9-3 Cardiovascular cases lab Flashcards

1
Q

—Where does the sympathetic innervation of the heart have its origins?

A

—Cord segments T1-5(6)
—Synapses occur in the upper thoracic and/or cervical chain ganglia

—Sympathetic fibers to the heart do have a right- and left-sided distribution
—Right sided fibers pass to the right deep cardiac plexus - innervate the right heart and sinoatrial (SA) node
—Left sided fibers pass to left deep cardiac plexus – innervate left heart and atrioventricular (AV node)

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2
Q

—What is the result of hypersympathetic activity (tone) to the right side of the heart (SA node)?

A

—Supraventricular tachyarrhythmias
—Sinus tachycardia
—Paroxysmal supraventricular tachycardia (PSVT)

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3
Q

—What is the result of hypersympathetic activity (tone) to the left side of the heart (AV node)?

A

—Ectopic foci
—Ventricular tachycardia
—Ventricular fibrillation

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4
Q

—What type of somatic dysfunction can increase sympathetic activity (tone) to the heart?

A

—Upper thoracic dysfunction (especially extended segments)
—Upper rib dysfunction, many times associated with upper thoracic dysfunction
—Cervical dysfunction – affecting the superior, middle and inferior cervical ganglia

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5
Q

—Where does the parasympathetic innervation of the heart have its origins?

A

—Vagus nerves (cranial nerve 10)

—Also have ipsilateral distribution:
—Right vagus – innervates the sinoatrial (SA) node
—Left vagus – innervates atrioventricular (AV) node

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6
Q

—What is the result of hyperparasympathetic activity (tone) to the right side of the heart (SA node)?

A

—Sinus Bradycardia
—

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7
Q

—What is the result of hyperparasympathetic activity (tone) to the left side of the heart (AV node)?

A

—AV Blocks

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8
Q

—What is the course of the vagus nerve (cranial nerve 10)?

A

—Originates on the medulla
—Exits the skull via the jugular foramen between the occipital and temporal bones
—Has connections with the first 2 cervical somatic nerves
—Enters the chest via the thoracic inlet

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9
Q

—What types of somatic dysfunction can affect the vagus nerves?

A

—Occipitomastoid compression affecting the jugular foramen
—Occiput, atlas and axis (upper cervical spine)

—Thoracic inlet
—Upper thoracics
—Upper ribs
—Clavicles
—Lower cervicals
—Cervical fascia
—ECT.

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10
Q

What is the path of lymph back to the heart? What drives it?

A

—Lymphatic drainage from heart and lungs primarily carried back to the heart via the right lymphatic duct (1/3 of body)
—Courses through the thoracic inlet on the way back into the heart

—Driven by synchronized diaphragmatic function and muscle activity – overall body movement

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11
Q

What improves lymphatic flow?

A

—OMM, in dog studies, can improve lymphatic flow by 4-5 times
—Exercise can improve lymphatic flow by 30+ times
—We can combine both for the benefit of the patient

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12
Q

—What are some areas of somatic dysfunction that can negatively affect lymphatic flow?

A

—Thoracic inlet
—Respiratory diaphragm
—Lower thoracics
—Lower ribs
—Upper lumbars (psoas major muscle)
—Sympathetics

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13
Q

How are Chapman’s reflexes good for CV cases?

A

They probably are not. Here’s what Ramey says:

—Chapman’s Reflexes
—A viscerosomatic reflex mechanism
—Associated with palpable nodules deep to skin and subcutaneous tissue
—Can be used for diagnosis and treatment
—Can be used to affect heart, renal and adrenal function

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14
Q

What are some palpatory changes associated with cardiac problems?

A

—Larson, Beal and Nicholas have reported palpatory changes at T2-T4 on the left with cardiac problems
—Can any situations mask a patient from developing palpable reflexes (tissue texture changes) with cardiac problems?

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15
Q

How does allostatic load cause disease?

