Cardiovascular System – Comprehensive Study Notes (Chapter 42)

Structure of the Heart

• Four chambers: right heart and left heart

• Each side has an atrium (upper) and a ventricle (lower)

• Auricles (ear-like extensions of the atria)

• Septum divides the heart into right and left sides

Blood Flow Into and Out of the Heart

• Right half:

  • Receives deoxygenated blood from the body via veins

  • Directs blood to the lungs via the pulmonary artery

• Left half:

  • Receives oxygenated blood from the lungs via the pulmonary veins

  • Directs blood to the aorta for systemic circulation

• Aorta delivers blood into systemic circulation via arteries

• Circulatory system contains about ~60,000 miles of interconnecting blood vessels

Blood Flow Into and Out of the Heart (Pathway Summary)

• Superior and inferior vena cava deliver deoxygenated blood to the right atrium

• Right atrium → Tricuspid valve → Right ventricle

• Right ventricle → Pulmonary valve → Pulmonary arteries → Lungs

• Lungs → Pulmonary veins → Left atrium

• Left atrium → Mitral valve → Left ventricle

• Left ventricle → Aortic valve → Aorta → Systemic circulation

Cardiac Cycle

• Two main phases:

  • Diastole: period of relaxation; blood returns to the heart

  • Systole: contraction; blood is ejected from the heart

• Synchronous (simultaneous) contraction of cardiac muscle

• Starling’s law of the heart relates to how the heart contracts based on stretch of the myocardium

Starling’s Law of the Heart (Concept)

• The heart’s contractile force increases with increased ventricular filling (preload) up to a limit

• The further the heart is stretched during filling, the stronger the subsequent contraction, until a point where it no longer responds

• Practical implication: stroke volume increases with increased end-diastolic volume (up to the physiological limit)

Conducting System of the Heart

• Key components in order of impulse travel:

  • SA node (sinoatrial, pacemaker)

  • Atrial muscle and atrial bundles

  • AV node (atrioventricular)

  • Bundle of His (atrioventricular bundle)

  • Right and left bundle branches

  • Purkinje fibers

• Diagram components (for reference): SA node → AV node → Bundle of His → Bundle branches → Purkinje fibers

Cardiac Conduction #1

• SA node contains pacemaker cells

• Atrial bundles conduct impulses through atrial muscle

• AV node slows the impulse to coordinate atrial and ventricular contraction

• Bundle of His conducts impulse into the ventricles

• Includes: Bundle branches and Purkinje fibers

Cardiac Conduction #2 (Automaticity and Action Potentials)

• Automaticity: cardiac cells can generate action potentials without external stimulation

• Action potential: phases are labeled 0–4

  • Phase 0: rapid depolarization

  • Phase 1: initial repolarization

  • Phase 2: plateau phase

  • Phase 3: repolarization

  • Phase 4: resting (diastolic) potential for most cells; pacing cells have gradual diastolic depolarization

• In pacemaker cells (e.g., SA node), the resting potential is not stable like ventricular myocytes

Action Potentials (Example Comparisons)

• SA node action potential timeline and ventricular muscle cell action potential timeline differ in shape and phase durations

• Key concept: phases reflect ion channel activity (mainly Ca2+ and K+ dynamics) that govern depolarization and repolarization

Cardiac Conduction #3 (Conductivity)

• The heart’s specialized cells conduct impulses rapidly to synchronize ventricular and atrial contraction

• Conduction velocity:

  • Slowest in the AV node

  • Fastest in the Purkinje fibers

Cardiac Conduction #4 (Autonomic Influences)

• Autonomic nervous system (ANS) modulates heart rate, rhythm, and contractility

• Sympathetic nervous system (SNS) effects:

  • Increases heart rate

  • Speeds conduction through the AV node

  • Increases strength of ventricular contraction

Cardiac Conduction #5 (Myocardial Contraction)

• When cardiac muscle is stimulated, Ca2+ enters via membrane channels and calcium storage sites

• Ca2+ helps regulate troponin activity

• Troponin allows actin-myosin cross-bridge cycling; cross-bridges form and break rapidly

• Result: coordinated contraction and pumping action of the heart

Sarcomere: The Functioning Unit of Cardiac Muscle

• Ca2+ ions regulate the interaction of actin and myosin within the sarcomere

• Structure components include: actin filaments, myosin filaments, Ca2+ channels, Z bands, troponin

• Contraction occurs as actin and myosin slide past each other within the sarcomere

Question #1

• What does Starling’s law of the heart address?

