Pulmonary, Cardiovascular, and Neurological Lecture Notes Flashcards

Pulmonary Gas Exchange and Respiratory Physiology

• Ventilation (V)

  • Defined as the flow of gases into and out of the alveoli of the lungs.

  • Pleural Space Dynamics: The pleural space maintains a negative pressure of $-4\,mmHg$, which allows the lungs to remain inflated.

  • Requirements: Ventilation requires an open airway and a pressure difference to facilitate air movement.

  • Pressure-Volume Relationship:

    • Inhalation: Increase in volume leads to a decrease in internal pressure, causing the lungs to expand.

    • Exhalation: Decrease in volume leads to an increase in pressure, causing the lungs to recoil or relax to their original shape.

  • Autonomic Influence:

    • Parasympathetic Nervous System (PSNS): Stimulates bronchoconstriction and increases secretions.

    • Sympathetic Nervous System (SNS): Stimulates bronchodilation and decreases secretions, while constricting blood vessels.

  • Pulmonary Surfactant: Reduces surface tension at the air-water interface in the alveoli. This prevents alveolar collapse at the end of expiration and reduces the overall work associated with breathing (Work of Breathing - WOB).

  • Ventilation Deviations:

    • Hypoventilation: Leads to respiratory acidosis.

    • Hyperventilation: Leads to respiratory alkalosis.

• Perfusion (Q)

  • Defined as the flow of blood within the pulmonary circulation (capillaries and vasculature).

  • V/Q Matching: Optimal gas exchange requires appropriate contact between ventilated alveoli and the pulmonary circulation.

• Diffusion

  • The transfer of gases across the alveolar-capillary membrane.

  • Hypoxia-Induced Vasoconstriction (HPV): A mechanism where pulmonary vessels constrict in response to low oxygen levels to optimize and increase oxygen exchange.

Efficiency and Work of Breathing (WOB)

• Work of Breathing (WOB): Depends on the effort needed to move air through airways and the ease of lung expansion.

• Lung Compliance: The ability of the lung to stretch.

• Lung Recoil: The ability of the lung to relax.

• Restrictive Lung Disease (Stiff/Noncompliant Lungs)

  • Examples: Pneumothorax, atelectasis, pulmonary fibrosis, pneumonia.

  • Mechanics: Increased recoil and decreased compliance ($\uparrow$ recoil, $\downarrow$ compliance).

  • Presentation: Low tidal volume ($V_T$ - shallow breaths) and increased respiratory rate ($\uparrow RR$) to meet oxygen demands.

  • Lung Volumes: Decreased Total Lung Capacity ($TLC$) and decreased residual volume.

• Obstructive Lung Disease (Compliant Lungs)

  • Examples: Asthma, COPD (often presenting with a barrel chest).

  • Mechanics: Increased compliance and decreased recoil ($\uparrow$ compliance, $\downarrow$ recoil). The lung can expand, but air movement through the airway requires more effort.

  • Presentation: High tidal volume ($V_T$ - deep breaths) and decreased respiratory rate ($\downarrow RR$) to achieve adequate ventilation.

  • Lung Volumes: Increased Total Lung Capacity ($TLC$) and increased residual volume due to air trapping.

Alterations in Ventilation and Perfusion (V/Q)

• A: Normal ($V/Q = 1:1$): A specific amount of blood passing an alveolus is matched with an equal amount of gas.

• B: Shunt (Low V/Q Ratio)

  • Status: Low ventilation with normal perfusion (Low V:Normal Q).

  • Definition: Perfusion exceeds ventilation. Blood passes alveoli without gas exchange occurring due to distal airway obstruction.

  • Causes: Pneumonia (PNA), atelectasis, tumors, COPD, or secretions.

• C: Dead Space (High V/Q Ratio)

  • Status: Normal ventilation with low perfusion (Normal V:Low Q).

  • Definition: Ventilation exceeds perfusion. Alveoli lack adequate blood supply for gas exchange.

  • Causes: Pulmonary emboli, infarction, or cardiogenic shock.

