Cardiac & Renal Disorders Flashcards

Question

2 types of true aneurysms

Answer 1

Saccular and Fusiform

Answer 2

Increased coagulation state

Answer 3

Symptoms are below the occlusion, cool and pale below

Answer 4

Symptoms are below the occlusion, warm and tender

Answer 5

Happens at the site of damage, Blood clot consisting of platelets, fibrin, erythrocytes, and leukocytes. DVT

Answer 6

Thrombus breaks loose and travels through the circulatory system eventually embedding in a smaller vessel. Starts out as DVT then to a Pulmonary Embolus.

Answer 7

Extremity fullness and edema distal to the thrombus

Answer 8

Pallor and coolness extremity distal to the thrombus

Answer 9

Pallor Paresthesia Paralysis Pain Polar Pulselessness

Answer 10

Swelling due to lymph obstruction. Connected by their own fluid system. Primary is rare r/t congenital abnormality. Secondary is r/t another condition (lymph node resection, radiation, cancer, infection, or injury)

Answer 11

Non-pitting, gradual onset, pt c/o heaviness in legs, unilateral or bilateral edema, key is recognizing early

Answer 12

Thickening and hardening of arterial wall due to loss of elasticity and collagen in vessel

Answer 13

Type of arteriosclerosis. The buildup of fats and cholesterol to form plaque in the artery wall. Can cause obstruction, decreased tissue perfusion, ischemia and necrosis and can occur in any artery

Answer 14

Accelerated LDL uptake into vessel lining, creation of foam cells, infiltration of macrophages and inflammatory mediators for a chronic inflammatory process, formation of fatty streaks (plaque composed of fibrous cap and fatty streaks) and plaque narrows the vessel lumen causing turbulent flow. Possible rupture and clot

Answer 15

Asymptomatic until at 70% reduction in vessel diameter

Answer 16

Total cholesterol \>200 Increases the risk of CAD, PAD, Hypertension and Cerebrovascular disease

Answer 17

Primary - Inherited - not related to external factors Secondary - Not inherited - related to environment (diet, obesity, sedentary lifestyle)

Answer 18

Shows inflammation in vessels want level \<1 if \>3 at high risk

Answer 19

Pain in legs when walking

Answer 20

To excrete drugs. So if all drugs use the same excretion system you would not get rid of the drugs effectively

Answer 21

The clearance of a filterable substance from the urine

Answer 22

There are two ways renin is stimulated: 1. The primary stimulus for secretion is renal hypoperfusion… when renal perfusion is decreased, renin release is stimulated. So, anytime renal blood flow is decreased, renin will be released. The second way... There are specialized cells in the distal tubule that sense Na+ and Cl-. When the concentration of Na+ and Cl- falls renin is released 2. Renin then enters the general circulation acting on angiotensinogen (which is a protein produced in the liver) to convert it to Angiotensin I. 3. Angiotensin I passes through the lung and is converted (by ACE…angiotensin converting enzyme) to Angiotensin II. 4. Angiotensin II is physiologically active and is a potent vasoconstrictor.... Increasing PVR (peripheral vascular resistance) leading to increased BP 5. Angiotensin II also stimulates the adrenal cortex to release aldosterone (a salt-retaining hormone) Aldosterone acts mainly on distal tubule…in the presence of aldosterone Na (and H2O) is reabsorbed and K is secreted

Answer 23

Voiding Involves both reflex and voluntary mechanisms Mediated by the micturition center in the pons

Answer 24

Allow for relaxing and filling of the bladder

Answer 25

From S2 to S4 parasympathetic nerves result in bladder contraction and relaxation of the internal sphincter to initiate bladder emptying

Answer 26

Used for diagnosing voiding dysfx, pt drinks a lot and the bladder is visualized when full, pt voids and the residual amount is then analyzed should be less than 50 - 100ml

Answer 27

Does not happen at night. Occurs when urine is involuntarily lost with increases in intraabdominal pressure (coughing, lifting, sneezing, BM, vomiting, or degenerative neurologic diseases)

Answer 28

Overactive or damaged **_detrusor muscle!_** Involuntary sudden leakage of urine along with or immediately following the sensation of a need to urinate. Sudden urge. Secondary to infection, radiation, stones. NO Warning or prompt

Answer 29

Bladder overflows. Obstruction (narrowing of urethra), large prostate, prolapsed uterus

Answer 30

Have to ask ?'s several type of disorders

Answer 31

Happens at night too. Increased daytime and nocturnal frequency. The bladder will not relax, always contracting

Answer 32

Related to physical or environmental limitiations. Cannot access the toilet in time. Nothing wrong with the bladder/no access to the bathroom

Answer 33

Sudden onset r/t infections, constipation, or impaction. Reversible

Answer 34

Nocturnal overactivity of the detrusor muscle Incontinence while sleeping, common with children Primary - child who has never achieved continence Secondary - develops after a period of at least 6 months of dryness

Answer 35

Caused by interruption of normal bladder innervation Stroke, Parkinson's, CP, Spinal Cord injury Manifests as overactive (incontinence) and spastic or inactive and flaccid (retention).

