Cardiovascular System Flashcards by Faith L

It is located in the middle mediastinum, tilted forward to the left

HEART

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Heart consist of 3 layers

EPICARDIUM
MYOCARDIUM
ENDOCARDIUM

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Covers the outer surface of the heart

EPICARDIUM

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Is the middle muscular layer of the heart

MYOCARDIUM

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Lines the chambers and the valves

ENDOCARDIUM

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The layer that covers the heart is the

PERICARDIUM

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Pericardium consist of two parts?

PARIETAL PERICARDIUM
VISCERAL PERICARDIUM

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It is the primary physiologic cardiac pacemaker, with firing rate of 60-100 bpm. It is located at the junction of the superior vena cave and right atrium

SA NODE

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It is the secondary cardiac pacemaker, it can sustain of 40-60bpm and it is located at the lower aspect of the atrial septum.

AV NODE

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It is located at the interventricular septum and branches into the right and left bundle branch and terminates at the Purkinje fibers

BUNDLE OF HIS

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Are a diffuse network of conducting strands located beneath the ventricular endocardium, they spread the wave of depolarization through the ventricles and can act as the pacemaker with a rate between 20 to 40 bpm when higher pacemaker fail.

PURKINJE FIBERS

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Normal range is 60-100 beats per minute
Tachycardia is greater than 100 bpm
Bradycardia is less than 60 bpm
Sympathetic system increase HR
Parasympathetic system (Vagus) Decrease HR

HEART RATE

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Cardiac output X total peripheral resistance
Control is neutral (central and peripheral) and hormonal

Blood pressure

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Heard as the AV valves close. Heard loudest at the apex of the heart

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Head when the semilunar valves close. Heard loudest at the base of the heart.

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May be heard if ventricular wall compliance is decrease and structures in the ventricular wall vibrate such as in heart failure or valvular regurgitation. May be normal in individuals younger than 30 years.

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May be heard on atrial systole if resistance to ventricular filling is present. Abnormal finding usually found in cardiac hypertrophy, disease or injury to the ventricular wall.

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Elevates in MI within 4 hours, peaks in 18 hours and then declines within 24 hours

CK-MB ( Creatine kinase)

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Normal CK MB

Female: 2-5 ng/ml
Male: 2-6 ng/ml

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Rises within 1-3 hours
Peaks in 4-12 hours
Return to normal in a day
Not used alone
Muscular and Renal disease can have elevated myoglobin.

MYOGLOBIN

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Elevates in MI in 24 hours, peaks in 48-72 hours
Normal value is 70-200 IU/L

LACTIC DEHYDRATION (LDH)

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Compose of 3 proteins: Troponin C, Cardiac Troponin I and Cardiac Troponin T
Elevates within 3-4 hours, peaks in 4-24 hours and persists for 7 days to 3 weeks

TROPONIN

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Lipid profile measure the serum cholesterol, triglycerides and lipoprotein levels
Assess the risk of developing coronary artery disease.

SERUM LIPID

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In RHD and ineffective endocarditis; RBC increases in condition characterized by inadequate tissue oxygenation

RBC DECREASE

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In infectious and inflammatory diseases of the heart and after MI because large numbers of WBCs are needed to dispose of the necrotic tissue resulting from the infarction.

WBC INCREASES

Can result from vascular volume depletion

ELEVATED HEMATOCRIT

Can indicate anemia

DECREASE HEMOGLOBIN AND HEMATOCRIT

Can occur during and after MI, which places the client at greater risk for thrombophlebitis and extension of clots in the coronary arteries.

INCREASE IN COAGULATION FACTORS

May increase the risk of cardiovascular diseases; level should be less than 14 mmol/dL

HOMOCYSTEINE

What are the Electrolytes

POTASSIUM SODIUM CALCIUM PHOSPHORUS MAGNESIUM

What are the 2 Potassium?

HYPOKALEMIA HYPERKALEMIA

Causes increased cardiac electrical instability, ventricular dysrhythmias, and increased risk of digoxin toxicity; the ECG shows flattening and inversion of the T wave, the appearance of a U wave and ST depression

HYPOKALEMIA

Causes asystole and ventricular dysrhythmias. The ECG may show tall peaked T waves, widened QRS complexes, prolonged PR intervals or flat P waves.

