Lecture 8 (Hypotension)-Exam 3 Flashcards
1
Q
What is hypotension? What are the values?
A
- Hypotension is a decrease in systemic blood pressure below accepted low values
- While there is not an accepted standard hypotensive value, pressures less than 90/60 are recognized as hypotensive
- It may be absolute with changes in systolic blood pressure to less than 90 mm Hg or mean arterial pressure of less than 65 mm Hg
2
Q
How do we calculate MAP?
A
2/3 diastolic pressure + 1/3 systolic pressure
3
Q
Blood pressure is continuously regulated via what?
A
via the autonomic nervous system as a balance of the sympathetic nervous system and the parasympathetic nervous system.
4
Q
How does parasympathetic and sympathetic nervous system act on the BP?
A
- The sympathetic nervous system acts to raise blood pressure by increasing heart rate and constricting arterioles.
- The parasympathetic nervous system lowers blood pressure by decreasing heart rate and relaxing arterioles to increase vessel diameter.
5
Q
Blood pressure modulation
* Blood pressure is modulated by what 2 primary mechanisms?
A
CO and total peripheral vascular resistance
6
Q
How do you calculate CO and SVR?
A
- Cardiac output = Stroke Volume x Heart Rate
- Systemic Vascular Resistance = 80 x (Mean Arterial Pressure - Mean Venous Pressure) / Cardiac Output
7
Q
Blood pressure modulation:
* Disease states that reduce stroke volume or heart rate will decrease what?
A
will decrease the total cardiac output of the heart, functionally decreasing the ability to generate blood pressure
8
Q
Various medications are also capable of inducing hypotension via what?
A
via augmenting these biologic parameters
* Disease states that reduce stroke volume or heart rate will decrease the total cardiac output of the heart, functionally decreasing the ability to generate blood pressure
9
Q
What are disease states that modulate BP? (6)
A
Disease states include arrhythmias, valvular regurgitation, valvular stenosis, diastolic or systolic heart failure, large volume losses of blood, and cardiac tamponade
10
Q
What is poiseuille’s law?
A
- Where L equals the length of the vessel and n equals the viscosity of blood. Functionally, vessel length is not subject to change in the body and viscosity does not rapidly adjust and can be accepted as standard value in most cases. Therefore, the only modifiable physiological value is the radius of the vessel.
- A decrease in arteriolar caliber increases the resistance to blood flow, thus increasing blood pressure. Conversely, increasing the diameter of terminal arterioles will decrease resistance to blood flow, thus decreasing blood pressure.
- Total peripheral vascular resistance is primarily controlled via autonomic neuronal responses to modulate fluctuations in blood pressure
- The natural state for arteriolar smooth muscle tone is to be relaxed with dilated arterioles. Therefore, the absence or blunting of autonomic input by medications or disease states will lead to hypotension.
11
Q
Blood pressure modulation
* Both cardiac output and total peripheral vascular resistance function as what?
* When cardiac output decreases, peripheral resistance should what? How?
* When peripheral resistance decreases, cardiac output will do what?
A
- Both cardiac output and total peripheral vascular resistance function as feedback compensation mechanisms for the other in healthy individuals.
- When cardiac output decreases, peripheral resistance should increase via constriction of terminal arterioles to decrease vessel caliber to maintain blood pressure
- When peripheral resistance decreases, cardiac output will increase via increased heart rate to maintain blood pressure.
12
Q
A decrease in arteriolar caliber increases what? increasing the diameter of terminal arterioles will what?
A
- A decrease in arteriolar caliber increases the resistance to blood flow, thus increasing blood pressure.
- Conversely, increasing the diameter of terminal arterioles will decrease resistance to blood flow, thus decreasing blood pressure.
13
Q
Total peripheral vascular resistance is primarily controlled via what?
A
via autonomic neuronal responses to modulate fluctuations in blood pressure
14
Q
The natural state for arteriolar smooth muscle tone is what?
