Cardiovascular Systems Physiology and Pathophysiology IV Flashcards
Can target the SNS (i.e. beta blockers); or can impede the activation of Ca2+, Na+, or K+ channels. In so doing, these compounds modulate depolarization and/or repolarization of cardiac tissues
Antiarrythmics
In addition, certain of the above listed cardiac arrhythmias can be studied and treated by an
Electrophysiologist
In general, an electrophysiologist can do what 3 things?
- ) Assess cardiac conductance system
- ) Characterize recurrent arrythmias
- ) Map and potentially destroy arrythmogenic foci
An area of necrosis which develops due to a sudden loss of blood supply
Infarct
Results from a severe impediment of blood supply (ischemia) to a region of the myocardium
Myocardial Infarction
The most common location for the development of an MI is the
Left ventricle
Represent ischemia and are not diagnostic for the MI
T waves
Becomes elevated following an MI and returns to normal several hours later. This elevation signals an MI
ST segment
The pathogenesis of ST elevation is complex and involves localized increases in
Extracellular K+
Resting membrane potential (RMP) of the damaged myocardium becomes less negative and the observed ST elevation is basically the difference between
Healthy RMP and ichemic RMP
Indicates irreversible myocardial death
-represent the misdirection of current away from the dead area
New Q waves
Appear within a few hours of the infarct, but may take a few days to develop
-Do not resolve
Q waves
The inferior and posterior regions of the heart are supplied by the
Right coronary artery
If the inferior myocardium is affected, electrical activity within which leads would reflect MI changes in the ECG
Inferior leads: II, III, and aVF
The posterior heart does not have a dedicated lead so we rely on
V1
A posterior infarct would show as reciprocal changes, such as a prominant R wave that is not present in a healthy ECG, in
V1
Which leads show electrical activity in the region that is supplied by the left circumflex artery?
Left lateral leads: I, aVL, V5, and V6
The anterior myocardium is supplied by the
Left anterior descending artery
Damage to the portion of the heart supplied by the left anterior descending artery would show in the
Precordial leads (V1-V6)
What are the 4 heart sounds that occur and can be coordinated with an ECG?
- ) S1
- ) S2
- ) S3
- ) S4
The first heart sound
-represents the onset of ventricular systole
S1
The first heart sound (S1) is caused following closure of the
AV valves (lub)
Heard following closure of the semilunar valves due to
vibrations of the ventricular and large vessel walls due to recoil of arterial and ventricular blood against the valve leaflets
S2 (2nd heart sound, dub)
S2 is split into which 2 components?
- ) Aortic valve component (A2)
2. ) Pulmonic valve comonent (P2)
A2 and P2 are most easily elucidated upon
Inspiration
Under normal conditions, A2-P2 is fused on expiration, but splits into a distinct A2-P2 pattern on inspiration; this is known as
Psychologic splitting
Occurs due to the decreased intrathoracic pressure that is generated during inspiration
Psychologic splitting
Decreased intrathoracic pressure allows for increased venous return to the right heart which allows for lengthened
Systolic ejection
Also, low intrathoracic pressure increases capacitance of pulmonary arteries and veins; this reduces
Intravascular pressures
During inspiration, diastolic back pressure against the pulmonic valve is reduced so that
Later closure occurs
The decrease in intrathoracic pressure lowers pulmonary vein pressure and reduces left heart diastolic filling. With less volume, the time for systole is reduced and the
Aortic valve closes earlier
An increase in the delay between A2 and P2 that is often caused by right bundle branch block, which prolongs the cardiac cycle in the right heart
Widened splitting
P2 can also be delayed by the less common
Pulmonic valve stenosis
When P2 occurs before A2 and the splitting occurs on expiration
Paradoxal splitting
Paradoxal splitting is caused by a delay in aortic valve closure. This can be the result of
