organs, creating a cycle of progressive damage that the body can't recover from

ventilation (v) - perfusion (q) ratios

3 types of v/q imbalances

- high (under perfused)

- alveolar unit is ventilated, but not perfused

- low (under ventilated)

- related to hypoxemia

- airwats are partially obstructed

- airflow rates are low

- shunt (no ventilation)

- passage of deoxygenated blood from the right to the left side of circulation, either through anatomic shunting where blood bypasses the lungs from veins to arteries

hypoventilation

air delivered to alveoli is insufficient to provide o2 & remove co2

- hypoventilation results in hypercapnia (increased paco2) and hypoxemia

- causes: morphine, barbiturates, obesity, myasthenia gravis, obstructive sleep apnea, copd, chest wall damage, paralysis of respiratory muscles, surgery of the thorax or abdomen

hyperventilation

increase of air entering the alveoli leads to hypocapnia (paco2 < 35 mmhg)

- causes: pain, fever, anxiety, obstructive & restrictive lung diseases, sepsis, high altitude, & brainstem injury

oxygenation issues

hypoxemia: deficient blood oxygen as measured by low arterial o2 & low hemoglobin saturation

hypoxia: a decrease in tissue oxygenation

types of hypoxia

hypoxic hypoxia: high altitude, hypoventilation, obstruction

anemic hypoxia: low hemoglobin

circulatory hypoxia: low cardiac output; shock

histotoxic hypoxia: decreased o2 carrying capacity from a toxic substance; cyanide poisoning

hypoxic vasoconstriction

alveolar hypoxia leads to vasoconstriction

blood is diverted from areas of low alveolar oxygen to areas of higher oxygen

by diverting blood to areas of higher oxygen concentration, the negative effects on gas exchange are reduced

can result in increased pulmonary vascular resistance

pneumonia: overview + common organisms

inflammation of the lower respiratory tract (alveoli & bronchioles) caused by viruses, bacteria, fungi, and gi content aspiration

- s pneumoniae, s aureus, rsv, influenza, group a strep

community acquired pneumonia (cap)

infection from organisms found in the community

- infection that begins outside the hospital or diagnosed within 48-hours of hospital