HEART PHYSIOLOGY
Complete Nursing Notes + High-Yield Concepts + Clinical MCQs
NORCET 12 Preparation
Nursing Officer Exams
25 MCQs
30-Minute Test
Understand the cardiac cycle, cardiac output, conduction system, ECG and heart sounds.
Learning objectives
- Explain the physiology of the cardiac cycle and circulation.
- Understand cardiac output, stroke volume and heart rate.
- Describe the cardiac conduction system and ECG waves.
- Differentiate systole, diastole, preload, afterload and contractility.
- Apply cardiac physiology to nursing exam scenarios.
📚 Table of Contents — Click to Jump
- Introduction to Heart Physiology
- Pulmonary and Systemic Circulation
- Cardiac Conduction System
- Cardiac Cycle
- Cardiac Output and Stroke Volume
- Heart Sounds
- ECG Physiology
- Blood Pressure and Hemodynamics
- Regulation of Heart Function
- Coronary Circulation and Oxygen Demand
- Clinical Applications and Nursing Points
- High-Yield Revision Table
- 25 MCQs — 30-Minute Test
1. Introduction to Heart Physiology
Heart physiology is the study of how the heart generates electrical impulses, contracts, pumps blood, maintains circulation and adjusts its activity according to the body's oxygen requirements.
The heart functions as a muscular pump with two coordinated sides:
- Right side: receives systemic venous blood and pumps it toward the lungs.
- Left side: receives oxygenated blood from the lungs and pumps it into systemic circulation.
Important physiological terms
| Term | Meaning | Exam point |
|---|---|---|
| Heart rate (HR) | Number of heartbeats per minute | Typical adult resting range: 60–100/min |
| Stroke volume (SV) | Blood ejected by one ventricle per beat | Often approximately 70 mL in a resting adult |
| Cardiac output (CO) | Blood pumped by one ventricle per minute | HR × SV |
| Preload | Ventricular filling/stretch before contraction | Related to end-diastolic volume |
| Afterload | Resistance/pressure the ventricle must overcome to eject blood | Increased arterial pressure can increase LV afterload |
| Contractility | Intrinsic strength of myocardial contraction at a given preload | Sympathetic stimulation usually increases it |
| Ejection fraction (EF) | Percentage of end-diastolic ventricular blood volume ejected per beat | Normal adult LV EF is commonly about 55–70% |
| Automaticity | Ability of cardiac cells to generate impulses spontaneously | SA node normally sets the rhythm |
| Conductivity | Ability to transmit electrical impulses | AV node delays conduction physiologically |
| Excitability | Ability to respond to a stimulus | Important for impulse generation and propagation |
NORCET pearl: The heart is both an electrical pump and a mechanical pump. Electrical activation normally precedes mechanical contraction.
2. Pulmonary and Systemic Circulation
A. Pulmonary circulation
Blood flows from the right ventricle through the pulmonary arteries to the lungs. Gas exchange adds oxygen and removes carbon dioxide. Oxygenated blood returns to the left atrium through the pulmonary veins.
B. Systemic circulation
Blood leaves the left ventricle through the aorta, supplies the body tissues, and returns through systemic veins to the right atrium.
Diagram 1: Simplified blood-flow pathway
Blue represents the venous/deoxygenated pathway; red represents the oxygenated pathway. The actual circulation is continuous.
BODY → VENA CAVAE → RIGHT ATRIUM → TRICUSPID VALVE → RIGHT VENTRICLE → PULMONARY VALVE → PULMONARY ARTERIES → LUNGS → PULMONARY VEINS → LEFT ATRIUM → MITRAL VALVE → LEFT VENTRICLE → AORTIC VALVE → AORTA → BODY
Mnemonic: Right = Respiratory; Left = Life to the body.
- Right ventricle pumps blood to the lungs.
- Left ventricle pumps blood to the systemic circulation.
- Pulmonary arteries carry deoxygenated blood.
- Pulmonary veins carry oxygenated blood.
