Module 2 - Altered Perfusion Flashcards
(18 cards)
Discuss the gross cardiac anatomy
The heart is located in the thoracic cavity, between the lungs, in the mediastinum, positioned slightly to the left of the midline
Exterior: The heart is encased in a double-walled sac called the pericardium, which provides protection and reduces friction as the heart beats. The heart has three distinct layers: the epicardium (outer layer), the myocardium (middle, muscular layer), and the endocardium (inner layer). The epicardium houses the coronary vessels, the myocardium is the thickest layer and is composed of cardiac muscle, the endocardium lines the inner chambers of the heart
Chambers: The heart is divided into four chambers - two atria (upper) and two ventricles (lower)
Atria: The right atrium receives deoxygenated blood from the body via the superior and inferior venae cavae, while the left atrium receives oxygenated blood from the lungs through the pulmonary veins.
Ventricles: The right ventricle pumps deoxygenated blood to the lungs through the pulmonary artery, and the left ventricle pumps oxygenated blood to the rest of the body through the aorta. The left ventricle has noticeably thicker myocardial muscle due to requiring more power than the right side to pump blood throughout the whole body.
Septum: a thick muscular wall, divides the heart into right and left sides
Valves: contains four valves that ensure unidirectional blood flow through its chambers.
The atrioventricular (AV) valves are located between the atria and ventricles to prevent backflow during ventricular systole. The right AV = tricuspid, the left AV = bicuspid (mitral). These valves are connected to ventricle walls by chordae tendineae connected to papillary muscles that contract during ventricular systole, pull back on the chordae tendineae and prevent the valves from inverting
Semilunar valves are located at the exits of the ventricles. Pulmonary valve = between the right ventricle and the pulmonary artery. Aortic valve = between the left ventricle and the aorta - prevent backflow into the ventricles after blood has been ejected
Coronary circulation: heart is supplied with blood through coronary arteries, which branch from the base of the aorta.
The left coronary artery divides into the LAD and the circumflex artery, supplying the left side of the heart. The right coronary artery supplies the right side. These arteries deliver oxygen-rich blood to the myocardium during diastole, coronary veins collect deoxygenated blood and drain it into the right atrium through the coronary sinus.
Discuss the features of one cardiac cycle
Discuss the features of regulating adequate blood pressure
There are three key mechanisms the body uses to regulate blood pressure: The Renin-Angiotensin-Aldosterone System (RAAS), Antidiuretic Hormone and the Baroreceptor reflex.
ADH
Triggers: ^plasma osmolarity detected by osmoreceptors in hypothalamus, decreased blood volume, or ^angiotensin II
=> release of ADH from posterior pituitary gland
=> binds to V2 receptors in kidneys to alter aquaporin proteins to promote water reabsorption
=> in high concn of ADH (e.g. in hypovolaemic shock), ADH can bind to V1 receptors on vascular smooth muscle causing vasoconstriction
Discuss the compensatory mechanism which regulate adequate cardiac output
Baroreceptor reflex
- Rapid mechanism
- Found within the aortic arch and carotid sinus
- Constantly monitor and detect changes in stretch of vessels and thus changes in MAP
- An increase in BP = ^baroreceptor activity (^firing rate in afferent/sensory neurons) -> medulla (cardiovascular centre) = ^PSNS and vSNS activity => vCO and vasodilation to vBP
OR//
- A decrease in BP = decreased baroreceptor activity (v afferent impulses -> medulla) = vPSNS and ^SNS activity => ^CO and vasoconstriction to ^BP
Discuss the features of the Renin- Angiotensin- Aldosterone System
RAAS system = Uses hormones to alter blood pressure through increasing blood volume and peripheral vascular resistance
Decreased Na+ concn, decreased renal blood flow, or SNS activating beta1 adrenergic receptors => Renin release from kidneys (juxtaglomerular cells)
Liver continuously producing angiotensinogen. => Renin converts angiotensinogen to angiotensin I
ACE (angiotensin converting enzyme) mostly found in lungs
=> ACE converts angiotensin I to angiotensin II
Angiotensin => vasoconstriction (systemic and renal) - ^SVR = ^BP
Angiotensin II stimulates release of aldosterone from adrenal cortex => promotes Na+ reabsorption, allowing for passive water reabsorption through osmosis => ^plasma volume = ^BP
Discuss the gross respiratory anatomy
- Respiratory system is made up of the upper airways: nose and nasal cavity, mouth and oral cavity, pharynx and larynx and the lower airways,: trachea, bronchi and bronchioles
- The conducting portion (pharynx, larynx, trachea, bronchi, bronchioles) humidify, warm, and filter air
- The respiratory portion (respiratory bronchiole, alveolar duct, alveolar sac, alveoli) performs gas exchange
- The diaphragm is the muscle that sits beneath the lungs, attached to the sternum/spine/bottom of ribcage and facilitates inhalation and exhalation
Discuss the features of the respiratory drive
Respiratory drive refers to the output of the brain’s respiratory centres that control the respiratory muscles
Respiratory centre is comprised of the three neuronal groups (dorsal, ventral, and pontine respiratory groups) - These function to regulate breathing, maintain oxygen and carbon dioxide levels and pH levels in the blood
Dorsal respiratory group is responsible for the timing of respiratory cycles - inspiratory neurons that travel from the DRG via the phrenic nerve to the diaphragm and external intercostal muscles.
