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Cardiac Study Guide
Cardiac Unit Study Guide WVC
| Question | Answer |
|---|---|
| The heart is located between the lungs in the | mediastinum |
| The apex is above the | diaphragm |
| The heart is tilted slightly to the | LFT of midline |
| What valve moves blood between the RT atrium and ventricle | The tricuspid valve does this |
| What valve moves blood between the LFT atrium and ventricle | The mitral valve does this |
| What is the sound of the tricuspid and mitral valves closing | The "lub" It is the ventricular systole and it is the loudest. |
| The RT ventricle uses what valve to help move blood into the pulmonary arteries | pulmonary valve |
| The LFT ventricle uses what valve to do the same for the aorta | the aortic valve |
| The "DUB" is the sound of what | the aoRTic and pulmonary valves closing. It is the second sound. Diastole |
| During this the atria and ventricles of your heart relax and begin to fill with blood | diastole |
| Your heart's atria contract and pump blood into the ventricles | atrial systole |
| The atria then begin to relax. Next | your heart's ventricles contract |
| During ventricular systole the heart pumps blood where | pumps blood out of your heart. |
| How does blood flow through the heart | V/C 2 RT ATRIUM( ATRIAL SYSTOLE) 2 TRICUSPID 2 RT VENTRICLE(VENTRICULAR SYST) 2 PULM VALVE (semilunar) 2 PULM ARTERIES 2 LUNGS, back 2 PULM VEIN 2 LFT ATRIUM(ATRIAL SYST) MITRAL VALVE 2 LFT VENTRICLE. (VENTRICULAR SYSTOLE) A/V (semilunar)2 AORTA |
| The vessels that deliver oxygen-rich blood to the myocardium are known as | coronary arteries they represent the only source of blood supply to the myocardium |
| the LFT coronary artery originates from the | LFT aortic sinus |
| the RT coronary artery originates from the | RT aoRTic sinus. |
| most myocardial perfusion occurs through the coronary arteries during heart relaxation or contraction | diastole/relaxation |
| Failure of the coronary arteries to deliver oxygen caused by a ↓ in blood flow in front of ↑d oxygen demand of the heart results in | tissue ischemia, MI or angina pectoris. |
| Ischemia is | A condition of oxygen debt |
| Brief ischemia is associated with intense chest pain known as | angina |
| Severe ischemia can cause the heart muscle to die from hypoxia. An example of this is | myocardial infarction MI |
| What sympathetic neurotransmitter constricts the heart and causes ↑ BP | norepinephrine |
| In the coronary circulation norepinephrine elicits | vasodilation due to the predominance of beta-adrenergic receptors in the coronary circulation. |
| BNP has what effect on the heart | vasodilation, ↑Na secretion in the urine to result in ↓ BP & ↓ CO |
| Where is BNP produced | It is produced in the ventricles |
| Where is ANP produced and what effect does it have on the heart | vasodilation, acts to reduce the water, sodium and adipose loads on the circulatory system, → ↓ BP ↓ CO |
| The RT coronary artery supplies blood to the | RT atrium and RT ventricle |
| Where is the RT coronary artery located | from the ascending aorta to under the RT atrium |
| What is the fluid filled sac that surrounds the heart and the proximal ends of the aorta | vena cava |
| What are the 3 layers of the pericardium | FIBROUS PERICARDIUM is the outer fibrous sac that covers the heart. PARIETAL PERICARDIUM lies between the visceral pericardium and the fibrous pericardium. VISCERAL PERICARDIUM also called the epicardium |
| What are the mechanical properties of the heart | HR Cardiac Output and Stroke Volume |
| Blood flow from the heart into the systemic arterial circulation is measured clinically as | cardiac output (CO) the amount of blood pumped from the LFT ventricle each minute. |
| CO depends on the relationship between | heart rate (HR) and stroke volume (SV) |
| How do you calculate CO | HR X Stroke Volume |
| In adults the CO ranges from | 4 to 7 L/min. |
| HR is the | number of times the ventricles contract in one minute. Normal is 60-100 |
| What system controls HR | ANS |
| What systems slow the heart | The parasympathetic (vagus nerve) system slows the HR (beta-blockers slow the heart) |
| What system speeds up the heart | sympathetic stimulation ↑s the heart rate (epinephrine and norepinephrine) |
| Stroke volume (SV) is the | amount of blood ejected by the LFT ventricle during each contraction. |