Answer 36

Chronic bladder pain without apparent cause. Inflammation of the bladder lining, often misdiagnosed as a infection. Have to do cultures to determine inflammation vs. infection

Answer 37

Prevents bacterial growth

Answer 38

Kills bacterial growth

Answer 39

Blockage in urinary flow partial or complete from the bladder to the urethra

Answer 40

Fifth most common cancer Most tumors originate from the transitional epithelium lining the urinary tract (traditional cell)

Answer 41

Bladder cancer hard to treat PAINLESS HEMATURIA

Answer 42

Renal pain generally at CVA (flank pain)

Answer 43

Down dirty cheap - shows general size and stones

Answer 44

Size of a kidney, comparison, always order bilateral (solid tissue or cyst)

Answer 45

Detailed information about the vascular and tissue in kidneys

Answer 46

Dye is nephrotoxic have to know renal fx

Answer 47

nuclear scan of kidneys which will show vasculature and neoplasms

Answer 48

Abnormal dilation of renal pelvis and calyces of one or both kidneys. Colicky intermittent spazmatic pain

Answer 49

kidneys do not develop in utero; bilateral - incompatible with life. Can be r/t nephrotoxic drugs

Answer 50

Nonmetastising growths, cystic No intervention, monitoring

Answer 51

Evident at birth; inherited Kidneys enlarged Severe systemic HTN (RAAS system) Liver disease - liver biopsy

Answer 52

Renal cell is very curable, the transitional cell is harder to treat Often metastasizes to lung Being obese is an increased risk factor for every type of CA

Answer 53

Most common CA in children. Hypertension is a unique sign Can palpate kidney tumor Tx Nephrectomy, radiation, chemo

Answer 54

Acute bacterial infection in kidney WBC's CASTS Nitrates

Answer 55

Repeated acute infections Results in loss of nephrons

Answer 56

Renal calculi - crystal aggregates composed of organic and inorganic materials within the renal tract Most stones are calcium-based but can be uric acid based

Answer 57

Non-malignant enlargement of prostate gland \>50 Unknown cause for prostatic stromal cell proliferation (estrogen, delayed apoptosis)

Answer 58

LUTS Lower urinary tract symptoms hesitancy, frequency am/pm, reduced stream, post void incontinence Slow onset of sx

Answer 59

3 layers: endothelial lining, basement membrane, epithelial cells

Answer 60

Diffuse \>50% Focal \<50%

Answer 61

Inflammatory disorder of the glomeruli Humoral and cellular mediated immune response Degradation of the basement membrane results in blood and protein passing

Answer 62

Immune response with **_inflammation_**-causing renal capillary damage More common in children Sx present 1-2 weeks after pharyngitis or up to 6 weeks after impetigo (strep throat strep A)

Answer 63

Tea colored urine Oliguria = Edema = HTN

Answer 64

Autoimmune IgG Glomerulonephritis with alveolar hemorrhages Rapid & progressive renal failure SOB, hemoptysis due to alveolar hemorrhage

Answer 65

Children Vasculitis related to immune response HEMATURIA, NO PROTEIN

Answer 66

Glomerular damage due to IgA protein deposits inside the filters (glomeruli) in the kidneys Occurs after a URI in adults Hematuria & Proteinuria Can lead to end-stage renal disease

Answer 67

Immune injury affecting mainly podocytes (barrier to protein passage) Massive amounts of PROTEIN in urine \>3.5grms /day Proteinuria leads to hypoalbuminemia and generalized edema (putting out so much protein in urine that it is not staying in vessels since albumin follows fluid the fluid shifts to interstitial = edema

Answer 68

Sudden loss of renal fx **_Acute tubular necrosis_** is most common cause

Answer 69

Disruption of blood flow to the kidney can be from: Hypotension, renal artery stenosis, dehydration MI, CHF, Diuretics, NSAIDs Prolonged ARF leads to acute tubular necrosis S/S concentrated urine (hanging onto Na+H20 makes serum osmolality high)

Answer 70

Damage to the structure of the nephrons and kidney Ischemia from renal vein thrombosis, internal vasoconstriction resulting in hypoxia Glomerulonephritis, cast formation in tubules obstructing urine flow Multiple myeloma IV contrast, IV abx

Answer 71

Blocked urine excretion

Answer 72

Sudden reduction of kidney fx Increased serum CREATINE 1.5x higher than baseline Increased serum creatine results in decreased GFR

Answer 73

RIFLE criteria The injury is defined by a doubling of serum creatinine or a reduction of urinary output below 0.5ml/kg per hour during at least 12h. Patients who develop injury \>50% will develop renal failure

