Lecture at UTRGV Friday, Sept. 22, 2017

Lecture: How to Interpret Arterial Blood Gases

The Power of "Why?"

Super post from the Harvard Macy Institute

http://www.harvardmacy.org/index.php/hmi/the-power-of-why

Reason Not To Have 4 Hours of Lectures In The Afternoon

QR codes for learning objectives

Will be embedded into future PowerPoint slides

A Case of Succinylcholine-Induced Hyperkalemia

A Case of Succinylcholine-Induced Hyperkalemia 

(Authored by Dr. Merrill Tarr, Department of Molecular and Integrative Physiology, University of Kansas Medical Center) 

Case History: The following case history relates to a patient who was treated at Saint Luke’s Hospital, Kansas City, Missouri and is condensed from the following paper (Matthews JM. Succinylcholine-Induced Hyperkalemia and Rhabdomyolysis in a Patient with Necrotizing Pancreatitis. Anesth Analg 2000;91:1552–4. 

“A 54-yr-old, 114 kg man presented to the hospital after the abrupt onset of abdominal pain accompanied by severe nausea and vomiting. A presumptive diagnosis of pancreatitis was confirmed by increased amylase and lipase. Abdominal computed tomography showed severe inflammation of the pancreas with probable necrosis. The pancreatitis was attributed to the presence of gallstones.” .... “On the fifth day of admission, respiratory failure necessitated orotracheal intubation and mechanical ventilation. Midazolam infusion provided adequate conditions for ventilatory support, and nondepolarizing muscle relaxants were not administered. Ventilatory support continued for 1 wk before it was successfully terminated and the trachea extubated. On the 35th day of hospitalization, the patient again developed respiratory failure associated with large bilateral pleural effusions. Anesthesia personnel were summoned to the intensive care unit (ICU) to perform an endotracheal intubation. Initial assessment revealed an obese man in obvious respiratory distress. Topical local anesthetic was applied to the oropharynx, and direct laryngoscopy was attempted. This was unsuccessful because of the patient’s confusion and inability to cooperate. Midazolam was titrated IV to a total dose of 8 mg without appreciable sedative effect. Because of the patient’s vigorous resistance to the procedure, his large body habitus with associated broad neck, his tolerance to standard sedatives, and the perceived need for expedient intubation, the decision was made to facilitate laryngoscopy with thiopental and succinylcholine. After breathing oxygen, thiopental 200 mg and succinylcholine 80 mg were given IV as cricoid pressure was applied. Successful endotracheal intubation was accomplished within 60 s, and the oxygen saturation increased to 96%. Approximately 2 min after intubation, the previously normal cardiac rhythm changed to a wide complex bradycardia. A presumptive diagnosis of hyperkalemia was made, and IV calcium chloride was given. The electrocardiographic complexes continued to widen to a sine-wave pattern followed by asystole. Cardiopulmonary resuscitation was performed. Epinephrine, sodium bicarbonate, and insulin/glucose were administered, and a blood sample was obtained to determine serum potassium. After 12 min of cardiopulmonary resuscitation, a narrow complex tachycardia resumed that was associated with good peripheral pulses. Defibrillation was not performed. Initial potassium level obtained during cardiopulmonary resuscitation was 9.8 mEq/L. Approximately 10 min after restoration of cardiac rhythm, the serum potassium had returned to a normal level of 4.1 mEq/L.” The patient died on the 41st day after admission due to rhabdomyolysis-induced kidney failure. 

Arterial Blood Gas Interpretation

Arterial Blood Gas Interpretation

The Four Most Important Equations in Clinical Medicine

Henderson-Hasselbalch Equation - Calculator

to calculate pH from PCO2 and HCO3-

Henderson-Hasselbalch Equation - Calculator

to calculate HCO3- and Base Excess from pH and PCO2

Henderson-Hasselbalch Base Excess Calculator

Inward Rectifying Potassium Current

http://tmedweb.tulane.edu/pharmwiki/doku.php/introduction_to_cardiac_physiology_
electrophysiology

The inward potassium rectifying current (Ik) is what distinguishes a cardiac muscle cell from other muscle cells and nerve cells.  It causes a delay in the refractory period which allows for the crucial entry of calcium during the plateau phase of the action potential.

How does it work?

Ionic basis for the resting and action potential in a ventricular heart cell. The action potential is divided into phases 0 through 4. Each phase results from a change in the balance of inward and outward ionic currents that become activated upon membrane depolarization. The primary currents underlying each phase are: phase 0: Na current (I_Na); phase 1: transient outward K current (I_to); phase 2: L-type Ca current(I_Ca); phase 3: delayed rectifier K currents (I_Kr & I_Ks); phase 4: inwardly rectifying K current (I_K1). The change in dominant conductance during each phase produce either net depolarization or hyperpolarization, and give the action potential its characteristic shape.

