Chapter 17: Function of the Heart Practice Flashcards

Pump Logic and the Fundamental Principles of Cardiac Function

• The Triple Goal of Cardiac Performance: The heart operates on a simple functional logic to maintain health: FILL, SQUEEZE, and DELIVER.

  • Fill: Occurs during Diastole when blood enters relaxed ventricles.

  • Squeeze: Occurs during Systole to create the pressure necessary to eject blood.

  • Deliver: Flow must reach the brain, kidneys, skin, and muscles to sustain life.

• The Dependency of Perfusion: Adequate perfusion is not guaranteed by a normal heart rate alone; it requires coordination of rate, rhythm, volume, pressure, and contractility.

• The Cardiac Cycle: Defined as one coordinated fill-and-eject sequence. It consists of three specific stages:

  1. Ventricular Filling: Relaxed ventricles receive blood, primarily through passive movement.

  2. Atrial Systole: Atrial contraction completes the final, variable portion of ventricular filling.

  3. Ventricular Systole: Ventricular contraction raises pressure to eject blood.

• Coordination vs. Simultaneity: Atrial and ventricular contractions are coordinated but are not simultaneous peak squeezes.

Mechanical Phases of Filling and Ejection

• Phase 1: Early Diastole (Passive Filling):

  • Both the atria and ventricles are relaxed.

  • Atrioventricular (AV) Valves: Open.

  • Semilunar Valves: Closed.

  • Pressure Dynamics: Atrial pressure exceeds ventricular pressure, causing blood to move through the open AV valves.

  • Significance: The ventricles receive the majority of their volume passively before atrial contraction occurs.

• Phase 2: Atrial Systole (The Atrial Kick):

  • Atrial contraction provides a final fill boost to the ventricles.

  • Atrial Fibrillation Impact: Disorganized atrial activity removes this coordinated kick. The severity of the effect depends on the heart rate and ventricular stiffness.

  • Variable Contribution: The atrial contribution is not a fixed $30\%$. It varies based on heart rate, age, rhythm, and ventricular compliance.

• Phase 3: Ventricular Systole (Ejection):

  • S1 (First Heart Sound): Occurs when ventricular pressure exceeds atrial pressure, causing the AV valves to close.

  • Isovolumetric Contraction: A brief period where all valves (AV and semilunar) are closed. Pressure rises rapidly while ventricular volume remains constant.

  • Semilunar Valve Opening: Occurs when ventricular pressure exceeds arterial (aortic or pulmonary) pressure, allowing blood ejection.

  • S2 (Second Heart Sound): Occurs at the end of systole when the aortic and pulmonary valves close.

  • Isovolumetric Relaxation: Follows S2; all valves are closed as pressure drops while volume remains constant.

Valve Logic and Structural Support

• Pressure Gradients: Valves operate based on pressure differences, not nerve impulses.

  • Valve Opens: When Upstream Pressure > Downstream Pressure.

  • Valve Closes: When Downstream Pressure > Upstream Pressure.

• Valve-Specific Features:

  • AV Valves: Supported by chordae tendineae and papillary muscles. These structures prevent valve prolapse during systole but do not pull the leaflets open.

  • Semilunar Valves: Aortic and pulmonary cusps lack chordae; their state is changed solely by pressure changes.

  • Pathology: Valve problems change the pressure pathway, thereby altering flow patterns.

Heart Rate, Cycle Length, and Coronary Perfusion

• Cycle Length Calculation: One cardiac cycle lasts $\frac{60}{HR}$ seconds.

  • At $70/min$, the cycle is approximately $0.86\text{ s}$.

  • At $150/min$, the cycle is only $0.40\text{ s}$.

• Limitations of Tachycardia: Extreme tachycardia can reduce output by shortening filling time.

  • Diastole Reduction: Diastole is the portion of the cycle that shrinks the most during high rates, reducing preload and stroke volume ($SV$).

  • Double Hit to the Heart: Increased heart rate raises oxygen demand, yet Left Ventricular ($LV$) coronary perfusion occurs mainly during diastole, which is shortened.

