pathophysiology/ cardiovascular function

Pathophysiology/ cardiovascular function 1


هذا العمل مقدم من الفريق الأكاديمي في فريق لجان الدفعات/ كلية

التمريض

يحتوي على ملخص من الكتاب ، بالإضافة إلى شرح من الدكتور

^^ و شروحات باللغة العربية

الملخص مرتب حسب ورود المادة في الكتاب


Cardiovascular function

Heart failure: -

Referred to as congestive heart failure

Is a condition in which the heart is unable to pump an adequate amount of blood

to meet the body's metabolic needs. Leads to decreased cardiac output, increased preload, increased afterload; these

three events result in decreased contractility and stroke volume. Causes include: Congenital heart defects, myocardial infarction, heart valve Disease,

dysrhythmias, thyroid disease (either hyperthyroidism or hypothyroidism), And severe anemia.

Compensatory Mechanism:

-Initially, the SNS is stimulated which increases heart rate, contractility, vasoconstriction, and antidiuretic hormone secretion, it increases cardiac output in the beginning, but eventually leading to excessive preload and afterload. -These mechanisms continue to struggle to meet the body's metabolic needs until

excessive myocardial oxygen demand and preload result in decreased contractility

and decompensation.

- Declining cardiac output also leads to decreased renal perfusion, which activates

the renin-angiotensin-aldosterone system. Which contributes to the vasoconstriction

and fluid retention.

- Ventricular hypertrophy is another compensatory mechanism, but the enlarged

myocardium eventually exceeds the oxygen supply and decreases contractility.

Heart failure can be categorized in several ways: Systolic dysfunction, Diastolic dysfunction and mixed. A. Systolic dysfunction: - -It is characterized by decreased cardiac output due to decreased contractility. -Causes of decreased contractility include; chronic ischemia from coronary artery disease, dysrhythmias, dilated cardiomyopathy, chronic alcohol abuse, myocarditis

B. Diastolic dysfunction: - -It is characterized by decreased ventricular filling from Abnormal myocardial relaxation and increased left ventricular pressure. -Caused by Conditions that stiffen the myocardium, such as coronary artery disease, Hypertrophic and restrictive cardiomyopathy and pericardial disease.

C. Mixed dysfunction: - -It is a combination of Systolic dysfunction and Diastolic dysfunction.


Heart failure can be classified as left or right sided heart failure. → Left sided heart failure: - - It is a result of ineffective left ventricular contractility. - When cardiac output falls, blood that is not being pumped out into the body backs up first in the left atrium and then in the pulmonary circulation which result in pulmonary congestion, dyspnea and activity intolerance. - If blood continues to accumulate, pulmonary edema and right sided heart failure will develop. - Causes include left ventricular infarction, hypertension, and aortic and mitral Valve stenosis

^^ ران و اتجاه الأسهمانتبهوا على سماكة الجدو لصورة بتوضحهم ^^ هاي ا


→ Right sided heart failure: - -It is a result of ineffective right ventricular contractility.

-As a result the blood does not move appropriately out of the right ventricle and blood

backs up in the right atrium and then in the peripheral circulation, causing increased

pressures in the peripheral capillary the patient begins to gain weight as Fluid is not

excreted by the kidneys, tissue becomes edematous as pressures in the capillaries push

fluid out of the circulatory system.

-Causes include: Increased pulmonary resistance because of respiratory disease (also

known as cor pulmonale), pulmonic and tricuspid valve stenosis.

Heart failure can present as an acute or chronic problem Acute heart failure: - may be related to a temporary condition and resolve with

treatment of that condition. Chronic heart failure: - is a progressive condition that may have exacerbations, or an

acute worsening, which will require additional treatment measures.

هاي الصورة

بينهم ^^ مقارنة


Clinical manifestaions:-

- It depends on the side affected and on the severity. - Right side reflect systemic fluid accumulation - Left side is characterized by pulmonary fluid accumulation

A grading system is used to classify the severity of heart failure (I-IV)

Diagnosis include: History, physical examination, Chest X-ray, Arterial blood

gases, echocardiogram, EKG, Brain natriuretic peptide (a hormone released by

the ventricles in response to over stretching).

