CVD - Chronic heart failure Flashcards
What is Chronic Heart Failure (CHF)
Syndrome of the inability of the heart to deliver adequate blood/oxygen to the body
What are the different heart failure (HF) - for each side
Left sided HF = failure to properly pump blood out to the body - systolic and diastolic failure
Right sided HF = back ups in the area that collects used blood
Congestive heart failure
Systolic HF is
Less blood pumped out of ventricles
Weakened heart muscle cant squeeze as well
Diastolic HF is
Less blood fills the ventricles
Stiff heart muscle cant relax normally
When does CHF occur
When heart is unable to pump sufficiently to maintain blood flow to meet body demands
What is affected by CHF
Reduced cardiac output - due to left/right ventricular dysfunction
Systolic dysfunction - due to impairment of left ventricle
Diastolic dysfunction - due to resistance to filling of one or both ventricles
Systolic dysfunction is when
The ventricles fill with blood and then can only pump out less than 40-50% of the blood
Diastolic dysfunction is when
The stiff ventricles fill with less blood
The ventricles then only can pump out 60% of the blood
What are the most common causes of CHF (3)
Conornary artery disease
Hypertension
Myocardial infarction
What causes systolic dysfunction (reduced ejection fraction)
Afterload
Impaired contractility
What is Afterload
What causes it
Chronic pressure overload
Advanced aortic stenosis
Uncontrolled severe hyptertension
What causes impaired contractility
Cononary artery disease
Chronic volume overload
Dilated cardiomyopathies
What causes diastolic dysfunction (preserved ejection fraction)
Impaired diastolic filling
Myocardial injury results in
Reduced cardiac output
Decreased carotid baroreceptor stimulation
Decreased renal perfusion
Reduced carotid BR stimulation and Renal perfusion results in
Activation of SNS and renin angiotensin aldosterone system (RAAS)
Activation of the SNS (from reduced carotid BR stimulation and Renal perfusion) results in
Increase HR and inotropy (contraction/force of muscle)
Myocardial toxicity
Activation of the RAAS results in
B type natriuretic peptides (BNP) released
A type natriuretic peptides (ANP) released
Vasconstriction - increases Afterload
Hemodynamic alterations - increases Preload
What causes vasoconstriction
Increased angiotensin 2
What causes hemodynamic alterations
Increased aldosterone
What does BNP and ANP both do
Decrease TPR and Central venous pressure
Where is BNP secreted and in response to what
By the ventricles in response to excessive stretching of cardiomyocytes
Where is ANP secreted and in response to what
By atria in response to high blood volume
What is the SNS then inhibited by
Which results in
Beta blockers
Negative remodeling
Worsened LV function
What is the RAAS inhibited by
ACE inhibitors
Angiotensin receptor blockers
Aldosterone antagonists
ADH antagonists
Negative remodeling and worsened LV function result in
Symptoms of HF
During exercise the neural pathway consists of
Arterial baroreceptors and skeletal muscle mechano receptors go brain
Brain creates sympathetic or parasympathetic to change HR and SV, also vasculature in muscle
Changes cardiac output
Changes in total vascular conductance
Resets BP
The rein angiotensin aldosterone system is made up of
Liver
Kidneys
Liver produces
Angiotensinogen
Kidney produces
Renin when there is a decrease in renal perfusion
Angiotensinogen and Renin create
Angiotensin 1
ACE is produced
On the surface of pulmonary and renal endothelium
Angiotensin 1 and ACE create
Angiotensin 2
Angiotensin 2 causes
Increase Sympathetic activity
Increase Tubular NA and CL reabsorption and K excretion = H2O retention
Stimulation of Adrenal gland cortex
Stimulation of arteriolar vasoconstriction - increases blood pressure
Stimulation of pituitary gland posterior lobe
All the stimulations of angiotensin cause what
Water and Salt retension
Effective circulating volume to increase
Perfusion of the juxtaglomerular apparatus to increase - inhibitatory signal to stop renin from being produced in kidney
What does the stimulation of the adrenal gland cortex cause
Aldosterone secretion
Which stimulates H2O retention
What does the stimulation of the pituitary gland posterior lobe cause
ADH secretion
Which stimulates H2O absorption in collecting duct
Regulation of stroke volume includes
EDV
Aortic blood pressure
Contractility of ventricles
What is EDV
End diastolic volume
