Cardiovascular Physiology Lecture 9
Objective 1: Understand the meaning of various changes in the ECG, why they occur, the consequences of these changes, and how they can be treated.
Interpretation of the ECG can provide information on HR, rhythm, and conduction velocity
Alterations in the shape, timing, or duration of various waves and/or segments can help clinicians diagnose electrical abnormalities in the hear
ECG: sum of all electrical activity in the heart
P wave: atrial depolarization
P-R segment: conduction through AV node and AV bundle
QRS complex: ventricular depolarization
T wave: ventricular repolarization
10 sec rhythm strip, 12 cycles = 12 x 6= 60 bpm
Brady Cardia= tom brady is slow, below normal HR
Tacacardia= above normal HR
Third Degree block= conduction b/t atria and ventricles through AV node isn't happening (extra p-waves)
Atrial fibrillation= electrical chaos, depol. everywhere, no coord. contraction of atria (no p-waves)
Ventricular fibrilation= electrical chaos in ventricles, heart quivers, cardiac arrest, treated with defib (shocks heart, stops electrical chaos)
Objective 2: Understand how the failure of cardiac valves affects CO and BP, as well as how heart valve dysfunction can be treated.
Objective 3: Understand how reductions in cardiac contractility can cause the development of heart failure, as well as the consequences of this condition.
Objective 4: Understand the causes, consequences, and treatment of atherosclerotic vascular disease.
Objective 5: Understand the causes, consequences, and treatment of hypertension (high blood pressure)
2:1 ratio of conduction between atria and ventricles
1/2 of atrial beats conducted to ventricle
Av node= frequency filter, many of atrial impulses reach AV node during its refractory period.
This protects the ventricles from dangerously high rates that compromise CO
Cardiac Abnormalities: Valve Disease
Stenotic Valves:
-Narrowing of valve opening
-Increased resistance to flow
-Increased velocity of flow
Turbulent flow -> heart murmur when valve should be open
Insufficient Valves:
-Valve leaflets do not completely seal when valve should be closed
-Causes regurgitation of blood (backward flow into proximal chamber)
Turbulent flow -> heart murmur when valve should be closed
Examples of these:
In Systole: Aortic Semilunar Valves should be open and mitral valve should be closed. With a stenotic murmur, the semilunar valve is partially closed. With an incompetent valve the mitral valve is slightly open.
Mitral Stenosis: During Diastole -> narrow mitral valve opening, increased resistance to flow from LA to LV. Increased pressure and volume in LA.
-> Backward transmission of elevated LA pressure to pulmonary circulation. PULMONARY EDEMA
-> Elevates hydrostatic pressure which favors filtration (leads to fluid in lungs)
Mitral Regurgitation
During Ventricular contraction the AV valves remain closed to prevent backflow. Mitral regurgitation blood flows back into atria (leaky)
->leads to high LA pressure -> pulmonary edema
-> CO is reduced because portion of SV is ejected back into LA
Cardiac Abnormalities: Heart Failure
Heart failure is present when CO fails to meet metabolic demands of the body (HF with reduced EF)
-> Less blood pumped out of ventricles because of weakened heart muscles can't squeeze as well.
Or when those demands can only be met when cardiac filling pressures are abnormally high (HF with preserved EF)
-> less blood fills the ventricles because stiff heart muscles can't relax normally (less known about this condition)
Heart failure is associated with diminished cardiac contractility
SV diminished (more blood in ventricle left)
Restores SV but more EDV -> decrease in ejection fraction
Also leads to inadequate arterial pressure:
Decrease in flow and resistance= Decrease pressure
Compensatory Responses in HF
Increase SNS activity
-Increase contractility and HR to maintain CO
-Increase TPR to maintain MAP
Actually detrimental in long term...
Leads to downregulation and desensitization of beta-adrenergic receptors
Augmented EDV (preload) to maintain SV via Frank-Starling mechanism
Best treatment: "get a new pump" (heart transplant, mechanical assist device, regenerative therapy?)
When the heart becomes an insufficient pump: Venous pressure becomes elevated
Tissue edema develops due to increased hydrostatic pressure at capillaries
Atherosclerotic Vascular Disease:
Fatty deposits (plaques) form along inside of arterial blood vessels.
May decrease vessel diameter and reduce blood flow due to increased resistance
Fatty Streak
Lipids build up
Stable plaque
Vulnerable plaque (microphages may release enzymes that dissolve collagen and convert stable plaques to unstable plaques
-> eventually leads to Atheothrombosis: rupture causes block
Can compromise blood flow throughout the body
Coronary Artery Disease
Cerebrovascular Disease
Peripheral Arterial Disease
Treatment:
Cardiac Catheterization= moves opposite direction of blood flow. Inserted at femoral artery.
Coronary Artery Bypass Graft (CABG) Surgery:
Bypass using an artery from another tissue, alternative path for blood to flow. Can do it with a vein or artery.
Coronary Stenting to Restore Vessel Diameter (Angioplasty):
Balloon catheter inserted between stenosis.
-Systolic BP: >140 mmHg or Diastolic BP: >90 mmHg
-Chronic (while Hypotension is more immediate)
-Risk of developing CVD doubles with each 20/10 mm Hg increase in BP over baseline 115/75
Essential (90-95%)= no clear identifiable cause
Secondary (5-10%)= known cause ( renal stenosis= narrowing of renal artery , decrease flow to kidneys, thinks BP is low, kidneys signal to increase BP)
Essential Hypertension:
-Cardiac output is usually normal
-Appears to be associated with increased peripheral resistance
Consequences:
Afterload= the "load" that the heart must overcome to eject blood (arterial BP is used as indirect indicator)
Carotid and aortic baroreceptors adapt: allows higher BP to persist with correction by autonomic nervous system
Kidneys are complicit: BP elevations could be corrected by decreasing blood volume (via increased urine output by kidneys)
Treatment: reduce TPR/blood volume?
-Calcium channel blockers, diuretics, beta-blocking drugs, ACE inhibitors, and angiotensin receptor blockers