| What variables influence stroke volume | HR, preload, afterload, and contractility. |
| Preload is | the degree of myocardial fiber stretch at the end of diastole and just before contraction. |
| What determines preload | determined by the amount of blood returning to the heart from both the venous system (RT heart) and the pulmonary system (LFT heart) (LFT ventricular end-diastolic [LVED] volume). |
| The ability of the heart to be able to equalize the amount of blood entering and exiting it is called | Frank-Starling’s law of the heart. |
| Stroke volume is ↑d by | stretching of the ventricular muscles during diastole ↑s the contractility of the muscle. It is involved in Starling’s Law |
| Excessive filling of the ventricles results in excessive LVED volume and pressure may result in | ↓d cardiac output. |
| Afterload is | the pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels. |
| What affects stroke volume and CO and is the force of cardiac contraction independent of preload | contractility |
| Contractility is ↑d by what factors | sympathetic stimulation, calcium release, and positive inotropic drugs. |
| How is contractility ↓d | hypoxia and acidemia. |
| Systolic BP is | the amount of pressure/force generated by the LFT ventricle to distribute blood into the aorta with each contraction of the heart. |
| Systolic BP measures | how effectively the heart pumps and is an indicator of vascular tone. |
| Diastolic BP is | the amount of pressure/force against the arterial walls during the relaxation phase of the heart. |
| What two properties determine BP | volume (cardiac output) and the resistance of the arterioles |
| BP | CO x PVR (peripheral vascular resistance) |
| BP is regulated by what body systems | ANS, Kidneys, Endocrine system |
| How does the ANS regulate BP | excites or inhibits sympathetic nervous system activity in response to impulses chemoreceptors and baroreceptors. |
| Chemoreceptors react to | to hypoxemia (a ↓ in the partial pressure of arterial oxygen [PaO2]) HYPOXIA |
| How do chemoreceptors work | stimulation send impulses along the vagus nerves to activate a vasoconstrictor response |
| Activated chemoreceptors do what to BP | ↑BP |
| How do baroreceptors work | arterial walls are stretched by an ↑d BP generate impulses that to the vasomotor center in the pons and the medulla. |
| Baroreceptors that ↓ BP are located in | the arch of the aorta and at the origin of the internal carotid arteries are stimulated when the arterial walls are stretched by an ↑d BP. |
| What happens when the arch of the aorta or at the origin of the internal carotid arteries are stretched | baroreceptors are stimulated and BP is reduced. |
| How do the stretch receptors in the superior vena cavae and the RT atrium and the RT atrium work | These sensitive to volume and pressure changes and aleRT the CNS to ↑ or ↓ HR |
| How do the kidney’s regulate BP | sense a change in blood flow activates the renin-angiotensin-aldosterone mechanism |
| What happens when RENAL BLOOD FLOW or PRESSURE ↓S | the kidneys retain sodium and water. BP tends to rise |
| Activation of the renin-angiotensin-aldosterone mechanism results in | vasoconstriction and sodium retention (and thus fluid retention). |
| Vascular volume is also regulated by the release | of antidiuretic hormone (vasopressin) from the posterior pituitary gland |
| How does the endocrine system regulate BP | releases various hormones (e.g. |
| Emotional behaviors (e.g. | excitement |
| What effect does hypothermia have on BP | tissues require fewer nutrients and blood pressure falls. |
| In hypeRThermia | the metabolic requirement of the tissues is greater and BP and pulse rate rise. |
| Postural hypotension is | A drop in blood pressure due to a change in body position when a person moves to a more veRTical position: from sitting to standing or from lying down to sitting or standing. |
| How do you diagnose POSTURAL HYPOTENTION | ↓ of MORE than 20 mm Hg of the SYSTOLIC pressure or MORE than 10 mm Hg of the DIASTOLIC PRESSURE |
| Areas to assess postural blood pressure | laying 3 minutes the to sitting or standing. After the position change |
| Paradoxical blood pressure is | an exaggerated ↓ in systolic pressure by more than 10 mm Hg during THE INSPIRATORY PHASE OF THE RESPIRATORY CYCLE (normal is 3 to 10 mm Hg). |
| Define hypertension | a systolic pressure of 140/90 mm Hg or higher or a diastolic pressure of 90 mm Hg or higher |