A

—Somatic dysfunction anywhere affects the individual locally and globally (entirely)
—Stressors/imbalance that takes them closer to the threshold of symptoms and disease-activates SNS-HPA couple

—Increased allostatic load may contribute to breakdown of the cardiovascular, immune, renal, gastrointestinal and central nervous systems

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16
Q

What activity is SD frequently associated with?

A

—Somatic dysfunction is frequently associated with hypersympathetic activity

—Example – upper thoracic dysfunction may be associated with local hypersympathetic tone to innervated structures but also a global increase in sympathetic tone throughout the body

—Overall, the entire individual is closer to their threshold for firing , more susceptible to imbalance and closer to the threshold for symptoms and disease

17
Q

What should we do to correct SD?

A

—Our job – to work knowingly with the system to allow health to manifest itself
—

As a result, multiple layers of dysfunction are removed to allow the underlying health to shine through
—It is not a sequence of wresting holds to mindlessly apply to disease conditions
—Osteopathy is art and science integrated into one

—The overall result of a competently applied Osteopathic treatment is to improve the health, function and motion of the individual

18
Q

—Epigenetics - do our genes (DNA) just randomly think for themselves?

A

—Probably not! Epigenetics look at the genes as responding to multiple environmental signals that go into them

—Positive signals may produce positive epigenetic expression and vice versa
—Epigenetic abnormalities may be passed on for multiple generations unless the environmental signals are altered

19
Q

—What are some negative environmental signals that may have a negative impact on gene expression?

A

—Poor nutrition
—Toxic thoughts/mental stress
—Physical stress
—Environmental toxins
—Somatic dysfunction
—Others???

20
Q

—What is the most common cause of hypertension?

A

—Essential
—We don’t know what causes it
—Harrison’s Principles of Internal Medicine describes multiple contributing factors including increased sympathetic activity
—Some antihypertensive medications work by reducing sympathetic effects
—Renin-angiotensin-aldosterone system – involved in the regulation of arterial pressure via:
—Angiotensin II (vasoconstrictor)
—Aldosterone (sodium retention)

21
Q

What does renin do? Where is it made?

A

—Renin is synthesized by the juxtaglomerular cells of the kidney in response to:

—Decreased pressure or stretch within the renal afferent arteriole (baroreceptor mechanism)

—Sympathetic nervous system stimulation of renin-secreting cells

22
Q

—How can somatic dysfunction contribute to elevated blood pressure and hypertension?

A

—Upper thoracic dysfunction can facilitate increased sympathetic tone to the heart
—Increased heart rate
—Increased stroke volume

23
Q

What can increase sympathetic tone to adrenal gland and kidney?

A

—Somatic dysfunction in the thoracic and lumbar regions (especially T6-L2) can facilitate increased sympathetic tone to the adrenal gland and kidney

24
Q

What can HTN and SD do hormonally?

A

—Will facilitate catecholamine release from adrenal – resulting in increased cardiac output and peripheral resistance

—Will activate renin-angiotensin-aldosterone system – resulting in vasoconstriction (increased vascular resistance) and sodium and fluid retention via aldosterone

25
Q

How can SD of the cranium alter BP?

A

—Somatic dysfunction affecting the cranium (SBS compression, occipitomastoid compression affecting jugular foramen), occiput, atlas and remainder of cervical spine may alter carotid receptor function and contribute to alterations in blood pressure

26
Q

What should you do when treating CV cases with OMM?

A

—Treat the entire patient Osteopathically to overall reduce the allostatic load
—Pay special attention to the cranial mechanism, cervicals, upper thoracics and thoracolumbar junction
—Don’t forget Chapman’s reflexes

27
Q

—A 30 year old male presents for an initial routine physical. He has not seen a physician for 12 years and has no complaints.
—Review of systems negative
—Medical histories noncontributory
—Vitals Temp 99.0F, BP 145/95, Pulse 70, Respirations 14
—Physical exam – normal
—What is the diagnosis?
—How will you manage it?