• D: Silent (Absence of Both)

  • Status: Absence or limited ventilation and perfusion.

  • Causes: Pneumothorax or Acute Respiratory Distress Syndrome (ARDS).

Oxyhemoglobin Dissociation Curve

• In the Lungs: Oxygen leaves the alveoli and binds to hemoglobin (Hgb). This leads to increased oxygen saturation ($SaO_2$) and increased affinity (Hgb "holds on" tightly to oxygen).

• In the Tissues: Oxygen leaves Hgb to enter the cells. This results in decreased $SaO_2$ and decreased affinity (Hgb puts down its "guard" to release oxygen).

• Affinity Factors: The affinity of Hgb for $O_2$ must change to meet the metabolic needs of the tissues.

• Decreased Affinity (Right Shift)

  • States: High $PCO_2$, high temperature, acidosis (Low pH), high altitude, COPD, heart failure, severe anemia, exercise, hypoxia, and high $2,3-DPG$.

  • Consequence: Oxygen is released more easily to the tissues. Hgb is "willing" to give up $O_2$, which may reduce $SaO_2$ but ensures vital organs receive oxygen.

Hypoxia, Hypoxemia, and Hypercapnia

• Hypoxia (Tissue level lack of oxygen):

  • Hypoxic: Poor diffusion at the alveoli (e.g., airway obstruction, COPD, high altitude).

  • Anemic: Inadequate Red Blood Cells (RBCs) to transport oxygen.

  • Circulatory: Poor perfusion and blood flow (e.g., low Cardiac Output, hypovolemia).

  • Histotoxic: Toxic substances (e.g., cyanide) preventing tissue oxygen utilization.

• Hypoxemia:

  • Defined as abnormally low arterial oxygen levels (PaO_2 < 60\,mmHg).

  • Clinical Presentation (Mild/SNS Compensation): Increased Heart Rate ($HR$), peripheral vasoconstriction to conserve oxygen for vital organs, sweating, and a slight increase in Blood Pressure ($BP$). Slight confusion may occur due to low cerebral oxygen.

  • Clinical Presentation (Severe): Significant neurological deficits including agitation, impaired judgment, and significant confusion.

• Chronic Hypoxemia Compensation:

  • Increased Ventilation: Increased $RR$ and $HR$.

  • Pulmonary Vasoconstriction: Alveolar hypoxia triggers local vasoconstriction, increasing pulmonary arterial pressure to improve V/Q matching.

  • Right Heart Workload: Pumping against increased afterload/pulmonary vascular resistance leads to Cor Pulmonale.

  • Polycythemia: Kidneys release erythropoietin to increase RBC production and oxygen-carrying capacity.

• Hypercapnia:

  • Defined as abnormally high arterial carbon dioxide levels (PaCO_2 > 50\,mmHg).

  • Mechanisms: Increased $CO_2$ production or impaired alveolar diffusion. Often co-occurs with hypoxemia.

  • Consequences: Respiratory acidosis, which causes peripheral and cerebral vasodilation.

  • Symptoms: Warm, flushed skin, lethargy, increased Intracranial Pressure ($ICP$), poor muscle contraction, and potential coma.

Hypoventilation and Hyperventilation

• Hypoventilation

  • Mechanics: Insufficient air delivery to alveoli to meet oxygen needs and $CO_2$ removal ($\downarrow RR, \downarrow V_T$).

  • Causes: Respiratory drive depression (opioids, brain injury, anesthesia), respiratory muscle diseases (Myasthenia Gravis, Guillain-Barre, spinal cord injury), or thoracic cage issues (scoliosis, obesity).

  • Manifestations: Hypercapnic/Hypoxemic Respiratory Failure.

  • Signs: Initially rapid/shallow breathing; late signs include cyanosis, nasal flaring, and chest retractions. Reversed with $O_2$ therapy.

• Hyperventilation

  • Mechanics: Excess air entering alveoli leading to hypocapnia (PaCO_2 < 35\,mmHg) via $\uparrow RR$ and $\uparrow V_T$.