| What are the 3 stages of HNT | (Stage 1) 140/90 to 159/99, (Stage 2) 160/100 to 179/109 (Stage 3) >180/110 |
| What are the 3 types of HTN | malignant HTN (comes on suddenly), essential HNT (r/t risk factors), secondary HTN |
| What is secondary HTN commonly associated with | renal disease(the most), meds, endocrine, brain tumors or encephalitis |
| What is malignant HTN | BP >200 systolic & >150 diastolic, symptoms: HA, blurr vision, dyspnea, uremia. Can lead to CVA or renal failure. IT IS A MEDICAL EMERGENCY |
| Most common type of HTN | essential 85%-90% |
| These patients with HTN are at ↑d risk of | stroke, heart disease and end-stage kidney disease |
| The difference between the systolic and diastolic values is referred to as | pulse pressure. |
| A narrow pulse pressure can result from | ↑D PERIPHERAL VASCULAR RESISTANCE or ↓D STROKE VOLUME in patients with HEART FAILURE or HYPOVOLEMIA or SHOCK |
| An ↑d pulse pressure may occur in patients with | slow heart rates |
| The ankle-brachial index (ABI) can be used to assess | the vascular status of the lower extremities. |
| How do you assess ABI | The higher of these two pressures (dorsalis pedis and posterior tibial pulses) is then divided by the higher of the two brachial pulses |
| What are the 10 risk factors of heart disease | Age 65 or older. Being male. Family history. Race. Smoking. High cholesterol. High BP. Inactivity. Overweight. Diabetes |
| What questions should you ask in your assessment regarding heart conditions | history of depression & anxiety/ demographics/diet/Co-morbidity |
| Signs & symptoms of heart disease | angina/dyspnea/fatigue/palpitations/weight gain/pain in extremities/slow cap refill/clubbing/edema. |
| The term for the unusual sound that blood makes when it rushes past an obstruction (called turbulent flow) in an artery when the sound is auscultated with the bell poRTion of a stethoscope | Bruit |
| Pulsus alternans is | a physical finding with arterial pulse waveform showing alternating strong and weak beats |
| Pulsus alternans is almost always indicative of | LFT ventricular systolic impairment and carries a poor prognosis. |
| Assessment of arterial pulses provides information about | vascular integrity and circulation. |
| An ↑ in JVP (causes JVD) and is usually caused by | RT ventricular failure. Other causes include tricuspid regurgitation or stenosis |
| RT ventricular failure is associated with | ↑d systemic venous pressures and congestion |
| What is hepatojugular reflux | hepatomegaly causes an elevation of RT atrial pressure that is visualized by JVD. |
| Inspection in an assessment looks at | JVD, PMI @ 5th intercostal ,edema and respiratory rate |
| Late signs of severe RT-sided heart failure are | ascites, jaundice and anasarca (generalized edema) as a result of prolonged congestion of the liver. |
| In what order do you assess the heart | Inspection, palpation, percussion, auscultation |
| S1 marks the beginning of | ventricular systole and occurs RT after the QRS complex on the electrocardiogram (ECG). |
| When auscultated, S1 is | low pitched and softer than S2 |
| S1 is best heard at | the lower LFT sternal border or the apex of the heart. It may be identified by palpating the carotid pulse while listening. |
| The second heart sound (S2) is caused mainly by | the closing of the aoRTic and pulmonic valves (semilunar valves). |
| S2 is | higher pitched |
| S2 is heard best at | the base of the heart at the end of ventricular systole. |
| What are abnormal heart sounds | Gallops, murmurs and pericardial friction rub |
| Murmurs reflect | turbulent blood flow through normal or abnormal valves. The valves not closing(prolapse) or opening (stenosis) properly |
| Where are murmurs heard | mitral regurgitation is on top & aoRTic stenosis on the bottom |
| S3 is called | a ventricular gallop |
| An S3 gallop is caused by | ↓ compliance, early HF or ventricle skeptical defect |
| S4 gallop is referred to as | atrial gallop. |
| S4 gallop is caused by | ↓ compliance, HTN,anemia, ventricular hypeRTrophy, MI, aorta pulmonary stenosis, pulmonary emboli or loss of compliance with age. |
| A pericardial friction | rub originates from the pericardial sac and occurs with the movements of the heart during the cardiac cycle. |
