Cardiac Physiology Refresher

The major role of cardiac physiology and the heart as an organ is simply to pump deoxygenated blood to the lungs in order to uptake oxygen into the blood, and then pump oxygenated blood to all of our organ systems and tissues to deliver oxygen to the tissues for energy production. 

The oxygen as a pump has two distinct features to consider:

1. The myocardium - muscle that is necessary to pump the blood

2. Electrical automaticity - System of spontaneous propagation of action potentials to produce a pulsatile and coordinated pumping system.

Organized pulsatility is important for coordinated filling of the ventricles by the atria prior to ejection to the tissues - "atrioventricular synchrony"

Definitions

Inotropy:

• Degree to which the heart can squeeze or pump with increased force. Agents that increase inotropy will make the heart pump stronger (epinephrine), and negative inotropes will decrease force of contractility (Beta blockade, calcium channel blockers)

Chronotropy:

• Changes in heart rate. 

Lusitropy: 

• Diastolic relaxation of the myocardium

Bathmotropy:

• The myocardial response to stimulation or the excitability (threshold of excitation) of a muscle fiber. How well does the heart respond to increases and decreases in stimulation.

Dromotropy:

• Conduction velocity of the cardiac conduction system through. Positive dromotropy increases conduction velocity and negative dromotropy decreases it. 

Cardiac Function

Stroke Volume

• Volume (in L or mL) ejected by the right or left ventricle with each beat

• Stroke volume for individual patients is determined by preload, afterload and contractility

Determinants of Cardiac Output

Clinical applications of the Frank-Starling Curve:

• Severely dehydrated patient who is hypotensive is likely all the way to the left of the curve - fluid administration should bring the patient up along the curve to the right in order to develop improved cardiac output

• Patient who is in heart failure or has myocardial dysfunction (myocarditis, acidosis), the entire curve is shifted downwards. Treating with inotropic support (epinephrine) will shift the curve upwards

• Patients in heart failure often also retain fluid to compensate for decreased cardiac output however might be all the way to the right of the curve. Diuretics will bring them back to the peak of the curve and optimize cardiac output

Laws of flow dynamics

Therefore, resistance of the tube can be determined if we know the pressure difference (driving pressure) and the flow (in liters per minute)

Vascular resistance can be measured in Woods units (WU∙m2) and dynes (dynes/sec/cm-5) 

WU is converted to Dynes by multiplying by 80

Flow through a compressible tube (like a blood vessel) also depends on the distension pressure on the inside of the tube and the inward pressure from the outside. This is referred to as transmural pressure. (Ptm = internal distension pressure - external surrounding pressure)

Oxygen Delivery and Consumption

Oxygen Delivery: Oxygen diffuses through the alveolar membranes in the lungs through the alveolar capillaries and enters the bloodstream via 2 distinct properties. Oxygen binds to hemoglobin molecules and is carried through the blood on hemoglobin to be released within the capillary bed of various tissues and organs. Oxygen is also dissolved directly into the plasma portion of blood. This dissolved oxygen slowly diffuses out of the bloodstream over time but does not play a large role in tissue and organ oxygenation. 

The oxygenated blood is pumped by the left ventricle of the heart through the body and as oxygenated blood arrives at the tissues it is dissociated from hemoglobin and released into the tissues to undergo oxidative phosphorylation. 

Therefore, in order to better understand oxygen delivery to tissues, we must be able to measure how much total oxygen is in the bloodstream.

The oxygen content equation takes into account both the saturated oxygen within hemoglobin and the dissolved oxygen

It is important to note that the majority of oxygen in our blood is saturated on hemoglobin and not dissolved in blood. The dissolved oxygen is the partial pressure of oxygen which depends on how much effect of atmospheric pressure (very different on mount Everest and in the Dead Sea. 

Oxygen Delivery is the rate of how much oxygen (based on oxygen content equation) is circulating to the tissues per unit of time, which is dependent on cardiac output. 

Oxygen consumption signifies how much oxygen is utilized per unit of time by the tissues. This requires knowing the content of oxygen in arterial blood as well as venous blood to demonstrate the difference between them, in addition to cardiac output. 

Oxygen consumption is increased with:

• Exercise, Stressful activities

• Illness

• Fever

• Hyperthyroid

• Catecholamines, inflammation

Since we don't often know the exact measurement of cardiac output, we cannot estimate VO2 at the bedside, however it is also helpful to think about the A-V O2 difference, which can be estimated by subtracting the O2 saturation in arterial blood by O2 saturation in venous blood. If you then divide that number by the O2 content in arterial blood, you will know your extraction ratio. This is the fraction of oxygen delivery that is utilized by tissues. 

Normal A-V O2 difference (arterial saturation minus venous saturation) should be around 25%

Note: we can estimate this effect using a venous saturation from anywhere. Central venous saturations are ideal, however require a central line and there will be a difference between central venous saturation from the SVC vs. IVC. Additionally, if a central line is sitting inside the right atrium, it could provide erronious central venous saturations if there is an ASD with left to right shunt (higher than SVC sat) or if the sample is sampling coronary sinus return (lower than SVC sat).

True "mixed venous saturation" which is the actual venous saturation of all of the blood combined that returns to the heart, can only be drawn from the main pulmonary artery.

Oxygen Delivery

The determinants of Oxygen delivery are therefore CaO2 (How much oxygen is in the blood) and cardiac output (how much blood is being pumped). The following diagram therefore will help determine why there might be impaired oxygen delivery to tissues. 

