Heart Failure & Thromboembolic Disorders Flashcards
What are factors that affect cardiac output?
Cardiac Output = Heart Rate X Stroke Volume
What are factors affecting HR?
- autonomic innervation
- hormones
- age
What are factors affecting SV?
- heart size
- contractility (force, duration) * preload (end diastolic volume)
- afterload (vascular resistance)
What causes an ↑ in SV & CO?
↑contractility
↑preload
↓afterload
What causes a ↓ in SV & CO?
↓contractility
↓preload
↑afterload
Why athletes generally have lower heart rate?
↑muscle wall thickness (left ventricle - needs more profusion of blood & O2 b/c has thicker wall) → ↑contractility
→ ↑stroke volume → ↑tissue blood supply
↑ heart size → ↑end diastolic volume → stronger
contractility (left ventricle) → ↑stroke volume
↑SV → ↓HR (still in normal range) → maintain normal resting CO
Preload:
(stretch, filling)
* volume of blood in ventricles at end of diastole (EDP)
When does preload increase in?
- hypervolemia
- regurgitation of
cardiac valves - heart failure
Afterload:
(vascular resistance)
* left ventricle must overcome resistance to circulate blood
↑afterload =
↑cardiac workload
When does afterload increase in?
- hypertension
- vasoconstriction
What are factors that affect preload, afterload, and contractility in heart?
Contractility
* SNS, PSNS stimulation
* hormones (e.g. epinephrine,
norepinephrine, thyroid)
* electrolytes (e.g. Ca2+,K+)
* hypoxia
* drugs
Preload
* venous return
* filling time
* electrolytes (Na+, K+, Ca2+) * hypoxia
* hormones (e.g. thyroid)
* drugs
Afterload
* vascular resistance
* valve damage
Ejection fraction:
The fraction of blood ejected from ventricle in each heart beat (contraction)
EF= SV/EDV =
(~70 ml) / (~140 ml) = (~ 50%)
↑end diastolic volume
–> ___ stretch in cardiac muscle –>
__ stroke volume
↑
↑
↑preload → __ stretch → __SV
↑
↑
What are determinants of ventricular function?
- CONTRACTILITY
- AFTERLOAD
- HEART RATE
- PRELOAD
–> STROKE VOLUME - LV wall integrity
- Valvular competence
–> CARDIAC OUTPUT
In congestive heart failure (CHF), the heart:
- fails to pump the blood efficiently
- not able to maintain normal blood flow to organs
- unable to provide adequate perfusion to meet metabolic needs of peripheral tissues
“ CHF represents a complex syndrome characterized by abnormalities of ____ _______ function and ____- ______ regulation, which are accompanied by ______ ______, ____ _______, and _______ ________”.
From Dr. Milton Packer
LEFT VENTRICLE
NEURO-HORMONAL
EXERCISE INTOLERANCE
FLUID RETENTION
REDUCED LONGEVITY
What are 2 major types of heart failure?
Systolic failure
Diastolic failure
Systolic failure:
The heart loses its ability to contract or pump blood
into the circulation.
Diastolic failure:
The heart loses its ability to relax because it becomes
stiff and cannot fill properly between each beat.
CHF is divided into 2 categories based on changes in EF:
- heart failure with PRESERVED EF (≥50%)
- heart failure with REDUCED EF (≤40%)
What are common causes of CHF?
- heart attack (myocardial infarction)
- coronary heart disease
- hypertension
- congenital heart defects
- heart valve defects (mitral, aortic)
- cardiac myopathy (heart muscle disease)
- lung disease
What are the 4 compensatory mechanisms in CHF?
