The cardiac cycle describes each heart beat, incorporating relaxation and contraction. Phase one describes diastole and you can see above that atrial & ventricular pressure are both low but atrial pressure is higher than ventricular pressure - this sets up the through through of blood when the atria end up contracting. You can also see how the ventricular pressure ends up below the atrial pressure after isovolumetric relaxation.The ventricular volume rises slightly during diastole and then to its peak at the end of atrial systole. Aortic pressure is always high but falls during diastole, then peaks during ventricular systole.There is a dicrotic notch after the first fall after peak aortic pressure - this is when the aortic valve closes and a backup of pressure (aorta > LV) leads to a second, smaller peak. During rapid inflow, the ventricular volume, but not pressure increases.
#Pathophys #Cardiology #CardiacCycle #Stages #Systole #Diastole #HeardSounds #Pressures #Phonogram #Electrocardiogram #Graphs
Perhaps quite too often, the knee-jerk reaction to an elevated Troponin is to call our friends from Cardiology. This becomes a flawed philosophy when taking into consideration the coronary circulation and its potential alterations in the setting of acute illness. The heart consumes a tremendous amount of O2 at baseline, despite receiving only 5% of the resting cardiac output. To compensate, O2 in the coronary circulation is extracted in the myocardium by a much higher degree than it is in any other tissues. In fact, myocardial oxygen extraction is so high, that in conditions imposing greater workloads on the heart (Sepsis, Shock, Hypoxia), the only way to increase myocardial O2 is by increasing coronary blood flow altogether. To do this, the coronary vessels are typically able to dilate significantly…typically.
Consider Sepsis, a condition characterized by PERIPHERAL VASODILATION. How can the coronary vessels dilate further if they are already maximally dilated? In many situations they cannot, coronary ischemia ensues, and the Troponin rises. Cardiology cannot help us with this beyond advising us to treat the primary cause. Now consider Tachycardia, often a physiological response to acute illness. Recall, little coronary blood flow occurs during Systole with the majority occurring in Diastole. Even during the Isovolumetric phase of Systole, the LV generates enough compressive force to effectively block off the coronary circulation. There is a bit more Systolic flow on the right side as the RV generates much less force. The faster the heart rate, the less time there is for Diastole and thus, less time for coronary perfusion. In a healthy heart, this may not be an issue as the vessels can easily dilate and respond. But in our patients with CAD with already dilated vessels, or acutely ill patients with systemic vasodilation, this may not be the case. Once again, other than dealing with the primary disturbance Cardiology may not provide much more insight.
There is no “one size fits all” in medicine and there are situations which may be similar where Cardiology may truly be needed. Just keep in mind the coronary circulation, the presenting illness, and predisposing conditions of the patient before making the call.
#diagnosis #management #cardiology #clinica l#foamed #algorithm #criticalcare
Perhaps quite too often, the knee-jerk reaction to an elevated Troponin is to call our friends from Cardiology. This becomes a flawed philosophy when taking into consideration the coronary circulation and its potential alterations in the setting of acute illness. The heart consumes a tremendous amount of O2 at baseline, despite receiving only 5% of the resting cardiac output. To compensate, O2 in the coronary circulation is extracted in the myocardium by a much higher degree than it is in any other tissues. In fact, myocardial oxygen extraction is so high, that in conditions imposing greater workloads on the heart (Sepsis, Shock, Hypoxia), the only way to increase myocardial O2 is by increasing coronary blood flow altogether. To do this, the coronary vessels are typically able to dilate significantly…typically.
Consider Sepsis, a condition characterized by PERIPHERAL VASODILATION. How can the coronary vessels dilate further if they are already maximally dilated? In many situations they cannot, coronary ischemia ensues, and the Troponin rises. Cardiology cannot help us with this beyond advising us to treat the primary cause. Now consider Tachycardia, often a physiological response to acute illness. Recall, little coronary blood flow occurs during Systole with the majority occurring in Diastole. Even during the Isovolumetric phase of Systole, the LV generates enough compressive force to effectively block off the coronary circulation. There is a bit more Systolic flow on the right side as the RV generates much less force. The faster the heart rate, the less time there is for Diastole and thus, less time for coronary perfusion. In a healthy heart, this may not be an issue as the vessels can easily dilate and respond. But in our patients with CAD with already dilated vessels, or acutely ill patients with systemic vasodilation, this may not be the case. Once again, other than dealing with the primary disturbance Cardiology may not provide much more insight.