| Rubs are usually transient and are a sign of | inflammation, infection, or infiltration. They may be heard in patients with PERICARDITIS resulting from MI, cardiac tamponade, or post-thoracotomy. |
| (S&S of CHF) ↓d perfusion is manifested as | cool, pale, and moist skin, cap refill <3 secs |
| (S&S of CHF) Pallor is characteristic of anemia and can be seen in areas such as the | nail beds, palms, and conjunctival mucous membranes in any patient. |
| ↓d blood flow results in ↓d skin temperature. It is lowered in several clinical conditions, including | heart failure, peripheral vascular disease, and shock. |
| Clubbing of the fingers and toes is caused by | chronic oxygen deprivation in body tissues. |
| Clubbing is common in patients with | advanced chronic pulmonary disease, congenital heart defects, and cor pulmonale (RT-sided heart failure) |
| Serum Markers of Myocardial Damage | CK-MB, myoglobin, Troponin (referred to as cardiac markers and detect cardiac injury |
| CK-MB is found in | myocardial muscle |
| Creatine kinase is | is an enzyme specific to cells of the brain, myocardium, and skeletal muscle. It is an marker for MI |
| Myoglobin is | a low-molecular-weight heme protein found in cardiac and skeletal muscle, is the earliest marker detected—as early as 2 hours after an MI with rapid decline after 7 hours. |
| Normal levels for myoglobin | <90 mcg/L |
| Troponin is | a myocardial muscle protein released into the bloodstream with injury to myocardial muscle. |
| Normal levels for CK are | Females: 30-135 units/L Males: 55-170 units/L |
| Troponins T and I are not found in healthy patients, so any rise in values indicates | cardiac necrosis or acute MI. |
| Normal values for Cardiac troponin | T <0.20 ng/mL Cardiac troponin I <0.03 ng/mL |
| What are the serum lipids | cholesterol, triglycerides, HDL, LDL |
| What are the normal TOTAL lipids | Total lipids 400-1000 mg/dL |
| Normal cholesterol e values | 122-200 mg/dL, or 3.16-6.5 mmol/L IN Older adult (> 70 yr): 144-280 mg/dL |
| Normal triglycerides | Females: 35-135 mg/dL Males: 40-160 mg/dL Older adult (>65 yr): 55-260 mg/dL |
| Normal HDL | Females: mean, 40 mg/dL Males: mean, 40 mg/dL Older adult range ↑s with age |
| What serum lipid protects against CAD | HDL |
| Normal LDL | 60-180 mg/dL Older adult (>65 yr): 92-221 mg/dL |
| HDL:LDL ratio | 3:1 |
| Homocysteine is | an amino acid that is produced when proteins break down. |
| Elevated homocysteine values may be an independent risk factor for | the development of CVD, CAD, PVD and venous thrombosis |
| High serum levels of homocysteine may block production of | nitric oxide on the vascular endothelium, making the cell walls less elastic and permitting plaque to build up |
| Blood coagulation studies (panels) evaluate | the ability of the blood to clot. |
| Why are blood coagulation panels impoRTant | in patients with a greater tendency to form thrombi (e.g., those with atrial fibrillation, prosthetic valves, or infective endocarditis).It can help predict disease |
| What test is primarily used, along with the creatinine test, to evaluate kidney function | BUN |
| Arterial blood gas (ABG) determinations are often obtained in patients with CVD. Why is it impoRTant | Determination of tissue oxygenation, carbon dioxide removal, and acid-base status is essential to appropriate intervention and treatment. |
| The most definitive but most invasive test in the diagnosis of heart disease is | cardiac catheterization. |
| Complications of Cardiac Catheterization on RT-SIDED HEART CATHETERIZATION | Thrombophlebitis, Pulmonary embolism, Vagal response |
| Complications of Cardiac Catheterization on LFT-SIDED HEART CATHETERIZATION | Myocardial, infarction, Stroke, Arterial bleeding or thromboembolism, Dysrhythmias |
| Angiography of the arterial vessels is an invasive diagnostic procedure that involves | fluoroscopy and the use of contrast media. |
| Angiography is performed when | arterial obstruction, narrowing, or aneurysm is suspected. |
| What are the radiographic diagnostic tests | Chest X-Ray, Angiograph, Cardiac Catherization |
| Standard preoperative tests are performed prior to a cardiac catherization | chest x-ray, complete blood count, coagulation studies, and 12-lead ECG. |
| The RT side of the heart is catheterized first. The cardiologist inseRTs a catheter through | the femoral vein to the inferior vena cava or through the basilic vein to the superior vena cava. It is advanced through the RT atrium, through the RT ventricle, and, at times, into the pulmonary artery |
