Cardiopulmonary, Metabolic, Renal & Hepatic Physiology – Key Vocabulary

Cardiovascular Responses to Acute Aerobic Exercise

Cardiac Output, Heart Rate, Stroke Volume

  • Fundamental relationship: Q = HR \times SV
    • "Q" (cardiac output) represents the volume of blood pumped per minute.
    • HR (heart rate) and SV (stroke volume) are the principal determinants.
  • Exercise Effects
    • HR rises almost linearly with %VO₂max until approaching maximal levels.
    • Question posed in lecture: "What is the implication for HR excursion if SV plateaus at a higher % of VO₂max?"
      • If SV plateaus early, HR must do more of the work to elevate Q → larger HR excursion.
    • SV increases sharply at exercise onset, then plateaus (~40–60 % VO₂max in untrained; higher in trained).
  • Rating of Perceived Exertion (RPE)
    • Strong positive correlation with HR during sub-max and max work.
    • Practical use: RPE can estimate HR when direct measurement isn’t feasible.

Blood Pressure & Total Peripheral Resistance (TPR)

  • Core equation: MAP = Q \times TPR
  • Systolic BP (SBP)
    • Rises proportionally to workload (≈10 mm Hg per MET for healthy adults).
    • Mechanisms
    • ↑ Myocardial contractility.
    • ↑ SV → ↑ Q.
    • Muscles demand higher driving pressure to receive blood.
  • Diastolic BP (DBP)
    • Shows minimal change (±10 mm Hg) during dynamic exercise.
    • Mechanism: arteriolar vasodilation within active muscle allows more runoff from arterial tree.
  • TPR
    • Falls because vasodilation in active beds > vasoconstriction in non-active beds.
  • Dynamic vs. Static Exercise BP Profiles
    • Dynamic (cyclic) work → large ↑ SBP, little DBP change.
    • Static (isometric) work → SBP & DBP both rise substantially because muscle contraction compresses vessels, impeding flow.

Blood Flow Redistribution

  • Rest: ~15–20 % of Q to skeletal muscle.
  • Heavy exercise: 80–85 % to muscle.
  • Governing forces
    • Sympathetic nervous system (SNS) & circulating epinephrine (EPI) → systemic vasoconstriction.
    • Local metabolites (↑PCO2, ↓PO2, ↑[H⁺], adenosine, ↑[K⁺], nitric oxide) → functional sympatholysis → vasodilation in working muscle.
    • Result: Overall vasoconstriction maintains MAP while local dilation supplies muscle.
  • Capillary Recruitment
    • More open capillaries increase surface area for exchange, lower diffusion distance.
  • Question posed: "Why doesn’t MAP decrease during exercise?"
    • ↑ Q offsets ↓ TPR, maintaining or slightly elevating MAP.

Summary of Acute CV Responses

  • ↑ Q, HR, SV.
  • ↑ SNS activity & catecholamines (NE/EPI).
  • ↑ Venous return (muscle pump, respiratory pump).
  • Vasodilation in active tissue; vasoconstriction in inactive beds.
  • Goal: Match O₂ delivery to metabolic demand.

Chronic Cardiovascular Adaptations to Aerobic Training

Left-Ventricular (LV) Remodeling

  • Eccentric hypertrophy: ↑ sarcomere number/length → ↑ LV internal volume (preload).
  • Outcomes
    • ↑ SV at rest & sub-max → ↓ resting HR for same Q.
    • ↑ Max SV allows greater Qmax without change in HRmax.

Blood Volume Adaptations

  • ↑ Plasma Volume (PV) (≈10–20 % within weeks).
    • Drives ↑ SV via ↑ EDV (Frank-Starling).
    • Benefit for thermoregulation: larger PV supports sweating without compromising venous return.
  • ↑ Red Blood Cell mass via erythropoiesis → maintains/raises Hct despite hemodilution.

