Fourteen Flashcards
What are three mechanisms that try to compensate when there is ventricular dysfunction? What happens when they can’t completely compensate?
Frank-Starling Mechanism-Increase preload, increase stretch, increase CO
Release of catecholamines (sympath.)
Myocardial hypertrophy and remodeling
Heart failure symptoms occur when they can’t quite compensate.
What specific things cause remodeling of the heart in cardiac dilation, pathological hypertrophy, and physiological hypertrophy? What happens regarding myocyte size/condition, fibrosis, and cardiac function in each?
Cardiac dilation can be caused by MI and dilated CM. Myocyte length increases (too much). Myoctyes die. Fibrosis occurs. Cardiac Dysfunction occurs.
In patholog. hypertrophy, it is caused by pressure loading. Myocytes width is increased, but they are increased in a way that makes them contract less effectively. There is fibrosis. There may or may not be cardiac dysfunction depending on compensation.
In physiol. hypertrophy, it is caused by development, exercise, or pregnancy. Myoctye length increases in a way that makes contraction more efficient. No fibrosis. No cardiac dysfunction.
What are 13 causes of predominant systolic dysfunction? 4 causes of diastolic dysfunction?
Predominant systolic dysfunction
- Myocardial infarction /severe coronary artery disease
- Hypertension (severe and prolonged exposure)
- Idiopathic or familial
- Toxicity[chemotherapy, cocaine, ETOH]
- Systemic or infiltrative process [amyloidosis, sarcoidosis, hemochromatosis, scleroderma]
- Myocarditis
- Catecholamine-induced ‘Takotsubo’
- Peri-partum
- Mitochondrial disease, muscular dystrophy, or glycogen storage disease
- Congenital or LV non-compaction syndrome
- Infectious [viral, Chagas]
- Valvular (aortic valve stenosis or insufficiency, mitral valve insufficiency)
- Nutritional deficiency (thiamine, selenium, carnitine )
Predominant diastolic dysfunction
- Hypertension
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy from a systemic or infiltrative process [amyloidosis, sarcoidosis,
hemochromatosis, eosinophilia/Loeffler’s, fibrosis] - High output failure (beri-beri, hyperthyroidism, anemia)
Describe how the neuro-humoral system tries to compensate for ventricular dysfunction.
Circulating catecholamines and NE from nerves bind to their receptor on the heart (Beta 1 likely), activating adenylate cyclase, leading to cAMP which activates protein kinases leading to more calcium, more efficient contracting.
While they due help ventricular function for awhile, they lead to worsened survival (decompensation) due to:
Causing necrosis/apoptosis
Regulating the beta receptor g protein adenylate cyclase complex
Causing arrhythmia
How does the RAAS try to compensate for ventricular dysfunction?
Low cardiac output leads to renin release leading to angiotensis I then II.
Angiotensin II is a potent vasoconstrictor. It also causes the released of ADH and aldosterone.
ADH causes water and salt retention to occur
Endothelin is a very marked vasoconstrictor.
Atrial natriuretic peptide assists in combating the vasoconstriction (causing salt and water to be secreted)
ALdosterone leads to myocardial fibrosis, remodeling, activation of symp. system and salt retention.
What things happen to the myocardium that cause ventricular dysfunction? What are some possible causes of these things?
Increased level of programmed cell death (apoptosis) and suicide gene expression. Likely due to excess catecholamines, angiotensin, oxygen free radicals, and inflammatory cytokines.
There is less intracellular calcium in the failing heart (abnormal contractile mechanisms)
Reversion to the fetal genotype with expression of abnormal proteins including myosin heavy chain-beta. This displays slower contraction velocity and weaker contraction strength from dysfunctional excitation-contraction coupling.
What adaptions occur as a result of myocardial dysfunction that lead to congestive symptoms?
VESV and VESP increase.