  • Causes: Pain, fever, anxiety, high altitude, and Cheyne-Stokes breathing in increased $ICP$.

  • Manifestations: Light-headedness, dizziness, and syncope due to cerebral vasoconstriction (local response to low $CO_2$).

Acute Respiratory Distress Syndrome (ARDS)

• Definition: Inflammatory lung injury or diffuse alveolar-capillary injury.

• Characteristics: Severe dyspnea of rapid onset, significant hypoxemia, and pulmonary infiltrates.

• Refractory Hypoxemia: The hypoxemia does not respond to supplemental oxygen.

• Etiology: Major trauma, sepsis, pneumonia, aspiration (near drowning, gastric contents), burns, smoke, or heroin/methadone overdose.

• Acute Lung Injury (ALI): A less severe form where severity is measured by the response to oxygen.

Common Pulmonary Disorders

• Aspiration

  • Passage of fluids or solids into the lungs; most frequent in the Right Lower Lobe.

  • Presentation: Sudden onset choking and intractable cough.

  • Interventions: Oxygen, fluid restriction (to minimize pulmonary edema), steroids within the first $72$ hours, and potentially antibiotics.

• Pneumothorax

  • Air enters the pleural cavity, restricting lung expansion and causing atelectasis.

  • Spontaneous: Rupture of an air-filled blister.

  • Traumatic: Chest injury or rib fracture.

  • Tension: Life-threatening "one-way valve" where air enters during inhalation but cannot leave during exhalation; can cause cardiac tamponade.

  • Open: Air enters during inhalation and leaves during exhalation.

• Atelectasis (Lung Collapse)

  • Compression: External pressure (e.g., rib fracture/pneumothorax).

  • Obstructive: Blocked/damaged alveoli or hypoventilation (COPD).

  • Adhesive: Decreased or inactivated surfactant (common in premature infants prior to $26$ weeks).

  • Post-Surgical Care: Deep breathing (Incentive Spirometer), frequent position changes, and early ambulation to prevent V/Q shunting from viscous secretions.

• Asthma

  • Chronic inflammatory disorder of bronchial mucosa with reversible airflow obstruction.

  • Intrinsic: Stress, cold/dry air, exercise, infections.

  • Extrinsic: Allergic triggers (dust, pollen, mold, dander).

• COPD (Chronic Bronchitis + Emphysema)

  • Characterized by airflow limitation that is not fully reversible.

  • Chronic Bronchitis ("Blue Bloater"): Cyanosis and edema due to Right Heart Failure. Defined by a productive cough for > 3 months in $2$ consecutive years. Changes include mucosal hypertrophy and hyperplasia of goblet cells.

  • Emphysema ("Pink Puffer"): Destructive changes of alveolar walls and enlargement of distal air sacs via elastin breakdown. Causes air trapping ($\uparrow$ CO2) and barrel chest.

  • Risk Factors: Smoking, pollutants, and genetic $\alpha 1$-antitrypsin deficiency.

Pulmonary Vascular Conditions

• Pulmonary Hypertension

  • Mean pulmonary artery pressure > 25\,mmHg at rest (Normal is $15 - 18\,mmHg$).

  • Causes: Idiopathic (Primary) or secondary to hypoxia-induced vasoconstriction, increased blood viscosity (Polycythemia), or Left Heart Failure.

• Cor Pulmonale

  • Right ventricular enlargement in response to chronic pulmonary hypertension.

  • Signs: Peripheral edema, Jugular Vein Distention (JVD), and decreased cardiac output with exercise.

• Pulmonary Embolus (PE)

  • Blockage of pulmonary vasculature, $90\%$ resulting from DVT.

  • Virchow Triad: Venous stasis, hypercoagulability, and endothelial injury.

  • Signs: Sudden pleuritic pain, dyspnea, tachycardia, and unexplained anxiety.

Infectious Respiratory Diseases

• Pneumonia

  • Typical: Bacterial (e.g., Streptococcus pneumoniae), infection inside alveoli. Common in smokers due to impaired mucociliary blanket.

  • Atypical: Viral or Mycoplasma pneumoniae, infection in the interstitial space causing alveolar septum thickening.