Aneurysms: -

It is a weakness in arterial walls because of high pressures, plaque and infection. This weakening happens much like a worn spot on a tire or a bulge in an old balloon,

an aneurysm can rupture when the pressure builds inside the wall or when the wall becomes too thin.

When it ruptures, blood spills out of the circulatory system, known as Exsanguination.

تكمن رته ب, و خطوتفاخ في الشريان أو زي كأنه بلون طالع منه ف في جدران الشرايين .. ف بصير زي انارة عن ضع^ هي عب^ و ممكن تسبب الموت تمزق و يصير في نزيف حاد إنه ممكن ي

Factors increase the risk of developing aneurysm: - Congenital weakening of the

arterial wall, Atherosclerosis, Hypertension, dyslipidemia, Diabetes mellitus, tobacco, advanced age, trauma, Infection (e.g., Syphilis).


Types of aneurysms: - True aneurysms and False aneurysms

True aneurysms: - شرايين قات البتأثر على كل طب

→ Saccular aneurysm: - is a bulge on the side of the vessel ^^ الضعف بكون بجهة بوحدة

→ Fusiform aneurysm: - affect entire circumference of the vessel. شريان محيط بكامل ال^^ الضعف بكون

False aneurysms: - طبقات الشرايينما بتأثر على كل

Does not affect all three layers of the vessel, and example of this type is a dissecting aneurysm (in which the weakening occurs in the inner layers).

قات الشرايين طبحدة من الطبقات و بصير يدخل الدم بين ^^ بصير في ضعف في وا

Clinical manifestaions

→ Common in the abdominal aorta, thoracic aorta, and cerebral, femoral and

popliteal arteries. → Most aneurysms are asymptomatic until they rupture. Symptoms may include a

pulsating mass, pain, respiratory difficulty, and neurologic decline. Diagnosis include; Physical examination or X-ray echocardiogram, CT, MRI. And

arteriography.

Dyslipidemia: - Also called as hyperlipidemia, it is an elevated level of lipids in the blood. Include cholesterol and triglycerides, which are necessary for cellular membrane

Formation. Increased lipid levels have been linked to multiple disease including atherosclerosis,

peripheral vascular disease, coronary artery Disease, hypertension, and stroke. Lipids are introduced into the bloodstream in two ways Diet and liver production. Dietary cholesterol is found in animal products, and dietary triglycerides are found in

saturated fats. The human liver makes more cholesterol than the body could possibly use, so it is not

necessary to eat it. Additional risk factors for dyslipidemia include excessive alcohol consumption,

smoking, sedentary lifestyle, obesity, diabetes mellitus, hypothyroidism, and renal disease.

Cholesterol moves through the bloodstream in large molecules much like cooking lard. But triglycerides move through versus ugh bloodstream in large sticky molecules, much like gum.

These sticky, fatty molecules travel through the circulatory system clogging small vessels and coating larger ones, like what happens when oils and grease are poured down a drain.


Lipoproteins are classified according to their density, which based on 1) the amount of triglycerides (which are low in density), 2) versus the amount of proteins (which are high in density).

The main classes of lipoproteins are chylomicrons: 1- very-low-density Lipoproteins. 2-low-density lipoproteins (LDLS). Bad cholesterol 3-high-density lipoproteins (HDLS). Good cholesterol

LDL and HDL the most significant of lipoproteins. انسدادات في بعض الشرايينو هاي المواد سهلة الالتصاق فبتصير تعمل دم .. في ال lipidsيعني هي زيادة مستويلت ال ^^

سبب أمراض مثل تصلب الشرايينمكن تخثرات في الشرايين الكبيرة و مالصغيرة و

Clinical manifestaions; it is often asymptomatic until it develops into other diseases

(e.g., atherosclerosis, coronary artery disease). Diagnosis include; Cholesterol screening and lipid profiles, angiography, ultrasound,

and nuclear scanning.

Atherosclerosis: - تصلب الشرايين It is a chronic inflammatory disease characterized by thickening and hardening of

the arterial wall. It is developed when lipid levels are not normalized in dyslipidemia Lesions (or plaques) composed of lipids develop on the vessel wall and calcify over

time. This development Causes vessel obstruction, platelet aggregation (collection), and

vasoconstriction. It can lead to peripheral coronary artery disease, thrombi, hypertension, renal

disease, and stroke.


