Advanced Pathophysiology and Physiology: Module 4 Cardiovascular Alterations

Terms in this set (58)

Secondary HTN is caused by any systemic disease process that raises peripheral vascular resistance or cardiac output. Causes include renal disease, adrenal disorders, vascular disease, and drugs (corticosteroids, oral contraceptives, and antihistamines). Fortunately, if the cause is identified and removed before permanent structural changes.
Complicated Hypertension: Complicated HTN is sustained primary HTN that has pathologic effects in addition to causing hemodynamic alterations and fluid and electrolyte imbalances. Complicated HTN compromises the structure and function of vessels, the heart, kidneys, eyes, and the brain. Cardiovascular complications include left ventricular hypertrophy, angina pectoris, congestive heart failure or left side heart failure, coronary artery disease, myocardial infarction, and sudden death.
Malignant Hypertension: Malignant HTN is a rapidly progressive HTN in which diastolic pressure usually exceeds 140mm Hg. It can cause profound cerebral edema, which disrupts cerebral function and causes loss of consciousness. High hydrostatic pressures in the capillaries cause vascular fluid to move into the interstitial space. If blood pressure is not reduced, cerebral edema. Encephalopathy occurs because high arterial pressure renders the cerebral arterioles incapable of regulating blood flow to the cerebral capillary beds. Capillary permeability is increased by high hydrostatic pressures in the capillaries, and vascular fluid exudes into the interstitial space. If blood pressure is not reduced, cerebral edema and cerebral dysfunction increase until death occurs. Organ damage resulting from malignant hypertension is life threatening. Besides encephalopathy, malignant hypertension can cause papilledema, cardiac failure, uremia, retinopathy, and cerebrovascular accident
Once injury has occurred, endothelial dysfunction and inflammation lead to the following pathophysiologic events:
1.Injured endothelial cells become inflamed and cannot make normal amounts of antithrombotic and vasodilating cytokines (see Figure 31-23).

2.Numerous inflammatory cytokines are released, including tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), interleukin-1 (IL-1), toxic oxygen radicals, CRP, and heat shock proteins.

3.Cellular Proliferation - Macrophages adhere to injured endothelium by way of adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1).

4.LDL Oxidation These macrophages then release enzymes and toxic oxygen radicals that create oxidative stress, oxidize LDL, and further injure the vessel wall. Oxidized LDL is toxic to endothelial cells and causes smooth muscle proliferation. Oxidized LDL also increases endothelial adhesion molecule expression, which recruits more monocyte/macrophages that penetrate the vessel wall. Fatty Streaks: Macrophages filled with Oxidized LDL that accumulate.

5.Growth factors also are released, including angiotensin II, fibroblast growth factor, TGF-β, and platelet-derived growth factor, which stimulate smooth muscle cell proliferation in the affected vessel.

6.Once formed, fatty streaks produce more toxic oxygen radicals and cause immunologic and inflammatory changes, resulting in progressive damage to the vessel wall. At this point, smooth muscle cells proliferate, produce collagen, and migrate over the fatty streak forming a fibrous plaque

7. The fibrous plaque may calcify, protrude into the vessel lumen, and obstruct blood flow to distal tissues, especially during exercise, which may cause symptoms (e.g., angina or intermittent claudication).
Complications/ Consequences:
--- Stable Angina: Angina pectoris chest pain (chest discomfort ranging from a sensation of heaviness or pressure to moderately severe pain) caused by myocardial ischemia. Stable angina is caused by gradual luminal narrowing and hardening of the arterial walls, so that affected vessels can't dilate in response to increased myocardial demand associated with physical exertion or emotional stress.

In other words, stable angina occurs when chronic coronary obstruction results in recurrent chest pains. The pain is transient and can last for 3-5 min. The pain is caused by lack of perfusion and anaerobic metabolism, which irritates the myocardial nerve fibers.

---- Prinzmetal Angina: also called variant angina, is chest pain due to transient ischemia of the myocardium that occurs unpredictably and almost exclusively at rest. Pain is caused by vasospasm of one or more major coronary arteries with or without associated artherosclerosis. The angina may result from decreased vagal activity, hyperactivity of the SNS, increase calcium reflux in the arterial smooth muscle and decreased nitric oxide activity.

---- Silent Ischemia and Mental Stress (Induced Ischemia): Myocardial ischemia does not always cause angina and may be associated only with nonspecific symptoms such as fatigue, dyspnea, or feeling of unease caused by induced ischemia and mental stress. More common in women and often undetected.
Acute mental stress triggers central and ANS activity. So you may have a flight or fight response to stress where the catecholamines increase HR/ b.p or coronary constriction and increase platelet activity may occur. If you already have artherosclerosis, MI or poor LV function sets up cardiac effects such as increased electrical instability, increase demand and decrease blood supply. This results in VF/ VT, ischemia, plaque rupture, coronary thrombosis. Perhaps even sudden cardiac death or MI.
Dysrhythmias, CHF, Cardiogenic Shock, Pericarditis.