• Tuberculosis (TB)

  • Caused by Mycobacterium tuberculosis (waxy cell wall).

  • Primary: Initial exposure.

  • Latent: Asymptomatic, not contagious, organisms are walled off.

  • Secondary: Reactivation of dormant disease.

  • Diagnosis: PPD skin test, sputum culture, chest radiographs, and blood tests. Requires Airborne Droplet Precautions.

Cardiovascular and Vascular Pathology

• Atherosclerosis Progression: Damaged endothelium $\rightarrow$ Inflammatory response $\rightarrow$ Macrophages engulf LDL (Foam Cells) $\rightarrow$ Fatty Streak $\rightarrow$ Fibrous Plaque (narrowed lumen) $\rightarrow$ Complicated Lesion (ulceration and coagulation cascade).

• Peripheral Artery Disease (PAD)

  • Systemic atherosclerosis distal to the aortic arch.

  • Signs: Intermittent claudication, dependent rubor (pallor when elevated), diminished pulses, and atrophic skin.

  • Diagnosis: Ankle-Brachial Index (ABI < 0.9).

• Acute Arterial Occlusion: Seven "Ps"—Pistol shot (onset), Pallor, Poikilothermia (cold), Pulselessness, Pain, Paresthesia, Paralysis.

• Chronic Venous Insufficiency (CVI)

  • Results from valvular incompetence or DVT. Causes venous hypertension and circulatory stasis.

  • Signs: Edema, brown skin pigmentation (hemosiderin deposits), and stasis ulcers (usually at the medial malleolus).

• Deep Venous Thrombosis (DVT): Unilateral clot formation. Prevention includes mobilization, anticoagulants (heparin, warfarin), and pneumatic devices.

• Acute Hypertension

  • Hypertensive Crisis: SBP > 180\,mmHg or DBP > 120\,mmHg.

  • Urgency: No target-organ damage.

  • Emergency: Target-organ damage (e.g., encephalopathy, renal failure, cardiac ischemia).

Pathophysiology of Shock

• General Signs: Hypotension, tachycardia, increased respiratory rate, and oliguria.

• Stages:

  • Initial: SNS activation (Increased HR, RR, cortisol, epinephrine) and RAAS activation to maintain BP.

  • Progressive: Shift to anaerobic metabolism (Metabolic Acidosis/Lactic Acid excess). Reduced perfusion to GI (sepsis risk), Pancreas ($\uparrow$ glucose), and Kidneys (oliguria/failure).

  • Irreversible: Failure of circulation to brain/heart; failure of $Na^{+}/K^{+}-ATPase$ pump leading to cellular edema, death, and hyperkalemia.

• Categories:

  • Cardiogenic: Heart failure to pump (SBP < 90\,mmHg, elevated preload/afterload).

  • Hypovolemic: Depletion of blood/fluid volume.

  • Distributive:

    • Neurogenic: Loss of SNS tone; specifically characterized by bradycardia and dry, warm skin.

    • Anaphylactic: IgE-mediated histamine release causing massive vasodilation and bronchospasm.

    • Septic: Systemic inflammatory response to infection; characterized by warm/flushed skin and hyperglycemia.

  • Obstructive: Mechanical obstruction (e.g., cardiac tamponade, PE, tension pneumothorax).

Coronary Heart Disease (CHD)

• Chronic Conditions:

  • CAD: Slow development of atherosclerotic plaques; collateral circulation may develop.

  • Stable Angina: Predictable pain with exertion, relieved by rest.

  • Ischemic Cardiomyopathy: Heart pumping ineffectively due to chronic ischemia and scarring.

• Acute Coronary Syndromes (ACS):

  • Unstable Angina: Incomplete obstruction, unpredictable, negative biomarkers.

  • MI (NSTEMI): T-wave inversion or ST depression; positive biomarkers (Troponin is most specific).

  • MI (STEMI): Transmural injury across all 3 heart layers; ST elevation ("tombstones"); positive biomarkers.