Volume of blood in ventricles = preload
What is aortic blood pressure
Pressure that heart must pump against to eject blood = afterload
What enhances contractility
Circulating Epi and NeoEpi
Direct sympathetic stimulation of heart
Coronary artery disease (CAD) is a result of
Ischemic heart disease (IHD)
Build up of plaque in the coronary arteries
Risk factors
What is the most common cause of death
Coronary artery disease
What does the build up of plaque in coronary arteries cause
Leads to limited blood flow to the heart (ischemia)
Leads to heart attack (MI)
What are the risk factos of CAD
High LDL
Low HDL
Hypertension
Family history
Diabetes
Smoking
Obesity
Medical management of CAD includes
Pharmacological treatment
Coronary intervention
Revascularisation
Pharmacological treatment of CAD involves
Statin (cholesterol lowering)
Beta blockers
Calcium channel blockers
Antiplatelet drugs (aspirin)
Coronary intervention of CAD involes
Angioplasty - unblocking blood vessel
Coronary stent - widening of blood vessel
Revascularisation of CAD involves
Coronary artery bypass grafting
4 different levels: Single Double Triple Quadruple
Myocardial infaraction occurs when
Blood flow stops to a part of the heart
Causes damage to cardiac muscle
Mostly due to coronary artery disease
Heart attack (MI) risk in monitored by
Atherosclerotic plaque
Inflammation indicated by high sensitivity C - reactive protein (hs-CRP)
Calcification from calcium deposit as part of plaque formation
rs-CRP risk levels are
<1 mg/L = low risk
1-3 mg/L = average risk
> 3 mg/L = high risk
Elevated levels of CRP predict
Risk of MI and stroke
Calcification can be detected by
CT scans
Detect calcium deposits from plaque formation
What produces CRP and in response to what
Liver
In response to factors released by macrophages and adipocytes
What are the typical signs of myocardial infarction
Discomfort in center of chest
Uncomfortable pressure, pain
Pain/discomfort in one or both arms, back, neck, jaw or stomach
Shortness of breath with or without chest discomfort
Breaking out in cold sweat, nausea or lightheadness
Medications and precautions during exercise (list of drugs)
Diuretics
Beta Blockers
Vasodilators, ACE inhibitors and angiotensin receptor blockers
Calcium channel blockers
CNS active drugs
Alpha receptor blockers
Diuretics result in
No impact on aerobic capacity
False positive test
Beta blockers result in
Decreased submax and max HR
Sometimes decreased exercise capacity
Vasodilators , ACE inhibitors and Angiotensin receptor blockers result in
Do not affect HR response
May experience Hypotension
Calcium channel blockers may result in
Decrease HR response at rest and during exercise
CNS active drugs result in
Attenuating effects on HR and BP during exercise
Alpha receptor blockers result in
Significantly lower BP
Minimal effects on HR and metabolic responses to exercise
True positive refers to
Positive exercise test
CVD
True negative refers to
Negative exercise test
No CVD
False positive refers to
Positive exercise test
No CVD
False negative refers to
Negative exercise test
CVD
Adrenalin and Noradrenalin affect on Alpha 1 leads to
Smooth muscle contraction
Adrenalin and Noradrenalin affect on Alpha 2 leads to
Inhibition of transmitter release
Smooth muscle contraction
Adrenalin and Noradrenalin affect on Beta leads to
Heart muslce contraction
Smooth muscle relaxation
Glycogenolysis
In patient aerobic frequency (FITT) with CAD and MI
2-4 times/day for 1st 3 days in hospital
2 times/day for day 4 in hospital
In patient aerobic Intensity (FITT) with CAD and MI
To tolerance if asymptomatic
RPE <= 13
Post MI/CHF = HR <=120 bpm or HRrest +20 bpm
Post surgery = HRrest +30 bpm
In patient aerobic Time (FITT) with CAD and MI
Begin intermittent bouts of 3-5 mins as tolerated
Rest period - slower walk
2:1 exercise/rest ratio
Progress to 10-15mins
In patient aerobic Type (FITT) with CAD and MI
Tolerate
Aerobic prescription with CAD and MI (FITT)
4-7 days/wk (short bouts of 1-10mins)
RPE 11 to 16
40-80%
HR below ischemic threshold
Warm up 5 -10min
20-60 min exercise
Tolerate
Muscular strength and endurance prescription with CAD and MI (FITT)
3-4 days/week
2-4 sets
12-15 reps
8-10 exercises
As long as it takes
Functional movements
Circuit training
Avoid straining and holding breath
What are the increasing effects of exercise training with CAD and MI
Maximal oxygen consumption
Ventilatory response