----Dysrhythmias (arrhythmias): disturbances of cardiac rhythm (most common complication). Dysrhythmia can be caused by ischemia, hypoxia, ANS imbalances, lactic acidosis, electrolyte abnormalities, alterations of impulse conduction pathways or conduction defects, drug toxicity or hemodynamic abnormalities.
---- Left ventricular (CHF): characterized by pulmonary congestion, reduced myocardial contractility, and abnormal heart wall motion.
---- Cardiogenic shock: Develops if cardiac output is insufficient to maintain normal arterial pressure and to perfuse the kidneys and other organs adequately.
---- Pericarditis: Inflammation of the pericardium is a common complication of acute MI. Pericardial friction rubs often are noted 2- 3 days after MI and are associated with anterior chest pain that worsens with respiratory effort.
---- Dressler postinfarction syndrome: is a delayed form of acute pericarditis, can occur from 1 week to several months after acute MI.
---- Organic brain syndrome: can occur in acute or chronic form if blood flow to the brain is impaired secondary to MI. TIA or an outright cerebrovascular accident may result from thromboemboli that have broken loose from the wall of the left ventricle or form cardiac valves.
---- Ventricular aneurysm: formation caused by weakening of the wall of the infarcted ventricle. Also rupture of heart structures.
---- Thromboembolism: may disseminate from debris and clots that collect inside dilated aneurysmal sacs or from the infarcted endocardium and travel to the pulmonary or systemic vascular systems.
---- Pulmonary emboli: may result from the breaking loose of deep venous thrombi of the legs in individuals who are confined to bed.
---- Sudden death: result from cardiac arrest is often caused by dysrhythmias, particularly V-fib.

Clinical Evaluations
ECG changes
Cardiac enzymes: -troponin most specific, - see in 2-4 hrs, remains elevated for 7-10 days.
CK-MB: see in 2-4 hrs, peak in 24hrs
LDH- hyperglycemia 72 hrs post MI

Look at Box 32.2 pg. 1160 in Huether
HF is the general term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood- borne nutrients.

Heart failure: is an inability of the heart to supply the metabolism with adequate circulatory volume and pressure.

Left heart failure (CHF) can be categorized as heart failure with reduced ejection fraction (systolic heart failure- insufficient contraction) or heart failure with preserved ejection fraction (diastolic heart failure- insufficient relaxation).

Systolic heart failure is defined as an inability of the heart to generate an adequate cardiac output to perfuse vital tissue. Treatment: ACE inhibitors, beta blockers, salt restriction, loop diuretics and aldosterone- blockers

4. Cardiac output depends on the heart rate and stroke volume. Stroke volume is influenced by contractility, preload, and afterload. MI is the most common cause of decreased contractility. Myocardial ischemia results in ventricular remodeling that cause progressive myocyte contractile dysfunction over time.

5. Preload LVEDV is increased when there is decreased contractility or excess plasma volume.

6. Increased afterload is most commonly the result of increased peripheral vascular resistance. This increase in resistance decreases ventricular emptying and makes more workload for the left ventricle, resulting in hypertrophy and ventricular remodeling. The vicious cycle of decreasing contractility, increasing preload, and increasing afterload causes progressive worsening.

7. Neurohumoral mechanisms of CHF include abnormalities in the SNS, RAAS, arginine vasopressin, natriuretic peptides, inflammatory cytokines and myocyte metabolism.

8. The clinical manifestations of left heart failure are the result of pulmonary vascular congestion and inadequate systemic perfusion,

9. Management of left heart failure relies on increasing contractility and reducing preload and afterload.
High-output heart failure is the inability of the heart
to adequately supply the body with blood-borne nutrients
despite adequate blood volume and normal or elevated
myocardial contractility. In high-output failure, the heart
increases its output, but the body's metabolic needs are
still not met.

Common causes of high-output failure are
anemia, septicemia, hyperthyroidism, and beriberi.

Anemia decreases the oxygen-carrying capacity of the
blood. Metabolic acidosis occurs as the body's cells switch
to anaerobic metabolism (see Chapter 4). In response to
metabolic acidosis, heart rate and stroke volume increase
in an attempt to circulate blood faster. If anemia is severe,
however, even maximum cardiac output does not supply
the cells with enough oxygen for metabolism.

In septicemia, disturbed metabolism, bacterial toxins,
and the inflammatory process cause systemic vasodilation and fever. Faced with a lowered SVR and an elevated
metabolic rate, cardiac output increases to maintain
blood pressure and prevent metabolic acidosis. In overwhelming septicemia, however, the heart may not be able to raise its output enough to compensate for vasodilation. Body tissues show signs of inadequate blood supply despite high cardiac output.

Hyperthyroidism accelerates cellular metabolism
through the actions of elevations of thyroxine from the
thyroid gland. This elevation may occur chronically
(thyrotoxicosis) or acutely (thyroid storm). Because the
body's demand for oxygen threatens to cause metabolic
acidosis, cardiac output increases. If blood levels of thyroxine are high and the metabolic response to thyroxine
is vigorous, even an abnormally elevated cardiac output
may be inadequate.

Huether, Sue E.; McCance, Kathryn L.; Parkinson, Clayton F. (2013-12-24). Study Guide for Understanding Pathophysiology (Page 168). Elsevier Health Sciences. Kindle Edition.
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