• The Useful Zone: A moderate increase in heart rate may raise Cardiac Output ($CO$), but an extreme increase typically lowers it.

Case Study 1: Unstable Tachycardia

• Cues: Patient presents with a regular narrow-complex rhythm at $168/min$, $BP 82/50$, chest pressure, cool skin, and new-onset confusion.

• Interpretation: The rapid rate is causing cardiopulmonary compromise, not just a high number on the monitor. Perfusion has failed.

• Immediate Actions:

  • Activate rapid response or ACLS protocols.

  • Support ABCs; initiate monitoring and IV access.

  • Obtain a 12-lead ECG if it does not delay definitive care.

  • Prepare for synchronized cardioversion per facility protocols.

  • Key Nursing Rule: Treat the clinical status of the unstable patient rather than the number on the monitor.

Autonomic Nervous System (ANS) Control

• Automaticity: The heart possesses a built-in spark; the SA node normally initiates impulses. The ANS modifies this performance but does not create the beats.

• Sympathetic Nervous System (The Accelerator):

  • Mediated by Norepinephrine and Epinephrine acting on Cardiac $\beta_1$ receptors.

  • Positive Chronotropy: Increases SA-node firing, raising heart rate ($HR$).

  • Positive Dromotropy: Speeds up AV-node conduction.

  • Positive Inotropy: Strengthens ventricular contraction (squeeze) at same loading conditions.

  • Positive Lusitropy: Speeds up ventricular relaxation to support filling at high rates.

  • Triggers: Pain, fever, hypovolemia, anxiety, and shock.

• Parasympathetic Nervous System (The Brake):

  • Mediated by the Vagus nerve releasing Acetylcholine (ACh) onto Muscarinic $M_2$ receptors.

  • Negative Chronotropy: Slows the SA-node firing rate.

  • Negative Dromotropy: Slows AV-node conduction (may lengthen the PR interval).

  • Limited Ventricular Effect: Vagal effects are strongest at the nodes (SA/AV) and atria; direct direct inotropic effects on the ventricles are limited.

  • Clinical Stimuli: Suctioning or straining can trigger bradycardia; in such cases, stop the stimulus and reassess perfusion.

Receptor Language and Cardiovascular Medications

• $\beta_1$ Activation: Increases $HR$, AV conduction, and contractility.

• $\beta_1$ Blockade (Beta-Blockers): Decreases $HR$, AV conduction, and contractility. Nursing checks include $HR$, $BP$, rhythm, and specific hold parameters.

• $M_2$ Activation: Decreases $HR$ and AV conduction.

• $M_2$ Blockade (Atropine): Blocks muscarinic effects to raise $HR$ and AV conduction in symptomatic bradycardia.

• Digoxin: Provides positive inotropy while slowing AV conduction. Requires monitoring of renal function, Potassium ($K$), Magnesium ($Mg$), rhythm, and toxicity signs.

• Safe Practice: A slow rate without evidence of poor perfusion is not necessarily an atropine emergency.

The Cardiac Output Equation and Calculations

• The Formula: $CO = HR \times SV$

  • $CO$ (Cardiac Output) is measured in $\text{mL/min}$ or $\text{L/min}$.

  • $HR$ (Heart Rate) is measured in $\text{beats/min}$.

  • $SV$ (Stroke Volume) is measured in $\text{mL/beat}$.

• Context of Output:

  • Normal resting $CO$ is often between $4\text{--}8\text{ L/min}$.

  • Cardiac Index: $CI = CO \div \text{Body Surface Area}$.

• Calculation Examples:

  • Example A: $72 \text{ bpm} \times 70 \text{ mL/beat} = 5,040 \text{ mL/min} \approx 5.0 \text{ L/min}$. (Adequate rate and stroke volume).

  • Example B: $120 \text{ bpm} \times 35 \text{ mL/beat} = 4,200 \text{ mL/min} = 4.2 \text{ L/min}$. (Faster rate, but total flow fell because $SV$ dropped lower than the rate could compensate for).

