Management of Hemodynamics

Referring back to the ASA Standard Guideline, anesthesia providers should be monitoring ventilation, oxygenation, temperature, and circulation. Hemodynamics is going to cover the circulation aspect for the patient. Majority of surgical cases with require some sort of hemodynamic treatment. Most often this is treating hypotension. But occasionally we also need to lower the blood pressure. Understanding how to compartmentalize the various components of hemodynamics will help you both diagnose the underlying cause of hypo- or hypertension and lead you to the correct treatment option.


Let’s start with where these components come from. When we say hemodynamics, we are really referring to blood flowing throughout the body, providing all of your organs with oxygen in order to stay alive. And flow is created by a pressure gradient. This pressure difference in blood flow is analogous to Ohm’s Law, which states that current (I) equals the voltage difference (ΔV) divided by the resistance (R). If you rearrange this, you get ΔV = I x R.


Now, let’s switch these physics variables for physiologic variables. We end up with the equation (MAP - CVP) = CO x SVR (MAP = mean arterial pressure; CVP = central venous pressure; CO = cardiac output; SVR = systemic vascular resistance). CVP can be replaced with ICP (intracranial pressure) if this number is higher.



Most people will simplify this equation to MAP = CO x SVR. MAP is typically the number we care most above in majority of cases. We know that this number is measured on NIBP measurements and that studies have showed that for most patients a MAP > 65 mmHg will prevent end-organ ischemia, ensuring adequate perfusion. Looking at the variables CO and SVR, we can extrapolate 5 factors that impact MAP. CO is the product of HR (heart rate) and stroke volume. So already we see HR as one factor. Stroke volume is determined by preload, rhythm, and contractility. And finally, SVR can also be reworded as afterload. And those are the 5 components! (1) Preload, (2) Afterload, (3) rate, (4) rhythm, and (5) contractility. Since we see hypotension the most, that’s what I am going to focus on the most.



Preload refers to the amount of blood that returns back to your heart from the venous system. This volume of blood stretches out your heart muscles prior to a contractile force. There are multiple ways to measure preload like with CVP tracing, PCWPs (pulmonary-capillary wedge pressure = left atrium pressure), and TEE (transesophageal echocardiogram). When I think about things that decrease preload, I usually think of hypovolemic causes (ie. dehydration, blood loss, “third-space” shifting) and obstructed venous return (ie. tension pneumothorax, pulmonary embolism, high PEEP). The best treat is going to be treating the underlying cause. So for blood loss or dehydration, usually blood products and IV fluids will help. For obstructed venous return, that becomes more specific to the obstruction such as a pericardiocentesis vs. TPA.   



Afterload is the resistance the blood flows against when leaving the heart. This is mainly determined by systemic vascular resistance, but also impacted by wall tension and blood viscosity. When I group hypotensive causes related to afterload, I think about anesthetic drugs, neuraxial anesthesia, and anaphylaxis or septic shock. If you believe your anesthetics are causing hypotension, the best start is to reduce your inhaled or IV agents if the situation permits. If not, you may be required to start a vasoactive medication. The pressor of choice for these situations is an alpha-agonist like phenylephrine or norepinephrine.



Heart rate can cause hypotension both from being too slow and from being too fast. Bradycardia related to second- or third-degree heart block can lead to symptoms of lightheadedness and syncope, which are both signs of low blood pressure. Typically this can be treated with a pacemaker. In the operating room, we use anticholinergics, like glycopyrolate, to increase the heart rate when it gets low from things like abdominal insufflation or sympathectomy created by neuraxial anesthesia. When the heart beats too fast, it decreases the amount the left ventricle can fill with blood during diastole, decreasing the the stroke volume pushed forward. To reduce HR, we typically use beta blockers such as labetolol or metoprolol.



Rhythm plays a crucial role in maintaining stroke volume. The abnormal rhythm we see most commonly is atrial fibrillation. When patient’s are in a-fib, you can see a lack of p-waves on their ECG. This p-wave signifies the atrial contraction of the cardiac cycle. Without the atrial contraction, left ventricular end-diastolic filling volumes decrease, leading to a decrease in cardiac output. Patients with afib lose around 10-20% of their cardiac output because of this. This number increases in patients with stiff ventricles from left ventricular hypertrophy leading to a decrease in compliance.



And finally, contractility can lead to hypotension. With weak heart muscle, patients may not be able to adequately pump the blood in their heart forward, leading to symptoms of congestive heart failure (ie. dyspnea, orthopnea, pleural effusions, pedal edema, jugular venous distension). Causes of decreased myocardial contractility include previous myocardial infarctions, current ischemia, cardiomyopathies, and anesthetic drugs. The treatment of choice for this is typically a inotropic agent, such as epinephrine or dobutamine, to increase the contractile force of the heart and move blood forward.


I’ll briefly leave you with 6 categories for causes of hypertension:

  1. Increased Sympathetic Tone: this can be related to light anesthesia, pain, autonomic dysreflexia, drug abuse (ie. amphetamines, cocaine), hypercarbia.

  2. Chronic Hypertension

  3. Elevated ICP (Intracranial Pressure): “Cushings Triad” - hypertension, bradycardia, irregular respirations.

  4. Hypermetabolic state: this includes malignant hyperthermia, thyrotoxicosis, neuroleptic malignant syndrome.

  5. Endocrine disorders: pheochromocytoma, hyperaldosteronism

  6. Drug-related: iatrogenic (ie. lidocaine + epinephrine) or unintentional (ie. drug error).

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