Anaerobic and ventilatory threshold
HDL
Self efficacy
Numbers of endothelial progenitors cells and cells that promote angiogensis and vascular regeneration
Vegal tone
What are the decreasing effects of exercise training with CAD and MI
Modest decrease in body weight, fat stores, BP, total blood cholesterol etc
Relief of angina
Protection against triggering MI by vigerous physical exertion
Coronary inflammatory markers (hs-CRP)
Adrenergic activity
What is the exercise response in CHF
Alterations in Central, Peripheral and Ventilatory abnormalities
Exercise testing considerations for CHF (table)*****
Exercise programming in CHF consists of
Referral to cardiac rehabilitation
Basic CCD4 recommendations
Re evaluate frequently
Prolong warm up and cool down
Perceived exertion and dyspnea scales > target heart rates
No isometric exercise
Electrocardiogram monitoring required when history
Resistance training safe in people with systolic dysfunction who are stable
What is the neural effect of exercise training in CHF
Central
Reflex
Neurohumoral
What is the muscular effect of exercise training in CHF
Biochemical
Metabolic
Structural
What is the cardiac effect of exercise training in CHF
Contractility
Hemodynamic
What is the vascular effect of exercise training in CHF
Vasodilatory
Overall exercise training in HF causes
RAAS to decrease
Chemoreceptors reducing stimulation of SNA
Arterial baroreceptors increasing inhibition of SNA
Exercise pressor reflex reducing stimulation of SNA
Overall reduction in ANG 2 - reduces SNA and ventilation
Reduction in RAAS causes
Less circulating and tissue ANG 2
Increase blood flow
Exercise pressor reflex causes
Reduced SNA stimulation
Increase TRPV 1 receptors
Increase CB1 recpetors
Decrease inflammation
Missing ____ reflects absence of atrial depolarization in atrial fibrillation
P Wave
Restoring the heart to a normal rhythm by pharmacologic agents is one way for the medical management of atrial fibrillation
False
Heart rate responses to exercise in individuals with atrial fibrillation can be affected by medication use
True
During exercise, stroke volume in individuals with atrial fibrillation is reduced due to limited atrial assistance during ventricular systole
False
Hs-CRP level 2mg/L classifies average risk for cardiovascular disease
True
______ happens when the blood flow to a part of the heart is blocked and cause cardiac muscle cell death
Heart attack
Which of following describes general pathophysiology of chronic heart failure
Increase in preload
If your patient (with heart failure) takes __________, it will lower BP significantly during exercise (or testing) and will have minimal effects of HR and metabolic response to exercise
Alpha receptor blockers
BNP is secreted by atria in response to high blood volume
False
Aldosterone is secreted from pituitary gland, and it increases water retention in collecting duct
False
Weakened heart muscle which cannot squeeze the ventricle well describes the typical characteristic of diastolic heart failure
False
Which of the following describes the effect of exercise training in patients with Coronary Artery Disease and Myocardial Infarction
Decreased Hs-CRP level
Coronary artery disease leads limited blood flow to the heart which causes ischemia, then it may lead ____
Heart attack
Ventilation perfusion mismatching is a typical characteristic of heart failure indicated by VE/VCO2 slope ≤34 as a poor prognosis
False
End diastolic volume in systolic heart failure will decrease with exercise training
True
True positive in testing indicates
Tested positive for CVD
Have CVD
False positive in testing indicates
Tested positive for CVD
But dont actually have CVD
True Negative in testing indicates
Tested negative for CVD
No CVD
False Negative in testing indicates
Tested negative for CVD
But you actually have CVD
Diuretics do what
Increase urine production
Have no impact on aerobic capacity
Can result in a false positive test
Beta blockers do what
Decrease submax and max heart rate
Sometimes decrease exercise capacity
Vasodilators, ACE inhibitors and angiotensin receptor blockers do what
Have no affect on HR response
May experience hypotension
Calcium channel blockers do what
Some may decrease HR response at rest and during exercise
CNS active drugs do what
Have attenuating effects on HR and BP during exercise
Alpha receptor blockers do what
Significantly lower BP
Have minimal effects on HR and metabolic responses to exercise