Stroke Volume Dynamics: Preload, Afterload, and Contractility

• Stroke Volume Components: $SV = EDV - ESV$

  • $EDV$ (End-Diastolic Volume): Volume at the end of filling (e.g., $120\text{ mL}$).

  • $ESV$ (End-Systolic Volume): Volume remaining after squeeze (e.g., $50\text{ mL}$).

  • Example: $120\text{ mL} - 50\text{ mL} = 70\text{ mL/beat}$.

• The Three Levers of SV:

  1. Preload (The Stretch): Ventricular stretch present at end-diastole. Increased preload usually raises $SV$.

     • Increases: Venous return, fluid retention, venoconstriction.

     • Decreases: Hemorrhage, dehydration, venodilation (e.g., Bleeding $\rightarrow$ Venous return $\downarrow \rightarrow$ Preload $\downarrow \rightarrow SV \downarrow \rightarrow CO \downarrow$).

  2. Afterload (The Resistance): The load the ventricle must overcome to eject blood.

     • Left Ventricle: Influenced by systemic pressure (SVR), arterial impedance, and aortic-valve obstruction.

     • Right Ventricle: Influenced by pulmonary vascular load and pulmonary pressure.

     • Effect: Increased afterload increases ventricular work and oxygen demand; usually lowers $SV$.

  3. Contractility (Inotropy): Intrinsic strength of the squeeze independent of preload.

     • Positive Inotropy: Stronger squeeze, higher $SV$. Risk: May increase dysrhythmia risk and oxygen demand.

     • Negative Inotropy: Weaker squeeze, lower $SV$.

• Frank-Starling Law: Matches cardiac output to venous return. Increased venous return causes increased stretch, usually resulting in increased contraction force.

  • The Ceiling: In a failing heart, the curve flattens. Extra filling increases pressure and edema (congestion) without gaining useful output.

Case Study 2: Postoperative Blood Loss

• Cues: Surgical drain shows $350\text{ mL}$ bright-red blood; $HR 118$, $BP 86/54$, cool skin, falling urine output, flat neck veins.

• Interpretation: Acute blood loss led to decreased venous return/preload, causing a drop in stroke volume and cardiac output.

• Actions:

  • Activate urgent help and notify the surgical team.

  • Assess ABCs and bleeding; trend vital signs and mental status.

  • Maintain or obtain IV access; prepare fluids or blood products as ordered.

  • Crucial Note: Do not dismiss compensatory tachycardia (high heart rate) as simple anxiety.

Ejection Fraction (EF) and Heart Failure Phenotypes

• Definition: Ejection Fraction is the percentage of $EDV$ ejected with each beat. It is a percentage, not a volume.

  • Formula: $EF = \frac{SV}{EDV} \times 100$

  • Example: $72\text{ mL} \div 120\text{ mL} \times 100 = 60\%$.

• Heart Failure Phenotypes:

  • HFrEF (Heart Failure with reduced EF): $EF \leq 40\%$.

  • HFmrEF (Heart Failure with mildly reduced EF): $EF\,41\text{--}49\%$\ plus evidence of increased filling pressures.

  • HFpEF (Heart Failure with preserved EF): $EF \geq 50\%$\ plus evidence of increased filling pressures.

• HFpEF Physiology: A stiff ventricle fills with less volume at higher pressure; it then ejects a normal percentage of that already small volume.

• Cardiac Reserve: The ability of the heart to increase output during activity. Patients may appear stable at rest but show low reserve (fatigue, dyspnea) during mild exertion like walking to the bathroom.

Pathophysiology of Heart Failure (HF)

• Definition: A syndrome of congestion (backup) and/or inadequate output (hypoperfusion). It is not cardiac arrest; the heart is still beating but inefficiently.

• Left-Sided Failure (Backup to Lungs):

  • Path: LV fails $\rightarrow$ Left atrial/pulmonary venous pressures rise $\rightarrow$ Fluid moves into lung tissue/alveoli.

  • Symptoms: Dyspnea, orthopnea, Paroxysmal Nocturnal Dyspnea (PND), crackles, cough.