• Angina Equivalents: Dyspnea, nausea/vomiting, back/jaw pain, and fatigue (more common in women).

• Prinzmetal (Variant) Angina: Result of vasospasm, occurs during rest (often between midnight and $8\text{ AM}$).

Heart Failure (HF) and Valve Defects

• Valve Defects:

  • Stenosis: Valve fails to open fully; creates resistance to flow.

  • Regurgitation: Valve fails to close fully; blood leaks backward.

• Ejection Fraction (EF):

  • $EF = \frac{SV}{EDV} \times 100$

  • Systolic Dysfunction (HFrEF): Weak heart muscle, baggy heart; reduced $EF$ ($40\%$ example).

  • Diastolic Dysfunction (HFpEF): Stiff muscle/LV hypertrophy; small filling space; preserved $EF$ ($66\%$ example).

• Failure Modes:

  • Left-Sided: Backs up to lungs (pulmonary edema, orthopnea, cough with frothy sputum). Causes decreased cardiac output/RAAS activation.

  • Right-Sided: Backs up to body (JVD, peripheral edema, liver congestion/ascites, GI distress). Often caused by left-sided failure or lung disease.

Pain, Neurological, and Neuromuscular Disorders

• Pain Pathways: Nociceptors (receptors); C-fibers and A-delta fibers; Spinothalamic tract (Neospinothalamic and Paleospinothalamic).

• Pain Types:

  • Nociceptive: Somatic (skin, bone) or Visceral (internal organs).

  • Neuropathic: Nerve dysfunction (e.g., Diabetic neuropathy, Shingles).

  • Central: CNS damage (e.g., stroke).

  • Referred: Convergent nerves (e.g., MI pain in left arm).

  • Phantom: Post-amputation perception.

• Myasthenia Gravis (MG): Autoimmune attack on Acetylcholine receptors. Symptoms ($Diplopia, Ptosis$) worsen with activity, improve with rest. Myasthenia Crisis involves compromised ventilation.

• Multiple Sclerosis (MS): Myelin sheath degeneration in CNS. Types include Relapsing-Remitting and Primary Progressive. Often involves vision and motor deficits.

• Parkinson Disease (PD): Loss of dopamine neurons in Substantia Nigra. Cardinal signs: Resting tremor, Cogwheel rigidity, Bradykinesia. Presentation: Masked face, shuffling gait.

• Spinal Cord Injury (SCI):

  • Spinal Shock: Immediate loss of all reflex activity below injury.

  • Neurogenic Shock: Occurs in injuries above $T6$ (Bradycardia and Hypotension).

  • Autonomic Dysreflexia: Life-threatening exaggerated SNS response; severe hypertension (up to $300\,mmHg$) and bradycardia ($30 - 40\,bpm$).

• Stroke:

  • Hemorrhagic: Burst vessel (high BP or aneurysm).

  • Ischemic: Thrombotic or Embolic blockage. Ischemic Penumbra is the salvageable region around the infarct. tPA must be given within $4.5$ hours of onset.

  • TIA: Symptoms resolve within $24$ hours.

• Increased Intracranial Pressure (ICP):

  • Cushing Triad (Late sign): Irregular respirations, Bradycardia, Systolic Hypertension.

  • Pupillary Reflex: Doll's Head Eyes (+ve indicates intact brainstem; -ve indicates dysfunction).

  • Posturing: Decorticate (flexor - cortex) vs. Decerebrate (extensor - brainstem; worse prognosis).

• Traumatic Hematomas:

  • Epidural: Arterial bleed; Unconscious $\rightarrow$ Lucid interval $\rightarrow$ Rapid decline.

  • Subdural: Venous bleed; gradual development (Acute, Subacute, or Chronic in elderly/alcohol users).

• Seizures: Generalized (Tonic-clonic/Absence) vs. Partial (Focal). Status involves increased ATP ($250\%$) and oxygen ($60\%$) demand.

• Dementia/Alzheimer's ($AD$): Progressive failure of cerebral functions. AD involves acetylcholine decrease, neurofibrillary tangles, and amyloid plaques (Neuritic plaques).