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280 Cards in this Set
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TL #3
Shock what is shock |
Failure to maintain adequate tissue perfusion
impaired tissue perfusion and impaired O2 delivery |
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what is the formula for the delivery of O2 to system
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DO2 = 1.39 x Hgb x SaO2 x CO
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list the 3 stages of shock
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1st Nonprogressive stage
2nd Progressive stage 3rd Irreversible stage |
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Name the stage of shock
Baroreceptor reflex stimulation sympathetic nervous system catecholamines released Alpha-/beta- receptor stimulation most pronounced in large vascular beds |
1st Nonprogressive stage
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name the stage of shock
Increased renin release (R-A-A system)- sodium/water reabsorption vasoconstriction Precapillary/postcapillary constriction- “transcapillary refill” |
1st Nonprogressive stage
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fill in the formula
BP = CO x ___ |
Systemic vascular resistance
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In the first stage of shock, non progressive, how does the body compensate
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tries to maintain BP= CO X SVR by:
1. increase CO- Increase preload, heart rate & contractility 2. maintain MAP-Increase CO & afterload |
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what 4 major events happen in progressive shock
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1st- Reduced CO & BP leading to tissue hypoperfusion
2nd Aerobic to anaerobic metabolism glycolysis = lactic acid production which leads to ATP depletion and then organelle/organ failure 3rd. Humoral/vasoactive agents released like adenosine, nitric oxide, serotonin, etc. 4th Lactic acid + agents = vasodilatation, which increased capillary permeability and reverse “transcapillary refill” |
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list 3 features that are ascribed to irreversible shock
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1. Vascular decompensation
resistant to therapy 2. Toxic free-oxygen radicals 3. Profound vasodilatation “vascular collapse” |
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what 4 criteria are used to clinically diagnose shock
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1. Hypotension- sBP < 90 mmHg or > 30% reduction from baseline (if know it)
2. Urine output < 0.5 cc/kg/hr 3. Metabolic acidemia (lactic acidemia) 4. Tissue hypoperfusion |
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how can you tell a tissue is hypoperfused
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Skin- pallor, diaphoresis, cyanosis, mottling
Cardiovascular- increased HR, SVR, contractility myocardial, ischemia/dysfunction or arrhythmias Brain restlessness, confusion, coma Kidney ischemia, dysfunction, acute renal failure Liver- dysfunction/injury Lungs- altered V/Q matching hypoxemia respiratory center stimulation tachypnea, hyperventilation |
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what do most people with shock die of
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RESPIRATORY FAILURE
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what are the 4 types of shock
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1. Hypovolemic
2. Cardiogenic 3. Distributive 4. Obstructive |
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describe the type of shock and the signs and symptoms associated (which parameters increased or decreased)
Loss of circulating blood volume Decreased CO from reduced preload caused by : whole blood loss, plasma loss, or protein-free fluid loss |
hypovolemic shock
Skin: cool, pale, clammy Decreased parameters: BP, CVP, PAP, PAWP, CI, SVI Increased parameters: HR, SVR |
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what is the first line of treatment for hypovolemic shock
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replace what pt lost. if lost blood give blood, if lost plama give plasma.
reverse hypoperfusion with Fluid resuscitation with rapid IV infusion of large volumes Fluid of choice- isotonic crystalloid (normal saline) |
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other than maintenance of fluid of pt in hypovolemic shock what other important factors must be carefully monitored since this is the reason most pt die
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adequate oxygenation
PaO2 > 60 mmHg; SaO2 > 90% adequate ventilation normalization of ABG’s |
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name the type of shock
Myocardial loss/dysfunction Decreased CO: Decreased contractility- Fast/slow heart rate Mortality = 50% - 80% 7% of AMI’s |
cardiogenic shock
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what is defined as acute cardiogenic shock
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> 40% loss of LV myocardium
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what are the 4 big causes of cardiogenic shock
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1. AMI
2. RVI 3. Acute mitral regurgitation 4. Ventricular septal rupture |
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how can we differential hypovolemic shock from cardiogenic shock since both pt have cool, clamy skin with hypovolemia
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cardiogenic Characteristic features:
JVD S3/S4 rales |
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what Hemodynamic parameters are increased or decreased in cardiogenic shock
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Decreased:
BP, CI, SVI Increased: HR, SVR, CVP, PAWP |
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what 4 components determine cardiac output
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Heart rate
Contractility Preload Afterload |
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in cardiogenic shock, the main problem is contractility. what is done to hopefully improve contractility.