Vascular Adaptations

  • ↑ Capillary density in muscle → greater O₂ extraction.
  • ↑ Endothelial release of nitric oxide, K⁺, adenosine → better local control.
  • ↓ Afterload (arterial stiffness, systemic BP) → augments SV.

Pulmonary & Ventilatory Responses

Ventilation ((\dot V_E))

  • Increases linearly with work rate until reaching the Ventilatory Threshold (VT) at ~50–75 % VO₂max.
    • Post-VT → exponential rise.
    • On-set/Off-set kinetics mirror Q.
  • Ventilatory Breakpoint
    • Disproportionate ↑ \dot V_E relative to VO₂ due to metabolic acidosis (↑[H⁺], ↑CO₂) → chemoreceptor stimulation.
    • VT ≈ Anaerobic Threshold but measured non-invasively.

Factors Elevating Ventilation at VT

  • ↑ Blood [CO₂], [H⁺], [K⁺].
  • ↑ Blood temperature & catecholamines.
  • ↑ Central motor command/motor-unit recruitment.

(a-v)O₂ Difference

  • Widens with intensity because muscles extract more O₂ (↑ mitochondrial O₂ use, ↑ capillary density).

Metabolic Foundations

Respiratory Exchange Ratio (RER)

  • Definition: RER = \frac{VCO2}{VO2} (steady-state requirement).
  • Interpretations
    • RER \approx 0.70 → predominately fat oxidation.
    • RER \approx 1.00 → predominately CHO oxidation.
    • RER = 0.85 → ~50 % fat / 50 % CHO.
    • RER > 1.00 → hyperventilation & bicarbonate buffering; indicates near-max effort.

Fuel Stores (≈80 kg adult male)

  • Carbohydrates ≈ 2,012 kcal (liver glycogen 400, muscle glycogen 1,600, blood glucose 12).
  • Fat ≈ 110,740 kcal (subcutaneous, intramuscular, plasma).

Energy Systems & ATP Resynthesis

  • ATP-PCr (phosphagen) – immediate, cytosolic.
  • Glycolytic (anaerobic) – cytosolic, 1–2 min dominant, produces lactate.
  • Oxidative – mitochondrial, sustained energy.

Lactate (Ventilatory) Threshold (LT/VT)

  • Exercise intensity at which blood [lactate] or \dot V_E rises non-linearly.
  • Relevance
    • Athletic: predicts endurance race pace; training (tempo, intervals) aims to shift LT rightward.
    • Clinical: deconditioned patients reach LT at low workloads → early fatigue; PT can use graded activity to elevate LT.

Nutrients

  • Six classes: CHO, fat, protein, vitamins, minerals, water.
  • Roles: energy (CHO/fat), structure (protein, Ca, P), regulation (vit/min/protein).
  • Energy yields: CHO & protein = 4 kcal g⁻¹, fat = 9 kcal g⁻¹.

Ancillary Pathways

  • Glycogenolysis, Glycogenesis, Gluconeogenesis, Lipolysis, Lipogenesis, Proteolysis.

Renal Physiology & Pathophysiology

Nephron Anatomy

  • ~1 million per kidney; functional unit.
  • Components
    • Renal corpuscle = glomerulus + Bowman’s capsule (filtration).
    • Tubule segments: PCT, loop of Henle (descending/ascending), DCT, collecting ducts.
  • Blood flow path: Aorta → renal artery → segmental → interlobar → arcuate → cortical radiate → afferent arteriole → glomerulus → efferent arteriole → peritubular/vasa recta → venous return.

Kidney Functions (Regulation Theme)

  • Fluid & electrolyte balance, acid–base balance.
  • BP regulation (renin–angiotensin–aldosterone, volume control).
  • Erythropoietin & thrombopoietin production.
  • Bone metabolism (vitamin D activation, Ca²⁺/PO₄³⁻ handling).
  • Excretion of wastes, toxins, drugs.

