Pathophysiology and Management of Shock and Hemodynamics

Comprehensive practice flashcards covering cellular hypoxia, acid-base buffering, hemodynamics, shock pathophysiology, compensatory mechanisms, classification, and management principles.

How does cellular hypoxia trigger metabolic acidosis and cellular dysfunction during shock?

A lack of oxygen forces cells into anaerobic metabolism, leading to lactic acid accumulation and a systemic pH drop below $7.35$ (e.g., $7.30$, $7.29$, $7.28$). This acidosis causes vasoconstriction, precapillary sphincter failure, and peripheral blood pooling.

What happens to cellular ion gradients when the sodium-potassium ($\text{Na}^+/\text{K}^+$) pump fails during shock?

Metabolic acidosis causes cell membrane dysfunction and pump failure, causing potassium ($\text{K}^+$) to leak out of the cell and sodium ($\text{Na}^+$) to become trapped inside, destroying the electrical gradient needed for cellular contraction and firing.

What cellular consequence occurs when intracellular lysosomes rupture during severe acidosis?

The lysosomes rupture and release digestive enzymes (the cell's "stomach acids") internally and into surrounding interstitial spaces, damaging neighboring cell membranes and capillary linings.

How many total units of energy ($\text{ATP}$) are produced by aerobic metabolism, and what are the primary byproducts?

Aerobic metabolism yields $36\,\text{ATP}$ per glucose molecule, producing carbon dioxide ($\text{CO}_2$) and water ($\text{H}_2\text{O}$) as clean byproducts.

How is energy ($\text{ATP}$) generated across each stage of aerobic cellular respiration?

Glycolysis in the cytoplasm produces $2\,\text{ATP}$, the Krebs cycle in the mitochondria produces $2\,\text{ATP}$ and $\text{CO}_2$, and the electron transport chain (ETC) produces $32\,\text{ATP}$ and $\text{H}_2\text{O}$.

Why is energy production drastically reduced during anaerobic metabolism?

Without oxygen, the three-carbon sugars (pyruvate) cannot enter the mitochondria for the Krebs cycle and the electron transport chain; the cell relies solely on glycolysis, yielding only $2\,\text{ATP}$ while accumulating lactic acid and pyruvate.

What is the primary instantaneous buffer system in the bloodstream, and what chemical equilibrium does it maintain?

The bicarbonate buffer system: circulating bicarbonate ($\text{HCO}_3^-$) binds hydrogen ions ($\text{H}^+$) to form carbonic acid ($\text{H}_2\text{CO}_3$), which breaks down into water ($\text{H}_2\text{O}$) and carbon dioxide ($\text{CO}_2$).

How does exhalation of $\text{CO}_2$ affect systemic acid-base balance?

Because carbon dioxide is a cellular waste product of buffering and respiration, exhaling $\text{CO}_2$ directly eliminates carbonic acid from the body, helping to normalize systemic $\text{pH}$.

What is the most common cause of airway obstruction, and how should a patient be positioned to prevent it?

The tongue. The patient should be placed in an ear-to-sternal-notch alignment with the head and neck elevated forward until the ears align horizontally with the sternal notch, followed by a head-tilt/chin-lift.

What is the formula and standard value for normal resting minute volume?

Minute Volume $=$ Tidal Volume ($\approx 500\,\text{mL}$) $\times$ Respiratory Rate ($10\text{--}12\,\text{breaths/min}$), yielding approximately $5{,}000\text{--}6{,}000\,\text{mL/min}$.

What is the baseline atmospheric fraction of inspired oxygen ($\text{FiO}_2$) in ambient air?

$21\%$ (or an atmospheric pressure concentration of $0.21$).

Which mineral is required for the heme group of red blood cells to transport oxygen and carbon dioxide?

Iron.

What is the core premise of the Fick principle in relation to tissue perfusion?