Left bundle branch block or aortic stenosis
If detectable, occurs during the beginning of the middle third of ventricular filling
S3
A low pitched sound that resembles S1 and S2 and has the cadence of the word Kentucky
S3
In adults, S3 can often be heard in the setting of elevated left heart filling pressures in adult patients with
Dilated cardiomyopathies
Can be ascultated in patients with left ventricular hypertrophy (a stiff ventricle)
S4
S4 sounds like S 1 and S2 and occurs in
Late diastole
The cadence of S1 + S2 + S4 is similar to the word Tennessee, where the first syllable is
S4
Heart murmur when the aortic valve resists blood flow and there is a dramatic increase in LVP
Aortic valve stenosis
Over time, aortic valve stenosis can result in
LV hypertrophy
Heart murmur when the pulmonic valve resists blood flow and RVP is much greater than pulmonary arterial pressure
-Results in RV hypertrophy over time
Pulmonic valve stenosis
The intensity of a pulmonic valve stenosis increases
During inspiration (loudest over 2nd intercostal space)
Murmur resulting from the left atrium having to work harder to eject blood through the resistant valve, resulting in left atrial hypertrophy
-rare
Mitral stenosis
Mitral stenosis is observed on an ECG as an increased amplitude and duration of the left atrial component of the P wave observed in leads
II and V1
Murmur resulting from blood leaking back into the left atrium, which causes the left atrium to have to work harder against elevated pressures
Mitral regurgitation
The increase in left atrial size accompanying a mitral regurgitation results in a
Notched P wave in the ECG
A murmur cause by the reflux of blood during RV systole that causes an abnormal increase in jugular venous pressure
Tricuspid regurgitation
Can cause pathologic systolic waveforms within the venous circulation
Tricuspid regurgitation
Because of reflux through the inferior vena cava, tricuspid regurgitation can result in a
Pulsative liver
-liver pulsations can be palpated
Patients with a murmur that intensifies during inspiration and present with a distended jugular vein likely have a
Tricuspid regurgitation
A murmur that causes the over taxed LV to perform more work to pump blood through a leaky valve and against the high pressure within the aorta
Aortic valve regurgitation
In an aortic regurgitation, LVV and LVP are increased and the result is
LV dilation and hypertrophy
The cornerstone of diagnosing and quantifying murmurs, and certainly directs medical and surgical interventions
Electrocardiography
In the event of low plasma volume (hypovolemia), the SNS triggers changes in cardiac, vascular, renal, and neuroendocrine function which raise
Intravascular volume, CO, and total peripheral resistance (TPR) (increase BP)
With elevated plasma volume (hypervolemia) inducing a
concomitant rise in BP, alterations in renal function, CO, and vascular smooth muscle tone serve to
Lower BP
Populations of high pressure sensory receptors (baroreceptors) are loated in the
Aortic arch and carotid sinus
Low pressure baroreceptors (type A and B) are found in the
Right atrium/vena cava and left atrium/pulmonary vein regions
Sensitive to stretch and therefore change firing rate with atrial systole and diastole
Low pressure baroreceptors
Relatively inactive at blood pressures below 50-60 mm Hg, but progressively increase the rate of firing between pressures of approximately 60-180 mm Hg
High pressure baroreceptors
Signals the medulla to increase SNS input to the heart if BP plummets below 60 mmHg
Low pressure baroreceptors
Signal the ANS to attenuate SNS activity concomitant with an increase in PSNS ton in order to slow HR if BP soars
High pressure baroreceptors
Located in the carotid sinus and aortic body where they sense decreases in blood partial pressure of O2 (PO2)
Chemoreceptors
Elevated PCO2 and decreased blood pH increase the sensitivity of chemoreceptors to
Hypoxia
Chemoceptors are exquisitely sensitive to tiny changes in PCO2; but are less sensitive to changes in
PO2
Occurs when BP falls below approximately 60 mmHg because deoxygenated blood is not being removed quickly enough