A
is to be relaxed with dilated arterioles. Therefore, the absence or blunting of autonomic input by medications or disease states will lead to hypotension
15
Q
What are different types of hypotension?
A
- Cardiogenic
- Orthostatic
- Vasovagal
16
Q
What is going on with orthostatic hypotension?
A
- In orthostatic hypotension, a combination of the blunting of the autonomic nervous system and mild hypovolemia from dehydration is the culprit.
- When lying flat, there is even distribution of fluid throughout the body.
- However, on standing heart rate fails to increase appropriately and peripheral resistance fails to increase appropriately leading to a rapid, transient decrease in blood pressure that improves with postural changes. This is classically symptomatic with dizziness and syncope.
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Q
Cardiogenic hypotension/shock
* What is it?
* What are some sxs?
* What labs?
A
- Cardiogenic shock is a failure to achieve sufficient cardiac output with maintained total peripheral resistance.
- Sxs: decrease BP, edema syncope
- Labs: EKG, lactic acid
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Q
Defining Cardiogenic Shock
* Defined as what?
A
Cardiogenic shock is defined as a primary cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion
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Q
Defining Cardiogenic Shock
* What is the clinical criteria?
A
Clinical criteria include a systolic blood pressure of less than or equal to 90 mm Hg for greater than or equal to 30 minutes or support to maintain systolic blood pressure less than or equal to 90 mm Hg and urine output less than or equal to 30 mL/hr or cool extremities
20
Q
Defining cardiogenic shock:
* Hemodynamic criteria include
A
Hemodynamic criteria include a depressed cardiac index (less than or equal to2.2 liters per minute per square meter of body surface area) and an elevated pulmonary-capillary wedge pressure greater than 15 mm Hg
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Q
Cardiogenic shock:
* What is the MCC cause?
* What are the mechanical defects?(5)
A
- Acute myocardial ischemia (most common)
- Mechanical defect: acute mitral regurgitation (papillary muscle rupture), ventricular wall rupture (septal or free wall), cardiac tamponade, left ventricular outflow obstruction (hypertrophic obstructive cardiomyopathy [HOCM], aortic stenosis [AS]), Left ventricular inflow obstruction (MS, atrial myxoma)
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Q
Cardiogenic shock causes:
* What are contractility defects? (5)
* What can happen (clot)?
* What _ _ failure?
* What can happen to the aorta?
A
- Contractility defect: ischemic and non-ischemic cardiomyopathy, arrhythmias, septic shock with myocardial depression, myocarditis
- Pulmonary embolus (right ventricular with or without left ventricular failure)
- Right ventricular failure
- Aortic dissection
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Q
Cardiogenic shock:
* What are other causes?(4)
A
Other causes include cardiotoxic drugs (doxorubicin), medication overdose (beta/calcium channel blockers), metabolic derangements (acidosis), electrolyte abnormalities (calcium or phosphate)
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Q
Pathophysio of cardiogenic shock dt MI
* Ischemia to the myocardium causes what? What happens in return?
A
- Ischemia to the myocardium causes derangement to both systolic and diastolic left ventricular function, resulting in a profound depression of myocardial contractility.
- This, in turn, leads to a potentially catastrophic and vicious spiral of reduced cardiac output and low blood pressure, perpetuating further coronary ischemia and impairment of contractility.
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Pathophysio cardiogenic shock:
* What are the compensatory processes from low BP, CO and impairment of contractility? (2)
* The activation of the sympathetic system leading to peripheral vasoconstriction may improve coronary perfusion at the cost of increased afterload, and
* Tachycardia which increases myocardial oxygen demand and subsequently worsens myocardial ischemia.
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Pathophysiology of Cardiogenic shock
* What do the compensatory mechanism do?
* These compensatory mechanisms are subsequently counteracted by pathologic vasodilation that occurs from the release of potent systemic inflammatory markers such as interleukin-1, tumor necrosis factor-a, and interleukin-6.
* Additionally, higher levels of nitric oxide and peroxynitrite are released, which also contribute to pathologic vasodilation and are known to be cardiotoxic.