Answer 74

Severity of disease

Answer 75

Patient outcomes

Answer 76

Increased creatinine x1.5 or GFR decrease \>25% UO \< 0.5 x6 hours

Answer 77

Increased creatinine x2 or GFR decrease \>50% UO \< 0.5 x12 hours

Answer 78

Increased creatinine x4 or GFR decrease \>75% or creatinine \>4mg per 100ml UO \<0.3 x24 hours or anuria x12 hours

Answer 79

Persistent ARF = complete loss of renal fx \>4 weeks

Answer 80

End Stage Renal Disease

Answer 81

Common cause of AKI Ischemia due to decreased renal perfusion Hypoxia, vasoconstriction, or nephrotoxic medications Results in necrosis of the tubules REVERSIBLE if caught early

Answer 82

Prodromal Oliguric Postoliguric

Answer 83

Early Normal or declining output Serum BUN or creatine begin to rise Insult to kidney has occurred and duration of this phase depends on cause, amt of toxin ingested, duration and severity of hypotension

Answer 84

May last up to 8 weeks with urine output 50-400ml/day Oliguria and progressive uremia; decreased GFR; hypervolemia Typically lasts 1-2 weeks Dialysis may be required

Answer 85

Renal recovery (5% don't recover) Urine volume increases May last 1 week with full recovery in 1 year Some degree of renal insufficiency may persist

Answer 86

Outcome of progressive and irrevocable loss of functional nephrons Progressive process: CKD then ESRD (requires dialysis) Comorbidities HTN, DM Decreased kidney fx or ***_kidney damage of 3 months GFR \<60 for 3 months_*** with or without indication of damage to kidney

Answer 87

Diabetes HTN Recurrent pyelonephritis Glomerulonephritis Polycystic kidney disease Family history of CKD Hx of exp to toxins \>65 YO African American

Answer 88

Can lose 75-80% of their nephrons before having issues

Answer 89

STAGE 1 - NORMAL : \>90 GFR ( Add 30 to 60) STAGE 2 - MILD : 60-89 GFR (Add 30) STAGE 3 - MODERATE : 30-59 GFR (Stage 3 = 30 GFR) STAGE 4 - SEVERE : 15-45 GFR (Stage 4 - 15) STAGE 5 = END STAGE : \<15 GFR (Stage 5 - 15 )

Answer 90

Stages of CKD Focus in stage 1 and 2; minimizing risk factors By stage 3: symptoms may be starting to appear requiring trmt In stage 4: planning for dialysis or transplant should begin In stage 5: transplant or death

Answer 91

-Hypertension and cardiovascular disease -Uremic syndrome -Metabolic acidosis

Answer 92

Hypervolemia, escalated atherosclerotic process, heightened RAAS and SNS activity

Answer 93

Retention of metabolic wastes; impaired healing, pruritus; dermatitis, uremic frost

Answer 94

Retention of acidic waste products; hyperkalemia

Answer 95

Retained K, Phosphorus, Magnesium

Answer 96

Elevated phosphorus and PTH causes altered bone mineral metabolism; kidneys unable to reabsorb calcium

Answer 97

Decreased intake from uremic syndrome, depression, dietary limitations, changes in taste, protein-energy wasting neg nitrogen balance

Answer 98

Lack of erythropoietin; uremia shortens RBCs life; combination of worsening CKD, anemia, and heart failure (cardiorenal anemia syndrome)

Answer 99

Comorbid conditions; disease itself ; disruption of social interactions and relationships

Answer 100

Partial or complete occlusion (stenosis) of the artery resulting in hypoxia to the tissues. Can be slow or fast onset. One or both extremities

Answer 101

SMOKING Age \> 70 Diabetes Dyslipidemia HTN

Answer 102

Extremity pain with activity with adv disease at rest too Claudication (intermittent pain with activity) **_Pain with elevation of the extremity and improved with dependant position_** Dimished pulses **_Decreased hair, cooler skin temp_** **_Non-healing ulcers on distal bony area (toes)_** **_Upper extremity - \> 15mmHg pressure difference in arms_**

Answer 103

* PALLOR * PULSELESSNESS * PARAESTHESIA * PARALYSIS * POIKILOTHERMIA (COLD) * PAIN

Answer 104

* Veins return blood flow back to the heart through negative thoracic pressure and muscle contraction with physical activity * Veins have one-way valves

Answer 105

Obesity Pregnancy DVT Liver Disease Prolonged sitting or standing

Answer 106

Venous valve dysfunctions lead to engorged and enlarged veins usually happens in the legs Increased hydrostatic venous pressure leads to capillary dilation and increased permeability Movement of fluid and pigments into the surrounding tissues results in edema and skin discoloration that can lead to tissue necrosis. remember the veins do not carry clean blood it carries all blood with waste product

