ICU hemodynamics review

Hemodynamics review

Cardiac Output and Cardiac Index

Cardiac Output  (CO)  is the amount of blood pumped by the ventricles each minute. It is the product of Heart Rate (HR) and Stroke Volume (the amount of blood ejected by the ventricle with each contraction).


Normal C.O. = 4-8 L/min

* These values are relative to size*- What may be normal for a 5ft tall 80 yo 40 kg woman may be totally inadequate for a 6 ft 100kg man. So we use Cardiac Index to adjust to individual body size.

Cardiac Index  = CO/the person's Body Surface Area

Image result for cardiac output

What happens when cardiac output is outside of the normal range?

Common Signs and Symptoms of low Cardiac Output

One of the first things you will see with a decreased cardiac output is a decrease in Urine Output. Never ignore a patient who has a sudden decrease in urine output! It is the poor man's predictor or cardiac output. 

What are some of the potential clinical clues that a patient's cardiac output is low?

  • Decreased urine output.
  • Decreased blood pressure
  • Decreased heart rate
  • Bounding peripheral pulses
  • Decreased mental status
  • Syncope and dizziness
Choose all correct answers

Heart rate and its effect on cardiac output

Increased Heart Rate effects on CO

In a normal, healthy individual, an increase in heart rate can lead to an increase in CO.

However, in a person with cardiac dysfunction or disease, increases in heart rate can lead to a decreased CO and sometimes even ischemia. Why?

            Increased heart rate decreases the ventricular filling time, by reducing preload, which decreases stroke volume and leads to decreased CO - in other words....

          The faster the heart beats the less time it has to fill with blood before it pumps it out. 

Decreased Heart Rate effects on CO

A lower heart rate does not necessarily result in a lower CO. Decreased heart rates are often found in athletes or healthy individuals and they have a normal CO.  Their heart muscle is strengthened and it causes an increase in the amount of blood pumped out with each beat (Stroke Volume). 

In individuals with Left Ventricular dysfunction, a slow heart rate can produce a decrease in CO. This is caused by a decrease in contractility (the muscle is weaker and not able to contract as well as it should). Also fewer heart contractions every minute causes decreased cardiac output simply because the heart is squeezing less often. Fewer squeezes = less blood pumped. 

Since CO is a product of Stroke Volume and Heart Rate, changes in HR can affect SV and changes in SV can affect HR. 

Stroke Volume increases - heart rate can decrease (as seen in athletes)

Stroke Volume falls - heart rate increases (to try and compensate)

Evaluating the cause of the tachycardia becomes an essential component of hemodynamic assessment. Bradycardia and tachycardia are potentially dangerous because they may result in a decrease in CO if adequate stroke volume is not maintained. Sudden onset bradycardia is almost always reflective of a falling Cardiac Output. The cause of tachycardia on the other hand  must be determined  because it may not reflect a low output state but rather a normal physiologic response (ex tachycardia due to fever).


Stroke Volume

Stroke Volume is the amount of blood ejected from each ventricle with each heart beat. The right and left ventricle eject nearly the same amount, which is normally from 50-100 ml/ heart beat. 

Ever see SVI and wonder what that means? Well it is the Stroke Volume Index. Just like Cardiac Index it takes into account the patient's size.

Normal SVI = 35-60 ml/beat

Stroke Volume is affected by Preload, Afterload, and Contractility. 



Image result for preload and afterload






Preload is the volume of blood that exerts a force or pressure (stretch) on the ventricles during diastole.


It may also be described as the filling pressure of the ventricles at the end of diastole or the amount of blood that fills the ventricles during diastole. 

Preload is determined primarily by the amount of venous return to the heart. Venous constriction or dilation,and alterations in the total blood volume all affect preload. Preload decreases with volume change. 

Decreased preload can occur in hemorrhage, diuresis, vomiting and diarrhea, third spacing, redistribution of blood flow and profound diaphoresis. Venous dilation also results in diminished preload. Etiologies  that increase venous pooling and decreased venous return to the heart can include hyperthermia septic shock, anaphylactic shock, and drug administration. 

Increased preload includes excessive fluid resuscitation and renal failure. Venous constriction results in teh shunting of peripheral blood to the central organs The increased venous return  results in an increased preload. This may happen in hypothermia, some forms of shock, and with drugs that stimulate alpha receptors. 

Starlings Law

Image result for starling's law of the heart

Frank Starling's Law of the heart states that the greater the stretch (preload) the greater the force of contraction.... to a point....

Think of it like a rubber band, the further you stretch the rubber band the farther it shoots when you let go. That is until you stretch the rubber band out so far that is can not bounce back. The same principle applies to the heart. The more amount of blood that fills before contraction (preload) the better cardiac output, until the heart becomes so stretched out it can't contract well anymore, like in some cardiomyopathies. 

So increasing preload helps improve cardiac output, but only to a certain point. 


Image result for preload and afterload

Afterload is the resistance to the ventricles emptying during systole (contraction). It is the pressure or resistance that the ventricles must overcome to open the aortic and pulmonic valves and to pump blood into the systemic and pulmonary vasculature.

Vascular resistance is determined by three things:

1. the length of a vessel

2. the diameter or radius of that vessel

3. the viscosity (the measure of a fluid's resistance to flow) of the blood

As afterload increases (vasoconstriction or obstruction)the heart must work harder to eject the volume.  With increased afterload the heart works harder to eject contents leading to increased myocardial oxygen demand. 