  • Severe Signs: Pink frothy sputum indicating acute pulmonary edema.

• Right-Sided Failure (Backup to Systemic Veins):

  • Path: RV fails $\rightarrow$ Pressure rises in venae cavae $\rightarrow$ Fluid backs up into systemic circulation.

  • Symptoms: Elevated Jugular Venous Pressure (JVP/JVD), hepatomegaly, ascites, abdominal fullness, early satiety.

  • Edema: Dependent pitting edema (ankles if walking; sacrum if bedbound).

  • Contributors: Left HF, pulmonary hypertension, lung disease, RV infarction, tricuspid disease.

• Forward Flow Failure (Systemic Hypoperfusion):

  • Brain: Confusion, restlessness.

  • Kidneys: Falling urine output (oliguria).

  • Skin: Cool extremities, weak pulses, delayed capillary refill.

  • General: Fatigue, weakness, hypotension when advanced.

Case Study 3: Acute Pulmonary Edema

• Cues: $RR 34$, $SpO_2 82\%$, $BP 176/104$, diffuse crackles, pink frothy sputum.

• Interpretation: An airway-breathing emergency due to fluid backup in the lungs.

• Actions:

  • Activate rapid response; do not leave the patient.

  • Sit the patient upright if tolerated.

  • Provide oxygen for hypoxemia; prepare noninvasive ventilation.

  • Initiate monitoring and prepare IV diuretics or vasodilators.

  • Avoid: Do not lay the patient flat; do not give routine oxygen if the patient is not hypoxemic; do not force oral fluids.

Clinical Assessment Frameworks for Heart Failure

• The Wet/Dry, Warm/Cold Matrix:

  • Dry + Warm: No major congestion; adequate perfusion.

  • Dry + Cold: Hypoperfusion present without obvious congestion.

  • Wet + Warm: Congestion present but perfusion is preserved.

  • Wet + Cold: High-risk pattern; congestion plus hypoperfusion.

• Assessment Keys:

  • Warm: Alert, warm skin, adequate urine.

  • Cold: Altered mentation, cool skin, weak pulses, oliguria.

  • Trend Monitoring: Follow weight, I&O, breathing, edema/JVP, BP, rhythm, renal function (creatinine), and electrolytes ($K$, $Mg$) together.

  • Weight Warning: A common provider notification threshold is a gain of $2\text{--}3\text{ lb}$ in $24\text{ hours}$ or $5\text{ lb}$ in a week.

Compensatory Mechanisms and Chronic Management

• Short-Term Compensation (The Cost):

  • Sympathetic Response: Increases $HR$, contractility, and vasoconstriction. Helps pulse/pressure briefly but increases afterload and oxygen demand.

  • RAAS + ADH Response: Causes sodium/water retention and vasoconstriction. This raises preload and afterload.

  • Long-Term: Leads to remodeling, congestion, and pump stress.

• Four Disease-Modifying Pillars for Chronic HFrEF:

  1. ARNI (Angiotensin Receptor-Neprilysin Inhibitor) or ACEI/ARB.

  2. Beta-Blocker (Evidence-based for HFrEF).

  3. MRA (Mineralocorticoid Receptor Antagonist - Aldosterone blockade).

  4. SGLT2i (Sodium-Glucose Cotransporter-2 inhibitors for cardiorenal protection).

• Loop Diuretics: Essential for congestion relief but not considered one of the four disease-modifying pillars.

Case Study 4: Right-Sided / Biventricular Pattern

• Cues: Weight gain of $2.7 \text{ kg } (6 \text{ lb})$ in $4$ days, $3+$ ankle edema, JVD, abdominal fullness; lungs are mildly clear, $SpO_2 95\%$.

• Interpretation: Dominant systemic venous congestion. Clear lungs do not mitigate the severity of the JVD and weight gain.

• Actions: Assess vitals and perfusion; notify provider; administer prescribed diuretics; monitor urine, $BP$, $K$, $Mg$, and renal function.

• Urgent Escalation Cues: Severe dyspnea, hypoxemia, chest pain, syncope, confusion, or signs of shock.