HYPERKALEMIA

Decreased with the use of diuretics Decreased in heart failure

SODIUM

What are the 2 calcium

Hypocalcemia Hypercalcemia

Can cause ventricular dysrhythmia, prolonged ST and QT intervals and cardiac arrest

HYPOCALCEMIA

Can cause a shortened ST segment and widened T wave, AV block , tachycardia or bradycardia, digitalis hypersensitivity and cardiac arrest.

HYPERCALCEMIA

Should be interpreted with calcium levels because kidneys retain or excrete one electrolyte in an inverse relationship to the other.

PHOSPHORUS

Low level can cause ventricular tachycardia and fibrillation. May show tall T waves and depressed ST segments High level can cause muscle weakness, hypotension and bradycardia. May show a prolonged PR interval and widened QRS complex.

MAGNESIUM

Released in response to atrial and ventricular stretch; it serves as a marker for heart failure. Should be lower than 100 of/ml; the higher the lever; the more severe the heart failure.

B-TYPE NATRIURETIC PEPTIDE

Reflects the electrical activity of cardiac cells and records electrical activity at a speed of 25 mm/ second.

ELECTROCARDIOGRAPHY

Non-invasive test which the client wears a holter monitor and ECG tracing is recorded continuously for 24 hours or more while the client performs his or her ADLs. Identifies dysrhythmias, location & extent of MI, cardiac hypertrophy and evaluation of effectiveness of cardiac medications.

HOLTER MONITORING

Noninvasive procedure which is based on the principles of ultrasound and evaluates structural and functional changes in the heart. Heart chamber size is measured, ejection fraction is calculated, and flow gradient across the valves is determined. Instruct the client to lie still.

ECHOCARDIOGRAPHY

Noninvasive test that studies the heart during activity and detects and evaluates coronary artery disease.

STRESS TEST (EXERCISE ELECTROCARDIOGRAPHY TESTING)

An invasive test involving insertion of a catheter into the heart and surrounding vessels. Obtains information about the structure and performance of the heart chambers and valves and the coronary circulation.

CARDIAC CATHETERIZATION

An invasive , non surgical technique in which one or more arteries is dilated with a balloon catheter to open the vessel lumen and improve arterial blood flow.

PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY

The occluded coronary arteries are by passed with the client’s own venous or arterial blood vessels. The saphneous vein, internal mammary artery, or other arteries may be used to by pass lesions in the coronary arteries Coronary artery by pass grafting is performed when the client does not respond to medical management of coronary artery disease or when vessels are severely occluded.

CORONARY ARTERY BYPASS GRAFTING

A.k.a ischemic heart disease/ Atherosclerotic heart disease. CAD result from the focal narrowing of the large and medium sized coronary arteries due to deposition of atheromatous plaque in the vessel wall.

CORONARY ARTERY DISEASE (CAD)

Risk factor of coronary artery disease

AGE ABOVE 45/55 SEX: MALES AND POST MENOPAUSAL FEMALES FAMILY HISTORY HYPERTENSION DM SMOKING OBESITY SEDENTARY LIFESTYLE HYPERLIPIDEMIA

Most important MODIFIABLE risk factors:

SMOKING HYPERTENSION DIABETES CHOLESTEROL ABNORMALITIES

It is a myocardial ischemia without cell death, Caused by vasospasm, decrease blood flow due to atherosclerosis of coronary arteries and increasing workload.

ANGINA PECTORIS

Death of myocardial tissue in regions of the Heart with abrupt interruption of coronary blood supply.

MYOCARDIAL INFARCTION

Caused by a coronary artery spasm Angina at rest after long exertion exercise and even sleep

PRINZMETAL ANGINA: (VARIANT ANGINA)

Occurs only at night associated with REM

NOCTURNAL ANGINA

Paroxysmal chest pain that occurs during sitting and standing.

ANGINA DECUBITUS

Chronic and severe incapacitating chest pain with no response to intervention

INTRACTABLE ANGINA

Occurs after MI when residual ischemia may cause episodes of angina.

POST INFARCTION ANGINA

What are the myocardial enzymes?

ELEVATED CK-MB ELEVATED, LDH ELEVATED TROPONIN LEVELS

Most reliable cardiac specific enzyme.

ELEVATED CK-MB

Increase only with cardiac damage 3-6 hrs after onset of MI

ELEVATED, LDH

Most definitive

ELEVATED TROPONIN LEVELS

May show elevated WBC count

CBC

Exercise tolerance test, thallium scans, and cardiac catheterization

TEST AFTER THE ACUTE STAGE.