There is no “one size fits all” in medicine and there are situations which may be similar where Cardiology may truly be needed. Just keep in mind the coronary circulation, the presenting illness, and predisposing conditions of the patient before making the call.
#diagnosis #algorithm #cardiology #echocardiogram #management #clinical #criticalcare #foamed #treatment
It is important to recognize Acute Decompensated Heart Failure (ADHF) as more than just simply a clinical diagnosis but rather as a condition with a wide range of possible clinical presentations. Patients presenting with ADHF typically fall into 1 of 4 recognized hemodynamic profiles that when appropriately identified, provide a particularly useful framework to guide therapy. The correct profile can be determined based on two clinical parameters: perfusion status and congestion.
The assessment of a patient suspected to be in ADHF starts with a good history & exam. Signs of poor perfusion include cool extremities, fatigue, altered mental status and low urine output. Signs of congestion include Crackles/Rales on auscultation, JVD, Orthopnea/PND and Peripheral Edema. Some exam findings may be more specific rather than sensitive making the diagnosis challenging. Imaging and more importantly, bedside ultrasound are excellent at evaluating hemodynamics and cardiac function (“the squeeze”) along with presence of pulmonary edema (“B-lines). ECG is vital while lab markers such as BNP/NT-proBNP and Troponin may be elevated and helpful in establishing a diagnosis.
Adequate perfusion without congestion (Warm & Dry) is the treatment goal with emphasis placed on prevention. Most patients, however, are adequately perfused but congested on presentation (“Warm & Wet”). They may benefit from LV afterload reduction (Vasodilators) which augment forward flow to the kidneys where excess volume can then be excreted using diuretics. The poorly perfused and non-congested profile (“Cold & Dry”) usually results from the overdiuresis of a Wet & Warm patient causing hypovolemia needing a little fluid. This is not uncommon and can be prevented by adjusting the dose and/or transitioning to oral therapy when our patients have achieved negative fluid balance and are clinically improved. Poorly perfused and congested (“Cold & Wet”) is essentially Cardiogenic Shock. These patients need inotrope therapy and afterload reduction. Cardiac cath if acute coronary syndrome is the determined cause and perhaps even mechanical support (Balloon pump, Impella, LVAD, ECMO). “Warm & Dry” is the treatment goal with emphasis then placed on prevention.
#diagnosis #differential #algorithm #management #cardiology #treatment #table #foamed #heartfailure #chf #criticalcare #icu #clinical #pharmacology
Mean Arterial Pressure (MAP)
Average arterial pressure throughout one cardiac cycle, systole, and diastole.
Surrogate indicator of blood flow and believed to be a better indicator of tissue perfusion.
To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg.
MAP = [Cardiac Output (CO) x Systemic Vascular Resistance (SVR)] + Central Venous Pressure (CVP)
MAP = (CO × SVR) + CVP
Because CVP is usually at or near 0 mmHg, this relationship is often simplified to:
MAP ≈ CO × SVR.
Cardiac output (CO) = Heart Rate (HR) X Stroke Volume (SV).
Stroke Volume is by ventricular inotropy and preload.
Preload is affected by blood volume and the compliance of veins.
Increasing the blood volume increases the preload, increasing the stroke volume and therefore increasing cardiac output.
Afterload also affects the stroke volume in that an increase in afterload will decrease stroke volume.
Heart rate is affected by the chronotropy, dromotropy, and lusitropy of the myocardium.
Systemic vascular resistance is determined primarily by the radius of the blood vessels.
Decreasing the radius of the vessels increases vascular resistance.
Increasing the radius of the vessels would have the opposite effect.
Blood viscosity can also affect systemic vascular resistance.
An increase in hematocrit will increase blood viscosity and increase systemic vascular resistance.
Viscosity, however, is considered only to play a minor role in systemic vascular resistance.
