#stroke volume

Where to begin?

Having realized I picked such a dynamic and elaborate topic, I figured I should start somewhat basic and work my way up.

If you are reading this, it is my hope that you already have a general background knowledge about the gross (and perhaps micro-)anatomy of the heart and large blood vessels coming off of it, as this will make the rest of my post more relevant and applicable to your understanding in critically ill suffering various forms of shock [i.e. cardiogenic, hypovolemic, distributive (septic), and obstructive (ex: PE, tension pneumothorax, cardiac tamponade)].

Let us begin with the equation for Cardiac Output, which will be the heart of this entire topic (pun very much intended), and something one should never forget during the initial stages of resuscitation. In times of physiologic stress, the body must compensate to meet the body’s increasing demands for perfusion and oxygenation, which is why understanding the equation below becomes indispensible. 

   Cardiac Output (mL/min) =  Stroke Volume (mL/beats) x Heart Rate (bpm)

        Average CO is 5 L/min;  Average SV 70 mL/beat, Average HR 70 bpm

Stroke volume is probably one of the most important aspects of hemodynamics in critical care resuscitation, so I feel it is vital to go in depth when breaking down stroke volume into its three main components:  Preload, Afterload, and Cardiac Contractility. 

Preload is the workload imposed on the heart before cardiac contraction begins; it is generated during diastolic filling and is maximized through stretching of cardiomyocytes to their fullest potential prior to kinetic ventricular cardiac contraction. Factors that increase preload include: volume (in the form of crystalloid, albumin, or blood products), exercise (wherein muscle contraction augments venous return toward the heart), reduced intrapleural pressure during inspiration (which allows thoracic veins to expand and increase venous return toward the right atrium - this becomes more relevant when discussing mechanical ventilation). Preload can be reduced in hemorrhage, hypovolemia, impaired filling in diastolic heart failure, as well as atrial fibrillation and other supraventricular tachycardias. Preload and volume status can best be assessed in the ICU by passive leg raise, transducing the CVP from a venous central line, POCUS of the inferior vena cava to evaluate volume status, echocardiography - TTE vs.TEE, FloTrac for SVV/SVI assessment, etc. 

Afterload is the pressure against which the heart has to pump in order to eject blood at the beginning of systole. Afterload of the right side of the heart is increased with pulmonary hypertension, while it is increased on the left side of the heart with aortic valve stenosis and systemic hypertension. In both right and left ventricular dilatation, afterload will also be elevated given increased wall tension that is required to stretch cardiomyoctes to provide adequate forward flow during systolic contraction (for further understanding, look up Frank-Starling law/curve). Decreases in afterload are caused by ventricular hypertrophy (less wall stress and increased strength of contractility), mitral regurgitation (wherein blood flows retrograde into the left atrium, and the left ventricle can eject less volume than normal out into the aorta), as well as distributive shock (seen with reduced systemic vascular resistance and hypotension following diffuse peripheral vasodilation). 

Myocardial contractility (inotropy) is the ability of the heart muscle to contract and forcefully eject blood from the right and left ventricles into the pulmonary arteries and aorta, respectively. Contractility can be augmented by sympathetic activation with catecholamine release/administration (epineprine, norepinephrine, etc.), hyperthyroidism, increases in HR, and abrupt increases in afterload. Contractility is reduced via parasympathetic activation (ex baroreceptor reflex, vasovagal episode), hypoxia (ex: myocardial infarct), hypercapnia, acidosis (reduced function of epi/norepi), hyperkalemia. 

Heart rate is the other important determinant of cardiac output. Normal heart rate falls between 60-100 beats per minute. Falling below 60 bpm, i.e. bradycardia, can significantly reduce cardiac output if the body cannot augment stroke volume by increasing preload, decreasing afterload, or increasing contractility as above. Increasing heart rate above 100, i.e. tachycardia, is oftentimes the body’s initial response to drops in cardiac output, for example in hypovolemia. However, tachycardia can also impede cardiac output by not allowing enough time for diastolic filling, reducing preload and thus, cardiac output. 

Pulmonary physiology in relation to cardiac output:

In normal ventilation, inspiration induces a drop in systolic blood pressure, an increase in right-ventricular preload, a septal shift toward toward the left ventricle, and reduced LV preload and LV stroke volume.

Below is an image that depicts intrathoracic pressure and its affect on cardiac output: 

In mechanical ventilation, when we supply positive airway pressure (i.e. PEEP), there is additional pressure that is supplied during exhalation to keep the alveoli in the airway open. This positive pressure increases intrathoracic pressure, which reduces right-sided venous return, especially in preload dependent patients who are hypovolemic.

In addition, increasing PEEP can lead to increased right-sided afterload, as the positive airway pressure during exhalation can surpass the pressures within the pulmonary artery, thus leading to pulmonary hypertension. 

With these above changes on the right side as a result of PEEP (decreased preload, increased afterload), the RV can become distended, and ultimately lead to reduced left sided filling via shifting of the septum toward the left side (decreased LV preload). Reduction in LV preload leads to reduced cardiac output. 

Despite the above, PEEP can actually reduce LV afterload and enhance cardiac output, thus why it becomes important in heart failure with subsequent pulmonary edema. This is a topic of discussion for another time in regards to BiPap. 

I will further delve into the above physiologic processes again and again, as they are of utmost important in post-cardiotomy patients. Additionally, I will save pulmonary hypoxic vasoconstriction as a separate topic in a subsequent post.

References: 

1: Website: https://www.physiology.org/doi/pdf/10.1152/advan.00190.2016 

2.  Text:  Human Physiology: From Cells to Systems, by Lauralee Sherwood

3. Website: https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system/Chapter%20523/effects-positive-pressure