Ventral respiratory group controls expiration and only activates during forceful breathing - works in coordination with the dorsal group, expiratory neurons located in the caudal region of the medulla oblongata activate expiratory muscles during active exhalation.
Pontine respiratory group is active during the transition between inhalation and exhalation to increase or decrease the duration and strength of breathing cycles - actions of the pontine group are dictated by pH/carbon dioxide levels picked up by chemoreceptors
- Peripheral chemoreceptors (carotid and aortic arch) send signals to the respiratory centre via the glossopharyngeal nerve
- Central chemoreceptors (medulla, cerebellum, hypothalamus, midbrain, and retrotrapezoid nucleus) transmit and receive signals via the glossopharyngeal and vagus nerves to modulate respiration
- During sleep, output from the respiratory controller in the brain declines and the respiratory centre becomes less responsive to changes in arterial oxygen and carbon dioxide. The pontine respiratory group aids sleep changes by switching the breathing pattern to ensue stable oxygen and carbon dioxide levels
Discuss the features of normal oxygen saturation
Oxygen saturation measures the ratio of oxygen bound to haemoglobin molecules to unbound haemoglobin molecules
- Normal levels in an adult are between 95-100%
- This can be measured by a pulse oximeter (non-invasive) or more accurately through ABG via an arterial line
- Considerations which may give unreliable results = poor perfusion, nail polish, anaemia or carbon monoxide poisoning
- The Bohr effect – Haemoglobin has a higher affinity for O2 at lower partial pressures of CO2, and a lower affinity for O2 at higher partial pressures of CO2 – therefore when there is a higher O2 demand, Hb can free up O2 to be utilised in the tissues
Discuss the mechanics of ventilation and apply the principles to pathological conditions
Boyles law
- According to Boyle’s law, volume and pressure are inversely proportional
- Increase in volume will result in a decrease in pressure inside the lungs compared to the outside atmospheric pressure and vice versa
- This produces a pressure gradient, forcing air to rush from the higher pressure of the atmosphere into the comparatively low pressure in the lungs allowing for inhalation
Inhalation
- Active process
- In inhalation, the external intercostal muscles contract and work together with the contraction of the diaphragm to expand the abdomen and create an increase in volume – see Boyle’s law
- Forced inhalation, present during exercise or respiratory distress, adopts the use of accessory muscles such as the sternocleidomastoid and the scalene muscles to elevate the sternum and upper ribs to allow for a further increase in volume and force more air into the lungs
Expiration
- Passive process - simply requires the relaxation of the diaphragm and intercostals which reduces the diameter of the chest due to the ribcage’s elasticity - results in an increase in pressure, forcing air back out of the lungs
- Expiration can also be an active process. Adopting the use of the internal intercostals and abdominal muscles pulls the ribs downward and forces the diaphragm up, allowing for air to be forced from the lungs quicker
Mechanics of Ventilation in Asthma
- Bronchoconstriction, or narrowing of the large airways, causes an increase in airflow resistance making it more difficult for air to flow into the alveoli
- Exhalation is made more difficult through gas trapping caused by obstruction of the small airways. This makes it nearly impossible to fully exhale, and with each subsequent inhale, the chest becomes hyperinflated
- Posturing plays an important role in asthma management, e.g., slumped position increases intraabdominal pressure, making it difficult for the diaphragm to descend downward during inspiration impacting the flow of air into the lungs.