Other factors may cause development of atherosclerosis include diabetes, HTN, stress, and smoking.

Atherosclerosis development is initiated by endothelial injury to the vessel wall. (This injury can cause by Dyslipidemia, hypertension, tobacco, diabetes, mellitus, elevated C-reactive protein levels, elevated homocysteine levels, autoimmune processes, and some bacterial infections).

The Injured cells become more permeable, suffer from free radical damage and become inflamed.

Leukocytes, macrophages, and cytokines are activated with the initiation of the Inflammatory process, which creates more damage.

The LDL becomes oxidized and permeates the vessel wall, exacerbating to the Injury and creating fatty streak.

Fibrous tissue and smooth muscle cells migrate to the site, increasing the size of the lesion and transforming it into fibrous plaque.

So, the arteries will become narrowed and hardened, and the heart must work harder to pump the blood through them.

ة في جرح بسيط بحدث في جدار الأوعية الدمويأكثر صلابة , و الي بصير إنه بخلي الشرايينتصلب الشرايين .. هو التهاب ^^

لهناك و بتتراكم هناك .. و بعدين ح الخلايا المناعية و بصير في التهاب مكان الجرح بترو ( ,,risk factors) بسبب واحد من

LDL ي اسمه و بتعمل اشم للإصابة بتنتشر هناك و بتسبب تفاقfatty streak صابة كمان نسيج ليفي و خلايا , و بروح لمكان الإ

صلب أضيق و أف بتصير الشرايين .. fibrous plaqueتتحول لاشي اسمه حجم الجرح و ب بسبب زيادة فيهذا و عضلية ملساء

جهد أكثر في ضخ الدم و بصير القلب بده يبذل

Clinical manifestaions; Atherosclerosis is often asymptomatic until complications

develop. Diagnostic procedures include: Lipids, C-reactive protein, and homocysteine levels,

Angiography, ultrasound, and nuclear scanning.


Peripheral vascular disease: - A narrowing of the peripheral vessels, caused by atherosclerosis, thrombus,

Inflammation (Thromboangitis obliterans), or vasospasm. Thromboangitis obliterans, or Buerger’s disease, is an inflammatory condition of the

arteries. Raynaud’s disease is a result of vasospasm of the arteries, most often of the hands,

that occurs because of sympathetic stimulation. It describes when vasospasm occurs association with an autoimmune disease.

When vessel occlusion increases the ischemia to the affected tissue worsens ( أسوء تصبح ).

Risk factors are the same as the atherosclerosis as well as autoimmune disease. Clinical manifestations; are tissue related and include: Pain, intermittent claudication

(pain that occurs the lower legs during activity), numbness burning, wounds that do not heal, pallor, cyanosis, rubor, such as the toes, impotency.

Diagnostic procedures include; history, physical examination, ankle-brachial index,

treadmill exercise test, angiography, ultrasounds, and MRI.

Coronary artery disease: - It develops when atherosclerosis develops in the artery supplying the myocardium. Blood flow temporarily diminishes in the coronary arteries, leading to reduction in

oxygen to the myocardium producing chest pain (angina). .. فبتقل كمية رايين التاجية( لب ) الشعضلة القايين الي بتغذي هذا المرض بحدث لما يصير في تصلب بالشر^^

ر بألم بالصدر يشع بصير الشخصتوصل للقلب و الدم الي ب

If blood flow decreased, it may cause permanent damage to the myocardium or infarction.

Causes include atherosclerosis (the most common cause), vasospasm, cardiomyopathy, diabetes, HTN, stress, tobacco, and thrombi.

Cardiovascular disease is the leading cause of death in United states fir men and women and also the leading cause of Myocardial infarction.

The left ventricle is the most susceptible to ischemic damage because more arteries supply it to meet its increased needs fir oxygen.

When oxygen supply is insufficient to meet this demand ischemia will happen, lactic acid and metabolic wastes accumulate, which causing angina and it stimulate other nerves causing pain to radiate to other parts of the body.

