1. Integrating concepts in Cardiovascular Physiology
Examples of normal physiology and pathophysiology:
Exercise
Heart failure
Hypovolemic shock
compensatory/decompensatory responses

2. Mohrman and Heller Skeletal muscle has B2 = vasodilation
More important for muscle dilation are the local factors that cause dilation
Top is initial response and bottom is how body responds to it.
Metabolic needs of the tissue is what drives CO
Mohrman and Heller

3. NEJM 2003 May

4. Law of LaPlace T = PD x r T PD PD
PD = distending pressure (or transmural pressure)
T = wall tension
r = radius of circle PD T PD
When walls are distended they cannot pump properly.
A baggier ht needs to have more pressure to contract it compared to a small heart chamber. A smaller chamber requires less work than a larger chamber.
Smaller vessel radius results in less distending pressure, thus requires less wall tension

5. Mechanically bad for dilated hearts Why?
Law of Laplace
Mechanically bad for dilated hearts
Why?
Normal
Hypertrophic
Dilated
 radius
Dilated hearts must do more work to generate same pressure as normal heart
Hypertrophic/dilated hearts are also compromised electrically

6. Hypertrophic and dilated cardiomyopathies present with prolonged action potential durations.
What are the consequences on heart rate, relaxation (diastole) time, potential for arrhythmias?
QT on hypertrophic ht gets longer.
Conductance is slower – QRS gets wider
Prolonged AP – prolonged refractory period – slower HR

7. Explain each symptom as it relates to congestive heart failure.
Your patient presents with shortness of breath upon exertion (dyspnea) and lying down (orthopnea) and has severe ankle swelling. Her heart and respiratory rates are elevated, her skin is pale, cold and sweaty.
Explain each symptom as it relates to congestive heart failure.
HR – compensation b/c tissue needs are not being met
SOB – edema in lung
RR –
Ankle – from edema as venous return is being backed up
Skin –
Cold –
Sweaty –

8. 1 4 2 3

9. Explain why each of the following result from reduced cardiac output1 2 3
1 – tissue needs are not being met
2 – inc HR and inc CO to better perfuse tissues/inc sympathetic tone
3 – increase blood volume – increase BP
4 – more fluid retention – more leaking
Whole r side trying to inc pressure and perfusion to tissues. On L getting congestion b/c of backup and result of actions of R side. Bad cluster of events that result in a pos feedback loop. The sooner you can break the cycle with B blockers the better 4
Distinguish the sequence of effects between LV versus RV failure
LV failure  tissue perfusion…  pulmonary congestion RV failure
RV failure  venous volume/pressure arterial-venous pressure gradient venous return vascular edema and congestion…

10. What reflexes would be involved in these responses?
During your first day of clinical rotations in the ER a patient comes in with severe femoral lacerations due to a motorcycle accident. The paramedics were unable to stop the bleeding, but you were able to do so upon admission (~1 hour after the accident).
What consequences would you anticipate on the following prior to cessation of bleeding?
Heart rate
Cardiac output
Blood pressure
Urinary production
What reflexes would be involved in these responses?
What would you do to stabilize this patient?
Compensate for venous return to compensate for blood loss
SV down b/c venous return is down
Not pumping efficiently
Wants to retain fluid to maintain blood volume/ decrease glomerular filtration b/c of dec CO
Reflexes – fast reflexes, baroreceptors, tissue needs
Stabilize – IV fluids

11. Dec cap pressure b/c they are closing
Dec cap pressure b/c they are closing. Wants to close down everything that is not needed for survival (kidneys etc).
Mohrman and Heller

12. Boron and Boulpaep Fig 24-8A
If intervention is soon enough it is reversible. If flow not returned to organs soon enough, irreversible.
If 10-20% total blood loss comes from large vein, significant decrease in intravascular volume, venous return, cardiac output…
If blood loss comes from peripheral artery, MAP does not fall until venous return is compromised
Boron and Boulpaep Fig 24-8A