Increased afterload causes:                                                            Decreased Afterload causes:

- pulomonic stenosis                                                                         - hyperthermia

- hypothermia                                                                                      - distributive shock (septic, anaphylactic,etc)

- hypertension                                                                                     - vasodilating drugs (nitro. Beta Blockers, CA -

- classic shock states                                                                                                 channel blockers, nipride) 

- drugs that stimulate alpha receptors 

          (epi, levo, dopamine, phynelephrine)

- the body's compensatory response to hypotension and decreased CO

After an MI what do we try to decrease by inserting an IABP?

  • Afterload
  • Preload


Image result for contractility of the heart cartoon

Contractility is the strength of the myocardial contraction, or the degree of myocardial fiber shortening with contraction. Contractility contributes significantly to cardiac output. if the other determinants of cardiac output were constant, then a heart with a greater contractile forcer would produce a greater cardiac output. However contractility depends on many variables including preload and afterload. 

Electrolyte levels also have a major impact on the contractility of the heart. Monitoring and treating abnormal Ca, Na, Mg, K, and Phos levels is essential to ensure optimal contractility. Other factors that contribute to contractility include myocardial oxygenation (ischemia), amount of functional heart muscle (ischenmia and cardiomyopathy), and positive and negative inotropic drugs. 

Clinical indicators for hemodynamic properties

Preload = CVP and WEDGE

Right ventricular preload is measured by Right Atrial Pressure aka  CVP. Normal value is 2-10 cmh2o.

Left ventricular preload is measured by the Pulmonary Artery Occlusion Pressure (PAOP) aka the wedge. Normal is 8 to 12 mm Hg.

 Afterload - can not be directly measured, however SVR and PVR are looked at.

Image result for normal hemodynamic parameters


PA pressures

Pulmonary Artery Pressure is determined  by the Right ventricular CO and the Pulmonary Vascular Resistance. Normal PA pressures are 20-30/10-15 mm Hg. 

Elevated PA pressures occur in pulmonary HTN, chronic pulmonary disease, mitral valve disease, LV failure, hypoxia, and pulmonary emboli. Below normal PA pressures primarily occur in conditions that produce hypovolemia. If blood valumes are reduced, less resistance to the ventricles emptying occurs resulting in a drop in arterial pressures. 

As a practical guideline, the pulmonary artery diastolic pressure is higher than left atrial pressure (wedge pressure)

Normal PA waveform:

Image result for normal PA waveform


SVR = Systemic Vascular Resistance. Normal SVR= 800-1200.

SVR is the resistance to the flow of blood through the body's vessels. It increases as vessels constrict and decreases when vessels dilate.

Any change in the diameter, elasticity, or number of vessels recruited can influence the measured amount of resistance to the flow of blood through the body.  If the SVR is elevated, the left ventricle faces an increased resistance to the ejection of blood.

The SVR commonly elevates as a compensatory response to hypertension or a low cardiac output (increased SVR increases preload), such as would occur in shock states. It is important for us to know why our patient's SVR is elevated if it is. 

EX: your patient's SVR is elevate to 1500 because their blood pressure is 198/95, you know to give a medication that reduces afterload. But lets say you have a patient who is in shock and the body clamps down to improve the cardiac output, you need to reduce the SVR to improve your cardiac output. 

If the SVR is low the left ventricle faces a lower resistance to the ejection of blood. Generally, the SVR only decreases as a pathological response to inflammatory conditions (ex sepsis, fever, etc). Generally if the SVR is reduced, fluids and vasopressors is the considered treatment. However, ultimately the underlying condition must be treated. 

PVR = Pulmonary Vascular Resistance. Normal PVR = 100-250 dynes/s/cm

Generally only and elevated PVR is considered a problem, because it produces strain on the right ventricle. If this strain is unrelieved, the Right Ventricle eventually fails. Failure of the right ventricle results in less blood entering the lungs and the left ventricle. This causes hypotension. 

The most common causes of elevated PVR are pulmonary hypertension, hypoxia, end stage COPD with cor pulmonale, and PE. 


Normal SVO2 is 60-80

Mixed venous oxygen saturation (SvO2) is the percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart.  This refects the amount of oxygen "left over" after the tissues remove what they need. It is used to help us to recognize when a patient's body is extracting more oxygen than normally. An increase in extraction is the bodies way to meet tissue oxygen needs when the amount of oxygen reaching the tissues is less than needed.

A true mixed venous sample (called SvO2) is drawn from the tip of the pulmonary artery catheter, and includes all of the venous blood returning from the head and arms (via superior vena cava), the gut and lower extremities (via the inferior vena cava) and the coronary veins (via the coronary sinus). By the time the blood reaches the pulmonary artery, all venous blood has "mixed" to reflect the average amount of oxygen remaining after all tissues in the body have removed oxygen from the hemoglobin. The mixed venous sample also captures the blood before it is re-oxygenated in the pulmonary capillary.


Image result for SVO2

EKG practice/ review

Normal Heart Rate is considered what?

  • 60-100 beats per minute
  • 50-120 beats per minute

What rhythm is this?

  • SVT
  • sinus tachycardia
  • afib

Name the rhythm

Junctional Rhythms - 

Abnormal p waves - retrograde (after the qrs), absent p waves, or inverted p waves = junctional rhythm

Remember they are broken down by the heart rate:

40-60 = junctional escape rhythm

60-100 = accelerated junctional

over 100 = junctional tachycardia

Identify the rhythm

Heart Rate = 70

  • atrial flutter
  • atrial fibrillation

identify the weird beats - Which one is a PVC, which one is PJC and which one PAC?

Choose everything that is correct about the rhythm:

  • This is Torsades De Pointes
  • This is V-fib
  • This is a polymorphic ventricular tachycardia
  • This is considered a lethal rhythm and usually results in decompensation to vfib
  • normal treatment for this is potassium
  • normal treatment for this is magnesium