Stagnant hypoxia (increase in PCO2:PO2 ratio and H+ concentration)
In this scenario, chemoceptors are activated and signal a sequence of events resulting in augmented SNS cardiovascular activity, in conjunction with a block in
Cardiac PSNS tone
Baroreceptors and chemoreceptors are designed to correct only
Acute changes in BP
-not chronic
Episodes of hypertension increase high pressure baroceptor activity. High pressure baroceptors
activate fibers within the
Afferent vagal and glossopharyngeal tracts
Within the medulla, the coordinated actions of stimulatory and inhibitory interneurons impair the activity of SNS preganglionic fibers that supply SNS tracts to the
Heart and vascular smooth muscle
In addition, there is also an activation of interneurons connecting to medullary
PSNS fibers
In response to hypertension, baroreceptors signals the medulla to downregulate SNS innervation while upregulating PSNS activity of the heart. The result is
Reduced TPR and slowed HR
In addition, signals to the kidneys lead to increased
Urine excretion
In an acute drop in BP, low pressure baroreceptors and chemoreceptors induce an upregulation in SNS activity. As a result, the following are increased
- ) Venous return to the heart
- ) HR
- ) Vascular resistance in skeletal muscle and splanchnic and renal tissues
Chronic low BP activates elaborate and integrated renal and endocrine compensatory mechanisms involving the hormones
Angiotensin II, aldosterone, and arginine vasopressin
What are the two types of hypertension (HTN)
Primary and secondary
The form of HTN which develops somewhat gradually commonly within the age range of approximately 20-50 years-old
Primary HTN
Around 95% of patients with HTN have which form?
Primary HTN
Renal malfunctions resulting in increased Na+ and H2O retention, and/or hyperactive RAAS activity can be a cause of
Primary HTN
Primary HTN can also be caused by the desensitization of baroreceptors to increased volume and pressure which results in the loss of
Normal feedback control
In part defined as uncontrolled BP despite the use of optimal doses of 3 BP medications, one of which is a diuretic
Resistant (or secondary) HTN
Secondary HTN usually manifests
Prior to age 20 or after age 50
Kidney disease such as renal artery stenosis and renal parenchymal disease and adrenocortical hormone excess can cause
Secondary HTN
Hypo- and hyperthyroidism and coarction of the aorta can cause
Secondary HTN
A protein hormone that is synthesized within the renin-angiotensin system
-A potent vasoconstrictor
Angiotensin II (An-II)
Angiotensin II bioactivity is regulated by which receptors?
AT1 and AT2
Known to mediate angiotensin II activity in vascular smooth muscle and cardiac muscle
AT1
Based upon what is known, AT1 is the predominant AnII receptor that mediates AnII-orchestrated
vasoconstriction
Angiotensin II is a potent vasoconstrictor and this action is mediated by
An-II binding to AT1
Has extra-vascular effects that can exacerbate renovascular hypertension
An-II
Can block high pressure baroreceptor input; therefore, the counter-response to elevated BP is neutralized, and SNS has free-reign to maintain increased TPR
An-II
An-II stimulates the adrenal cortex to secrete the steroid hormone
Aldosterone
Augments kidney-mediated Na+ reabsorption from the forming urine
Aldosterone
Increased Na+ resorption results in
H2O retention
A vasoconstrictor that can modulate Na+ and K+
currents that regulate ventricular myocyte function in the heart
Aldosterone
Directly linked with promoting ventricular hypertrophy, the induction of proinflammatory cascades, and profibrotic remodeling
Aldosterone
Can directly stimulate the release of norepi from post-ganglionic SNS fibers
An-II
Collectively then, An-II-induced vasoconstriction, An-II-dependent block in high pressure baroreceptor activity, increased aldosterone levels, and An-II-directed secretion of norepi, all factor into increased TPR and thus
Elevated BP
Counteract transient increases in AII and aldosterone, as well as high BP
Renal and other mechanisms
In the normotensive patient, urinary output is directly correlated with
Mean arterial Pressure (BP)