Mechanics of Ventilation in Emphysema
- Emphysema is a chronic airway disease which leads to the obstruction of expiratory air flow & abnormal enlargement of the airways caused by destruction of the septa in the alveoli
- Alveolar septa destroyed = reduction in surface area
- Alveoli loss of shape and integrity = collapse of alveoli = gas trapping
- Decreased elasticity = decreased chest recoil, thus ability to push air out from the lungs = over-inflation, appearance of “barrel chested”, need for active exhalation (use of accessory muscles)
- Decreased airflow due to narrowed airways and in increased resistance especially during exhalation
- Due to this increased work of breathing, they are at risk of respiratory fatigue and joined with impaired gas exchange they can become easily dyspnoeic
- The use of airways devices such as continuous positive airway pressure can aid the mechanics of ventilation through splitting open the alveoli helping to alleviate difficulties in breathing and reduce fatigue
Discuss the features of a VQ mismatch
- V represents alveolar ventilation, Q represents perfusion of the pulmonary capillaries
- A compromise to either pulmonary ventilation or pulmonary perfusion causes a V/Q mismatch, resulting in decreased oxygenation of blood
- Factors affecting ventilation include airway lumen size, airway obstruction (choking, mucus plugging), and alveolar surface area (alveolar collapse, APO, pneumonia)
- Factors affecting perfusion include restricted pulmonary blood flow (pulmonary vasospasm, pulmonary embolism), or dysregulated hypoxaemic pulmonary vasoconstriction (such as inflammatory vasodilation)
E.g. PE - The presence of an embolism in the pulmonary circulation will obstruct the flow of blood to a portion of the lungs.. The size of the affected area corresponds to the size and quantity of the emboli. The lack of blood flow through the affected area prevents any gas exchange despite normal ventilation of the alveoli. This is referred to as “dead space” The reduction in perfusion reduces the value of “Q”, resulting in an increased V/Q.
Discuss the features of respiratory failure
Respiratory failure = a state of inadequate gas exchange
Type 1 - hypoxaemic
- Cannot adequately oxygenate the blood - caused by mechanisms that restrict oxygenation of blood but permits elimination of carbon dioxide
- Carbon dioxide levels usually normal/low
- (Low CO2 levels can occur because CO2 is more soluble than oxygen so diffuses more easily across the respiratory membrane, and hypoxia and its sequelae can stimulate the respiratory drive, which permits carbon dioxide elimination)
Three main factors cause T1RF:
1) Decreased alveolar oxygenation
- Reduced fraction of inspired oxygen (FiO2) reduces the pressure of alveolar oxygen. This reduces the pressure gradient between alveolar and capillary oxygen levels, reduce the rate of diffusion of oxygen into the blood.
2) V/Q mismatch
- A compromise to either ventilation or perfusion causes a V/Q mismatch, resulting in decreased oxygenation of blood. If carbon dioxide elimination is still adequate, this will cause T1RF
- Factor affecting ventilation include airway lumen size, airway obstruction, and alveolar surface area
- Factors affecting perfusion include restricted pulmonary blood flow or dysregulated hypoxaemic pulmonary vasoconstriction
3) Diffusion issue
- O2 has low solubility in water, but high affinity for Hb - Hb can draw dissolved oxygen out of the blood at low pressure - this maintains a low pressure of oxygen dissolved in the blood, maintaining an adequate pressure gradient between capillary and alveolar oxygen levels to allow for adequate diffusion
- Reduced ability of haemoglobin to take up oxygen will therefore reduce oxygenation
- Caused by carbon monoxide poisoning, low Hb levels in the blood, and deformed Hb structure
Type 2 - hypercapnic
- Cannot adequately oxygenate the blood but also cannot remove carbon dioxide efficiently
- High CO2 and low O2
- Caused by conditions that impair the ability of the lungs to ventilate adequately
- Accumulation of CO2 = decrease in blood pH, leading to respiratory acidosis
- Normal blood pH = 7.35 and 7.45
- In respiratory acidosis, decrease in pH can impair enzyme function and disrupt cellular processes, affecting the entire body.