3. Cardiac Conduction System
The conduction system generates and transmits electrical impulses that coordinate atrial and ventricular contractions.
Diagram 2: Electrical conduction pathway
Electrical impulses normally originate at the SA node, pass through the atria, pause at the AV node, and travel through the His–Purkinje system.
| Structure | Function | Important fact |
|---|---|---|
| Sinoatrial (SA) node | Normally initiates each heartbeat | Primary pacemaker; located in the right atrium near the SVC opening |
| Atrial conduction pathways | Spread impulses across the atria | Promote coordinated atrial depolarization |
| Atrioventricular (AV) node | Slows conduction before ventricular activation | Allows time for ventricular filling |
| Bundle of His | Carries impulses from the AV node into the ventricular conduction system | Passes into the interventricular septum |
| Right and left bundle branches | Conduct impulses toward the ventricles | Travel along the interventricular septum |
| Purkinje fibers | Rapidly distribute impulses through ventricular myocardium | Support coordinated ventricular contraction |
Typical intrinsic pacemaker rates:
- SA node: approximately 60–100 impulses/min.
- AV junction: approximately 40–60/min.
- Ventricular escape pacemakers: approximately 20–40/min.
Mnemonic: S-A-H-B-P
SA node → Atria → His bundle → Bundle branches → Purkinje fibers.
Remember: the AV node introduces the physiological delay between atrial and ventricular activation.
SA node → Atria → His bundle → Bundle branches → Purkinje fibers.
Remember: the AV node introduces the physiological delay between atrial and ventricular activation.
Autonomic control of heart rate
| Sympathetic stimulation | Parasympathetic stimulation |
|---|---|
| Increases heart rate | Decreases heart rate |
| Increases AV conduction | Slows AV nodal conduction |
| Increases myocardial contractility | Effects on ventricular contractility are relatively limited under normal conditions |
| Predominantly mediated by beta-1 receptors in the heart | Vagus nerve; predominantly muscarinic M2 receptors |
4. Cardiac Cycle
The cardiac cycle is the sequence of electrical and mechanical events occurring during one heartbeat. At a heart rate of 75/min, one cycle lasts approximately 0.8 seconds.
Cardiac cycle duration = 60 ÷ Heart rate
Example: at 75 beats/min, 60 ÷ 75 = 0.8 seconds per beat.
Diagram 3: Simplified phases of the cardiac cycle
Phases of the cardiac cycle
| Phase | What happens? | Valve status |
|---|---|---|
| 1. Atrial systole | Atria contract and complete ventricular filling | AV valves open; semilunar valves closed |
| 2. Isovolumetric ventricular contraction | Ventricular pressure rises; volume remains constant | All four valves closed |
| 3. Ventricular ejection | Ventricular pressure exceeds aortic/pulmonary arterial pressure; blood is ejected | Semilunar valves open; AV valves closed |
| 4. Isovolumetric relaxation | Ventricles relax; pressure falls without a volume change | All four valves closed briefly |
| 5. Ventricular filling | Ventricular pressure falls below atrial pressure; blood enters ventricles | AV valves open; semilunar valves closed |
High-yield concepts
- During isovolumetric contraction, ventricular pressure rises but ventricular volume does not change.
- During ventricular ejection, semilunar valves are open.
- During isovolumetric relaxation, all four valves are closed.
- Most ventricular filling occurs passively during early diastole at a normal resting heart rate.
- Atrial contraction contributes the final portion of ventricular filling and becomes more important in some patients with impaired ventricular relaxation.
End-diastolic and end-systolic volumes
- End-diastolic volume (EDV): blood present in a ventricle at the end of filling, just before contraction.
- End-systolic volume (ESV): blood remaining in a ventricle after ejection.
- Stroke volume: EDV minus ESV.
SV = EDV − ESV
Example: EDV = 120 mL and ESV = 50 mL. Stroke volume = 70 mL.
5. Cardiac Output and Stroke Volume
Cardiac output is the volume of blood pumped by one ventricle per minute. It depends mainly on heart rate and stroke volume.