Pulse Pressure

Pulse Pressure

Definition: Systolic BP - Diastolic BPExample: 120 - 80 = 40 mmHg

Variations in Pulse Pressure are due to:

• changes in compliance of aorta
• changes in stroke volume

Factors that determine pulse pressure

It is helpful to think of the definition of compliance C = ∆V/∆P and rearrange this to think about factors governing ∆P (stroke volume).

∆P = ∆V/C

Factors affecting systolic pressure

1. Compliance of the aorta
• A highly compliant aorta (i.e., less stiff) has a smaller pulse pressure for a given stroke volume into the aorta.
• A larger stroke volume (not shown in the figure) produces a larger pulse pressure at any given compliance.
• Aortic compliance decreases with age due to structural changes, thereby producing age-dependent increases in pulse pressure.
• For a given stroke volume, compliance determines pulse pressure and not mean aortic pressure.
• However, because vessels display dynamic compliance, increasing the rate of ventricular ejection (as occurs with increased ventricular inotropy) will increase the pulse pressure compared to the same volume ejected at a lower rate.

2. Stroke Volume

Factors affecting diastolic pressure

3. Rate of runoff

3.  Runoff time

References: http://www.cvphysiology.com/Blood%20Pressure/BP002.htm

John Wood, PhD,  KUMC, lecture Power Points

Mitral Stenosis - Pathophysiology

emedicine

Pathophysiology

The normal mitral valve orifice area is approximately 4-6 cm². As the orifice size decreases, the pressure gradient across the mitral valve increases to maintain adequate flow.

Patients will not experience valve-related symptoms until the valve area is 2-2.5 cm² or less, at which point moderate exercise or tachycardia may result in exertional dyspnea from the increased transmitral gradient and left atrial pressure.

Severe mitral stenosis occurs with a valve area of less than 1 cm². As the valve progressively narrows, the resting diastolic mitral valve gradient, and hence left atrial pressure, increases. This leads to transudation of fluid into the lung interstitium and dyspnea at rest or with minimal exertion. Hemoptysis may occur if the bronchial veins rupture and left atrial dilatation increases the risk for atrial fibrillation and subsequent thromboembolism.

Pulmonary hypertension may develop as a result of (1) retrograde transmission of left atrial pressure, (2) pulmonary arteriolar constriction, (3) interstitial edema, or (4) obliterative changes in the pulmonary vascular bed (intimal hyperplasia and medial hypertrophy). As pulmonary arterial pressure increases, right ventricular dilation and tricuspid regurgitation may develop, leading to elevated jugular venous pressure, liver congestion, ascites, and pedal edema.

Left ventricular end-diastolic pressure and cardiac output are usually normal in the person with isolated mitral stenosis. As the severity of stenosis increases, the cardiac output becomes subnormal at rest and fails to increase during exercise. Approximately one third of patients with rheumatic mitral stenosis have depressed left ventricular systolic function as a result of chronic rheumatic myocarditis. The presence of concomitant mitral regurgitation, systemic hypertension, aortic stenosis, or myocardial infarction can also adversely affect left ventricular function and cardiac output.

Buffers

Buffers

The body has a very large buffer capacity.

This can be illustrated by considering an experiment where dilute hydrochloric acid was infused into a dog

(Pitts RF. Mechanisms for stabilizing the alkaline reserves of the body. Harvey Lect 1952-1953; 48 172-209. PubMed.)

In this experiment, dogs received an infusion of 14 mmols H+ per litre of body water. This caused a drop in pH from 7.44 ([H+] = 36 nmoles/l) to a pH of 7.14 ([H+] = 72 nmoles/l) That is, a rise in [H+] of only 36 nmoles/l.

SO: If you just looked at the change in [H+] then you would only notice an increase of 36 nmoles/l and you would have to wonder what had happened to the other 13,999,964 nmoles/l that were infused (14 mmolsH+/L = 14,000,000 nmoles/L.)

Where did the missing H+ go?

They were hidden on buffers and so these 13,999,964 nmoles/L of hydrogen ions were hidden from view.

Buffering hides from view the real change in H+ that occurs.

Because of the large buffering capacity, the actual change in [H+] is so small it can be ignored in any quantitative assessment, and instead, the magnitude of a disorder has to be estimated indirectly from the decrease in the total concentration of the anions involved in the buffering. The buffer anions, represented as A-, decrease because they combine stoichiometrically with H+ to produce HA. A decrease in A- by 1 mmol/l represents a 1,000,000 nano-mol/l amount of H+ that is hidden from view and this is several orders of magnitude higher than the visible few nanomoles/l change in [H+] that is visible.) - As noted above in the comments about the Swan & Pitts experiment, 13,999,994 out of 14,000,000 nano-moles/l of H+ were hidden on buffers and just to count the 36 that were on view would give a false impression of the magnitude of the disorder.