Common formula:
MAP = Diastolic blood pressure + 1/3 (Systolic Blood pressure – Diastolic Blood Pressure)
= DBP + 1/3(SBP – DBP) or
MAP = DBP + 1/3(Pulse Pressure)
MAP = [Systolic Blood Pressure + (2 x Diastolic Blood Pressure)]
3
Example, if blood pressure is 82 mm Hg/50 mm Hg,
MAP = SBP + 2 (DBP) = 82 +2 (50) = 182 = 60.67 mmHg; or
3 3 3
MAP = 1/3 (SBP – DBP) + DBP = 1/3 (82-50) + 50 = 10.67 + 50 = 60.67 mmHg
In sepsis, vasopressors are often titrated based on the MAP.
In the guidelines of the Surviving Sepsis Campaign, it is recommended that MAP be maintained ≥ 65 mm Hg.
#meanarterialpressure #MAP #Afterload #afterload #Heartrate #chronotropy #dromotropy #lusitropy #Pulsepressure #strokevolume #cardiacoutput #Co #SV #lvdv
Fluid Responsiveness and Fluid Tolerance Testing - OnePager Summary
Fluid resuscitation can be beneficial when required or harmful in excess. Methods to predict fluid responsiveness enable parsimonious administration of fluids, resulting in reduced fluid shorter duration pf vasopressors and lower risk of renal failure.
Fluid responsive (FR) - a 10-15% increase in cardiac output (CO) when fluid administered; fluid responsiveness does not mean fluid is "needed" only the CO will increase with volume.
Arterial Line:
• Pulse Pressure Variation (PPV): Variation in pulse pressure (PPV) with the respiratory cycle suggests fluid responsiveness due to heart lung interactions.
• Pulse Contour Cardiac Output: Analysis of the waveform can be used to estimate stroke volume variation (SW) or cardiac output (CO) using proprietary formulas.
Central Venous Line:
• Central Venous Pressure (CVP): Measures CVP as a surrogate for RV filling pressure.
Pulmonary Artery Catheter:
• Thermodilution CO/CI: Thermodilution measurement of CO via a PAC, which can be either continuous (via heating) or intermittent (via cold saline injection).
• PAOP/PCWP: PAOP/PCWP approximates LAP.
• Mixed Venous O2 Saturation (SvO2): An increase in SvO2 suggests improved CO, however high baseline Sv02 does not preclude FR.
Point of Care Ultrasound:
• IVC Size & Distensibility: IVC size reflects RA pressure, similar to CVP. Thus measuring the IVC size & phasic variation with respiration might predict FR.
• LV End Diastolic Area (LVEDA): Measure the cross sectional area of the LV at the end of diastole (reflects adequate filling); "kissing papillary muscles" is the extreme
• LVOT VTI: Measure outflow of blood from the LV. Variability in VTI is analogous to PPV, absolute values can be compared before/after a challenge maneuver.
• Carotid VTI: Similar to L VOT VTI but easier to measure carotid facilitating repeat measurements.
Minimally Invasive:
• BIOREACTANCE/NICOM: Detection of blood flow in the chest by application of an external electric field. Averages blood flow over 8-30 seconds. Combine with a challenge (PLR, microbolus) to measure ΔSV.
• END TIDAL CO2: An increase cardiac output causes increases delivery of CO2 to the lungs, increasing exhaled CO2.
• PULSE OXIMETRY WAVEFORM ANALYSIS: Analysis of the plethysmographic waveform is analogous to PPV measurement using arterial line: a high degree of respiratory variation predicts FR.
• PULMONARY A vs B-LINE PATTERN: Sonographic lung changes precede other signs of volume overload. An A-line predominant lung US pattern suggests fluid tolerance (FT).
Challenges:
• PASSIVE LEG RAISE (PLR): Positioning a patient flat (00), then raising legs to 450) quickly (30-90 sec) returns a reservoir of ~300 ml of venous blood to the central circulation.
• MINI-BOLUS & MICRO BOLUS: Observing the hemodynamic response to the rapid infusion of a small volume 50-100m!) of fluid can predict the response to a larger bolus
• HIGH PEEP CHALLENGE: For patients on MV increasing PEEP can identify FR by identifying a decrease in MAP.
• END EXPIRATORY OCCLUSION (EEO): For MV patients, each breath increases intrathoracic pressure & impedes venous return. Interrupting MV at end expiration transiently increases preload. Decrease in CO during a 15 sec expiratorv hold maneuver predicts FR
by Nick Mark MD @nickmmark
#Fluid #Responsiveness #Tolerance #testing #diagnosis #criticalcare #comparison #challenges #management