Inability of the heart to pump sufficiently to maintain adequate circulation to meet the metabolic needs of the body. Classified according to the major ventricular dysfunction left or Right.

CONGESTIVE HEART FAILURE ( CHF)

Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion Necrosis of more than 40% of the left ventricle occurs, usually as a result of occlusion of major coronary vessels. The goal of treatment is to maintain tissue oxygenation and perfusion and improve the pumping ability of the heart.

CARDIOGENIC SHOCK (“POWER PUMP FAILURE”)

A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac. This condition restricts ventricle filling resulting to decreased cardiac output. Acute tamponade may happen when there is a sudden accumulation of about 20-50 ml in the pericardial sac.

CARDIAC TAMPONADE

A systolic BP greater than 130mmHg and diastolic pressure greater than 80mmHg get over a sustained period based on two or more BP measurement.

HYPERTENSION

What are the types of hypertension?

PRIMARY OR ESSENTIAL AGING FAMILY HISTORY BLACK RACE, WITH HIGHER PREVALENCE IN MALES OBESITY SMOKING STRESS EXCESSIVE ALCOHOL HYPERLIPIDEMIA

3 Major conditions concerns secondary hypertension

KIDNEY DISEASE DM DYSLIPIDEMIA

What are the Drug Therapy for Hypertension

DIURETICS ACE INHIBITORS BETA BLOCKERS ANGIOTENSIN II RECEPTOR BLOCKERS CALCIUM CHANNEL BLOCKERS

Diuretics 1st line of drugs for treatment of mild hypertension

LOOP -FUROSEMIDE OSMOTIC -MANNITOL THIAZIDE -HYDROCHLOROTHIAZIDE POTASSIUM SPARING- SPIRONOLACTONE (ALDACTONE)

ACE inhibitors- inhibits vasoconstriction, suppressed conversion of angiotensin I to Angiotensin II

CAPTOPRIL (CAPOTEN) QUINAPRIL (ACCUPRIL)

Beta Blockers- PNS, decreases heart rate may lead to bradycardia (count HR before administering the drug) to watch out for hypotension, wheezing, hypoglycemia (glucagon: antidote).

PROPRANOLOL (INDERAL) METOPROLOL (LOPRESSOR) ATENOLOL

Angiotensin II receptor blockers- prevent peripheral vasoconstriction and secretion of aldosterone and block the binding AII to type AII receptor

LOSARTAN (COZAAR) TELMISARTAN (MICARDIS) CANDESARTAN (CANDEZ) IRBESARTAN (AVAPRO)

Calcium channel blockers- blocks entry of calcium into smooth muscle cells causing a decrease in contractility and arteriolar contriction.

VERAPAMIL DILTIAZEM (DILZEM) NIFEDIPINE AMLODIPINE (NORVASC/AMVASC

Any clinical condition requiring immediate reduction in BP An acute and life threatening condition

HYPERTENSIVE CRISIS

Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis. Usually found in males age 50 and above The legs are most often affected.

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE (PAOD)

A.K.A thromboangitis obliterans A disease characterized by recurring inflammation of the medium and small arteries and veins of the lower extremities. The distal, upper and lower limbs are affected most commonly.

BUEGER’S DISEASE

A form of intermittent arteriolar vasoconstriction that result in coldness, pain and pallor of the finger tips or toes. Vasospasm of the Arterioles and arteries of the upper and lower extremities which causes constriction of the cutaneous vessels.

REYNAUD’S DISEASE (Blue-White-Red Disease)

A sac formed by dilation of an artery secondary to weakness and stretching of an arterial wall. The dilation may involve one or all layers of the arterial wall.

ANEURYSM

Inflammation of the vessel wall with formation of a clot (thrombus); may affect superficial or deep veins. Most frequent veins affected are the saphenous, femoral, and popliteal. Can result in damage to the surrounding tissues, ischemia and necrosis

THROMBOPHLEBITIS

Blocks conversion of prothrombin to thrombin and reduces formation of thrombus. Prevents thrombin from converting fibrinogen to fibrin. Prevents formation of new thrombus formation.

HEPARIN

Blocks synthesis of clotting factors X,IX, VIII, and prothrombin which are Vit. K dependent clotting factor. Prolongs clotting time and is monitored by PT and INR

WARFARIN

Dilated veins that occur most often in the lower extremities and trunk. As the vessels dilates, the valves become stretched and incompetent with the resultant venous pooling/edema.

VARICOSE VEINS