  • Options:

  • Automatic properties of the heart

  • Conductive properties of the heart

  • Contractile properties of the heart

  • Pressure properties of the heart

• Answer: C. Contractile properties of the heart

• Rationale: Starling’s law describes how increasing stretch of the cardiac muscle (preload) enhances contractile force up to a limit, affecting the contractile force and stroke volume

Electrocardiography (ECG)

• Definition: Process of recording electrical impulses as they move through the heart; diagnostic tool for cardiac patients

• ECG machine translates electrical impulses into waveforms (electrocardiogram)

• Purpose: measure electrical activity of the heart

Normal ECG Waveform

• Five main waves: P, QRS, T (and related segments/intervals)

  • P wave: atrial depolarization (originates in SA node/pacemaker)

  • QRS complex: ventricular depolarization (Q wave = bundle of His depolarization; R and S waves = ventricular depolarization)

  • T wave: ventricular repolarization

• Approximate normal intervals:

  • PR (P–R) interval: ext{PR} \, \approx \, 0.16\,\text{s}

  • QT interval: \text{QT} \, \approx \, 0.30\,\text{s}

  • QRS interval: \text{QRS} \, \approx \, 0.08\,\text{s}

  • P wave duration: \text{P duration} \, \approx \, 0.08\,\text{s}

• Time scales on ECG:

  • Each vertical square represents 0.1\,\text{mV} of electrical charge

  • Each horizontal square represents 0.04\,\text{s} of time

• Note: Atrial repolarization occurs during the QRS complex and is typically obscured

Normal Electrocardiogram (ECG) Details

• P wave: atrial depolarization

• PR (PR) interval: conduction delay through AV node

• QRS complex: ventricular depolarization

• QT interval: depolarization and repolarization of ventricles

• ST segment: interval between ventricular depolarization and repolarization

• The QRS complex and T wave define ventricular electrical events

Critical Points of the ECG

• P–R interval reflects: normal delay of conduction at the AV node and the electrical progression from atria to ventricles

• Q–T interval reflects: timing of ventricular depolarization and repolarization

• S–T segment reflects: information about ventricular repolarization

Arrhythmias

• Factors that can change heart rate and rhythm:

  • Drugs

  • Acidosis

  • Hypoxia (low oxygen)

  • Electrolyte imbalances

  • Buildup of waste products

• Arrhythmias arise from changes in automaticity or conductivity

• Significance: disturbances can disrupt cardiac output

Types of Arrhythmias

• Sinus arrhythmias

• Supraventricular arrhythmias:

  • Premature atrial contractions (PACs)

  • Paroxysmal atrial tachycardia (PAT)

  • Atrial flutter

  • Atrial fibrillation

• Atrioventricular (AV) block

• Ventricular arrhythmias

Question #2

• Statement: When reading an ECG, a nurse knows that the P–R interval reflects the normal delay of conduction at the AV node.

• Answer: True

• Rationale: The P–R interval spans from atrial activity to the start of ventricular activity, encompassing AV node delay and the atrial-to-ventricular conduction

Courses of Circulation of the Blood

• Two main circuits:

  • Pulmonary circulation (heart–lung): right heart sends blood to the lungs; CO2 and wastes removed; O2 picked up by red blood cells

  • Systemic circulation: left heart sends oxygenated blood to all body cells

Blood Flow Through the Systemic and Pulmonary Vasculature Circuits

• Vessel characteristics:

  • Veins: distensible, thin walls

  • Pulmonary vessels: distensible, thin walls

  • Arteries: elastic, thick walls

• Diagram concept: PULMONARY CIRCULATION vs SYSTEMIC CIRCULATION

Pulmonary Circulation Details

• Deoxygenated blood flows into the right atrium from the superior/inferior venae cavae and great cardiac vein

• Right atrial pressure rises, pushing blood into the right ventricle when the pressure in the right atrium exceeds that in the right ventricle

• The right ventricle contracts; pressure opens pulmonic valve; blood to pulmonary artery toward the lungs

• In the lungs: blood exchanges gases (O2 loading, CO2 unloading) in alveolar capillaries

• Oxygenated blood returns to the left atrium via the pulmonary veins

Systemic Circulation Details

• When pressure in the left atrium exceeds that in the left ventricle, oxygenated blood flows into the left ventricle

• The left ventricle contracts; blood is pumped into the aorta and distributed to the body

• The resistance system responds to body needs; blood flows from arterioles to capillaries; exchange of oxygen, nutrients, and fluids with tissues occurs at the capillary level

Fluid Shift Within the Capillaries (Capillary Exchange)

• Arterial end and venous end capillary dynamics involve hydrostatic pressure (HP) and oncotic pressure (OP)

• Driving forces:

  • Hydrostatic pressure (HP) tends to push fluid out of capillaries

  • Oncotic pressure (OP) due to plasma proteins tends to pull fluid into capillaries

• Filtration pressure example (arterial end): ext{Filtration pressure} = HP - OP \rightarrow \text{typically positive (fluid leaves capillary)}