Answer 107

Persistent Edema Heaviness in legs Rope like varicosities Stasis pigmentation Induration Lipodermatosclerosis Venous Ulcers ABOVE THE ANKLE Inflammation may lead to thrombophlebitis

Answer 108

CHF DVT Cellulitis

Answer 109

Changes in BP are mediated through stimulation of the alpha receptors (epinephrine and norepinephrine) of the sympathetic nervous system (SNS) Neurotransmitters epinephrine and norepinephrine cause vasoconstriction

Answer 110

Parasympathetic nervous system stimulation slows the heart rate using the vagus nerve

Answer 111

Cardiac Output (SVxHR) and systemic vascular resistance

Answer 112

Baroreceptors are in the aortic arch to detect pressure in the heart and arteries and make adjustments quickly.

Answer 113

Chemoreceptors detect chemical changes in the blood and stimulate the medullary vasomotor center to increase SNS activity

Answer 114

Regulated by neural, hormonal and renal An increase in ECF volume causes increased CO and SVR to raise BP and causes kidneys to excrete excess sodium and fluid An increase in serum sodium level causes increased osmolality, increased ADH secretion, and causes the kidneys to reabsorb water

Answer 115

Renin-angiotensin-aldosterone system (RAAS) important regulator of BP ## Footnote * Low BP stimulates Juxtaglomerular cells to release renin * Renin activates angiotensinogen to produce angiotensin I. * Angiotensin I contacts with ACE to activate angiotensin II (vasoconstriction) * Angiotensin II stimulates release of aldosterone. * Aldosterone causes reabsorption of sodium and water passively follows.

Answer 116

Potent vasodilator Vigara

Answer 117

ANP causes kidneys to increase sodium and water excretion by increasing the glomerular filtration rate resulting in urination If the L/R atrium is stretched (could be volume overload) so the kidneys kick in

Answer 118

Potent vasoconstrictor

Answer 119

* Circadian Rhythm (body’s internal clock) in the brain govern daily variations in bodily functions. * Rises before awaking (morning surge) * Highest in the middle of the morning * Lowest at night (nocturnal dip)

Answer 120

Hypertension increases morbidity and mortality associated with heart disease, kidney disease, peripheral vascular disease, and stroke

Answer 121

2017 AHA/ACC Guidelines No more term "Prehypertension" Stage 1 has been lowered 2 or more NP readings on 2 or more consecutive visits

Answer 122

Idiopathic disorder Most common form of HTN Rare prior to age 10 Systolic BP major risk factor for cardiovascular disease

Answer 123

Dietary factors - Na intake; DASH diet Sedentary lifestyle Obesity/weight gain Metabolic syndrome Elevated blood glucose levels/diabetes Elevated total cholesterol Tobacco Stress

Answer 124

HR SVR Stroke volume

Answer 125

Hypertension attributed to a specific identifiable pathology or condition. Infant/Child - most common cause renal disease and coarctation of the aorta and sleep apnea Adult - r/t renal artery stenosis, pheochromocytoma, pregnancy, obesity/OSA, hyperaldosteronism - most common cause

Answer 126

Hypertensive emergency - sudden increase in S or D BP with end-organ damage Hypertensive urgency - sudden increase in S or D BP without evidence of end-organ damage

Answer 127

Criteria: Excessive increase in HR (by 20 to 30/BPM) Dizzyness, blurred vision, confusion, syncope Assoc with CVD and is a risk factor for stroke, cognitive impairment, and death Causes: problem with vasomotor or baroreceptor response adverse drug therapy arterial stiffness volume depletion vasovagal reaction cardiac dysrhythmias

Answer 128

Preload (120ml) Amount returned to the heart between contractions Ventricular filling pressure prior to contraction

Answer 129

The resistance to eject blood during a cardiac contraction. SVR is afterload SVR is determined by the radius of arteries and degree of a vessel compliance

Answer 130

The amount of blood ejected with each contraction of the ventricle (S + EDV-ESV)

Answer 131

Amount of blood that remains in the ventricle after ejection 50ml

Answer 132

SV/EDV normal 60-80%

Answer 133

Left main coronary artery divides into left anterior descending and circumflex branches (widow maker)

Answer 134

Supplies the septal; anterior, lateral, and apical left ventricle; anterior of the right ventricle

Answer 135

Supplies the lateral and posterior left ventricles, left atrium

Answer 136

Supplies right atrium, right ventricle, and posterior left ventricle (SA and AV node)

Answer 137

* reduced driving pressure * reduced vessel diameter * reduced perfusion time (due to tachycardia) * increased metabolic demand (activity determines)

Answer 138

Conduction problems or heart block because of the SA and AV node

Answer 139

The measure of the amount of blood pumped out of the heart each minute Normal resting is 5-6L CO = stroke volume X heart rate

