More of an audutory learner? Click the link to listen to a podcast on  this summary, material covered on midterm exam 2:

https://notebooklm.google.com/notebook/3b157349-9d3e-4c1e-8a11-5add2c4f5b9b/audio

I've taken the liberty of making flashcards from this summary :

https://quizlet.com/ca/965178446/boysen-lectures-flash-cards/

Cardiac cycle, Electrical conduction, ECG's

Podcast for this lecture: https://notebooklm.google.com/notebook/8276ea4b-a3f2-4a90-a6e7-ba6f9a168d6c/audio

1. Cardiac Cycle

The cardiac cycle refers to the sequence of events that occurs from the beginning of one heartbeat to the next. It consists of two main phases:

• Systole: Ventricular contraction where blood is ejected from the heart.

• Diastole: Ventricular relaxation, allowing the chambers to fill with blood.

• Pause b/w systole and diastols (if present)

The heart valves, including the atrioventricular (AV) valves (mitral and tricuspid) and semilunar valves (aortic and pulmonary), open and close in response to pressure changes. The cardiac cycle is divided into six phases:

1. Atrial Contraction: Adds 20% of blood volume to ventricles. You can life w/o contraction of atria.

2. Isovolumetric Ventricular Contraction: beginnign of contraction, AV valves close, ventricular pressure increases but no blood is ejected. 

3. Rapid Ventricular Ejection: Semilunar valves open, and blood flows out of the ventricles.

4. Isovolumetric Ventricular Relaxation: Semilunar valves close, and ventricular pressure decreases.

5. Rapid Ventricular Filling: AV valves open, and blood rapidly fills the ventricles.

6. Reduced Ventricular Filling: Ventricular filling slows as they approach capacity.

Clinical Relevance: Damage to the chordae tendinea, such as rupture, can result in acute heart failure, particularly in the left side, causing blood to flow back into the atrium and leading to pulmonary edema (shortness of breath, coughing). Turbulent backflow into atrium can be heard on oscillation. 

2. Electrical Conduction System of the Heart

The heart has a specialized conduction system that ensures coordinated contraction. This system includes:

• Sinoatrial (SA) Node: The natural pacemaker, located in the right atrium, initiating each heartbeat.

• Atrioventricular (AV) Node: Slows down the electrical signal to allow time for ventricular filling. Electrical barrier keeping atrial and ventricular contraction seperate - allowing ventricles to fill. Think of it like a toll booth on the highway!

• Bundle of His and Purkinje Fibers: These rapidly conduct the signal through the ventricles, ensuring coordinated contraction and ejection of blood.

Cardiac Cells:

Have long refractory periods, each electrical impulse from SA node should only trigger one muscle contraction. 

• Contractile Cells: Majority of the heart muscle responsible for generating force (cells of atria/ventricles). Have self-automaticity but it's slower, especially as you move towards ventricles. 

• Conducting Cells: Specialized cells like the SA node, AV node, bundle of His, etc., that ensure rapid conduction of electrical impulses.

The heart's automaticity allows it to self-initiate impulses, but the SA node usually controls this under normal conditions as automaticity is slower than SA rate - known as overdrive surppression. Pathologies may alter normal conduction, and automaticity firing rate surpasses SA rate. This is termed latent pacemaker initiation and can lead to arrhythmias (this is ectopic - outside of normal).

3. Electrocardiography (ECG)

An ECG measures the heart's electrical activity through several characteristic waves:

• P wave: Atrial depolarization (before ventricles)

• QRS complex: Ventricular depolarization.

• Atria repolarize while ventricles are depolarizing (not visible on ECG)

• T wave: Ventricular repolarization.

These events reflect the coordination of atrial and ventricular contractions and are crucial for diagnosing heart rhythm abnormalities.

Note: you can live without atrial contraction (P-wave) but you can't live without ventricular contraction and repolarization (QRS and T-waves)

Solution to these issues: Pacemaker 

• • • Can take on the role of cardiac contractions if a patient has problems with coordinated rythmic contraction across the heart. Note: there is coordination between normal electrical activity of heart and a pacemaker.

5. Heart Sounds

Heart sounds, often described as "Lub-Dub," result from valve closure:

• 1st Heart Sound ("Lub"): Closure of AV valves at the onset of systole.

• 2nd Heart Sound ("Dub"): Closure of semilunar valves at the onset of diastole.

Murmurs: Abnormal heart sounds caused by turbulent blood flow. Sounds like a loss of crisp closure ("wooshing"). Murmurs are graded based on intensity (1-6) and can indicate underlying conditions like valve insufficiency, stenosis, or congenital defects.

6. Murmurs and Clinical Cases

Murmurs can be classified as:

1. Innocent: Not related to heart disease (ex: can dissapear with age)

2. Physiologic: Related to conditions like anemia or fever but not heart disease (ex: decreased viscosity of blood leads to turbulence)

3. Pathologic: Due to heart disease like septal defects, valve stenosis, or valve insufficiency.

• Holes in heart (atrial/ventricular septal defects)

• Absormal arterial venous connections (patent ductus arteriosus that closes before birth - creates a murmur if not)

• Stenotic heart valves

• Insufficient heart valves

You should try to characterize murmurs based on the location (which valve) and timing (systolic/diastolic).