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Poor contractility
inotropic agent dobutamine, dopamine, digoxin |
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in cardiogenic shock, a major problem is increased preload, what is done to decrease the preload
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loop diuretics- furosemide
vasodilator agent- nitroglycerin |
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for the high afterload in cardiogenic shock. what is done to hopefully reverse this effect
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vasodilator agent (if sBP > 100)- nitroglycerin, sodium nitroprusside
vasoconstrictor agent (if sBP < 90) |
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t/f thrombolytic agents or
PTCA should be considered in pts with hypovolemic shock |
false- should be considered in pt with cardiogenic shock
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what are 4 causes of distributive shock and how does it present
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Septic shock
Anaphylactic Spinal Drug/toxin ingestion Most common site of infection- pneumonia Warm type - most common hypotension, fever, warm/pink skin, confusion |
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most common causes of septic shock are due to which class of organism
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60% Gram (-) rods
Gram Negative Rods 1. Anaerobes-Bacteroidaceae (e.g. Bacteroides fragilis) 2. Facultative Anaerobes Enterobacteriaceae (e.g. Escherichia coli) Vibrionaceae (e.g. Vibrio Cholerae) Pasteurellae (e.g. Haemophilus Influenzae) 3. Aerobes Pseudomonadaceae (e.g. Pseudomonas aeruginosa) Gram Negative Cocci Aerobes Neisseriaceae (e.g. Neisseria Meningitidis) Gram Negative Obligate Intracellular Parasites- Rickettsiae (e.g. Rickettsia) |
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Describe the pathophysiology of septic shock-
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Infectious material released from organisms like endotoxin, exotoxin
Cytokines released from macrophages like TNF, interleukins -1, -2 Neutrophils, platelets, endothelial cells release- nitric oxide, free O2 radicals Activation of humoral defenses- coagulation, compliment, kinins Secondary mediator release prostaglandins, leukotrienes, endorphins, |
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in septic shock, what is the effect of the inflammatory response to an organism
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Vasodilatation (redistribution of blood flow) to Decreased afterload and Decreased preload
Myocardial depression which Decreased contractility Increased endothelial permeability leading to Decreased preload Altered cellular metabolism |
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list 4 causes for obstructive shock
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Cardiac tamponade
Tension pneumothorax Massive pulmonary embolus Thoracic aortic dissection |
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Chapter 26 Heart Failure
what is the definition of heart failure |
the heart is unable to pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body.
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what does the term congestive heart failure more clearly suggest
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the subset of HF patients who have biventricular failure, with elevated filling pressures of both ventricles, causing pulmonary and systemic venous hypertension.
Clinically, the term CHF best describes those HF patients with decreased effort tolerance, dyspnea, jugular venous distention (JVD), hepatic engorgement, and peripheral edema |
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in the prognosis of heart failure, which factors will worsened survival is predicted by: (4)
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1. Increasing severity of LV dysfunction (typically assessed by LV ejection fraction)
2. Reduced cardiac output / index 3. Elevated ventricular filling pressures 4. Reduced exercise capacity |
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New York Heart Association Functional Class describes class 1 as __
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Patients with cardiac disease but without symptoms during routine activity
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New York Heart Association Functional Class describes class 2 as __
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Class II: Asymptomatic at rest.