Answer 140

The levels of Na, K, and Ca affecting the electrical impulse to initiate contractility. Availability of ATP (need energy) Preload Afterload

Answer 141

Afterload is the impedance to ejection from the ventricle and is determined primarily by the aortic blood pressure. Aortic valve narrowing can significantly increase afterload * Increase in afterload increases the ventricular pressure which requires greater tension development within the walls of the chamber (wall stress) * Increases myocardial workload * Increases oxygen consumption * Increases chance of hypertrophy

Answer 142

Atrial natriuretic peptide (ANP) synthesized by myocytes and released in response to atrial stretch ANP and BNP cause enhanced excretion of sodium and water by the kidneys

Answer 143

B-type natriuretic peptide (BNP) produced and released by ventricles in response to chronic overdistention BNP is elevated in congestive heart failure

Answer 144

An impulse that cardiac cells initiate to cause contractility

Answer 145

Sympathetic innervation is widespread to all areas of the heart Parasympathetic innervation via the vagus is localized to the SA and AV nodal areas Right vagus nerve supplies SA node Left vagus nerve supplies AV node

Answer 146

Sympathetic activation binds norepinephrine to Beta-1 receptors Increases heart rate (chronotropic effect) Increases force of contraction (inotropic effect)

Answer 147

Parasympathetic stimulation binds acetylcholine to muscarinic receptors Reduction in heart rate Slower speed of action potential conduction Vasovagal response

Answer 148

Starts at the pacemaker site and spreads throughout the myocardium, electrical current is transmitted to the body surface Electrical impulse shortens cardiac muscle fibers and causes contraction

Answer 149

identifies irregularities in conduction rate or pathways

Answer 150

Atrial depolarization - contraction

Answer 151

Ventricular depolarization - contraction

Answer 152

Ventricular repolarization Recovery

Answer 153

in slow heart rate and low potassium

Answer 154

* Uses ultrasound to provide an image of cardiac structure and motion within the chest * Useful in diagnosis of heart enlargement, valvular disorders, collections of fluid in the pericardial space, cardiac tumors, and abnormalities in left ventricular motion * Provides estimations of ejection fraction and assessments of ventricular systolic and diastolic function

Answer 155

Risk of tachycardia

Answer 156

Can cause ventricular arrhythmias

Answer 157

* Shunting of blood through abnormal pathways in the heart or great vessels * Obstruction of blood flow because of abnormal narrowing

Answer 158

Development of the atrial and ventricular septum Division of the main outflow tract (truncus arteriosus) into the pulmonic and aortic arteries Development of the valves

Answer 159

* Congenital heart disease is the most common heart disorder in children. * May be attributed to * Maternal rubella during first trimester of pregnancy * Exposure to cardiac teratogens * Genetic influences

Answer 160

Shunt: abnormal path of blood flow through the heart or great vessels Right to left: cyanotic (unoxygenated blood going into left side) Left to right: acyanotic Obstruction: interference with blood flow because of abnormal narrowing leading to increased workload of affected chamber Acyanotic

Answer 161

Systemic vasculitis resulting from infection or toxin stimulus genetic component Seen in children under the age of 5 M \> F

Answer 162

Fever \> 5 days \>101 degrees Conjunctivitis, oral mucositis with strawberry tongue, truncal rash, erythematous palms and soles, cervical lymphadenopathy Other manifestations – joint pain, cyanotic extremities Diagnosis : fever and 4 of the 5 above manifestations

Answer 163

Failure of a valve to open completely resulting in extra pressure workload for the heart

Answer 164

Insufficiency - the inability of a valve to close completely resulting in extra volume workload for the heart Murmurs result from the abnormal flow through the valve

Answer 165

The pericardium is the sac that covers the entire heart providing support and protection and maintains the heart in a secure position in the thorax. Made of collagen and elastin fibers sac consists of 30 to 40ml of serous fluid

Answer 166

* Idiopathic * Viral infections (cytomegalovirus, coxsackie virus, hepatitis C, IV, flu, Epstein Barr virus) * Myocardial Infarction * Aortic Dissection * Trauma to chest wall * Surgery * Autoimmune disease (SLE, RA) * Metabolic disorders (Uremia) * Radiation * Chemotherapy * Immunosuppressants * Causative medications (Hydralazine) * Malignancy (breast, lung, lymphoma)

Answer 167

Inflammation of the mycardium Infectious Viral - influenza, CMV, HSV, Adenovirus, Parvovirus Bacterial - Lyme, mycoplasma Parasite - Chagas disease Non-infectious agents - radiation, inf. disorders or sarcoidosis

Answer 168

Clinical manifestations Asymptomatic or flulike symptoms Chest pain, palpitations, syncope Heart failure in severe cases