CARDIAC OUTPUT = HEART RATE × STROKE VOLUME
Example:
HR = 75 beats/min; SV = 70 mL/beat.
CO = 75 × 70 = 5250 mL/min = 5.25 L/min.
Factors affecting stroke volume
| Factor | Effect | Example |
|---|---|---|
| Preload | Increasing preload generally increases SV within physiological limits | Increased venous return |
| Contractility | Increased contractility generally increases SV and reduces ESV | Sympathetic stimulation |
| Afterload | Increased afterload can reduce SV if other factors remain unchanged | Markedly increased arterial pressure |
Frank–Starling law
Within physiological limits, greater ventricular filling stretches myocardial fibers and generally produces a stronger contraction, increasing stroke volume.
Clinical caution: The Frank–Starling relationship has limits. In significant heart failure, additional fluid may cause congestion without a useful increase in cardiac output.
Ejection fraction
Ejection fraction is the percentage of end-diastolic ventricular volume ejected during a heartbeat.
EF (%) = (Stroke volume ÷ EDV) × 100
Example: SV = 70 mL; EDV = 120 mL.
EF = (70 ÷ 120) × 100 = approximately 58%.
A typical normal left ventricular ejection fraction is approximately 55–70%, depending on the laboratory and measurement method.
Remember CO–SV–EF:
- CO = HR × SV
- SV = EDV − ESV
- EF = SV ÷ EDV × 100
6. Heart Sounds
Normal heart sounds are mainly produced by vibrations associated with valve closure and the resulting movement of blood and cardiac structures.
| Heart sound | Cause | Timing |
|---|---|---|
| S1 — “Lub” | Closure of mitral and tricuspid valves | Beginning of ventricular systole |
| S2 — “Dub” | Closure of aortic and pulmonary valves | Beginning of ventricular diastole |
| S3 | Associated with rapid ventricular filling | Early diastole; may be normal in children, young adults and pregnancy, but can indicate volume overload or heart failure in other adults |
| S4 | Atrial contraction against a stiff, less compliant ventricle | Late diastole; generally abnormal in adults and absent in atrial fibrillation |
Mnemonic: “M-T = 1; A-P = 2”
- S1: Mitral + Tricuspid close.
- S2: Aortic + Pulmonary close.
Important distinction: S1 is associated with the onset of ventricular systole; S2 is associated with the onset of ventricular diastole. Heart sounds are not caused simply by blood striking the valves.
7. ECG Physiology
An electrocardiogram (ECG) records electrical potential differences generated by cardiac depolarization and repolarization. It does not directly measure the mechanical force of contraction.
Diagram 4: Basic ECG waveform
| ECG component | Physiological meaning |
|---|---|
| P wave | Atrial depolarization |
| PR interval | From onset of atrial depolarization to onset of ventricular depolarization; includes AV nodal conduction time |
| QRS complex | Ventricular depolarization |
| ST segment | Period when the ventricles are largely depolarized; normally near the baseline in many leads |
| T wave | Ventricular repolarization |
| QT interval | Overall duration of ventricular depolarization and repolarization; varies with heart rate |
Exam pearl: Atrial repolarization usually cannot be identified separately because it is obscured by the QRS complex.
Electrical versus mechanical events
- Electrical depolarization normally occurs before the associated mechanical contraction.
- The P wave represents atrial depolarization; atrial contraction follows.
- The QRS complex represents ventricular depolarization; ventricular contraction follows.
- The T wave represents ventricular repolarization.
8. Blood Pressure and Hemodynamics
Blood flow through the cardiovascular system is influenced by pressure differences, resistance, blood viscosity and vessel diameter.
Mean Arterial Pressure (MAP) ≈ DBP + ⅓ (SBP − DBP)
This approximation is most useful at a usual resting heart rate; the relationship changes as heart rate and the duration of systole change.
Example: BP = 120/80 mmHg.