Chronic ischemia causes EKG changes (usually ST segment depression) Stable angina pectoris: ischemia that is initiated by increased demand (activity) and

relieved with the reduction of that demand (rest).


The cascade of events in which plaque ulcerates, Inflammation occurs, platelets aggregation, thrombi form further diminishes the blood supply. So, platelets release thromboxane A2, which causing arteries to spasm. These spasms trigger an unrelenting cycle of more platelet's aggregation and more spasm. So, chest pain eventually becomes unpredictable, occurs at rest, or increases in frequency or intensity.

Unstable angina: -The change in pain when chest pain eventually becomes unpredictable, occurs at rest, or increases in frequency or intensity.

CAD could cause HF, dysrhythmias, and sudden death. Clinical manifestations include;

• Angina that can radiate to other locations,

• Indigestion like sensation,

• Nausea and vomiting, cool, clammy extremities.

• Diaphoresis

• Fatigue Diagnostic procedures include; history, physical examination, exercise stress test,

echocardiogram, and EKG Lipids profile, angiography, and nuclear imaging.

Thrombi and emboli: - A thrombus is a blood clot that consists of platelets, fibrin, erythrocytes, and leukocytes. Promoting factors include endothelial injury, sluggish blood flow, and increased

coagulopathy Endothelial injury >> when a vessel wall is injured, the endothelial damage attracts

platelets and inflammatory mediators to the site, thereby stimulating clot formation. Sluggish blood flow >> stagnant blood flow allows platelets and clotting factors to

accumulate and adhere to the vessel wall. Increased coagulopathy >> Hyper coagulopathy states promote clot formation

inappropriately Thrombus formation may result in occlusion of a blood vessel or embolus development.


^^thrombus ممكن تحدث لثلاث أسباب الحمراء ,, و خلايا الدم الدموية و خلايا الدم البيضاء و ائح كون من الصف.. هي خثرة بتت.. بشكل غير مناسب حدوث تخثر في الدم الي هي coagulopathy الدم أو بسبب البسبب ركود في جرح في الأوعية الدموية أو

لدموية ا أو تعمل انسداد في الاوعية embolusو تكمن خطورتها إنها ممكن تصير

An embolus occurs when a portion or all of the thrombus breaks loose and travels through the circulatory system until it becomes embedded in a smaller vessel.

Thrombi, air, fat, tissue, bacteria, amniotic fluid, tumor cells, and foreign substances can become an embolus.

Emboli that originate in venous circulation can travel to the right atrium and then to the pulmonary circulation causing pulmonary embolism.

Emboli in arterial system which originate in the left side of the heart travel to the brain or the heart causing infarction.

في الجانب الأيمن ممكن ترجع ع إذا كانت إنها بتكمن خطورتها هي عبارة عن خثرة بتتحرك في الدورة الدموية و embolus^^ ال

روح على يسر ممكن ت.. و إذا كانت على الجانب الأ .pulmonary embolismرئتين و تعمل الأذين الأيمن و تطلع بعدها على ال

infarctionالدماغ و تعمل القلب أو على

Clinical manifestations; depend on the place the occlusion occurs.

Diagnostic procedures include arteriography, ultrasound, echocardiogram, and MRI.

Varicose veins: - Are dilated, tortuous, engorged veins that develop because of improper venous valve

function. Most common in the legs, can happen in the esophagus and the rectum. Increased pressure in the veins and blood pooling lead to enlarge in veins and more

stretch to valves, which become incompetent, blood flow is reversed, and venous pressure and distension are further increased.

Increases in the capillary pressure leading the fluid and pigment to leak out causing edema and skin discoloration. As a result, stasis pigmentation (brown skin discoloration), subcutaneous induration (thick and hardened skin), dermatitis (skin inflammation) and thrombophlebitis (vein inflammation resulting from a thrombus).