DO2 / VO2 Relationship

Oxygen consumption under normal conditions is independent of supply, which means that no matter how much oxygen is pumped throughout the body and delivered to tissues, consumption will remain stable. This is because we have a surplus of oxygen content being delivered to tissues and only what is needed in the given situation is extracted. 

There is a critical point after which if oxygen deliver falls below a certain level (for the specific clinical scenario), consumption starts to decline, and when consumption decreases, this causes tissue hypoxia, ischemia and organ dysfunction. Under these conditions, the fraction of extracted O2 increases signficantly and VO2 becomes supply dependent. When this occurs, anaerobic metabolism begins to take place, and lactate will rise, mixed venous saturation will drop. 

Measuring Cardiac Output

1. Cannot easily measure cadiac output but we have several ways of estimating CO

2. Can use the laws of conservation of mass, conservation of dye

3. Thermodilution = in the cath lab or using a Swan Catheter or PICCO catheter - instill ice cold water into one central vessel and measure the change in temperature downstream to estimate the cardiac output

4. Fick Equation: 

Right Ventricular Afterload

The right ventricle pumps deoxygenated blood to the lungs to receive oxygen, after which the blood enters the left atrium. 

Obstruction to flow from the right ventricle to the left ventricle can occur at several different levels. If flow is obstructed proximal to the left ventricle, LV filling decreases and cardiac output goes down. In addition to decreased cardiac output, the RV struggles to pump against a much higher pressure than it is used to and becomes strained, leading to congestion of the systemic venous return system (elevated JVD, hepatic congestion, ascites). RV strain can lead to RV failure.

Determinants of RV afterload:

• Obstruction of the pulmonary valve (PV stenosis, subvalvar or supravalvar stensosis)

• Constriction of one or both of the branch pulmonary arteries (pulmonary artery atresia or stenosis)

• Thromboembolic disease (pulmonary embolism)

• Pulmonary vein stenosis

• Mitral valve stensosis (Cor Triatrium = membrane in the LA that is obstructing flow through the MV) 

• Left ventricular dysfunction causing left atrial hypertension and backup to the right heart

• Increased pulmonary vascular resistance / Pulmonary hypertension

Determinants of pulmonary vascular resistance:

The pulmonary capillary bed spreads through the lungs in two different ways. 

1. The alveolar vessels line up right against the alveoli and are most efficient with gas exchange

2. The Extra-alveolar (ciorner) vessels run between 2-4 alveoli and essentially create a bypass without much gas exchange

When alveoli are atelectatic, the alveolar vessels are dilated and have very low PVR, but when the lungs are hyperinflated, they become compressed and have elevated vascular resistance

The opposite occurs with corner vessels. Atelectasis increases PVR and hyperinflation decreases it. 

Since these vessels work together to create the entire system, the point of lowest pulmonary vascular resistance is when the lungs are at FRC

Shock

Typically oxygen delivery (DO2) is-5x greater than oxygen demand/consumption (VO2) and there is significantly more O2 available than the body needs

Shock occurs when oxygen delivery (DO2) does not meet oxygen demand/consumption (VO2). With either enough decrease in DO2 or increase in VO2, the “Critical DO2” point is reached where cells no longer have enough oxygen and will begin to depend on aerobic respiration 

• Clinically, an important marker of O2 delivery and consumption is the mixed venous saturation (SvO2) since that is something we can measure in the PICU, unlike CO.

• If arterial blood is 100% saturated and the extraction ratio is 25%, SvO2 will be ~75%. If the extraction ratio is increased to 33%, SvO2 will be 67%. In other words, if the SvO2 is falling or lower than expected, either more O2 is being consumed or delivery is inadequate…not ideal

•  Summary: Shock = VO2 > DO2 = VO2 > (HR x SV) x (1.34 x Hb x SaO2)

○  How do you fix it? Decrease your metabolic demand (VO2) and/or increase your oxygen delivery (DO2)

Types of Shock

Generally classified into 4 categories 

Cardiovascular (Vasoactive) Drugs

ECG Basics

Congenital Heart Disease

This will be a very brief and simplified overview of congenital heart disease to help in better understanding what to be concerned about with each lesion.

Congenital heart defects or malformations come in several varying types, classifications and levels of severity with varying outcomes. 

This disease is often classified by broadly splitting into two categories: "Cyanotic" or "Acyanotic", however this starts to get confusing because in each category there are some malformations that have "Not enough pulmonary blood flow", "Normal pulmonary blood flow" or "too much pulmonary blood flow". For example, hypoplastic left heart syndrome is considered to by a cyanotic lesion, however after birth there is usually "too much pulmonary blood flow". There are also obstructive lesions that depending on additional factors can either be cyanotic or acyanotic. 

CHD is also sometimes classified as simple, moderate and complex. 

Therefore, we will split up our classifications as follows: 

• Septal defects: 

  • Lesions of the atrial and ventricular septum

• Obstructive lesions:

  • Right sided inflow or outflow obstructed lesions

  • Left sided inflow or outflow obstructed lesions

• Vascular connections:

  • Lesions of the great arteries, veins and coronaries

• Situs abnormalities:

  • Discordance between atria to ventricles and ventricles to arteries

Pulmonary and systemic cardiac outputs

Septal Defects

Obstructive lesions

Vascular Connections

Situs abnormalities