MAP ≈ 80 + ⅓(40) = approximately 93 mmHg.
Important concepts
- Systolic blood pressure: peak arterial pressure during ventricular systole.
- Diastolic blood pressure: lowest arterial pressure during ventricular diastole.
- Pulse pressure: systolic BP minus diastolic BP.
- Systemic vascular resistance (SVR): resistance to blood flow through systemic circulation.
- Venous return: blood returning to the heart through the veins.
Pulse Pressure = SBP − DBP
For BP 120/80 mmHg, pulse pressure = 40 mmHg.
Hemodynamic relationship: MAP is approximately related to cardiac output multiplied by systemic vascular resistance, with central venous pressure contributing to the full pressure-gradient equation.
Factors that can increase venous return
- Skeletal muscle pump during movement.
- Respiratory pressure changes during breathing.
- Venoconstriction mediated by sympathetic activity.
- Appropriate circulating blood volume and venous tone.
9. Regulation of Heart Function
A. Autonomic nervous system
- Sympathetic stimulation generally increases heart rate, AV conduction and contractility.
- Parasympathetic stimulation through the vagus nerve slows SA node firing and AV nodal conduction.
B. Baroreceptor reflex
Baroreceptors in the carotid sinus and aortic arch sense stretch associated with changes in arterial pressure.
- When arterial pressure rises, baroreceptor firing generally increases, reducing sympathetic output and increasing parasympathetic influence.
- When arterial pressure falls, baroreceptor firing generally decreases, increasing sympathetic activity to support heart rate, contractility and vascular tone.
C. Hormonal and chemical influences
| Factor | General effect |
|---|---|
| Adrenaline/noradrenaline | Increase heart rate and contractility through sympathetic mechanisms |
| Thyroid hormones | Increase metabolic demand and can increase heart rate and cardiac responsiveness |
| Increased potassium (hyperkalemia) | Can impair cardiac electrical conduction and cause dangerous arrhythmias |
| Reduced oxygen supply to myocardium | Can impair myocardial function and provoke ischemia |
| Acidosis | Can impair contractility and electrical stability, particularly when severe |
Nursing priority: Severe hyperkalemia can cause life-threatening ECG changes and dysrhythmias. Follow emergency protocols, obtain urgent clinical assessment and institute prescribed treatment without delay.
10. Coronary Circulation and Myocardial Oxygen Demand
The myocardium requires a continuous supply of oxygen and nutrients. Coronary arteries arise from the aortic root and supply the heart muscle.
Major coronary arteries
- Left coronary artery: commonly divides into the left anterior descending (LAD) and circumflex arteries.
- LAD: supplies much of the anterior left ventricular wall and anterior interventricular septum.
- Circumflex artery: supplies portions of the left atrium and lateral/posterior regions of the left ventricle, depending on coronary anatomy.
- Right coronary artery (RCA): commonly supplies much of the right atrium and right ventricle and may supply the inferior left ventricular wall.
- Coronary sinus: drains most venous blood from the myocardium into the right atrium.
Important: Coronary dominance and the exact distribution of coronary arteries vary between individuals. Do not assume every patient has identical coronary anatomy.
Why is left ventricular coronary perfusion important during diastole?
During ventricular systole, contraction of the left ventricular myocardium compresses intramyocardial vessels, particularly in the subendocardium. Much of left coronary perfusion therefore occurs during diastole.
Tachycardia shortens diastole and can reduce the time available for coronary perfusion while increasing myocardial oxygen demand.
Factors increasing myocardial oxygen demand
- Increased heart rate.
- Increased contractility.
- Increased ventricular wall stress, often related to pressure or volume load.
Clinical link: Myocardial ischemia occurs when oxygen supply is inadequate for myocardial oxygen demand. Coronary artery disease is a major cause of reduced myocardial oxygen supply.
11. Clinical Applications and Nursing Points
A. Tachycardia and cardiac output
A higher heart rate can increase cardiac output initially, but very rapid rates shorten ventricular filling time and may reduce stroke volume. The net effect depends on the rhythm, rate and patient's cardiac function.