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Cardiogenic shock patho:
* Unless interrupted by adequate treatment measures, this self-perpetuating cycle (aka compensatory measures) leads to what?
Unless interrupted by adequate treatment measures, this self-perpetuating cycle leads to global hypoperfusion and the inability to effectively meet the metabolic demands of the tissues, progressing to multiorgan failure and eventually death.
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What are the cardiogenic shock SCAI stages?
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Physical exam findings in cardiogenic shock
* What are the sxs? (7)
* What happens with the heart sounds?
* What can be congested?
* Altered mental status, cyanosis, cold and clammy skin, mottled extremities
* Peripheral pulses are faint, rapid, and sometimes irregular if there is an underlying arrhythmia.
* Jugular venous distension
* Diminished heart sounds, S3 or S4, may be present, murmurs in the presence of valvular disorders such as mitral regurgitation or aortic stenosis.
* Pulmonary vascular congestion may be associated with rales.
* Peripheral edema may be present in the setting of fluid overload
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Diagnostic evaluation of cardiogenic shock
* What are the orders that you need to do?(10)
* Complete blood picture, comprehensive metabolic panel, magnesium, phosphorous, coagulation profile, thyroid-stimulating hormone
* Arterial blood gas
* Lactate
* Brain natriuretic peptide
* Cardiac enzyme test
* Chest x-ray
* Electrocardiogram
* Two-dimensional echocardiography
* Ultrasonography to guide fluid management
* Coronary angiography
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Treatment and management of cardiogenic shock
* Rapid diagnosis with prompt initiation of pharmacological therapy to do what?
to maintain blood pressure and to maintain respiratory support along with a reversal of underlying cause plays a vital role in the prognosis of patients with cardiogenic shock
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Treatment and management of cardiogenic shock
* How do you manage?
* What do you monitor?
* What do you need to support?
* Medical Management
* Procedures/Monitoring: CVL Placement, arterial line and PCI
* Mechanical circulatory support
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Treatment and management of cardiogenic shock
* What medicine is widely used? What does it cause?
Dobutamine is widely used, has beta-1 and beta-2 agonist properties, which can improve myocardial contractility, lower left ventricular end-diastolic pressure, and increased cardiac output.
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Treatment and management of cardiogenic shock
* What else is used besides dobutamine? What does it cause?
* What is preferred for patients with severe hypotension or hypotension unresponsive to other medications? Why?
* Milrinone, also a widely used inotrope, has been shown to reduce left ventricular filling pressures.
* Norepinephrine is preferred over dopamine in patients with severe hypotension (systolic blood pressure less than 70 mm Hg) or hypotension unresponsive to other medications as dopamine has been associated with higher rates of arrhythmias and a higher risk of mortality in this patient population. However, norepinephrine should be used with caution as it can cause tachycardia and increased myocardial oxygen demand in patients with recent myocardial infarctions.
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Besides dobutamine, milrinone, NE, dopamine, what else can you use? What does it do?
Diuretics such as furosemide play a role in decreasing plasma volume and edema
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orthostatic hypotension:
* What is it defined as?
* Clinically this is diagnosied by?
* Orthostatic hypotension is defined as a sudden drop in blood pressure upon standing from a sitting or supine position.
* Clinically, this is diagnosed by a sustained reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within three minutes of standing after being supine for five minutes or at a 60-degree angle on the tilt table.
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Pathophysiology of orthostatic/postural hypotension
* The sudden drop in blood pressure is usually secondary to what?
to failure of the autonomic reflex, volume depletion, or adverse reaction to a medication
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Hypovolemia:
* Cannot pump when?
* What is the CO formula?
* If SV low, even w/ increased HR, may what?
* Can’t pump blood if the tank is empty!
* CO=SVxHR
* If SV low, even w/ increased HR, may not be enough to overcome
47
Dx hypovolemia:
* What test can you do?
* What is the patho behind it?
* What is it a predictor of?
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Passive leg raise (PLR)
* How do you do this?