و بتزيد زيد , و الي بصير فيه إنو الضغط في الاوردة بالي في الاوردة ,مامات ^^ هو مرض الدوالي و الي بحدث بسبب مشكلة في الص

للخلف و مدد أكثر و بصير فيها خلل و بصير الدم يرجعفبتزيد الضغط على هاي الصمامات بتف بزيد حجم الأوردة دم المتجمعة فة الكمي

ردة تهاب في الأوتحت الجلد و و التهاب في الجلد و ال تصلب لجلد وف بتغير لون ا.. وردة بزيد الضغط في الأ

Edema caused a pressure can decrease circulation resulting in metabolic needs not

being met (oxygen and nutrients needs) so necrosis as well As venous stasis ulcers. Factors increase a person's risk for developing varicosities include genetic

predisposition, pregnancy, obesity, prolonged sitting or standing Alcohol abuse and liver disorders (esophageal varices), constipation (hemorrhoids).


Clinical manifestations include; irregular, purplish, bulging veins, pedal edema,

fatigue aching in the legs Shiny, pigmented, hairless skin on the legs and feet, and skin ulcer formation.

Diagnostic procedures include; visualization during physical examination, doppler

ultrasound and venogram.

Lymphedema: - Refers to swelling, in the arms and legs, because of lymph obstruction.

مفية اللي اكم للسوائل بسبب انسداد الاوعيةر^^ هو ت

This swelling can occur on its own (primary) or because of another disease or condition (secondary).

Primary lymphedema is rare and related to a congenital absence or decreased number of lymphatics.

Secondary lymphedema is usually related to one of the following which might affect the lymph nodes and are surgery, radiation, cancer, infection, or injury.

Clinical manifestations include edema and skin changes

Edema may be unilateral or bilateral and it usually occurs in the extremities. The skin changes include hyperpigmentation, ulceration, thickening and it begins to

appear like elephant skin, thick and rough. Diagnostic procedures include physical examination, MRl, CT, Doppler ultrasound,

and nuclear imaging.

Hypertension

It is prolonged elevation in blood pressure (Blood pressure refers to the force that

blood exerts on the wall of blood vessels). It is the leading factor for Cardiovascular diseases. In hypertension, the heart must work harder than normal to pump the blood to all the

parts of the body, in part due to vasoconstriction that increase afterload, and decreases renal blood flow which results in an inappropriate activation of the renin-angiotensin-aldosterone system.

Risk factors:

1) Age

• vessel compliance

• in middle age high blood pressure is more common in men

• Women are more likely to develop high blood pressure after menopause

2)Race

• Hypertension is more prevalent in African Americans


3) Family history

4)Overweight

more weight increase oxygen and nutrients needs so to meet this needs blood

volume increases which exerts more pressure on the artery walls.

5)Physical inactivity

heart rate increases so cardiac workload increase

6) Tobacco use

• Nicotine raise blood pressure.

• The chemical in tobacco can damage artery walls overtime.

7)Low- potassium diet

potassium helps balance the amount of sodium in cells; without enough

potassium, too much sodium accumulates in the blood.

8)High vitamin D intake: -

vitamin D may affect the renin-angiotensin-aldosterone system.

9)Excessive alcohol consumption: -

heavy drinking can damage the heart

10)Stress

high levels of stress can lead to increase blood pressure.

Hypertension divided into 2 major types primary hypertension and Secondary Hypertension ▬ Primary hypertension → It called essential hypertension → There is no identifiable cause for this type of hypertension. → Tends to develop gradually over many years ▬ Secondary Hypertension → This type of hypertension caused by underlying condition. → Tends to appear suddenly and cause higher blood pressure than does primary

hypertension. → Conditions and medications can lead to Secondary Hypertension: - → Renal disease // Adrenal gland tumors // certain congenital heart defects //certain

medications (birth control pills, hormone replacement thereby, antihistamine, decongestants and glucocorticoid steroids) //illegal drugs.


Malignant hypertension: - It is an especially intense form if hypertension that may not respond well to treatment efforts.

Hypertension classified as Systolic or Diastolic depending which measurement increase, but elderly persons have high systolic readings and low diastolic readings because of aging changes.

Pregnancy – induced hypertension (PIH): -

→ Hypertension occurs during pregnancy → It may called toxemia and preeclampsia → Indicators of PIH include high blood pressure, proteinuria, and edema → PIH can worsen leading to eclampsia, in eclampsia seizures often occur because of PIH. → Risk factors for developing PIH include a history of PIH, renal disease, diabetes

mellitus, multiple fetuses, and maternal age younger than 20 years or older than 40 years.