A

—What is it? MI
—Many demonstrate autonomic imbalance

—Dysfunction at T2-3 on left in patients with anterior wall MI
—Dysfunction at C2 and cranial base (vagus) with inferior wall MI

—Most common cause of death within the 1st 24 hours is ventricular fibrillation (50% occur within 1st hour)
—Treat them sooner versus later

28
Q

What is a goal of OMM treatment of CV cases?

A

—Goals
— Bring autonomic balance back to the cardiovascular system
—Prevent ventricular fibrillation
—Reducing sympathetic tone will cause dilation of the coronary arteries – improved myocardial perfusion
—Improve arterial supply and venous and lymphatic drainage to heart

29
Q

Should you use HVLA with CV cases?

A

—Avoid HVLA technique (especially to the upper thoracics) during the initial management. Why?
—HVLA can cause a short-term increase in sympathetic activity
—May result in vasoconstriction of coronary arteries and extend infarct

30
Q

What should you pay special attention to when treating CV cases with OMM?

A

—Again, treat the whole patient Osteopathically to improve function and motion but pay special attention to the:
—Cranial mechanism (CV 4 helps balance autonomics)
—Cervical spine (Vagus)
—Upper thoracic spine and upper ribs
—Thoracolumbar junction
—Chapman’s reflexes affecting heart, adrenals and kidneys
—Gentler techniques are initially a better option!

31
Q

—A 48-year-old male is brought to your emergency department via ambulance with chest pain of 45 minutes duration. A 12-lead EKG is suggestive of an inferior wall MI
—What do you do?

A

don’t know yet

32
Q

What are the symptoms and associations with CHF?

A

—Clinical syndrome associated with:
—Intravascular and interstitial volume overload
—Inadequate tissue perfusion

—Symptoms
—Fatigue and SOB most common

—Also see anorexia, nausea, early satiety associated with abdominal pain/fullness, confusion, disorientation, sleep/mood disturbances and nocturia

33
Q

What is the pathogenesis of CHF?

A

—Pathogenesis – progressive disorder
—Something damages the heart muscle or reduces its ability to generate force (contract)
—

Many causes including coronary artery disease, MI, hypertension, toxic damage (excessive alcohol), viral infection, etc.
—Regardless of cause, result is overall decline in pumping capacity of heart

—Vicious downward spiral develops due to activation of neurohormonal systems

34
Q

What is the spiral associated with CHF?

A

—Decreased CO – unloading of high-pressure baroreceptors in left ventricle, carotid sinus and aortic arch

—Afferent signals to CNS – releases ADH (antidiuretic hormone)
—Reabsorption of free water

—Activation of sympathetic efferents to heart, kidney, peripheral vasculature and skeletal muscles

—Sympathetic stimulation of kidney associated with
—Release of renin and activation of renin-angiotensin-aldosterone pathway
—Salt and water retention
—Vasoconstriction and increased vascular resistance
—Myocyte hypertrophy
—Myocyte death
—Myocardial fibrosis

35
Q

What is the goal of OMM when treating CHF?

A

—Goal is to break into the downward spiral
—Reduce intravascular and interstitial volume overload (improve renal function)
—Improve tissue perfusion
—Optimize cardiac function

36
Q

How should patients with CHF be treated with OMM?

A

—Treat entire patient Osteopathically but especially pay attention to:
—Cranial mechanism
—Cervical spine
—Upper thoracics
—Thoracolumbar junction (kidneys and adrenals)
—Lymphatics (thoracic inlet, respiratory and other diaphragms)
—Proceed slowly - these patients can be very fragile!

37
Q

What are important elements of treatment other than OMM? Other than the obvious medicine/surgery/science?

A

—Exercise is a key and improves:
—Autonomic nervous system function
—Regional blood flow
—Endothelial function
—Skeletal muscle function
—Quality of life
—Exercise training can improve exercise duration as much as pharmaceutical agents (digoxin and ACE inhibitors)
—We combine exercise, pharmacologic management and OMM for best possible outcomes

—Manage other comorbid conditions including hypertension, diabetes, thyroid disease, etc.