* Sit patient at 45 degrees head up semi-recumbent position
* Lower patient’s upper body to horizontal and passively raise legs at 45 degrees up
* Maximal effect occurs at 30-90 seconds
* Assess for a 10% increase in stroke volume (cardiac output monitor) or using a surrogate such as pulse pressure (using an arterial line)
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What are the pros of PLR?
* Reversible
* Non-invasive
* Easy to perform in patients breathing spontaneously and with arrhythmias (but must use measures other than stroke volume variation and pulse pressure variation)
* Can be repeated many times to reassess preload responsiveness without any risk of inducing pulmonary edema or cor pulmonale in potential nonresponders
50
What are the cons of PLR?
* Unreliable in severely hypovolemic patients— the blood volume mobilized by leg-raising (which is dependent on total blood volume) could be small and can show minimal to no increase in CO and blood pressure, even in fluid responsive patients
* Need to stop any other interventions during the test
* Positional changes may be contra-indicated in some patients
* Not useful in patients with raised intra-abdominal pressure
51
What is the treatment of hypovolumic hypotension?
* Fill the tank!
* Remove any offending agents
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What medications could contribute to orthostatic hypotension specifically?
Antihypertensive Medications and Other Cardiovascular Drugs Predisposing to Orthostatic Hypotension (OH)
* Diuretics
* α-Receptor Blockers
* Nitrates
* β-Blockers
* Clonidine
* Calcium Channel Blockers
Drugs Acting on Central Nervous System Predisposing to OH
Antidepressants
* OH is the most common cardiovascular adverse effect of tricyclic antidepressants (TCA)
* Serotonin-selective reuptake inhibitors (SSRI) are reported to cause OH less frequently than TCA
* It is well known that serotonin-norepinephrine reuptake inhibitors (SNRI) may induce BP and heart rate increase.
* Benzodiazepines
* Antipsychotics
* Opioids
* The N-methyl-d-aspartate (NMDA) antagonist, memantine
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Postural Tachycardia Syndrome (POTS)
* What is the primary symptom?
* What it is?
* Postural orthostatic tachycardia syndrome (POTS) is one of a group of disorders that have orthostatic intolerance (OI) as their primary symptom
* OI is a condition in which an excessively reduced volume of blood returns to the heart after an individual stands up from a lying down position. The primary symptom of OI is lightheadedness or fainting
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## Footnote
For example, autoantibodies that target cardiac receptors may produce an abnormal response during orthostasis, whereas those that target vascular receptors may lead to venous pooling, relative hypovolemia and reflex tachycardia on standing. Note: EDS = Ehlers–Danlos syndrome, MCAS = mast cell activation syndrome, RAAS = renin–angiotensin–aldosterone system
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POTs diagnostic criteria:
* HR?
* Absence of what?
* Very frequent symptoms of orthostatic intolerance that are worse while what?
* What is the duration?
* Absence of what?
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What are other dx criteria that can explain sinus tachycardia?
* Acute hypovolemia (from dehydration or blood loss)
* Anemia
* Orthostatic hypotension
* Endocrinopathy
* Adrenal insufficiency
* Carcinoid tumour
* Hyperthyroidism
* Pheochromocytoma
* Adverse effects from medication
* Panic attacks and severe anxiety
* Prolonged or sustained bed rest
* Recreational drug effects
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POTs treatment:
* What are the nonpharm txts?
* Water 3 L/d
* Salt 5 mL/d (2 tsp/d)
* Waist-high compression garments
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POTS treatment: Pharm
* May start when?
* If standing heart rate very high?
* If standing heart rate very high and β-blocker is contraindicated?
* If standing heart rate is not too high and blood pressure is low?
* May start at initial visit if symptoms are severe
* If standing heart rate very high: propranolol 10–20 mg, 4 times per day
* If standing heart rate very high and β-blocker is contraindicated: ivabradine 5 mg 2 times per day
* If standing heart rate is not too high and blood pressure is low: midodrine 5 mg orally every 4 hours, 3 times per day (8 am, noon, 4 pm)
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* What is midodrine?