- Elevated heart rate (activation of SNS)
- Elevated preload
- Ventricular hypertrophy (enlarged heart)
- Vasoconstriction (endothelin, RAAS, SNS)
Describe the elevated HR (activation of SNS) pros and cons
- Pros: helps maintain cardiac output
- Cons:↓filling time, ↑O2 demand, ↑risk of arrhythmias
(b/c heart is beating faster, therefore resting/filling time is shorter)
Describe the elevated preload pros and cons
↑renin/angiotensin/aldosterone system → Na+ and water retention
- Pros: ↑stroke volume; ↑cardiac output
- Cons: pulmonary/peripheral edema, ↑O2 demand
Describe the ventricular hypertrophy (enlarged heart) pros and cons
- Pros: helps to maintain cardiac output
- Cons: ↑risk of ischemia, arrhythmias, fibrosis
Describe the vasoconstriction (endothelin, RAAS, SNS) pros and cons
- Pros: maintains BP, recruit blood to heart and brain - Cons: ↑afterload (resistance) → ↓stroke volume
Norepinephrine mechanism of action:
↑heart rate (tachycardia), ↑contractility, vasoconstriction
Angiotensin II (RAAS) mechanism of action:
vasoconstriction, Na+ retention in kidney, aldosterone release
Aldosterone mechanism of action:
Na+ and water retention in kidney
Anti-diuretic hormone mechanism of action:
↑water retention,↑vasoconstriction
Natriuretic peptides atrial (ANP), brain (BNP) mechanism of action:
diuretic (hypotensive) effects
- released from atrium & ventricles
Where are Natriuretic peptides atrial (ANP) RELEASED from?
atria
Where are Natriuretic peptides brain (BNP) RELEASED from?
ventricles
What are the signs & symptoms of CHF?
- Fluid retention and edema (peripheral/pulmonary)
- Shortness of breath (dyspnea, orthopnea, cough) - b/c of buildup of fluid in lungs & decrease O2 b/c of edema
- Fatigue (especially with activity) - can’t get to 2nd floor as easily as before
- Cyanosis (insufficient oxygen in blood)
- Confusion (if blood flow to brain is reduced)
(need more pillows at night to feel comfortable)
What are signs of Fluid retention and edema (peripheral/pulmonary) in CHF?
– WEIGHT GAIN (mainly due to edema)
– PITTING EDEMA (squishy feet/ankles) - indent stays there after you release finger
– ELEVATED JVP (jugular venous pressure)
– CRACKLING SOUNDS IN LUNGS (on auscultation)
What do symptoms of CHF depend on?
Symptoms depends on the type of heart failure (left-sided or right-sided).
- might see in both
What are symptoms of CHF mostly related to?
Symptoms are mostly related to compensatory mechanisms to improve reduced cardiac output.
What are the 2 types of CHF?
- Left-sided CHF
- Right-sided CHF
Left-sided CHF:
left side of heart (mainly left ventricle) fails; blood back up in lungs
(enough blood isn’t leaving heart)
Right-sided CHF:
- also called “Cor Pulmonale”
- right side of heart fails; blood back up in (areas that are easier to have fluid build-up like…) abdominal organs and peripheral tissues
What are the signs/symptoms of LEFT-sided CHF?
- paroxysmal nocturnal dyspnea
- ↑pulmonary capillary wedge pressure
- ↑pulmonary congestion
- cough
- crackle
- wheeze
- blood-tinged sputum
- tachypnea (b/c can’t get enough O2 exchange, so they try to compensate with increase HR)
- restlessness
- confusion
- orthopnea
- exertional dyspnea
- tachycardia
- fatigue
- cyanosis - ending of toes, fingers, lips get darker –> indication of decrease O2 levels in blood
What is the diagnosis of CHF using the PHYSICAL ASSESSMENT?
- Assessment of JVP
* indirect measure of central venous
pressure
* normal <4 cm above sternal angle
* ↑JVP indicates VOLUME OVERLOAD (doesn’t indicate HF - but commonly seen in volume overload) - Presence of ascites (fluid accumulation in peritoneal space)
- b/c abdominal has more room - Peripheral edema (pitting edema)
What is the diagnosis of CHF using IMAGING?
- Chest X-ray (CXR):
* evaluate heart size and pulmonary edema
* cardio-thoracic ratio >50% indicates enlarged heart
(ratio of heart:chest is increased in those patient) - Echocardiogram (ECHO):
CHF heart chest
* ultrasound waves used to image heart
* detect heart structural & functional abnormalities
* assess left ventricular EF (normal = 55-70% ; HF = <40%)
(never gets 100% or close to that)
What are strategies used to improve CHF?
