Human Physiology Week 4 - Cardiovascular (Transcripts Pt. 2)

Cardiac Contractility

• Contractility refers to the strength of ventricular contractions and the force produced by cardiac myocytes.
• The sympathetic nervous system plays a significant role in modulating contractility, while the parasympathetic system primarily influences heart rate.
• Sympathetic activation increases heart rate and contractility by releasing norepinephrine, which interacts with beta adrenergic receptors in cardiac muscle.

Calcium Ions and Cardiac Function

• Calcium ions are crucial for cardiac muscle contraction and play a central role in contractility.
• Increased calcium influx into cardiac myocytes enhances contraction strength, improving cardiac performance.
• Drugs that mimic sympathetic activity enhance contractility (positive inotropic agents) while those that block beta adrenergic receptors diminish contractility (negative inotropic agents), such as beta blockers.

Influencing Cardiac Contractility

• Agents that affect calcium levels also modify contractility; calcium channel blockers reduce calcium entry, thus decreasing contractility.
• Contractility is influenced by systemic factors like preload and afterload, which dictate the volume of blood in the ventricles and the resistance against which the heart must pump.

Preload and Afterload

• Preload is the volume of blood filling the ventricles before contraction, directly affecting stroke volume due to the Frank-Starling mechanism.
• Afterload represents the resistance the ventricles must overcome to eject blood. Increased afterload requires greater contraction force to maintain cardiac output.
• Normal systolic pressure in the aorta is approximately 120 mmHg, while diastolic pressure averages 80 mmHg.

Frank-Starling Mechanism

• As the ventricles fill with more blood, there’s an optimal overlap of actin and myosin filaments, leading to increased force during contraction (greater end-diastolic volume enhances stroke volume).
• Excessive stretching or overlap, however, can diminish contractile force.

Pathophysiology of Afterload

• High diastolic blood pressure leads to increased afterload; the left ventricle must exert greater force to overcome elevated resistance.
• Conditions like pulmonary hypertension elevate right ventricular afterload, necessitating stronger contractions for proper blood flow.

Calcium Homeostasis and Cardiac Function

• Blood calcium levels impact both contractility and electrical rhythm of the heart; low calcium can weaken heart contractions, while elevated levels can cause arrhythmias and heightened contractility.
• Long-term dysregulation of calcium levels can stem from endocrine issues affecting parathyroid hormone or calcitonin.

Integrating Cardiac Physiology

• Understanding how heart rate and contractility converge helps clarify their roles in regulating cardiac output and, subsequently, blood pressure.
• Changes in heart function through pharmacological or pathological means can impact overall cardiovascular health and efficiency.### Cardiac Output and Blood Pressure
• Cardiac output is the volume of blood the heart pumps per minute and is crucial for maintaining systemic arterial blood pressure.
• Blood pressure is determined by the product of cardiac output and total peripheral resistance.
• Systemic blood pressure refers to blood flow from the left side of the heart through the aorta, distinct from pulmonary blood pressure.

Components of Cardiac Output

• Cardiac output is influenced by heart rate and stroke volume (CO = HR × SV).
• Stroke volume is the amount of blood pumped from the ventricle with each heartbeat.

Stroke Volume Factors

• Stroke volume is determined by:
  • End diastolic volume (EDV): The total volume of blood in the left ventricle at the end of diastole, before contraction.
  • End systolic volume (ESV): The volume remaining in the left ventricle after contraction.
• Stroke volume can be calculated as SV = EDV - ESV.
• The Frank-Starling mechanism states that increased EDV leads to stronger contractions due to better muscle stretching, enhancing stroke volume.

Cardiac Contractility Influences

• Cardiac contractility is affected by:
  • The degree of stretch in the ventricle (via EDV).
  • Calcium ion availability in the heart muscle.
• Afterload is the resistance the heart must overcome to eject blood into the aorta. Higher diastolic pressure in the arteries increases afterload.

Preload and Afterload

• Preload corresponds to the Frank-Starling mechanism, while afterload refers to the resistance faced during heart contractions.
• A high afterload reduces stroke volume, leaving a higher end systolic volume.

Heart Rate Regulation

• The SA node serves as the natural pacemaker, controlling heart rate through automatic depolarization and repolarization.
• Parasympathetic nervous system activation (via acetylcholine) slows the heart rate.
• Sympathetic nervous system activation (via norepinephrine and epinephrine) increases heart rate and enhances cardiac contractility.

Role of Nervous Systems

• The autonomic nervous system plays a pivotal role in managing heart rate:
  • The parasympathetic system slows the heart down.
  • The sympathetic system accelerates heart rate and strengthens heart contractions.

Interconnection of Factors

• Together, these factors—cardiac output, heart rate, stroke volume—control systemic arterial blood pressure.
• Understanding these relationships is essential for assessing cardiovascular health and conditions like hypertension.

Explore the essential concept of contractility in cardiac physiology, focusing on how the ventricles contract and produce force. This quiz will help you understand the mechanics of cardiac myocytes and their role in heart function.