Answer 169

Invasion and colonization of the endocardial structures by microorganisms with resulting inflammation. More common at valvular structures resulting in vegetation growth Most common bacteria - Staphylococcus or Enterococcus from GI tract Vegetation breaks loose and becomes emboli

Answer 170

Implanted cardiac devices, invasive procedures, IV drug use

Answer 171

Endocardium lines the chamber and it at the valves

Answer 172

Clinical Manifestations: Fever and chills Myalgias, arthralgias New or worsened heart murmur CHF Symptoms associated with arterial emboli

Answer 173

* Acute inflammatory disease that follows infection with group A β-hemolytic streptococci * Immune attack on connective tissue in joints, heart, skin. * Occurs mainly in children – 5-15 yo * Fever; sore throat; joint inflammation; a distinctive truncal rash * Inflammation causes valve scarring and dysfunction - Mitral and Aortic Not commonly seen as we use abx to treat strep. The damage can been seen in older adults as a result of this in childhood

Answer 174

Age-related calcium deposits on the aortic cusps or rheumatic fever Reduced outflow from the LV into the aorta during systole resulting in decreased cardiac output and LVH develops due to increased workload Not enough blood going into the systemic circulation with each squeeze. not a big deal at rest but with exertion it is. Coronary arteries is right outside aortic valve if there is a lack of blood flow the coronary arteries will not get what it needs resulting in angina

Answer 175

DOE dyspnea on exertion Fatigue Angina Syncope on exertion Myocardial ischemia and left-sided heart failure Systolic crescendo decrescendo murmur ***Right sternal border 2nd intercostal space very loud murmur***

Answer 176

* Incompetent aortic valve allows blood to leak back from the aorta into the LV during diastole * Increased volume of blood to be pumped out with the next contraction * Increased cardiac workload Valves are loose doesn't close completely allows blood to flow backward

Answer 177

Manifestations * Fatigue * DOE - Dyspnea on EXERTION * Angina * Syncope * Palpitations * Leads to **LVH and dilation with eventual left-sided HF** * Diastolic high-pitched blowing murmur - Right sternal boarder 2nd intercoastal space

Answer 178

Reduced outflow from the Left Atrium to the Left Ventricle during **_Ventricular DIASTOLE_** Increased pressure of the LA leads to atrial chamber enlargement and hypertrophy Cause: calcification or rheumatic fever

Answer 179

Manifestations: * Fatigue * Palpitations * DOE, **PND (go to bed normal wake up gasping)**, Orthopnea •Leads to **pulmonary hypertension and eventually RV hypertrophy and right-sided HF - will see sx in lungs sooner due to proximity** **Diastolic low-pitched, rumbling murmur**

Answer 180

Incompetent mitral valve allows the backflow of blood from the left ventricle to the left atrium during ventricular systole. LV and LA both dilate and develop hypertrophy due to extra blood volume Caused by MI damaging supporting valve tendons damaged chordae tendae

Answer 181

Manifestations: Fatigue Dizziness Dyspnea Palpitations Leads to left-sided heart failure **Pansystolic (hear it through systole and diastole) high-pitched, blowing murmur**

Answer 182

Displacement (prolapsing) of the mitral valve leaflets into the left atrium during ventricular systole W \> M adolescent middle age Can lead to mitral regurgitation **Clicking pop murmur**

Answer 183

Typically asymptomatic Chest pain Palpitations Dyspnea Can lead to mitral regurgitation **_MIDSYSTOLIC click or systolic murmur_**

Answer 184

Coronary heart disease (CHD) also called ischemic heart disease and coronary artery disease (CAD) Characterized by insufficient delivery of oxygenated blood to the myocardium caused by atherosclerotic coronary arteries (CAD) Risk factors: DM, HTN, Hyperlipidemia, Smoking

Answer 185

Vulnerable plaques may rupture or become eroded which stimulates clot formation. Vulnerable plaques have large lipid core, thin cap, and high shear stress

Answer 186

Stable plaques have more collagen and fibrin and a stable cap

Answer 187

Large stable atherosclerotic plaque acute platelet aggregation and thrombosis vasospasm poor perfusion pressure

Answer 188

Plaque disruption and thrombus formation and results in unstable angina or MI Abrupt Life Threatening

Answer 189

* coronary vasospasm * hypoxemia (high altitude, pulmonary disease) * low perfusion pressure from volume depletion or shock

Answer 190

Chest pain associated with intermittent myocardial ischemia Ischemia causes a build-up of lactic acid and metabolic wastes in the cardiac tissue causing sx NO permanent damage occurs Dx ECG - ST depression

Answer 191

1. Stable or typical angina 2. Unstable or cresecendo angina 3. Prinzmental or variant angina

Answer 192

Most common aka classic Stenotic atherosclerotic coronary vessels 65-70% narrowing Predictable onset by similar stimuli Lasts 3-5 min