Become symptomatic with routine activity, resulting in slight limitation of activity |
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New York Heart Association Functional Class describes class 3 as __
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Class III: Comfortable at rest, but symptomatic with less-than-routine activity, resulting in marked limitation of activity
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New York Heart Association Functional Class describes class 4 as __
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Class IV: Unable to carry on any activity without symptoms. Often symptomatic at rest
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what is the difference in a pt with acute HF vs chronic heart failure
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Acute HF: Occurs with an abrupt onset, as after acute myocardial infarction (MI) or severe valvular dysfunction after chorda tendinae rupture
Chronic HF: Clinical features of HF often begin insidiously and progress to a chronic state |
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what is the most common presenting symptom of LV failure and why
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Dyspnea (difficulty breathing) is the most common presenting symptom of LV failure. Dyspnea is a direct consequence of elevated LV filling pressure and pulmonary congestion.
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what is the most common presenting symptom of RV failure
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Systemic venous congestion and peripheral edema are the predominant clinical findings
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what is the most common cause of RV heart failure and what causes this
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left sided heart failure due to
1. Pulmonary hypertension 2.Failure of shared myocytes in the ventricular septum |
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describe the clinical findings of biventricular heart failure
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biventricualr is both left and right HF, which cause pulmonary and systemic HTN (CHF)
Clinical findings of CHF: - Decreased exercise tolerance - Dyspnea; shortness of breath (SOB) - JVD - Hepatic congestion - Peripheral edema |
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describe high output cardiac failure
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HF in which the circulation remains brisk and the skin and extremities remain warm, despite increased venous pressures and a decreased cardiac output (CO) that existed prior to the onset of HF
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list 5 caused of high output failure
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- Anemia
- Hyperthyroidism (thyrotoxicosis) - Beriberi (thiamine deficiency) - A-V fistula - Paget’s disease of bone (hypercalcemia) |
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list 5 causes of low output failure
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1. Hypertension; hypertensive heart disease
2. Myocardial ischemia or infarct (i.e. Coronary atherosclerosis) 3. Valvular heart disease 4. Pericardial disease 5. cardiomyopathy |
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which type of heart failure (systolic or diastolic)
decreased contractility, causing a reduction in stroke volume (SV), leading to a decreased CO |
systolic
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how is ejection fraction calculated
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the volume of blood ejected from the ventricle (SV) divided by the LV end diastolic volume (LV EDV)
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which type of heart failure (systolic or diastolic)
Pulmonary and/or systemic venous congestion with resulting clinical findings in the presence of normal or near-normal systolic function |
diastolic
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what can cause diastolic heart failure
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Increased chamber stiffness
Chamber dilation Impaired ventricular relaxation Chamber hypertrophy |
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pts with diastolic HF has 1 or more of which conditions
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LVH : due to HTN, aortic stenosis , hypertrophic cardiomyopathy (increase chamber stiffness)
or Ischemic Heart Disease (IHD): (impairs ventricular relaxation )- or Infiltrative disease: amyloidosis, sarcoidosis, hemachromatosis (Chamber hypertrophy) |
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pt with which condition in his past med hx is 4 times more likely to have a systolic dysfunction than a diastolic dysfunction
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valvular heart disease
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on EKG, a pt with low voltage is more likely to suggest which type of dysfunction (systolic or diastolic)
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systolic
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on echocardiogram, a pt with which 2 conditions will indicate a systolic dysfunction rather than a diastolic dysfunction
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left ventricular dilation and reduced ejection fraction
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although HTN can indicate both systolic and diastolic dysfunction, which one is it more likely suggestive of
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diastolic dysfunction
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left ventricular hypertrophy indicates more of which type of dysfunction (systolic or diastolic)
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diastolic dysfunction
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an S3 gallop on auscultation indicates more of which type of dysfunction (systolic or diastolic)
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systolic
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an S4 gallop on auscultation indicates more of which type of dysfunction (systolic or diastolic)
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diastolic
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on chest roentfenogram indicating cardiomegaly, is suggestive of which type of dysfunction (systolic or diastolic)
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systolic
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cardiac causes of HF include :
1. Hypertensive heart disease, Myocardial ischemia or infarction accompanied by LV dysfunction, Valvular heart disease, Cardiac dysrhythmias and Cardiomyopathies: List 3 different types of cardiomyopathies that cause HF and which one is more likely due to infection, or alcohol related causes |
1. dilated (congestive) - more likely due to infection (parasite or viral), alcohol or connective tissue disease
2. hypertrophic- concentric LVH 3. Restrictive- from amyloidosis, hemachormoatosis, or sarcoid |
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t/f alcohol can precipitate heart failure
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ture
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how can fever precipitate Heart failure
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for every 1 degree increase in core body temp,there is an increase of 10% of metabolic demand placed on the body
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why can hypoxemia precipitate HF
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o2 is a vasodilator...