→ PIH can lead to multiple problem, including miscarriages, poor fetal development, and placental abruption.

→ Management focuses on prevention and nonpharmacologic measures to protect the fetus.

→ Treatment include bed rest and magnesium sulfate.

HTN is called the silent killer because it can begin to cause problems without any symptoms.

Hypertension causes excessive pressure on artery walls, which damages blood vessels and organs.

Complications:

1- Atherosclerosis 2- Aneurysm 3- heart failure 4- stroke 5- hypertensive crisis 6- renal damage 7- vision loss 8- metabolic syndrome 9- problems with memory and understanding

Clinical manifestations; fatigue, headache, malaise, dizziness.

Diagnostic procedures: history, physical examination, multiple blood pressure reading

at varying times of the day, EKG and lab tests (e.g., CBC, urinalysis, lipid panel and creatinine test.)


Shock Shock is a clinical syndrome resulting from inadequate tissue and organ perfusion

because of decrease blood volume or circulatory stagnation. Shock classified into three categories based on its precipitating factors:

Distributive (neurogenic, septic and anaphylactic), Cardiogenic and hypovolemic. Shock progresses through three stages that are common to all types of shock:

1) Compensatory 2) progressive 3) irreversible.

Compensatory Mechanisms: - are bodily responses that become activated when arterial pressure and tissue perfusion decrease, and that represent an effort to Maintain cardiac and cerebral function

These compensatory mechanisms include; activation of the SNS and renin-angiotensin-aldosterone system.

The progressive stage: - of begins when these compensatory mechanisms fail to maintain cardiac output.

Tissues become hypoxic, cells switch to anaerobic metabolism, lactic acid builds up, and metabolic acidosis develops.

This acidotic state further impairs cardiac functioning, causing sluggish blood Flow, and increases the risk for disseminated intravascular coagulation.

Irreversible stage: - occurs as the shock progresses, leading to respiratory and cardiac failure.

In distributive shock, vasodilation causes hypovolemia. Three types of distributive shock are distinguished neurogenic, septic, and Anaphylactic. First type: - Neurogenic shock:

→ Massive vasodilation causes by loss of sympathetic tone in vascular smooth muscle

and autonomic function → Blood pools in venous system, leading to decrease venous return, cardiac output and

blood pressure. Second type: - Septic shock

→ A bacterium's endotoxins activate an immune reaction. → Inflammatory mediators are triggered, increasing capillary permeability and causing

fluid shifts from the vascular compartment to the tissue. Falling cardiac Output then leads to multisystem organ failure.

Third type: - Anaphylactic shock → Consequence of an allergic reaction. → The allergic reaction leads to a cascade of events similar to that of septic shock, except that the

mediators differ. → Additionally, bronchospasm and laryngeal edema occur that can Impair respiratory status.


Cardiogenic shock: -

→ Results when the left ventricle cannot maintain adequate cardiac output. → Compensatory mechanisms of heart failure are triggered, but these mechanisms

increase cardiac workload and oxygen consumption, resulting in decreased contractility.

→ Consequently, tissue and organ perfusion decreases leading to multisystem organ failure.

Hypovolemic shock: - → Venous return declines because of external blood volume losses (e.g., hemorrhage

and dehydration). → Preload drops, decreasing ventricular filling and stroke volume. → As cardiac output falls, tissue and organ perfusion decreases.

Clinical manifestations of shock reflect the decreased cardiac output and impaired

tissue perfusion and may vary depending on the type of shock. And it include; General manifestations include the following signs and symptoms:

• Thirst

• Tachycardia

• Restlessness and irritability

• Tachypnea progressing to Cheyne-Stokes respirations

• Cool pale skin

• Hypotension

• Cyanosis

• Decreased urinary output

Complications of shock can be serious: -

• Acute respiratory distress syndrome

• Renal disease

• Disseminated intravascular coagulation

• Cerebral hypoxia

• Death

Diagnostic procedures for shock consist of a CBC, cultures, coagulation studies, cardiac

biomarkers, arterial blood gases, chest X-ray, hemodynamic monitoring, EKG, and echocardiogram.

pathophysiology/ cardiovascular function

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