| In a LFT-sided heart catheterization, the cardiologist advances the catheter | against the blood flow from the femoral or brachial artery up the aorta, across the aoRTic valve, and into the LFT ventricle. |
| What calculations are made from catherization | end-systolic volume, end-diastolic volume, stroke volume, and ejection fraction. |
| Digital subtraction angiography (DSA) is | type of fluoroscopy technique used in interventional radiology to clearly visualize blood vessels in a bony or dense soft tissue environment. |
| How is DSA accomplished | Images are produced using contrast medium by subtracting a 'pre-contrast image' or the mask from later images, once the contrast medium has been introduced into a structure. Hence the term 'digital subtraction angiography'. |
| An invasive procedure during which programmed electrical stimulation of the heart is used to cause and evaluate lethal dysrhythmias and conduction abnormalities | Electrophysiologic study (EPS) |
| This test assesses cardiovascular response to an ↑d workload. The stress test helps determine the functional capacity of the heart and screens for asymptomatic coronary artery disease | Exercise Stress Test |
| This test It helps assess and diagnose cardiomyopathy, valvular disorders, pericardial effusion, LFT ventricular function, ventricular aneurysms, and cardiac tumors | Echocardiography |
| This test examines cardiac structure and function with an ultrasound transducer placed immediately behind the heart in the esophagus or stomach | Transesophageal echocardiography (TEE) |
| A slightly more aggressive using either dobutamine or dipyridamole. This test is usually used when patients cannot tolerate exercise. | pharmacologic stress echocardiogram |
| What are the lifestyle choices that contribute to risks for heart disease | hypolipidemia, HTN, diabetes, diet, stress, smoking, obesity and sedentary lifestyle |
| What does a focused cardiac assessment consist of | Patient History( nutritional, smoking, exercise, alcohol and drugs), Family History (diabetes, obesity, HTN, CAD, sudden death) Cardiovascular Signs/Symptoms (pain PQRST), dyspnea, cough, fatigue, nocturia, edema, cyanosis, pallor |
| Electophysiologic Properties of cardiac cells regulate heart rate and rhythm. They are | Automaticity, excitability, conductivity, contractibility |
| The electrophyisologic property(EP) that is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively | Automaticity |
| What EP is the ability of non-pacemaker heart cells to respond to an electrical impulse generated from pacemaker cells and to depolarize. | Excitability |
| Depolarization occurs when | the normally negatively charged cells within the heart muscle develop a positive charge. |
| What EP is the ability to transmit an electrical stimulus from cell membrane to cell membrane. | Conductivity. As a result, excitable cells depolarize in rapid succession from cell to cell until all cells have depolarized. |
| The wave of depolarization causes | deflections of the electrocardiogram (ECG) waveforms that are recognized as the P wave and the QRS complex. |
| What EP is the mechanical activity of the heart. | Contractility |
| What EPis the ability of atrial and ventricular muscle cells to shoRTen their fiber length in response to electrical stimulation, generating sufficient pressure to propel blood forward. | Contractility |
| How is mild hyperkalemia seen on an ECG | reduction of the size of the P wave and development of peaked T waves. |
| Severe hyperkalemia results in a (on the ECG) | widening of the QRS complex |
| The conduction system begins with the | sinoatrial (SA) node (also called the sinus node). The action potential of the heart is staRTed |
| The SA node is the heart's | primary pacemaker. It can spontaneously and rhythmically generate electrical impulses at a rate of 60 to 100 beats per minute and therefore has the greatest degree of automaticity. |
| T waves may become tall and peaked, inveRTed (negative), or flat as a result of what electrolyte impalances | potassium or calcium imbalances |
| A constant blood calcium level is required for | A normal rhythmic heartbeat |
| What is the effect of Na on the heart | Too much or too little causes the body to retain water resulting in changes in BP |
| What is the effect of Mg on the heart | regulate BP |