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what is the effect of Na+ and H2O retention on ventricular function and ventricle size
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increase in Na and H20, increase preload which will increase ventricular function leading to volume overload causing metabolic stress and hypertrophy
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what is the effect of Na+ and H2O retention on ventricular function and ventricle size
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increase in Na and H20, increase preload which will increase ventricular function leading to volume overload causing metabolic stress and hypertrophy
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describe the effect of increase sympathetic activity on the vasculature, RAAS and afterload
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increase in sympathetic activity activates the RAAS to hold on to Na which will hold on to H2O, increasing preload and increasing ventricular function
increase sympathetic activity also increases vascular resistance and increase ventricular preload |
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Frank-Starling mechanism during HF increases preload to compensate for what
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a decreased contractility and therefore decreased cardiac output,
FS helps to sustain cardiac performance As preload is increased, heart’s contractility is increases. Stretching the muscle fiber to an optimal length produces a more forceful contraction |
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which type of hypertrophy (eccentric or concentric)
thickened ventricular walls with the potential for reduced chamber volume. Increases ventricular stiffness, necessitating higher-than-normal diastolic pressures to fill the ventricle, leading to diastolic dysfunction and diastolic HF. |
concentric
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which type of hypertrophy (eccentric or concentric)
ventricular walls are not thickened, but the chamber is dilated. hypertrophy impairs ventricular relaxation, leading to diastolic HF. |
eccentric
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which type of heart failure ( eccentric of concentric HF)
LVH (caused by IHD, MI and other conditions resulting in dilated LV) impairs relaxation of the ventricle, causing diastolic dysfunction |
eccentric
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which type of heart failure ( eccentric of concentric HF)
LVH ( as occurs in HTN, aortic stenosis, and hypertrophic cardiomyopathy) results in increased ventricular stiffness, necessitating higher-than-normal diastolic pressures to fill the hypertrophied ventricle. |
concentric LVH
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Name the symptom in LV failure
breathlessness predominant symptom, usually associated with tachypnea, due to increase blood volume and alveolar congestion |
dyspnea
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Name the symptom in LV failure
dyspnea that occurs soon after lying flat and is relieved by sitting up. what causes this |
orthopnea- caused by increases venous return to the right heart and lungs in recumbent position
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Name the symptom in LV failure
severe dyspnea may awaken a pt from sleep, relief urgently sough by sitting up or finding an open window |
paroxysmal nocturnal dyspnea
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Name the symptom in LV failure
decreased renal flow with upright activity this gives way to more normal renal perfusion and diuresis while in supine at night |
nocturia
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Name the symptom in LV failure
pulmonary venous and capillary pressure can increase abruptly, resulting in rapid accumulation of fluid in the alveoli and interstitial space of the lungs. what symptoms are seen |
acute pulmonary edema
symptoms: nonproductive cough, wheezing, severe dyspnea |
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Name the symptom in LV failure
rust colored sputum containing alveolar macrophages |
hemoptysis
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Name the symptom in LV failure
in advanced HF, may be accompanied by periodic breathing with alternating apnea and hyperventilation |
cheynes- stokes respiration
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describe the general appearance and Signs of LV Failure in a pt
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Anxious; sitting up if acute pulmonary edema
- Respiratory distress - Pale - Dusky - Sweaty - Cool skin / extremities |