Volume and pressure in atrium behind ventricle
Atrium contracts more vigorously
Pressure increases in the venous and capillary beds behind (and upstream) to the failing ventricle.
Transudation of fluid from capillary bed into the interstitial space leading to pulmonary congestion and/or peripheral edema and ascites
What are the low output sequelae of cardiac dysfunction?
Brain: Mental obtundation
Skeletal muscle weakness
Kidneys: Sodium and water retention
What are some causes of Right sided heart failure
left-side heart failure (most common), pulmonic valve stenosis, right ventricular infarction
COPD, interstitial lung disease, ARDS, Chronic lung infection or brochiecstasis
Pulmonary Embolism, Primary pulmonary hypertension
What is the difference between systolic and diastolic failure? What causes diastolic failure? How common is it?
Diastolic failure is when the LV can’t accept blood as well as it should. It may be the sole cause of HF in 1/3-1/2 pts. LV is usually small and thick with good overall ejection fraction.
May be seen in pts. with ischemic heart disease, HTN, LVH, and infiltrative diseases. Most with systolic dysfunction will have some diastolic dysfunction.
How is CHF diagnosed? What symptoms exist?
Syndromic clinical definition of cardinal symptoms. Dyspnea, pulmonary congestion, systemic congestion, heart enlargement, abnormal ausculation, jugular venous pressure abnormalities, HR and rhythm/BP abnormalities
What are some different aspects of dyspnea that come along with CHF?
- Pulmonary congestion is associated with dyspnea (difficult or labored breathing) only with exertion
in mild heart failure. W/worse HF progressively less exertion and finally even at rest. - Orthopnea: When a subject is supine, the fraction of the blood volume contained in the lungs is increased.
- PND: In its worst form, it is accompanied by cough, sometimes productive of white or pink frothy sputum which is occasionally blood stained.
- Cough: 1 a respiratory symptom. However cough, on assuming the supine position or on performing exercise, is an important symptom of cardiac disease and is related to pulmonary congestion.
What other evidence of pulmonary congestion can be found aside from dyspnea?
Chest X-ray: Redistribution of the blood in the lungs is noted as engorgement of the pulmonary veins
and to fluid in the interstitial spaces of the lungs or in the alveoli.
Normal standing subject:
upper lung zones are lucent (blood flow is least and the veins are almost collapsed)
blood lower lung zones flow is greatest.
In HF the normal distribution of blood flow from top to bottom of the lungs is abolished and
eventually even reversed in cardiac failure appearance of lung fields on X-ray (will view xrays in future lecture).
Enlarged heart: some forms of HF have cardiac enlargement. See as enlarged heart shadow on X-ray.
If a patient presents with new onset severe CHF and a normal heart size, think of a recent AMI.
What evidences of systemic congestion usually exist in CHF? What causes them?
Pulmonary circulation: Normally is a low pressure, low resistance system. 5-10 mmHg suffices to
drive blood from the head of the pulmonary circulation (the pulmonary artery) to its termination (the
left atrium).
If have increased LV diastolic pressure as in HF – the normal mean pulmonary arterial pressure of
approximately 11 mmHg will not suffice to perfuse the pulmonary vascular bed. Thus obligatory
pulmonary arterial HTN occurs to compensate.
systolic RV dysfunction, hypertrophy and possibly dilation/failure can occur leading to congestion
of systemic tissues and organ:
- liver becomes congested and eventually its function is grossly impaired
- subcutaneous fluid appears as edema
- effusions in the peritoneum (ascites) and in the pleural and pericardial cavities.
How is heart enlargement manifested? What if someone has new onset severe CHF w/o enlarged heart?
Enlarged heart: some forms of HF have cardiac enlargement. See as enlarged heart shadow on X-ray.
If a patient presents with new onset severe CHF and a normal heart size, think of a recent AMI.
Heart Enlargement: Manifested by clinical examination, the chest radiograph, the electrocardiogram, and the echocardiogram.