| Where is the cardiac control center located | Medulla oblongata |
| What other 2 areas control the heart | SA node and AV node |
| Where is the SA node located | located close to the surface of the RT atrium near its junction with the superior vena cava. The SA node is the heart's primary pacemaker |
| The SA node leads to | atrial depolarization. It’s the P wave |
| What is the normal BPM of the SA node | 60-100 BPM and therefore has the greatest degree of automaticity. |
| A heart controlled by the SA node is said to be in | normal sinus rhythm. |
| The AV node is located | lies just beneath the RT atrial endocardium, between the tricuspid valve and the ostium of the coronary sinus. (floor of the RT atrium) |
| What does the AV node do | T-cells (transitional cells) cause impulses to SLOW DOWN or to be delayed in the AV node before proceeding to the ventricles. |
| The activity of the AV node is reflected as (ECG) | PR segment. This slow conduction provides a shoRT delay, allowing the atria to contract and the ventricles to fill. |
| The AV node has its own intrinsic pacemaker activity at of (BPM) | 40-60 BPM. |
| The bundle of His connects with | AV node & continues thru the interventricular septum. It extends as a RT bundle branch down the RT side of the interventricular septum to the apex of the RT ventricle. On the LFT side, it extends as a LFT bundle branch, which fuRTher divides |
| What is the intrinsic value for rate of the bundle of His | 40-60 BPM |
| Where are the perkinje fibers located | At the ends of both the RT and the LFT bundle branch systems |
| Purkinje cells make up | the bundle of His, bundle branches, and terminal Purkinje fibers. |
| Perkinje fibers are responsible for | ventricular depolarization and the subsequent ventricular muscle contraction. |
| Perkinje fibers are the last line in conduction/contractility. If all other cells fail, they can beat (BPM) | 20-40 BPM |
| What does each small square on a 6 min ECG represent | 0.04 seconds |
| What does the P Wave represent | Atrial depolarization. |
| What does each big square on a 6 min ECG represent | 0.20 seconds |
| What does the QRS complex represent | ventricular depolarization, coincides w/mitral & tricuspids closing. |
| Where does the impulse for the QRS complex travel | down the bundle of His to the perkinje system |
| What does the T wave represent | ventricular repolarization, follows the same deflection as P wave |
| How is hyperkalemia reflected on the ECG | the T wave is peaked with prolonged QRS and PR intervals |
| How is hypokalemia reflected on the ECG | the T wave is low and rounded w/ST depression and U wave |
| What is the absolute refractory period | is the time for lethal arrhythmias |
| What does the J point stand for | The point where the QRS ends and the ST begins |
| What represents the time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to the Purkinje fibers | The PR INTERVAL |
| What does the ST segment represent | early ventricular repolarization (from J point to beginning of T wave) |
| What does a normal ST segment look like | no more than 0.5 mm elevation. |
| Elevation or depression of the ST segment can be caused by | myocardial injury, ischemia or infarction, conduction abnormalities, or the administration of medications. |
| What does the QT interval represent | depolarization and repolarization of the LFT and RT ventricles. |
| The QT interval varies with | age, sex and HR |
| A prolonged QT interval is a biomarker | for ventricular tachyarrhythmias (hypomagnesia) |
| QT interval can be lengthened with | meds, electrolyte imbalances (hypomagnesia), subarachnoid hemorrhage. |
| Common causes for Torsades de Pointes include | diarrhea, hypomagnesemia and hypokalemia (all cause tachycardia) |
| How do you check the atrial rhythm on an ECG | assessing the PP interval, are they smooth/rounded and up RT, one for each QRS, similar |
| Check the regularity of the ventricular rhythm by assessing | the RR intervals |
| The PR interval normally measures between | 0.12 and 0.20 second and s/b consistent across the strip |
| The QRS duration normally measures between | 0.04 and 0.10 second (Gloria stated .06-.12) |
| When the QRS duration is less than .10, it indicates | that the impulse was formed above the ventricle |
| When the QRS duration is more than .10, it indicates | that the impulse is either of ventricular origin or of supraventricular origin with aberrant conduction |