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describe the vital in a pt with LV failure
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Tachypnea
Tachycardia Narrowed pulse pressure- Diastolic BP may be increased - Systolic BP often low, but may be normal |
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describe the heart sounds and location in a pt with LV failure
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Cardiomegaly
Muffled heart sounds Accentuated pulmonic component of S2 Muffled heart sounds S3 gallop S4 gallop Murmurs Pulsus alternans- |
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what is Pulsus alternans in a pt with LV failure
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alternating strong and weak pulse in an underlying regular rhythm usually indicating a progressed HF
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Isolated RV failure is uncommon in adults, and is usually caused by (other than LV heart failure):
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1. - Cor pulmonale secondary to intrinsic lung disease
2. Congenital intracardiac left-to-right shunt (e.g. Atrial septal defect) with chronic volume overload |
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what causes the SYMPTOMS described by pt (sign: by examiner) in RV failure
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Caused by the elevation of systemic venous pressure
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Describe the 2 big symptoms of RV failure
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1. Hepatic and G.I.congestion and edema
- Anorexia - Nausea - Vomiting - Abdominal discomfort / pain - Ascites 2. Symptoms due to systemic venous congestion Peripheral edema Weight gain Venous stasis |
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what are the SIGNS of RV failure
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Cyanosis (usually absent in LV failure unless pulmonary edema)
JVD Hepatic engorgement with hepatomegaly and tenderness. Hepatojugular reflux- push on liver and increases distention in neck Peripheral Edema Oliguria |
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why is prevention of HF preferred over treatment of HF
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since high rates of mortality and mobidity persist in pt with HF, despite advance in treatment
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to prevent HF, pt should reduce which risk factors for coronary heart disease
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HTN, diabetes mellitus, dyslipidemia, obesity, smoking, increase exercise
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Acute HF is A medical emergency, what are the ABCs
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ABC’s: Airway, Breathing, Circulation
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how does O2 help in a pt with RV failure
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a) Increases arterial oxygenation in hypoxemic patient
b) O2 is a potent vasodilator of pulmonary arterial circulation (improves RV failure) |
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what is used to measure the Saturation of O2 (arterial oxygen saturation)
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pulse oximeter
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what 6 pharmacological agent classes are used in HF and why
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1. I.V. Diuretics- to decrease preload
2. Nitroglycerin (sublingual, intravenous, topical) 3. Morphine sulfate- decrease pain and anxitety 3. Intropic agents (dobutamine, amrinone, digoxin): to improve cardiac contractility 4. Pressors (e.g. Dopamine): to raise SBP and to improve renal/gut perfusion 5. Vasodilators (ACE inhibitors, hydralazine)- to decrease afterload |
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which cardiac glycoside is used in heart failure
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digoxin
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which 3 types of diuretics are used in heat failure and give examples of each type
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1. loop diuretics- bumetanide, furosemide
2. thiazides- hydrocholothiazide, metolazone 3. K+ sparring diuretics- spironolactone, amiloride, triamterene |
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list the 6 types of vasodilators used in heart failure
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1. hydralazine-interferes with the action of the second messenger IP3, limiting calcium release from the sarcoplasmic reticulum of smooth muscle. This results in an arterial and arteriolar relaxation.