Answer 193

May progress to acute ischemia Pain occurrence is not predictable Increasing severity and frequency of sx

Answer 194

Unpredictable attacks of anginal pain Onset of sx is unrelated to physical or emotional exertion, heart rate, or other obvious causes of increased myocardial oxygen demand Characterized by vasospastic chemicals by local mast cells, and abnormal calcium flux across vascular smooth muscle causing hypercontractility Minimal to no atherosclerosis **PAIN AT REST OR AT NIGHT** **Younger \<50 years of age**

Answer 195

Chest pain \>15 min Plaque rupture with acute thrombus development Unstable angina - occlusion is partial MI - occlusion is complete

Answer 196

ECG - ST elevation Biomarkers: Myoglobin - elevated at 1 hour, normalizes quickly CPK-MB - elevates at 4-6 hours Troponins - develop at 2-6 ours and peaks at 18-24 hours can last 10 days. Doesn't detect a MI onset less than 6 hours

Answer 197

* Chest pain \>15 min not relieved by rest or nitro * Asymptomatic MI : Silent MI * Women, the elderly, and patients with diabetic neuropathies * Atypical sx, including fatigue, nausea, back pain, and abdominal discomfort * ECG changes * ST- segment elevation, large Q waves, and inverted T waves

Answer 198

+ Biomarkers Chest pain with evidence of acute ischemia on ECG Candidates for acute **_REPERFUSION_** therapy

Answer 199

* availability and adequacy of collateral blood flow. * relative workload * length of time that flow is interrupted

Answer 200

Reduced ventricular contractility Decreased cardiac output Decreased cardiac output triggers compensatory responses including sympathetic activation

Answer 201

heart rate contractility blood pressure

Answer 202

* How quickly treatment is sought * Extent and location of the infarct * Previous cardiovascular health * Age * Presence of other disease processes

Answer 203

After 18-24 hours area of infarction becomes paler than the surrounding tissue 5-7 days yellowish and soft with rim of red vascular tissue 1-2 weeks necrotic tissue progressively degraded and cleared away **At 1-2 weeks infarcted myocardium weekend and susceptible to rupture** **By 6 weeks: Necrotic tissue replaced by tough fibrous scar tissue**

Answer 204

Diseases of the heart muscle Anything that changes the structure or function of the heart Dilated, hypertrophic, or restrictive types

Answer 205

Primary cause is genetic abnormalities Secondary Causes * Ischemic - CAD * Valvular – stenotic or insufficiency * Hypertensive – LVH with dilation * Inflammatory – myocarditis

Answer 206

* Dilation of one or both ventricular chambers * Slow progression of biventricular heart failure with a reduced ejection fraction **_•Systolic dysfunction (cannot squeeze effectively)_**– dyspnea, orthopnea, exertional intolerance

Answer 207

Thickened so much the LV is tiny **Genetic abnormality** Cause of sudden cardiac death in young patients NORMAL EJECTION FRACTION Not a problem with ejection problem with muscle for filling and diastole

Answer 208

Rarest form of cardiomyopathy **Stiff, fibrotic, rigid, noncompliant ventricle** with impaired diastolic filling Commonly associated with SLE, AMYLOIDOSIS, SARCOIDOSIS, SCLERODERMA (autoimmune) Affects collagen Decreased cardiac output and heart failure can result

Answer 209

The inability of the heart to maintain sufficient cardiac output to meet metabolic demands of tissues and organs Problem with impaired contractility 50% die within 5 years of diagnosis

Answer 210

Cause: * CAD and HTN - Most common * Valvular abnormalities, Sarcoidosis * Chemotherapy, appetite suppressants * Chronic lung disease Can be right or left sided or bilateral LV failure is most common and often leads to RV failure the worse outcomes are those with low EF

Answer 211

insufficient cardiac pumping manifested by poor cardiac output

Answer 212

Congestion of blood behind the pumping chamber

Answer 213

Baroreceptor (in carotids and aorta) reflex stimulation due to detecting fall in pressure - increased HR, increased contractility and vasoconstriction (makes the L side of the heart work harder increasing the afterload) Juxtaglomerular cells release renin, activating the RAAS cascade, resulting in Aldosterone release (increased Na and H20 retention) that increases volume and workload of the heart These changes result in increased cardiac output temporarily causing increased preload and afterload Eventually, the myocardial demand cannot be met and the heart decompensates

Answer 214

MI is a common cause of systolic dysfunction - whenever you have a MI you have permanent damage of the heart muscle which prevents it from contracting effectively (systolic/squeeze) Reduced contractility results in **_low EF_** Loss of cardiac muscle cells and reduced ATP production (no energy for cells to contract. This is called HFIEF - Heart failure with impaired EF Low EF \<35%

