Lecture 8 (Hypotension)-Exam 3 Flashcards
What is hypotension? What are the values?
- 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
How do we calculate MAP?
2/3 diastolic pressure + 1/3 systolic pressure
Blood pressure is continuously regulated via what?
via the autonomic nervous system as a balance of the sympathetic nervous system and the parasympathetic nervous system.
How does parasympathetic and sympathetic nervous system act on the BP?
- 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.
Blood pressure modulation
* Blood pressure is modulated by what 2 primary mechanisms?
CO and total peripheral vascular resistance
How do you calculate CO and SVR?
- Cardiac output = Stroke Volume x Heart Rate
- Systemic Vascular Resistance = 80 x (Mean Arterial Pressure - Mean Venous Pressure) / Cardiac Output
Blood pressure modulation:
* Disease states that reduce stroke volume or heart rate will decrease what?
will decrease the total cardiac output of the heart, functionally decreasing the ability to generate blood pressure
Various medications are also capable of inducing hypotension via what?
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
What are disease states that modulate BP? (6)
Disease states include arrhythmias, valvular regurgitation, valvular stenosis, diastolic or systolic heart failure, large volume losses of blood, and cardiac tamponade
What is poiseuille’s law?
- 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.
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?
- 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.
A decrease in arteriolar caliber increases what? increasing the diameter of terminal arterioles will what?
- 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 what?
via autonomic neuronal responses to modulate fluctuations in blood pressure
The natural state for arteriolar smooth muscle tone is what?
is to be relaxed with dilated arterioles. Therefore, the absence or blunting of autonomic input by medications or disease states will lead to hypotension
What are different types of hypotension?
- Cardiogenic
- Orthostatic
- Vasovagal
What is going on with orthostatic hypotension?
- 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.
Cardiogenic hypotension/shock
* What is it?
* What are some sxs?
* What labs?
- Cardiogenic shock is a failure to achieve sufficient cardiac output with maintained total peripheral resistance.
- Sxs: decrease BP, edema syncope
- Labs: EKG, lactic acid
Defining Cardiogenic Shock
* Defined as what?
Cardiogenic shock is defined as a primary cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion
Defining Cardiogenic Shock
* What is the clinical criteria?
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
Defining cardiogenic shock:
* Hemodynamic criteria include
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
Cardiogenic shock:
* What is the MCC cause?
* What are the mechanical defects?(5)
- 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)
Cardiogenic shock causes:
* What are contractility defects? (5)
* What can happen (clot)?
* What _ _ failure?
* What can happen to the aorta?
- 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
Cardiogenic shock:
* What are other causes?(4)
Other causes include cardiotoxic drugs (doxorubicin), medication overdose (beta/calcium channel blockers), metabolic derangements (acidosis), electrolyte abnormalities (calcium or phosphate)
Pathophysio of cardiogenic shock dt MI
* Ischemia to the myocardium causes what? What happens in return?
- 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.
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.
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.
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.
What are the cardiogenic shock SCAI stages?
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
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
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
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
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.
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.
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
Dx hypovolemia:
* What test can you do?
* What is the patho behind it?
* What is it a predictor of?
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
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?
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
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
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
Endocrine Shock
* What is this due to?
Due to underlying endocrine etiologies such as adrenal failure (Addisonian crisis) and myxedema.
What is the sepsis, severe sepsis, and septic shock criteria?
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.
Neurogenic shock:
* What are the sxs?
Hemorrhagic:
* What are some of the causes?
Non-Hemorrhagic:
* What are some of the causes?(4)
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