2. angiotensin converting enzyme inhibitor 3. angiotensin II receptor antagonists 4. nitrovasodilators- isosobide, nitroglycerin, nitroprusside 5. nesiritide 6. phosphodiesterase 3 inhibitor- inamrinone, milrinone |
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which 2 sympathetic amines can be used in heart failure
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dopamine or dobutamine
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which 3 beta blockers are used in heart failure
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carvedilol, metoprolol, bisprolol
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what type of diuretic is the following: mannitol
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
osmotic along with urea
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what type of diuretic is the following: acetazolamide
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
carbonic anhydrase inhibitor
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what type of diuretic is the following: furosemide
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
trade name is Lasix- loop diuretic
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what type of diuretic is the following: bumetanide
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
loop diuertic
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what type of diuretic is the following: hydrocholothiazide
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
thiazide-
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what type of diuretic is the following: spironolactone
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
K+ sparring
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what type of diuretic is the following: triamterene
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
K+ sparring
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what type of diuretic is the following: amiloride
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
K+ sparring
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what type of diuretic is the following: urea
a. potassium sparring b. thiazide c. loop diuretic d. carbonic annhydrase inhibitor e. osmotic |
osmotic
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which diuretics are used to reduce the vascular volume in pt
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hydrocholorothiazide and chlorthalidone
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which centrally acting sympatholytics alpha adreneric agonist were used to reduce sympathetic tone but the side effects of postural HTN and sexual dysfunction lead to its discontinuation for use as antihypertensives
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methldopa or clonidine
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which centrally acting sympatholytics alpha adreneric ANTAGONISTS were used to reduce sympathetic tone but the side effects of postural HTN and sexual dysfunction lead to its discontinuation for use as antihypertensives
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prazosin, doxazosin, terazosin
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name 6 beta adrenergic blockers that are used as antianginal, antihypertensives and adjuncts to MI therapy by non selectively blocking beta 1 adrenergic receptors and thus decreasing the O2 requirement.
What are the clinical effects of blocking the beta receptors |
carteolol, carvedilol, labetalol, propanolol, sotalol, timolol
clinical effects: decrease in sinus node HR, decrease cardiac output and decrease in BP |
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name 4 beta adrenergic blockers that are used as antianginal, antihypertensives and adjuncts to MI therapy by selectively blocking beta 1 adrenergic receptors and thus decreasing the O2 requirement.
What are the clinical effects of blocking the beta receptors |
acebutolol, atenolol, betaxolol, metoprolol
clinical effects: decrease in sinus node HR, decrease cardiac output and decrease in BP |
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which drug is a combined alpha and beta blocker
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labetalol
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name 2 vasodilators
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hydralzine and minoxidil
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what are the 3 modes of action for angiotensin-converting enzyme inhibitors and the results of their 3 actions
|
1. block the conversion of angiotensin 1 to angiotensin 2 ( Agio2 is a major vasoconstrictor)
2. ACEI inactivate the pulmonary bradykinin- a major vasodilator but causes cough 3. increase plasma renin level and reduce aldosterone levels so their systemic effect is to vasodilate resulting in lower BP, decrease afterload in CHF, and decrease development of CHF, increased survival of MI pt and decrease progression of diabetic nephotoxicity |
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name 3 angiotensin-converting enzyme inhibitor
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captopril, lisonopril, benazepril
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angiotensin II antagonists share many of the same features as angiotensin-converting enzyme inhibitor. how are ARBs different than ACEI
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ARBs- block the binding of angiotensin II to the recptor but do not prevent the degradation of bradykinin so there is less cough
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list 2 angiontenin II receptor blockers (ARB)
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losartan, valsartan
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what is the mechanism of action for calcium channel blocker in the heart and what are they used for
|
MOA: inhibit influx of intracellular Ca+2 through L-type channels so
1. decrease TPR 2. reduce contractility of smooth cardiac muscle 3. |