B. Bradycardia and perfusion
A slow heart rate does not always indicate disease. However, bradycardia accompanied by hypotension, altered mental status, chest discomfort, syncope or signs of shock requires urgent assessment.
C. Reduced preload
Severe blood loss or dehydration can reduce venous return and ventricular filling, lowering stroke volume and potentially cardiac output.
D. Increased afterload
Markedly increased systemic arterial pressure increases the pressure the left ventricle must overcome to eject blood. Over time, sustained pressure overload may contribute to ventricular hypertrophy.
E. Heart failure
Heart failure is a clinical syndrome in which structural or functional cardiac abnormalities cause impaired filling, impaired ejection, or both. Patients may develop breathlessness, fatigue, fluid retention and reduced exercise tolerance.
F. Nursing assessment
- Assess pulse rate, rhythm, blood pressure, oxygen saturation and level of consciousness.
- Ask about chest pain, breathlessness, dizziness, palpitations and syncope.
- Assess peripheral perfusion, skin temperature, capillary refill and urine output in the appropriate clinical context.
- Review ECG findings and prescribed investigations.
- Escalate promptly for chest pain suggestive of acute coronary syndrome, hemodynamic instability, severe dyspnea or a dangerous dysrhythmia.
Emergency reminder: A patient with suspected acute coronary syndrome or unstable dysrhythmia needs immediate clinical assessment and management according to institutional emergency protocols. Do not delay escalation while attempting to interpret a single physiological measurement.
12. High-Yield Revision Table
| Question | Answer |
|---|---|
| Primary pacemaker of the heart? | SA node |
| Typical adult resting heart rate? | 60–100 beats/min |
| Which node delays conduction? | AV node |
| Which ECG wave represents atrial depolarization? | P wave |
| Which ECG component represents ventricular depolarization? | QRS complex |
| Which ECG wave represents ventricular repolarization? | T wave |
| S1 is caused by closure of which valves? | Mitral and tricuspid |
| S2 is caused by closure of which valves? | Aortic and pulmonary |
| Formula for cardiac output? | HR × SV |
| Formula for stroke volume? | EDV − ESV |
| Formula for ejection fraction? | SV ÷ EDV × 100 |
| Which side pumps blood to the lungs? | Right ventricle |
| Which side pumps blood into systemic circulation? | Left ventricle |
| Which arteries supply the myocardium? | Coronary arteries |
| What does the AV nodal delay help accomplish? | Allows time for ventricular filling after atrial activation |
| What happens during isovolumetric contraction? | Ventricular pressure rises while volume remains constant |
| What happens during isovolumetric relaxation? | Ventricular pressure falls while volume remains constant |
| Which phase generally provides most LV coronary perfusion? | Diastole |
| What is pulse pressure? | SBP − DBP |
| What is preload related to? | Ventricular filling and myocardial stretch before contraction |
Final 1-minute memory tricks
- SA → AV → His → Bundle branches → Purkinje: normal electrical pathway.
- S1 = Mitral + Tricuspid; S2 = Aortic + Pulmonary.
- P = atrial depolarization; QRS = ventricular depolarization; T = ventricular repolarization.
- CO = HR × SV; SV = EDV − ESV.
- Preload = filling; Afterload = resistance to ejection; Contractility = strength.
- Right ventricle → lungs; Left ventricle → body.
13. NORCET 12 Practice Test — Heart Physiology
📝 Heart Physiology MCQ Test
25 Questions | 30 Minutes | One Question at a Time
Includes clinical scenarios, concepts, ECG and priority-based questions.
Instructions
- Select one best answer for each question.
- Use Previous and Next to navigate.
- Submit to see your score, correct answers and explanations.
- Unanswered questions are counted as incorrect.
- The timer submits the test automatically when it reaches zero.
Educational practice test. Questions are original practice questions, not claimed to be official previous-year questions.
Time Left: 30:00
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