** Bohr effect - haemoglobin’s ability to bind to and release oxygen is affected by the drop in pH, therefore, acidosis caused by T2RF can impair O2 delivery to tissues, exacerbating tissue hypoxia
Main causes of T2FR
Hypoventilation, airway obstruction, and CNS depression
- Hypoventilation: COPD, chest wall deformity, muscle fatigue, obesity, narcotic overdose etc.
- Airway obstruction: airway obstruction e.g. production excess mucus, inflammation, thickening of bronchial walls and bronchoconstriction seen in COPD and Asthma - prevent the lungs’ ability to effectively ventilate, causing air trapping and impaired gas exchange leading hypercapnia and respiratory acidosis
- CNS depression: Narcotic overdose, brain injuries, or conditions affecting the brainstem can also reduce the respiratory drive, leading to hypoventilation
Recognising respiratory failure
- Assessing respiratory obs to determine level of respiratory distress – RR, WOB, colour, auscultation, SpO2, ETCO2, conscious state, posturing
- ABG at hospital for markers including: Pa02, PaCO2, pH, bicarbonate, lactate, and carboxyhaemoglobin
Discuss the features and principles relating to administering oxygen therapies
Discuss the features, diagnosis, and out-of-hospital management of asthma
Asthma = reversible chronic inflammation disorder of the airway
Features
- Most commonly extrinsic (or allergic asthma) – meaning triggered by external allergens e.g., dust, pollen, smoke
- Characterised by airflow obstruction, broncho-hyperresponsiveness, inflammation
- Symptoms: SOB, wheeze, chest tightness, dry irritated cough
Pathophysiology
- CELLULAR PATHO
- IgE antibodies bind to mast cell to form mast cell-IgE complex -> this complex with recognise allergens and release histamine
- Normal lungs have more T-helper 1 cells (promote cell mediated immunity), in asthma -> upregulation of T-helper 2 cells in lungs – T-helper 2 cells promote inflammation through antibody production
- Allergen inhaled by asthmatic person => dendritic cells activated by allergen, dendritic cells release chemokines to activate T-helper 2 (Th2) and attract them to the bronchioles
- Th2 cells then release cytokines (interleukin 4 and 5)
- Th2 stimulate plasma cells to promote IgE production by plasma cells
- ^in IgE-mast cell binding
- Th2 also promotes eosinophil production in bone marrow, eosinophils damage lung endothelium
- Mast cell complex releases inflammatory mediators stimulating airway smooth muscle to constrict
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- Bronchospasm and increased mucous secretion cause airway obstruction
- Increased vascular permeability and release of immune cells occurs
- Over years, odema, scarring and fibrosis lead to thickening of the basement membrane – permanently reduces airway diameter
Treatment
- Depends on severity of asthma exacerbation
- Mild – salbutamol MDI 12 puffs
- Moderate – Salbutamol MDI 12 puffs and ipratropium MDI 8 puffs OR// nebulised salbutamol 5mg & ipratropium 500mcg => repeat salbutamol PRN, oral prednisolone if tolerated
- Severe – nebulised salbutamol 15mg & ipratropium 500mcg, repeat salbutamol PRN & ipratropium every 20 mins max 3 doses, oral prednisolone if tolerated
- Life-threatening - nebulised salbutamol continuous & ipratropium 500mcg, repeat ipratropium every 20 mins max 3 doses, IV saline 250mL aliquots up to 20mL/kg, consider IM adrenaline 500mcg (10mcg/kg) every 5 mins PRN – inline neb if IPPV required (BVM or SGA), slow ventilation rates, small tidal volume
Discuss the features, diagnosis, and out-of-hospital management of anaphylaxis
Anaphylaxis = a potentially severe and life-threatening systemic hypersensitivity reaction to an external trigger that can present with a rapid onset and life-threatening symptoms of airway swelling, circulatory compromise and altered conscious state or death.
Features
- Systemic allergic reaction to an external trigger
- Can be triggered by foods, medications, insect bites, etc.