* What is ivabradine?
* Midodrine is a pure alpha-agonist
* Ivabradine (Corlanor) is a hyperpolarization-activated cyclic nucleotide-gated channel blocker (HCN), this controls the spontaneous diastolic depolarization in the sinoatrial (SA) node and hence regulates the heart rate
61
Explain the pathophysio of baroreceptor reflex
Vagus nerves releases acetycholine on the heart, two types of effects, cardioinhibitory effect
* ACH will hit muscarinic receptors on the heart and decrease the HR, thus decreasing CO
* Vasodepressor effect on the vasculature shut off sympathetic and amplify parasympathetic resulting in vasodilatation and decreased SVR
When decreasing perfusion cerebral blood flow goes down and syncope occurs
Increased pain, phobias, standing
* Activates vagal outflow tract
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Diagnosing vasovagal syncope
* What is essential for diagnosis?
* In-depth history and detailed examination are essential for diagnosis
* The identification of life-threatening conditions in which syncope is only the indicator of an underlying cardiovascular disease is paramount
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What is the treatment of vasovagal synope
* Counterpressure maneuvers such as hand-grip and leg crossing may inhibit vasovagal syncope by increasing the venous return.
* Leg crossing combined with tensing of muscles at the onset of prodromal symptoms can delay or even prevent vasovagal syncope
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What are the four types of shock?
Distributive
* Septic, anaphylactic, neurogenic, endocrine-mediated
Cardiogenic
Hypovolemic
Obstructive
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Endocrine Shock
* What is this due to?
Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.
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Distributive shock:
* Characterized by what?
* What is happening? (2)
* Multiple types of distributive shock, characterized by peripheral vasodilation
* Inadequate perfusion of tissues through misdistribution of blood flow
* Cardiac pump function and blood volume is normal, tissue is not being adequately perfused
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Sepsis:
* What is it?
Sepsis is defined as life-threatening organ dysfunction resulting from dysregulated host response to infection. Septic shock is a subset of sepsis with severe circulatory, cellular, and metabolic abnormalities resulting in tissue hypoperfusion manifested as hypotension which requires vasopressor therapy and elevated lactate levels (more than 2 mmol/L)
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Sepsis:
* What is the most common pathogens?
The most common pathogens associated with sepsis and septic shock in the United States are gram-positive bacteria, including streptococcal pneumonia and Enterococcus
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What is the sepsis, severe sepsis, and septic shock criteria?
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Anaphylactic shock:
* What is it?
Anaphylactic shock is a clinical syndrome of severe hypersensitivity reaction mediated by immunoglobulin E (Ig-E), resulting in cardiovascular collapse and respiratory distress due to bronchospasm.
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Anaphylactic shock:
The immediate hypersensitivity reactions can occur when?
What is the treatment?
* The immediate hypersensitivity reactions can occur within seconds to minutes after the presentation of the inciting antigen
* Treatment: Epi
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Neurogenic shock:
* Can occur when?
* What is the underlaying mechanism?
* Neurogenic shock can occur in the setting of trauma to the spinal cord or the brain.
* The underlying mechanism is the disruption of the autonomic pathway resulting in decreased vascular resistance and changes in vagal tone.
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Neurogenic shock:
* What are the sxs?
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Hypovolemic shock
* What is it characterized by?
* What are the two types?
* Hypovolemic shock is characterized by decreased intravascular volume and increased systemic venous assistance (compensatory the mechanism to maintain perfusion in the early stages of shock). In the later stages of shock due to progressive volume depletion, cardiac output also decreases and manifests as hypotension
* Hemorrhagic vs non-hemorrhagic
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Hemorrhagic:
* What are some of the causes?
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Non-Hemorrhagic:
* What are some of the causes?(4)
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Obstructive shock:
* Mostly due to what?
* Pulmonary vascular due to what?
* Mechanical - impaired filling of right heart or due to decreased venous return to the right heart due to what?