Tissue perfusion equals red blood cell oxygen onloading in the pulmonary capillaries plus the effective transport and offloading of that oxygen to peripheral tissues.

Why does a massive pulmonary embolism (PE) cause an acute ventilation-perfusion ($\text{V/Q}$) mismatch?

The patient can ventilate adequately, but the blood clot blocks pulmonary capillary flow; without blood reaching the alveoli, gas exchange (respiration) is zero, resulting in rapid circulatory collapse.

What are the three essential components of the cardiovascular circuit?

The pump (the heart), the fluid (blood: plasma, red blood cells, white blood cells, platelets), and the container (vasculature: arteries, veins, capillaries).

Why is administering massive crystalloid boluses (normal saline or lactated Ringer's) referred to as making "bad Kool-Aid"?

Crystalloids increase intravascular volume but dilute red blood cells and clotting factors, creating thin, washed-out blood that cannot effectively carry oxygen or form clots.

Why are septic shock and anaphylactic shock classified fundamentally as "container" problems rather than "fluid" problems?

Neither involves initial fluid loss from the body; systemic inflammatory responses cause diffuse endothelial permeability and massive vasodilation, resulting in a leaky container where plasma escapes into interstitial tissues.

What is the clinical definition of cardiac preload?

The volume and pressure of blood in the ventricles (specifically left ventricular end-diastolic pressure or volume) at the end of diastole, immediately after atrial contraction and before ventricular ejection.

Why does extreme tachycardia ($>190\,\text{bpm}$) diminish cardiac preload and overall cardiac output?

The ventricles do not have adequate diastolic filling time between beats; the drastic reduction in ventricular filling decreases stroke volume beyond the compensatory ability of the rapid heart rate.

How does the Frank-Starling Law of the heart describe myocardial stretch?

Like a rubber band, greater end-diastolic filling stretches myocardial fibers, generating greater contractile force and stroke volume up to an optimal physiological limit, beyond which overstretching diminishes contractile strength.

What is cardiac afterload?

The resistance or pressure within the aorta that the left ventricle must overcome to open the aortic valve and eject blood into systemic circulation.

What is the mathematical relationship between Cardiac Output ($\text{CO}$), Stroke Volume ($\text{SV}$), and Heart Rate ($\text{HR}$)?

$\text{CO} = \text{HR} \times \text{SV}$. For example, an $80\,\text{mL}$ stroke volume at $80\,\text{bpm}$ circulates $6{,}400\,\text{mL/min}$, replenishing the body's entire $5\text{--}6\,\text{L}$ blood volume roughly once every minute.

What physiological factors determine Blood Pressure ($\text{BP}$)?

Blood pressure is the product of cardiac output and peripheral vascular resistance: $\text{BP} = \text{CO} \times \text{PVR}$ (where $\text{CO} = \text{HR} \times \text{SV}$).

What is the target Mean Arterial Pressure ($\text{MAP}$) in permissive hypotension for a patient in shock, and why?

A $\text{MAP}$ of $65\,\text{mmHg}$. This pressure is sufficient to sustain perfusion to vital core organs (brain, heart, lungs, and kidneys) without over-diluting blood or dislodging nascent blood clots.

Where are the primary vascular baroreceptors located, and where do they transmit pressure signals?

In the aortic arch and carotid sinuses (nuchal arteries); they transmit pressure data to the medulla oblongata (cardioacceleratory, cardioinhibitory, and vasomotor centers).

What are the physiological effects of stimulating Alpha-1 vs. Alpha-2 adrenergic receptors?

Alpha-1 stimulation induces direct arteriolar vasoconstriction; Alpha-2 stimulation acts as a background self-limiting feedback loop to prevent excessive vasoconstriction.

What three myocardial properties are enhanced by stimulating Beta-1 adrenergic receptors?

Chronotropy (heart rate), inotropy (contractile force), and dromotropy (electrical conduction velocity and excitability).

What is the primary physiological action of Beta-2 adrenergic receptor stimulation?