Urine Formation Processes

  • Filtration in glomerulus.
  • Secretion in tubules/collecting ducts.
  • Reabsorption along nephron.
  • Overall: \text{Excretion} = \text{Filtration} + \text{Secretion} - \text{Reabsorption}.

Cardio-Renal Interrelation

  • Chronic HTN → 2nd leading cause of CKD.
  • CKD → volume overload, anemia, and ↑ cardiovascular morbidity.

Kidney Failure

  • Acute Renal Failure (ARF): sudden, reversible if treated; causes – ischemia, toxins, obstruction.
  • Chronic Renal Failure (CRF): progressive → End-Stage Renal Disease (ESRD); causes – diabetes, HTN, lupus, obstruction.
  • Uremia: toxic accumulation of nitrogenous waste → anorexia, nausea, cognitive changes; dialysis/transplant required.

Abdominal Quadrants & Visceral Anatomy

RUQ

  • Liver (right lobe), gallbladder, portions of colon & small intestine, right kidney.

RLQ

  • Appendix, lower ascending colon, small intestine, right ureter/ovary/spermatic cord.

LUQ

  • Stomach, spleen, pancreas, liver (left lobe), left kidney, transverse/descending colon.

LLQ

  • Descending colon, small intestine, left ureter/ovary/spermatic cord.

Hepatic Physiology & Disease

Liver Overview

  • ~2.5 % body mass, only organ that regenerates.
  • Dual supply: 25–30 % hepatic artery, 70–75 % portal vein.
  • 70–80 % cells = hepatocytes.

Multifunctional Roles

  • Drug detoxification (penicillin, erythromycin, sulfonamides, etc.).
  • Hormone metabolism (thyroxin, aldosterone, estrogen, cortisol, insulin, glucagon, GH, GI hormones).
  • Energy metabolism
    • Glycogen storage & breakdown (glycogenolysis).
    • Gluconeogenesis, ketogenesis.
    • Triglyceride storage.
  • Protein synthesis (albumin, clotting factors) & micronutrient handling.
  • Immune contribution (Kupffer cells).

Pancreas Functions

  • Endocrine (≈5 %)
    • Insulin → ↑ glucose uptake.
    • Glucagon → glycogenolysis ↑ blood glucose.
    • Somatostatin → inhibits both insulin & glucagon.
  • Exocrine (≈95 %)
    • Digestive enzymes: trypsin family (proteins), amylase (CHO), lipase (fats), nucleases (DNA/RNA).
    • Bicarbonate secretions neutralize chyme.

Referred Pain Patterns

  • Esophagus ↔ mid-thoracic spine.
  • Liver/diaphragm/pericardium ↔ shoulder.
  • Stomach, gallbladder, pancreas, small intestine ↔ mid-back, scapular region.
  • Colon, appendix, pelvic viscera ↔ low back, pelvis, sacrum.
  • Spleen ↔ left shoulder (Kehr’s sign) & left Abd; can impair breathing.

Hepatitis

  • HAV
    • Fecal–oral, food/water; acute only; vaccine available.
  • HBV
    • Blood & body fluid transmission; vaccine available; can co-infect with HDV (worse prognosis).
  • Prevention strategies: hygiene, PPE, needle protocols, immunization.

Cirrhosis

  • Irreversible fibrosis from chronic hepatitis, alcohol, etc.
  • Signs/Sx
    • Jaundice, peripheral edema, hepatosplenomegaly, ascites.
    • Dupuytren’s contracture (4th/5th digit), palmar erythema (↑ estradiol), spider angiomas.

Clinical & Practical Connections

  • PTs must monitor SBP responses (drop or excessive rise = termination criteria).
  • RPE & talk/sing tests provide low-tech intensity gauges: easy to sing → below LT; can’t talk → above LT.
  • Chronic deconditioning lowers LT & VT → patients fatigue with ADLs; progressive aerobic training shifts thresholds right.
  • Knowledge of referred pain critical for differential diagnosis (e.g., shoulder pain of hepatic origin).