* Mostly due to extracardiac causes leading to a decrease in the left ventricular cardiac output
* Pulmonary vascular - due to impaired blood flow from the right heart to the left heart. Examples include hemodynamically significant pulmonary embolism, severe pulmonary hypertension.
* Mechanical - impaired filling of right heart or due to decreased venous return to the right heart due to extrinsic compression. Examples include tension pneumothorax, pericardial tamponade, restrictive cardiomyopathy, constrictive pericarditis.
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Management of shock
* treat how? (general)
Treat your underlying cause, support the patient with medications (and/or machines) i.e. vasopressors, ECMO
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Management of shock: Will vary based on type of shock you encounter
* Cardiogenic i.e. pump failure=
* Hypovolemic:
* Distributive:
* Obstructive:
* Cardiogenic i.e. pump failure=Inotropes, mechanical pump
* Hypovolemic: fill the tank
* Distributive: Treat your underlying infection while protecting end-organs
* Obstructive: Relieve or bypass your obstruction
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Fill in what is covered
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Fill in
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ShoCK Review
* What is shock?
* What are the four types of shock?
* An accurate diagnosis requires what?
* Shock is a clinical manifestation of circulatory failure and is associated with high morbidity and mortality.
* There are broadly four types of shock: distributive, cardiogenic, hypovolemic, and obstructive.
* An accurate diagnosis requires a good understanding of underlying pathophysiology, clinical, biochemical, and hemodynamic manifestations of the different types of shock.
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Shock review:
* Serum lactate level is useful for what?
* Timely diagnosis and initiation of appropriate therapy are what?
* Treatment includes what?
* Serum lactate level is a useful risk stratification tool in managing undifferentiated shock.
* Timely diagnosis and initiation of appropriate therapy are of paramount importance as it can prevent progression to the reversible shock, multiorgan failure, and death.
* Treatment includes hemodynamic stabilization and correction of underlying etiology of shock.
90
A 41 year-old involved in a motorcycle accident complaints of abdominal pain and Lightheadedness. Blood pressure is 94 / 60 supine and 86 / 48 standing; pulses are weak but symmetric. The extremities are cool. Pulse oximetry supports low oxygenation. Which of the following will best assist in diagnosis and prognosis at this time?
* Cardiac Biomarkers
* Chest radiography
* lactic acid levels
* serum creatinine
* Serial glucose levels
C) lactic acid is a fairly sensitive marker for the diagnosis and monitoring of hypovolemic shock, identified by the orthostatic blood pressure.
91
Which of the following is NOT a pillar of guideline directed medical therapy (GDMT)?
* SGLT 2 inhibitor
* ARNI
* Calcium-channel blocker
* Beta-Blocker
* Alpha-agonist
* Mineralocorticoid Receptor Agonist
* Alpha-agonist
92
Which of the following changes in blood pressure is defined as orthostatic hypotension? Patient is supine, measurements take after patient stands
* systolic blood pressure dropped 10mmHg 2 minutes after standing up
* diastolic blood pressure drop 12mmHg 2 minutes after standing up
* systolic blood pressure dropped 25mmHg 3 minutes after standing up
* diastolic blood pressure drop 8mmHg 6 minutes after standing up
* diastolic blood pressure drop 12mmHg 2 minutes after standing up
* systolic blood pressure dropped 25mmHg 3 minutes after standing up
93
Which of the following is the most common cause of acute cardiogenic shock?
* Myocardial infarct
* cardiac amyloidosis
* congenital defect
* non ischemic cardiomyopathy
Myocardial infarct
94
A 33-year-old male is brought to the ED with complaints of diarrhea, fever and vomiting for three days. The patient has features suggestive of severe dehydration and shock. Lactic is 4, BP 86-46. Which of the following is the appropriate initial volume of fluid resuscitation administered to this client at the onset of shock?
* 30mL/kg lactated ringers
* 2L normal saline
* 250mL concentrated albumin
* 50mL/hr x24h normal saline
30mL/kg lactated ringers