- Risk factors: asthma, COPD, CVD, older age
- airway oedema, bronchoconstriction, SOB, GI symptoms (nausea, diarrhoea, cramping etc.), urticaria, hoarse throat, dyspnoea, cardiovascular symptoms (tachycardia, hypotension), syncope, altered conscious state or death
Pathophysiology
- Type 1 hypersensitivity reaction mediated by IgE antibodies that bind to and sensitise mast cells and basophils
- Mast cells and basophils degranulate – release mediators such as histamine, bradykinin, typtase
- Histamine and bradykinin cause systemic vasodilation and increase vascular permeability allowing fluid to shift from intravascular to interstitial compartment => oedema
- Tryptase causes local tissue damage
- Prostaglandin D2 as well as leukotrienes and platelet activating factor can all have bronchoconstrictor effects causing airway obstruction
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- Anaphylactic shock
- INITIAL – systemic vasodilation = v venous return = vCO ..body cells not well perfused -> anaerobic metabolism -> lactic acid production … vpH
- COMPENSATORY – SNS increases activity to compensate for v perfusion, acid-base compensatory mechanisms activate
- PROGRESSIVE – compensatory mechanisms begin to fail -> lactic acid build-up in blood => worsening metabolic acidosis
- REFRACTORY – cellular death and multiple organ damage => can be fatal
Treatment
- DRABCs
- IM adrenaline 500mcg (or 10mcg/kg) repeat every 5 mins PRN
- Remove allergen
- High flow O2
- Clinical support for paeds essential
- Bronchodilators for bronchospasm
- Nebulised adrenaline 5mg for upper airway oedema
- Permissive hypotension – IV saline for SBP<100 up to 20mg/kg
- (ICP) Adrenaline infusion may be considered for persistent hypotension
- Oral prednisolone 50mg if tolerated
- Notify
Discuss the features, diagnosis, and out-of-hospital management of acute cardiogenic pulmonary oedema
Discuss the features, diagnosis, and out-of-hospital management of chronic obstructive pulmonary disease
Discuss the features, diagnosis, and out-of-hospital management of sepsis
Sepsis is life-threatening organ dysfunction as a result of a dysregulated host response to an infection
Features
- Symptoms may differ depending on site of infection – e.g., urinary tract – increased frequency of urination, burning sensations, colour, smells etc. or respiratory – cough, sputum, runny nose etc.
- Signs may include hyperthermia/fever, hypothermia, tachycardia, and tachypnoea and more late stage symptoms may include altered mental state, hypoxia, cyanosis, oliguria or anuria, hypotension, delayed capillary refill, cold extremities
- At risk populations: Older people, neonates, pregnant women, and people with weakened immune systems, chronic illness etc.
Pathophysiology
- Organ dysfunction results from increased metabolic demand + insufficient circulation
- In a dysregulated immune response, one of the main features is the release of nitric oxide, a potent vasodilator => decreasing MAP, …HR^ to compensate -> eventually fails => end result is decreased MAP and thus decreased perfusion
- Insufficient perfusion = septic shock
- Nitric oxide can also reduce cardiomyocyte function
- Other features of sepsis include ^Vessel permeability, ^procoagulants and v in anticoagulants => DIC, v in RBC flexibility (so, even if an organ is perfused, O2 delivery can still be impaired)
- 50% bacterial, but also viral, fungal, parasitic possible
Diagnosis
- Hospital management involves measuring serum lactate levels that measure acidosis (>4mmol/L), a sign of severe sepsis
- SIRS criteria = temperature, HR, RR, WBC count
- Prehospitally, the qSOFA score is used as it is quick, and feasible for prehospital: involves altered mental state (GCS<15), tachypnoea (>/=22), hypotension (systolic BP<100) presence of 2 or more symptoms suggests a high likelihood of sepsis and risk of a poor outcome
- Septic shock = sepsis with profound hypotension, OR serum lactate >2mmol/L and requirement of vasopressors to maintain MAP>65
Out-of-hospital management
- Early recognition using qSOFA or SIRS
- Oxygenation - high flow O2 titrated to 94-98%
- Targeted fluid resus – rapid IV saline 250mL aliquots up to 20mL/kg – reassess - aim for MAP>65 or SBP>100, monitor for signs of fluid overload
- Vasopressors for septic shock
- Early wide spectrum antibiotics (for some ambulance services, otherwise early notification for hospital)
- Notify
- IV benzylpenicillin for suspected meningococcal septicaemia
Discuss the principles and practices relating to intravenous fluid therapy for the non-traumatic hypotensive patient