| Dysrhythmia can be seen by the QRS complex duration that is more than | 0.12 second |
| Normal Sinus Rhythms originating from the SA are characterized by what | Rates: normal & contant. Rhythm: regular. Present P waves, consistent, smooth, one P wave before each QRS complex |
| Name 3 different dysrhythmias that cause ↓d cardiac output | Tachycardia, atrial fibrillation and atrial flutter |
| What are obvious signs of tachycardia | ↑pulse rate, fatigue, weakness, SOB, oRThopnea, JVD, ↓O2 sat, ↓BP, ↓ urine output anginal pain and palpitations. BP> |
| What does the ECG pattern in tachycardia | may show T-wave inversion or ST-segment elevation or depression in response to myocardial ischemia. |
| What is the most common type of dysrhythmia | Atrial fibrillation (AF) |
| What is AF | multiple rapid impulses depolarize the atria in a totally disorganized manner at a rate of 350 to 600 times per minute,no atrial contractions, loss of atrial kick, and an irregular ventricular response |
| What does AF look like on the ECG | The result is a chaotic rhythm with no clear P waves, |
| What is atrial flutter | a rapid atrial depolarization occurring at a rate of 250 to 350 times per minute, resulting in poor atrial pumping and ↓ CO because the ventricles don’t fill properly b4 contraction |
| Why does tachycardia reduce CO | ShoRTen the diastolic time and therefore the coronary perfusion time. HR ↑s and CO and BP ↓ |
| What are the effects of aging on the cardiac valves | Calcification and mucoid degeneration occur, especially in mitral and aoRTic valves. |
| What are the effects of aging on the conduction system | Pacemaker cells ↓ in number. Fibrous tissue and fat in the sinoatrial node ↑. Few muscle fibers remain in the atrial myocardium and bundle of His. Conduction time ↑s. |
| What are the effects of aging on the LFT Ventricles | size of LFT ventricle ↑s. It becomes stiff and less distensible. Fibrotic changes in the LFT ventricle ↓ the speed of early diastolic filling by about 50%. |
| Aging on the aorta and other large arteries | Thickes $ become stiffer& less distensible. Systolic BP ↑s to compensate for stiffness. Systemic vascular resistance ↑s as a result of less distensible arteries; →LFT ventricle pumps against greater resistance, contributing to LFT ventricular hypeRTrophy. |
| Baroreceptors become | less sensitive. |
| Symptoms & symptoms of HTN | Confusion: Ear noise or buzzing:Fatigue: Headache:Irregular heartbeat: Nosebleed:Vision changes: ↑BP |
| Pathophisiology of HTN | The basic explanation is that blood pressure is elevated when there is increased cardiac output plus increased peripheral vascular resistance. |
| Medical treatment for HTN | Alpha blockers: Angiotensin-converting enzyme (ACE) inhibitors: Angiotensin receptor blockers (ARBs): Beta blockers: Calcium channel blockers: Central alpha agonists: Diuretics: Renin inhibitors: Vasodilators |
| The 3 types of diuretics used to treat HTN | Thiazides: Loop Diuretics: Potassium sparing diuretics |
| Hydrochlorothiazide | reduces the volume of the blood, decreasing blood return to the heart and thus cardiac output and, by other mechanisms, is believed to lower peripheral vascular resistance |
| How does hydrochlorothiazide act on the kidney | ↓ sodium (Na) reabsorption in the distal convoluted tubule |
| What type of diuretic is hydrochlorothiazide (Hydordiuril) | Thiazides |
| What type of diuretic is Chlorothiazide (Diuril) | Thiazides |
| Name 2 loop duiuretic | Lasix (furosemide), ethacrynic acid (edecrin) |
| How does Lasix work | Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule. Increases renal excretion of H2O, Na, Cl, Mg, K, and Ca |
| Side effects of Lasix | dehydration, hypocalcemia, hypochloremia, hypokalemia, hypomagnesemia, hyponatremia, hypovolemia, metabolic alkalosis. |
| What are 2 K sparing diuretic | spironolactone (aldactone), triamterene (Dyrenium) |
| What is the action of spironolactone | Causes loss of sodium bicarbonate and calcium while saving potassium and hydrogen ions by antagonizing aldosterone |
| Major side effect of spironolactone | hyperkalemia |
| What do beta blockers do | slow the heart, ↓ its workload, and ↓ BP. In atrial fibrillation, they are used to control the heart rate |
| What are beta blockers used for | treat high blood pressure, angina, heart failure, and abnormal heart rates. |
