Lecture 25: Flashcards
Define and classify hypertension
Define:
- Level of BP above which investigation and treatment do more harm than good
- 140/90 –> Mild = grade 1
- > 180/>110 –> severe = grade 3
Classify:
1) Primary (Essential) (Cause is unknown) Types: -Benign --> slow, most common -Malignant --> rapid, medical emergency -MAP = CO X TPR
2) Secondary
- Specific Disease or abnormality
Define chronic congestive cardiac failure
- Caused by uncontrollable hypertension (maintenance by the kidneys)
- Failure of the heart to pump blood at a specific rate
- Increase of End Diastolic work load of the LV
Clinical Features:
1) Exercise intolerance
2) Breathlessness
3) Fatigue
Describe the compensatory responses in severe Heart failure
Compensatory response in general: Both pathways 1) Reduced cardiac output 2) Reduce SV, increasing EDV, increase force of contraction 3) Neurohumoral activation --> Sympathetic nervous system: -Renin Angiotensin Aldosterone system -Vasopressin system -Endothelin system 4) Pathway splits into two
Path to increase Blood volume:
(Bc system thinks its low) –> makes heart work harder
1) Sodium and water retention
2) Increased Intravascular volume
3) Increased blood pressure and cardiac work
4) Myocyte loss/hypertrophy
5) Heart failure
Path to increase TPR:
(Bc system thinks its low) –> makes heart work harder
1) Vasoconstriction
2) Increased afterload
3) Increased blood pressure and cardiac work
4) Myocyte loss/hypertrophy
5) Heart failure
Describe the major cardiovascular changes that occur with ageing (i.e. compliance changes)
x
What are the long term
consequences? Their treatment?
1) Increased Blood volume –> Pulmonary edema
Treatment = Diuretics
2) Increased TPR –> Increased Afterload, Decreased SV and CO
Treatment = Beta blockers
3) Increased HR –> Increased Metabolic demand
4) Continuous sympathetic activity –> Down regulation of B receptors
5) Increased Angiotension II
–> Increased cytokines and fibrobasts, adverse remodeling of the heart
Treatment: ACE inhibitors, Ang II rec antagonists
Explain hypertension and old age
1) Arterisclerotic changes in blood vessels
- Increase Systolic Bp –> Increase Pulse pressure, workload of heart –> cardiac failure
2) Decrease Baroreceptor sensitivity
3) Decrease Cardiac performance in exercise
Theories of Essential Hypertension
1) Neurogenic or stress Hypothesis
- Longterm Alerted response (Stress) –> Symp response –> bouts of reversible hypertension (But frequent) –> Eventually Can lead to hypertropy of vascular SM –> Vasoconstriction –> Chronic Increasing TPR
2) Salt Imbalance or Renal Hypothesis
-Salt intake > Salt excreted
-Increases more water –> Increases Blood volume –> Increase VR –> Increase CVP –> Vascular SM Hypertrophy –> Vasoconstriction –> Increase TPR
-Renal artery pressure increases = increase excretion of Na+ and H2O
(Sustained blood volume results = Sustained BP)
What is the role of Baroreceptors in HTN?
- Baroreceptor firing rate increases when BP increase
- -> vagal response
-But after 1-2 days baroreceptor goes back to normal (Hypertension person wont benefit if it’s in a chronic state)
How do we know the heart is failing?
1) Stroke volume
- Contractility
- Preload
- Afterload
Systolic
-Reduced ejection fraction
Diastolic
-Preserved ejection fraction
How do we know the heart is failing?
1) Stroke volume
- Contractility –> Decreased (Can cause edema)
- Preload –> Decreased
- Afterload –> Increased
Systolic
- Reduced ejection fraction
- Eccentric hypertrophy
- Increased EDV
- Increased blood volume, wall stress, work for heart
Diastolic
- Preserved ejection fraction
- Increased EDC
- Reduced ventricle filling
- Near normal EF
- Reduced SV
Consequences of decreased contractility?
-Edema
- Ventricle failure:
1) Right ventricle failure: - Peripheral edema –> Ankle swelling –> Pitting edema
2) Left ventricle failure:
- Pulmonary edema –> Breathlessness (Dyspnea) –> Worse when supine (Orthopnea)
(Note: When one ventricle starts to fail, the other one will too eventually)
Describe the compensatory responses to mild cardiac failure
Explain the outcomes of moderate to severe cardiac failure
Compensatory responses to mild cardiac failure:
1) Low SV and CO
2) Baroreceptor reflex will kick in increasing sympathetics
3) Increases renin, venoconstriction, contractility/HR –> Restoring SV and CO = Increase EDV
4) Salt/water retention increase = increase Blood volume = increase CVP = Increase EDV
outcomes of moderate to severe cardiac failure:
-Ventricular Hypertrophy to help sustain CO –> Increase EDP –> Increased atrial and venous pressure
Different types of Essential Hypertension?
1) Pump-based Hypertension: ↑ CO
(Younger people)
2) Vascular Resistance-based Hypertension: ↑ TPR
(Older people)
3) Volume-based Hypertension: ↑ retention of Na and H2O
(Renal disease pt’s)
Hypertension and Heart failure:
hypertension = Increase TPR (Resistance heart has to do to pump blood to organs)
Baroreceptors (Ex: Kidney response) come in when hypertension occurs, which can sometimes put the system back to normal
-At this point would TPR decrease or increase and why?
If chronic hypertension sustained and leads to Heart failure –>
-Initially = Decrease contractility, Decrease CO and VR, increase TPR
Body will try to respond and compensate and maintain contractility by increasing fluid volume
- Why does it want to maintain fluid volume, How would this benefit the system?
- Would TPR increase or Decrease, why?
If baroreceptors will not be able to keep up –> leads to chronic heart failure = causing blood vessels to hypertrophy to maintain contractility needed to pump blood and this in term would increase TPR?
Hemorrhage:
-Loss of blood –> Decreased CO and VR
After compensation
Baroreceptors try to compensate by increasing blood volume from the kidneys
-At this point would TPR decrease or increase and why?
If compensation doesn’t work then