Bronchodilation of the airways, which expands alveolar surface area to maximize oxygen onloading and carbon dioxide removal.

How do the adrenergic receptor profiles of Epinephrine and Norepinephrine (Levophed) differ?

Epinephrine stimulates alpha and beta receptors (predominantly beta-1 and beta-2 with moderate alpha-1); Norepinephrine is almost exclusively an Alpha-1 agonist, producing potent peripheral vasoconstriction with minimal direct cardiac stimulation.

What sequential steps constitute the Renin-Angiotensin-Aldosterone System (RAAS) compensatory cascade?

Decreased renal perfusion prompts the kidneys to release renin, which converts angiotensinogen to angiotensin I. In pulmonary capillaries, angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II, causing vasoconstriction and triggering aldosterone secretion.

What is the physiological role of aldosterone released from the adrenal cortex?

Aldosterone targets the distal tubules and collecting ducts of the kidneys to increase sodium reabsorption; water follows sodium, expanding intravascular volume and raising systemic blood pressure.

What triggers the release of Antidiuretic Hormone (ADH / Arginine Vasopressin), and what is its effect?

Released by the posterior pituitary gland in response to hypovolemia or hyperosmolarity, ADH stimulates the renal tubules to reabsorb water and sodium, conserving vascular volume.

Where is Erythropoietin (EPO) produced, what prompts its release, and what is the lifespan of a red blood cell?

EPO is secreted by renal interstitial fibroblasts in response to renal hypoxia, stimulating bone marrow stem cells to produce red blood cells; red blood cells have an average lifespan of $120\,\text{days}$.

How does pancreatic glucagon support the body's compensatory fight-or-flight response?

Pancreatic alpha cells release glucagon to stimulate hepatic glycogenolysis (the breakdown of liver glycogen into glucose), providing necessary fuel for cellular ATP generation during stress.

What two clinical assessment parameters differentiate compensated shock from decompensated shock?

Blood pressure and mentation (level of consciousness). Compensated shock presents with relatively normal blood pressure and intact mentation; decompensated shock is marked by falling blood pressure ($\text{MAP} < 65\,\text{mmHg}$ or systolic drop) and altered mental status.

What is irreversible shock, and what misleading clinical phase often precedes death?

A terminal phase of microvascular collapse and extensive cellular damage where death is inevitable despite medical interventions; patients often display a brief, deceptive 24-hour period of apparent clinical recovery just before dying.

What occurs during the Ischemic stage of microcirculatory shock?

Precapillary sphincters constrict to shunt blood flow toward vital central organs, causing downstream capillary tissues to become ischemic, hypoxic, and reliant on anaerobic metabolism.

What characterizes the Stagnant stage of microcirculation during shock progression?

Precapillary sphincters relax and open while postcapillary sphincters remain closed; incoming blood pools in the capillary beds, causing severe acidosis and microclot formation (rouleaux).

What occurs during the Washout stage of capillary sphincter regulation?

Postcapillary sphincters fail and open wide, flushing accumulated stagnant blood, lactic acid, toxins, and microthrombi into systemic circulation, worsening metabolic acidosis and triggering widespread inflammation.

What degree of left ventricular damage typically precipitates cardiogenic shock, and what is the mortality rate?

Cardiogenic shock typically occurs when the left ventricle sustains $40\%$ or more myocardial damage (such as from acute myocardial infarction), carrying an expected mortality rate of $40\text{--}50\%$.

How does blood pressure distinguish typical congestive heart failure (CHF) from end-stage cardiogenic shock?

Typical CHF presents with systemic hypertension from sympathetic compensation, whereas progression into cardiogenic shock causes severe hypotension (e.g., systolic BP $70\text{--}80\,\text{mmHg}$, $\text{MAP} < 65\,\text{mmHg}$) alongside pulmonary crackles/edema.