Answer 215

Right sternal border 2nd intercoastal space

Answer 216

Right sternal border second intercostal space very loud harsh murmur

Answer 217

Right sternal border 2nd intercostal space diastolic high pitched blowing murmur

Answer 218

Mid clavicular line 5th intercostal space under breast tissue diastolic low pitched rumbling murmur

Answer 219

CAD & HTN main causes More common in elderly women and those with no history of MI Disorder of the myocardial relaxation and the ventricle is stiff and does not fill effectively (can't pump out what you don't have) Low cardiac output, vascular congestion, and edema formation with NORMAL EF \>40% HFpEF - Heart failure with preserved EF

Answer 220

Accumulation of blood within the pulmonary circulation, pulmonary congestion and eventually edema. Dyspnea, DOE Orthopnea (has to sleep with multiple pillows) Paroxysmal Nocturnal Dyspnea (PND) can fall asleep with 1/2 pillows then wake up gasping when the pulmonary system backs up Cough, respiratory rales (crackles), hypoxemia and high left atrial pressure, circumoral cyanosis, hemoptyisis

Answer 221

Results in insufficient cardiac output with decreased oxygenation to peripheral tissues and organs S3 gallop Fatigue, weakness, activity intolerance Tissue hypoxia, renal dysfunction (less blood flow into the kidneys)

Answer 222

LV heart failure leads to RV heart failure or Pulmonary disorders cause increased pulmonary vascular resistance leading to high RV afterload causing right ventricular hypertrophy - caused by issues in the lungs backs up into the RV **(cor pulmonale)** then RV failure

Answer 223

Caused by congestion in the systemic venous system Dependant edema, ascites, jugular veins distended (JVD), hepatomegaly, splenomegaly Hepatogular reflux text; decreased GFR

Answer 224

Low output to the left ventricle leading to low cardiac output S4 gallop (blood dropping into a stiff right ventricle) Fatique and Confusion

Answer 225

Right-Sided Heart Failure ## Footnote * congestion of peripheral tissues * dependant edema and ascites * liver congestion - signs related to impaired liver fx * Gi tract congestion - Anorexia, GI distress, weight loss

Answer 226

Left heart failure * Decreased cardiac output - act intolerance, s/s decreased tissue perfusion * Pulmonary congestion * Impaired gas exchange * cyanosis and signs of hypoxia * Pulmonary edema * Orthopnea - has to sleep elevated on pillows * Cough with bloody sputum * Paroxysmal nocturnal dyspnea

Answer 227

Most often the result of primary left-sided HF progressing to right-sided HF Reduced cardiac output Pulmonary congestion caused by left-sided HF Systemic venous congestion caused by right-sided HF

Answer 228

H&P ECG - LVH, RVH ST depression (heart is being strained) CXR - pulmonary congestion/effusion Echo - size of heart chambers, valve abnormalities, EF Labs: BNP (ventricles dilate), troponins (ischemia), BNP (renal/electrolytes), Thyroid (controls metabolism)

Answer 229

FACES ## Footnote **F**atigue **A**ctivity limitations **C**ongestion **E**dema **S**hortness of breath

Answer 230

Definite Symptoms 1. Class I - No limitation of physical activity 2. Class II - Slight limitation of physical activity, comfortable at rest 3. Class III - Marked limitation of physical activity, comfortable at rest 1. Class IIIa - no dyspnea at rest Class IIIb - recent dyspnea at rest 4. Class IV - Inability to carry on any physical activity without discomfort, symptoms present even at rest

Answer 231

ACCF/AHA * Stage A - High risk for developing CHF, no structural disorder or the heart (CAD, MI, Diabetics) * Stage B - Structural disorder of the heart - Never had symptoms of CHF (Decreased contractility, valve abnormality) * Stage C - Past or current symptoms of CHF, symptoms associated with underlying heart disease * Stage D - End-stage disease, requires specialized treatment strategies

Answer 232

A dull pain that improves when you lay down. Fact: It is a shart pain that improves when you sit up. Patients will tripod

Answer 233

Hypertension Urgency

Answer 234

Because the EF is 30% it is a systolic disfunction b/c the problem is with the "squeeze" of the heart and a 3b the person still has min sx. A person would be a stage C with systolic dysfunction

Answer 235

b. hypoaldosterone Aldosterone makes you save salt and water which could make you hypertensive. If you are low (hypo) on aldosterone it would not cause htn

Answer 236

Stage III Stage IV is \< 30

Answer 237

Lateral MI

Answer 238

Anterior MI

Answer 239

A man with emphysema It's the lungs that stress the right side of the heart

Answer 240

False If you are failing there is not enough blood moving forward to give you HTN

Answer 241

b. albumin is being pushed out in the kidneys so you won't see it in the vascular system you will have hypoalbuminemia you will see a lot of Proteinuria over 3grams in Nephritic syndrome you will not see protein in urine

Answer 242

backs up into the pulmonary system

Answer 243

Vascular resistance in the large arteries