The Major Body Buffer Systems
Site	Buffer System	Comment
ISF	Bicarbonate	For metabolic acids
	Phosphate	Not important because concentration too low
	Protein	Not important because concentration too low
Blood	Bicarbonate	Important for metabolic acids
	Haemoglobin	Important for carbon dioxide
	Plasma protein	Minor buffer
	Phosphate	Concentration too low
ICF	Proteins	Important buffer
	Phosphates	Important buffer
Urine	Phosphate	Responsible for most of 'Titratable Acidity'
	Ammonia	Important - formation of NH4+
Bone	Ca carbonate	In prolonged metabolic acidosis

Henderson-Hasselbalch Calculator

Henderson-Hasselbalch Calculator



calculates pH from values for PCO₂ and HCO₃⁻





Online Acid Base Physiology

High Yield Medical Physiology

LaPlace's Law for the Heart

(from Hurst's, The Heart)

The impedance to ejection of blood by the ventricles includes blood viscosity, vascular resistance, vascular distensibility, and myocardial wall tension. The afterload is the total load that the heart must work against during contraction. Much of the afterload is made up of ventricular myocardial wall tension. In the ventricle, the tension on the walls increases as ventricular chamber volume increases even if intraventricular pressure remains constant. As the ventricle empties, tension is reduced, even as pressure increases. Calculations of myocardial wall tension are defined by the Laplace equation and are expressed in terms of tension, T, per unit of cross-sectional area (dynes per centimeter [dyn/cm]).

Within a cylinder, the law of Laplace states that wall tension is equal to the pressure within the cylinder times the radius of curvature of the wall:

T = P R

where T is wall tension (dyn/cm), P is pressure (dyn/cm2), and R is the radius (cm). Basically, wall tension is proportional to the radius. Because the heart has thick ventricular walls, wall tension is distributed over a large number of muscle fibers, thereby reducing tension on each. The equation for a thick-walled cylinder such as the heart is:

T = (P x R)/h

where h is wall thickness. 

Because the geometry of the ventricles is more complex than that of a cylinder, ventricular wall tension cannot be measured with precision. Wall stress, the force distributed across an area, is actually more correct but is seldom measured.

Two fundamental principles stem from the relationship between the geometry of the ventricular cavity and the tension on its muscular walls:

1. Dilatation of the ventricles leads directly to an increase in tension on each muscle fiber.
2. An increase in wall thickness reduces the tension on any individual muscle fiber. Therefore, ventricular hypertrophy reduces afterload by distributing tension among more muscle fibers.

Dilatation of the heart decreases cardiac efficiency unless hypertrophy is sufficient to normalize wall stress. In heart failure, wall tension (or stress) is high, and thus afterload is increased. The energetic consequences of the law of Laplace can have some role in progressive deterioration of energy-starved cardiac myocytes in the failing heart.

Ventricular dilatation, although initially adaptive as an attempt to sustain SV, eventually becomes a substantial disadvantage and contributes importantly to impaired myocardial performance. As the left and right ventricles dilate, functional mitral and tricuspid regurgitation can occur, adding to circulatory congestion. Stretched myocardial cells can induce programmed cell death (apoptosis), thereby contributing to further disease progression.31 Any treatment that slows progressive dilatation of the heart, such as angiotensin-converting enzyme (ACE) inhibitors or β−adrenergic blockers, will likely have a powerful role in the treatment of heart failure. The plasticity of progressive dilatation is now more apparent, with remarkable reversal of dilatation observed in response to ACE inhibitors and β−adrenergic blockers, cessation of alcohol use in patients with alcoholic cardiomyopathy, and spontaneous improvement in patients with inflammatory myocarditis.

EKG Memory Tools & Mean Electrical Axis

Leads I II & III

Count the "L's"
I = RA LA  = 1 L
II = RA LL = 2 Ls
III = LA LL = 3 Ls

Normal electrical axis 
Leads I & II both positive
Mean electrical axis = -30 to + 90

2nd degree Mobitz type 1 (Wenckebach) = "going, going, gone"

Why is the T wave positive if it is repolarization of the ventricles?

because the repolarization is going in the opposite direction.  A is negative charges going towards positive electrode.  B is positive charges going towards positive electrode.  C is positive charges going away from positive electrode (what happens in the ventricles).

Pulmonary Practice Questions

Pulmonary Practice Questions

General Principles I - spirometry, gas exchange, etc.

General Principles II

ventilation

gas exchange

blood flow

mechanisms of hypoxemia

blood gas transport

mechanics of breathing

control of breathing