What clinical hallmark distinguishes neurogenic shock from hypovolemic or cardiogenic shock?

A clear line of demarcation: skin above the spinal cord injury is cool, pale, and diaphoretic (sympathetic compensation intact), while skin below is warm, dry, and pink (loss of sympathetic tone, flaccid vasodilation, absence of sweating), accompanied by bradycardia.

What are the two diagnostic criteria required to define septic shock?

Persistent hypotension requiring vasopressors to maintain a $\text{MAP} \ge 65\,\text{mmHg}$ and a serum lactate level greater than $2\,\text{mmol/L}$ despite adequate fluid resuscitation.

Why should clinicians avoid artificially slowing ventilations in a tachypneic septic shock patient with a low End-Tidal $\text{CO}_2$ ($\text{EtCO}_2$)?

The rapid respiratory rate is a vital compensatory mechanism blowing off carbonic acid to offset severe metabolic acidosis; forcing ventilations to slow traps $\text{CO}_2$, worsening systemic acidosis.

What are the prehospital quick SOFA (qSOFA) criteria used to screen for sepsis?

Respiratory rate $\ge 22\,\text{breaths/min}$, altered mental status (Glasgow Coma Scale $< 15$), and systolic blood pressure $\le 100\,\text{mmHg}$.

What ECG rhythm in a pulseless trauma patient strongly points to an obstructive shock etiology (such as cardiac tamponade or tension pneumothorax)?

A well-organized, tachycardic Pulseless Electrical Activity (PEA).

Why is preventing hypothermia essential in bleeding and shock patients?

Every degree of core body temperature lost inhibits the coagulation cascade and impairs platelet function, directly accelerating hemorrhagic blood loss.

Why must patients in cardiogenic shock never be placed in a flat supine or Trendelenburg position?

Laying the patient flat allows accumulated pulmonary edema to spread across the entire posterior surface area of both lungs, eliminating functional gas exchange; they must be kept upright or semi-Fowler's.

What is the standard isotonic fluid resuscitation protocol for hypovolemic or septic shock?

Administer up to $30\,\text{mL/kg}$ given in rapid $500\,\text{mL}$ boluses pressure-infused in less than $15\,\text{minutes}$, titrating strictly to maintain a $\text{MAP} \ge 65\,\text{mmHg}$ and stopping if pulmonary edema appears.

What is the recommended first-line vasopressor and infusion dose for septic and neurogenic shock?

Norepinephrine administered at an IV/IO infusion dose of $0.05\text{--}0.5\,\mu\text{g/kg/min}$.

What is the recommended dosing for Epinephrine as an infusion and as a push-dose vasopressor in refractory shock?

Continuous infusion: $0.05\text{--}0.3\,\mu\text{g/kg/min}$; Push-dose: $0.1\,\mu\text{g/kg}$ per dose, up to a maximum single push dose of $10\,\mu\text{g}$.

What is Multiple Organ Dysfunction Syndrome (MODS), and what is its associated mortality rate?

The progressive impairment of two or more organ systems resulting from an uncontrolled inflammatory response to severe illness, trauma, or shock; it carries an overall mortality rate of $60\text{--}90\%$.

What is the difference between Primary MODS and Secondary MODS?

Primary MODS is the direct result of a specific primary insult; Secondary MODS occurs when an initial insult primes immune cells (neutrophils, macrophages), and a subsequent, even minor, insult triggers an uncontrolled systemic inflammatory cascade.

What clinical organ failure milestones occur over the chronological progression of MODS?

$24\,\text{hours}$: low-grade fever, tachycardia, hyperdynamic state; $24\text{--}72\,\text{hours}$: pulmonary failure and alveolar edema; $7\text{--}10\,\text{days}$: hepatic, GI, and renal failure begin; $14\text{--}21\,\text{days}$: intensified renal/hepatic failure and immune collapse; $>21\,\text{days}$: hematologic/cardiac collapse, brain edema, and death.