• Net force on fluid (from slide):

  • Arterial end: HP > OP (fluid leaves capillary)

  • Venous end: HP < OP (fluid reabsorbed into capillary)

Coronary Circulation

• The heart muscle requires a constant oxygen supply

• Coronary arteries receive blood predominantly during diastole

• Pulse pressure denotes the filling pressure of the coronary arteries

• Oxygenated blood reaches every cardiac muscle fiber

• The coronary circulation pattern is called end-artery circulation

Main Forces Determining the Heart’s Oxygen Consumption

• Heart rate: more pumping increases oxygen demand

• Preload: amount of blood returned to the heart; higher preload increases work needed

• Afterload: systemic vascular resistance; higher afterload increases contraction effort

• Contractility: increased influx of Ca2+ enhances contractile strength

Coronary Arteries and Veins (Anatomy Overview)

• Notable vessels include: right coronary artery, left coronary artery and branches (e.g., circumflex, anterior descending), coronary sinus, and cardiac veins

• Blood flow pathways through the coronary vessels are influenced by the heart’s activity and pressure conditions

Systemic Arterial Pressure

• Measurement reflects pumping pressure of the ventricle and generalized pressure in the circulation

• Clinical states:

  • Hypotension

  • Hypertension

• Humoral control mechanisms of blood pressure include natriuretic peptides

Renin-Angiotensin-Aldosterone System (RAAS)

• Trigger: reduced renal blood flow or decreased oxygenation can stimulate renin release

• Sequence of events:

  • Renin released from juxtaglomerular (JG) cells of the nephron

  • Renin converts angiotensinogen (liver-derived) to Angiotensin I

  • Angiotensin-converting enzyme (ACE) converts Angiotensin I to Angiotensin II

  • Angiotensin II acts via angiotensin receptors to cause vasoconstriction and stimulate aldosterone release from the adrenal gland

  • Aldosterone promotes Na+/H2O retention (increased blood volume), raising blood pressure

  • Angiotensin III and other peptides influence hypothalamic osmoreceptors and ADH release, further affecting fluid balance

• Effects of RAAS activation: increased血 pressure, increased blood volume, improved renal perfusion

Venous Pressure and Heart Failure

• Blood in the veins can rise above normal pressure, causing backup or congestion behind the heart

• Heart failure situations:

  • If the heart cannot effectively pump blood through the system, congestion occurs

  • Left-sided failure → pulmonary edema

  • Right-sided failure → peripheral, abdominal, and liver edema

Question #3

• Premature atrial contraction signifies a change in focus in which of the following?

  • Automaticity

  • SA node

  • AV node

  • Contractility

• Answer: B. SA node

• Rationale: PACs reflect ectopic pacemaker activity shifting from the SA node to another atrial site, generating impulses out of the normal rhythm

Summary of Key Formulas and Values

• Filtration pressure concept:

  • Filtration pressure = HP - OP

  • At arterial end: HP > OP → fluid filtration out of capillary

  • At venous end: HP < OP → fluid reabsorption into capillary

• ECG interval references (normal):

  • PR ext{ interval} \approx 0.16\text{ s}

  • QT ext{ interval} \approx 0.30\text{ s}

  • QRS ext{ interval} \approx 0.08\text{ s}

• Waveform interpretation:

  • P wave: atrial depolarization

  • QRS complex: ventricular depolarization

  • T wave: ventricular repolarization

• Angiotensin II–mediated effects include vasoconstriction and aldosterone-mediated fluid retention, increasing blood pressure

• End-artery circulation: pattern where the myocardium receives blood from end arteries without significant collateral supply

Connections to Foundational Principles and Real-World Relevance

• Oxygen delivery and waste removal depend on effective cardiac pumping and intact conduction pathways

• Heart rate, preload, afterload, and contractility are core determinants of myocardial oxygen demand and supply balance

• ECG is a cornerstone diagnostic tool for assessing rhythm, conduction delays, and potential ischemia

• RAAS regulation links renal function, fluid balance, and systemic blood pressure, with wide clinical implications for hypertension and heart failure

• Understanding the pulmonary vs systemic circulations clarifies how oxygenation status and systemic perfusion are maintained

Ethical, Philosophical, and Practical Implications

• Accurate interpretation of ECGs and hemodynamic measures is critical for patient safety; misinterpretation can lead to misdiagnosis or delayed therapy

• RAAS-targeted therapies (e.g., ACE inhibitors, ARBs, aldosterone antagonists) have broad implications for cardiovascular and renal health

• Knowledge of preload/afterload and contractility informs decisions about fluid management and inotropic support in critical care

• End-artery vulnerability highlights the importance of coronary perfusion timing (diastole) and protection against ischemia