Summary of Lecture on Cardiac Output and Shock:

Podcast for this lecture: https://notebooklm.google.com/notebook/d6a9dc43-94dc-4e3b-9436-4c3e1dba1908/audio

Cardiovascular system's primary function: delivering oxygenated blood to tissues for cellular metabolism and removing waste products. 

Key components include: the heart, which acts as a pump, and blood vessels, which distribute blood to the body. 

The amount of blood pumped by each ventricle per minute—is crucial for oxygen delivery (DO₂), which depends on cardiac output (CO) and arterial oxygen content (CaO₂). Cardiac output of the left heart should = cardiac output of the right heart. 

• Left side of the heart pumps blood to: the body

• Right side of the heart pumps blood to: the lungs

Oxygen Delivery is calculated as:

DO2 = CO x CaO2 where,

CaO2 is influenced by partial pressure of oxygen in arteries, hemoglobin saturation, and hematocrit (number of RBC’s). Can increase with RBC transfusion (if hematocrit is low) or oxygen supplementation (if Hemoglobin/arterial oxygen pressure is low)

If oxygen delivery (DO2)  to tissues is inadequate, organ failure can occur = Shock: Not a disease, but a consequence of decreased delivery (common) or increased demand (less common).

Cardiac output (CO) is calculated as:

CO = HR x SV where,

Heart rate is the number of contractions per minute, and Stroke volume (SV) is the amount of blood ejected per heartbeat, influenced by:

1. Preload: The blood volume returning to the heart. 

• Starling's law: 

• As you increase venous return, you increase ventricular contractility (to a point) so preload is very important for improving cardiac output. 

• As you decrease venous return, you decrease the volume of blood returning to heart (preload) which decreases ventricular contraction and hence cardiac output, which decreases oxygen delivery and can lead to shock. 

  • Decrease venous return can be caused by: hemorrhage, thromboembolism,  Gastric dilatation volvulus (GDV)

• How does the body increase preload? Sympathetic stimulation constricts and shifts blood away from veins (70% of blood volume), kidneys and skin to the heart to increase preload. Also selectively constricts BF to the brain but this is not relevant to preload. This mechanism can maintain normal Cv even when 25% of BV is lost.

• How can we increase preload? Increase blood volume: blood transfusion or hydration (IV fluids in vascular space, increases vascular return and hence contractility)

2. Contractility: The strength of heart contractions. Higher contractility increases CO, while decreased contractility (e.g., in heart disease) reduces CO. 

• Ejection fraction: Normally the heart ejects 50% of ventricular volume with each heartbeat

  • Increased contractility (positive intropy) can eject a greater proportion of blood and increase CO. This can be induced with drugs. Results in greater stroke volume. 

  • Decreased contractility = decreased stroke volume, may result in shock.

3. Afterload: The resistance the heart must overcome to pump blood. Increased afterload (e.g., due to high blood pressure) can reduce CO. 

• Greater constriction, in BV’s =  harder to pump against = greater afterload. 

• Need resistance to maintain BP (if we dilate the arteries, we decrease afterload, and BP)

If the stroke volume is low (ex: patient is in shock) the patient may increase their cardiac output by increasing the HR or the heart's contractility and vasoconstriction. Goal: maintain systolic BP (90mmHg), but don't be fooled by normal BP (can be compensated). Low blood pressure can be observed if compensation mechanisms aren’t sufficient, and beyond this the patient is terminal. 

Types of Shock:

1. Hypovolemic Shock: Caused by a drop in blood volume (e.g., severe vomiting or bleeding).

2. Hemorrhagic shock: Extreme blood loss (injury)

3. Cardiogenic Shock: From heart problems reducing CO (e.g., heart attack, heart failure).

4. Vasodilatory Shock: Seen in conditions like sepsis or anaphylaxis, where blood vessels dilate, lowering blood pressure.

5. Obstructive Shock: Due to physical obstructions to blood flow, such as in pulmonary embolism.

6. Anemic: severe reduction in the number of red blood cells or hemoglobin levels in the blood leads to insufficient oxygen delivery to tissues, despite normal cardiac output and arterial oxygen content (CaO₂)

7. Hypoxemic and Cytotoxic Shock: Resulting from low oxygen content in blood or cellular inability to utilize oxygen, respectively.

Clinical Application Example

A case study involves a Husky in potential shock after a car accident, presenting symptoms like elevated pulse, low blood pressure, weak pulses, and pale mucous membranes. These findings suggest shock, with the animal's body compensating by increasing heart rate and peripheral vasoconstriction to maintain CO and DO₂.

Key takeaways: Physiological Compensations in Shock

• Sympathetic Activation: Raises heart rate and contractility, constricts veins to increase preload, and maintains blood flow to vital organs.

• Treatment: IV fluids or blood transfusions to increase blood volume (for preload), oxygen therapy to improve CaO₂, and medications to support heart contractility.