| What is carvedilol (Coreg) | a beta-blocker |
| What are calcium channel blockers used for | to treat high blood pressure HTN, angina (chest pain), heart failure, and some arrhythmias (abnormal heart rhythms). |
| What is diltiazem (Dilacor XR) | a calcium channel blocker |
| What do ACE inhibitors do | block the conversion of angiotensin I to the vasoconstrictor angiotensin II. ACE inhibitors also ↑ plasma renin levels and ↓ aldosterone levels. Net result is SYSTEMIC VASODILATION |
| What are ACE inhibitors used for | HTN to ↓BP & Heart failure to ↓ afterload and symptoms & pain |
| What are central alpha agonists used for | ↓blood pressure by stimulating alpha-receptors in the brain which open peripheral arteries easing blood flow. They prevent reuptake of norepinephrine in the CNS. They are usually prescribed when all other anti-hypertensive medications have failed. |
| What are the side effects of a central alpha agonist | dry mouth, drowsiness, and withdraw potential |
| List 2 examples of a central alpha agonist | clonidine & methyldopa |
| List 5 examples of vasodilatos | nitroglycerin, terazonsin, nitroprusside, doxazosin & minoxidil |
| What would the rationale used for administering aspirin | Decreased incidence of transient ischemic attacks and MI |
| What do angiotensin II blockers do(ARB) | INHB vasocontraction & aldosterone by INHB binding of angio-II to receptors BUT they do not INHB ACE |
| What are ARB’s used for | they protect against renal failure in patients w/ DM II and don’t cause a cough |
| What are 2 examples of ARB’s | losartan (Lozaar), olmesartan (Benicar), candesartan (Atacand) |
| Vasodilation refers to | the widening of blood vessels resulting from relaxation of smooth muscle cells within the vessel walls, particularly in the large arteries, smaller arterioles and large veins. |
| A temporary imbalance between the ability of the coronary arteries to supply oxygen and the demand for oxygen by the cardiac muscle. As a result, the patient experiences chest discomfort. | Angina Pecoris |
| It is caused by a temporary imbalance between the coronary arteries' ability to supply oxygen and the cardiac muscle's demand for oxygen. | Angina. Can be caused by CAD |
| Angina is a symptom of a condition called | myocardial ischemia |
| Onset of angina | Sudden, usually in response to exertion, emotion, or extremes, in temperature |
| Onset of MI | Sudden, without precipitating factors, often in early morning |
| Drugs for angina | Nitroglycerin, aspirin and clopidogrel (Plavix) or prasugrel (Effient) |
| Disease affecting arteries that provide blood, O2, and nutrients to the myocardium; partial/complete blockage of the blood flow thru the coronary arteries, causing ischemia and infarction of the myocardium, angina pectoris, and acute coronary syndromes. | Coronary Artery Disease |
| What are signs and symptoms of CAD | Angina, SOB, fatigue, weakness, dysrhythmias, generalized edema, ↓urination, ↑urination at night, weight gain, ↑girth at diaphragm, ↓LOC |
| What diagnostic tests are done for chest pain | 12 lead ECG, serum markers & other blood tests (electrolytes), stress tests, chest x-ray, ECG, angiography and cardiac cauterization |
| Findings of the patient with left-sided heart failure may include | S3, wheezing or crackles & Paroxysmal nocturnal dyspnea |
| Assessment findings of a patient with right-sided heart failure may include | are ascites, jaundice, and anasarca (generalized edema) |
| Heart failure can cause a number of symptoms | SOB , typically worse when lying flat (orthopnea), coughing, chronic venous congestion, ankle swelling, and exercise intolerance |
| New York Heart Association Functional Classification of Cardiovascular Disability | Class 1 to 5. Mild symptoms to full blown cardiac disease. |
| Heart failure is caused by | any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading |
| Brief patho of Heart Failure | ↓ force of contraction, due to overloading of the ventricle. A ↓stroke volume, as a result of a failure of systole, diastole or both.↓ spare capacity ↑ HR ↓CO, Hypertrophy, Enlargement of the ventricles |
| Physiological compensations for heart failure | ↓ BP→ arterial vasoconstriction→ CO, ↑ sympathetic stimulation→ ADH & Angiotensin →↑fluid→↑BP &↑blood volume; hormones ↑BP, but put more strain on heart |
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