- control diet
- salt (Na+) restriction
- fluid restriction (~2L/day) (will increase fluid build-up in body) - modify lifestyle:
- stop smoking
- weight loss in obese patients (b/c will be less work on heart)
- exercise (after symptoms are controlled)
Note: rapid weight gain maybe due to water/salt retention (build-up of fluid)
(asking what they eat (diet) wouldn’t be appropriate b/c not due to food - pharmacotherapy: treatment is chosen based on underlying problem, type, and severity of CHF
What is rapid weight gain maybe due to? What should we ask the patient?
rapid weight gain maybe due to water/salt retention (build-up of fluid)
- asking what they eat (diet) wouldn’t be appropriate b/c not due to food
Thrombosis:
Formation of blood clot comprised of platelets, fibrin, & entrapped RBCs in the vascular system which is attached to vascular endothelium.
Embolism:
A small portion of the clot breaks off, travels, and becomes trapped in a small vessel, causing occlusion leading to ischemia and infarction.
What is the Virchow’s Triad?
Three factors that promote venous thrombosis:
- Venous Stasis
- abnormality of blood flow - Endothelial Injury
- abnormality of surfaces in contact with blood - Hypercoagulability
- abnormality in clotting components
What is a thrombosis in heart like?
Thrombus on the wall of a heart chamber (ventricle or atria) is called MURAL THROMBUS.
What is a thrombosis in arterial system like?
Common locations (of clot formation) include:
* cerebral
* coronary
* mesenteric
* renal arteries
What is a thrombosis in venous system like?
Common locations include:
* large deep veins of pelvis & lower extremities
* is referred to as deep venous thrombosis (DVT)
* may result in pulmonary embolism
What is a thrombosis in venous system like?
Common locations include:
* large deep veins of pelvis & lower extremities
* is referred to as deep venous thrombosis (DVT)
* (consequence) may result in PULMONARY EMBOLISM
Arterial thrombosis disease:
- It usually results from endothelial injury & platelet activation
(main cause: atherosclerosis)
What are the complications of Arterial thrombosis disease?
- vessel occlusion
- ISCHEMIC INJURY
- ORGAN INFRACTION (myocardial infarction,
cerebrovascular accident)
(cause major damages in tissue)
Venous thrombosis disease:
- Common sites:
It usually develops in large veins of pelvis & lower
extremities.
What are the complications of Venous thrombosis disease?
Pulmonary embolism, is the most significant consequence of venous thrombosis.
Explain Pulmonary embolism
- Blood clot (or fat, air, tumor) forms in a vein and breaks free from vessel wall.
- Embolus travels through the bloodstream to the heart.
- Embolus travels through the heart & blocks blood vessels in the lung.
What are the clinical features of Deep Vein Thrombosis?
- pain
- edema
- diaphoresis (lot of sweating b/c SNS system is activated and is trying hard)
- erythema
What are the clinical features of Pulmonary embolism?
- shortness of breath
- chest pain
- cough
- syncope (can be severe enough that patient can’t breathe anymore)
- hemoptysis
What are ways you can diagnosis deep vein thrombosis?
- Ultrasonography
- Duplex ultrasonography
- Ventilation-Perfusion Scan (see if it’s traveled into pulmonary system)
A) Ventilation scan: INHALATION of radioactive compound (should get to all areas of blood)
B) Perfusion scan: INJECTION of radioactive compound (colour will change if there or not)
What is the treamtent of pulmonary embolism?
- anticoagulants
- vena cava filters
- thrombolysis (try to lyse clot)
- embolectomy (surgery to remove clot if can’t lyse or anything else)
- prevention strategies for high risk patients (ex: anticoagulants)
CO regulatory mechanisms
on slide 37
What are consequences of impaired LV function?
- Impaired LV function
- ↓cardiac output
- neurohumoral imbalance
- ↑systemic vascular resistance
- ↑ afterload
Thrombosis:
Formation of blood clot attached to the vascular endothelium.
Embolism:
Clot breaks off, travels, and becomes trapped in small vessels causing ischemia / infarction.
What is Thrombosis caused by?
abnormalities in blood flow, blood vessel surfaces, or blood clotting process.
Where can Thrombosis occur in?
in heart, arteries, veins.
What does Arterial thrombosis usually result from?
endothelial injury (antherosclerosis)