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list 2 dihrydropyridine calcium channel blockers
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amlodipine, ifedipine
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list 2 non-dihrydropyridine calcium channel blockers
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diltiazem, verapamil
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in a hypertensive emergency, what 3 drugs could be given
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1. nitroprusside- NO analougue
2. diazoxide- causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions. This switches off voltage-gated calcium ion channels 3. trimethaphan- counteracts cholinergic transmission at the ganglion type of nicotinic receptors of the autonomic ganglia and therefore blocks both the sympathetic nervous system and the parasympathetic nervous system |
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which cardiac glycoside can be given to a pt in heart failure. and how does it work
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digoxin, - inotropic
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which drug can be given in case of a digitalis overdoes as an antidote
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digoxin
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t/f amrinone or milrinone are 2 positive inotropic agents can be given to pt in heart failure
|
true
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t/f dopamine, dobutamine are 2 beta-blockers that can be given to a pt in heart failure
|
false- dopamine, dobutamine are sympathomimetics
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t/f captopril, enalapril are 2 angiotensin converting enzyme receptor blockers that can be given to a pt in heart failure
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false- captopril, enalapril are ACE INHIBITORS not receptor blockrers
|
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which type of anti-arrhythmics are the following:
quinidine, procainamide, disopyramide, lidocaine, phenytoin, mexiletine a. calcium channel blockers b. drugs to prolong repolarization c. beta blockers d. sodium channel blockers e. vasodilators |
d. sodium channel blockers
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which type of anti-arrhythmics are the following:
propranolol, pindolol,bisoprolol and HCTZ combo a. calcium channel blockers b. drugs to prolong repolarization c. beta blockers d. sodium channel blockers e. vasodilators |
c. beta blockers
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which type of anti-arrhythmics are the following:
bretylium, amiodarone a. calcium channel blockers b. drugs to prolong repolarization c. beta blockers d. sodium channel blockers e. vasodilators |
b. drugs to prolong repolarization
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which type of anti-arrhythmics are the following:
verapamil, diltiazem a. calcium channel blockers b. drugs to prolong repolarization c. beta blockers d. sodium channel blockers e. vasodilators |
a. calcium channel blockers
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which type of anti-anginal drugs are the following:
nitroglycerin, isosorbide dinitrate a. calcium channel blockers b. drugs to prolong repolarization c. beta blockers d. sodium channel blockers e. vasodilators |
e. vasodilators
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which beta blocker is used as an anti-anginal drug
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propranolol
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what are the 6 top selling calcium channel blocking drugs sold in the us for anti-angina
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verapamil, diltazem, nifedipine, amlodipine, lisinopril+HCTZ, benazepril+HCTZ
|
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what are the 3 main goal in the management of CHF
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1. normalize bp
2. promote regression of LVH 3. prevent tachycardia |
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what is the standard therapy for a systolic CHF pt
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ACEI + Loop + Digoxin
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which drugs are beneficial for reducing preload (choose up to 2)
a. diuretics b. sympathomimetics c. beta blockers d vasodilators e. ACEI f. ARBs g calcium channel blocker h. phosphodiesterase inhibitor |
1. diuretics- to reduce pulmonary congestion in order to reduce preload and SV can also use K+ sparring diuretics like spironolactone
2. vasodilators like nitrates or hydralize or minoxidil |
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which drugs are beneficial for reducing afterload (choose up to 2)
a. diuretics b. sympathomimetics c. beta blockers d vasodilators e. ACEI f. ARBs g calcium channel blocker h. phosphodiesterase inhibitor |
1. ACEI- cause regression of LVH, lower bp, prevent cardiac remodeling
2. beta blockers- to decrease HR, increase diastolic filling time, decrease O2 consumption, lower BP and cause regression of LVH |
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which drugs are beneficial for reducing preload AND afterload (choose up to 2)
a. diuretics b. sympathomimetics c. beta blockers d vasodilators e. ACEI f. ARBs g calcium channel blocker h. phosphodiesterase inhibito |
1. sympathomimetic amines like dobutamine or dopamine
2. phosphodiesterase inhibitors like amrinone or milrinone |
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how is the heart muscle affected by digoxin
|
cardiac glycoside like digoxin, inhibit the Na/K ATPase pump on cardiac cell membranes which results in an increase in intracelluar Na+. This increase in Na+ is exchanged for Ca+2 by the Na/Ca exchanges so then there is more Ca+2 intracellularly. this increase in Ca+2 increases the contractility of the heart
|
|
which 4 Factors affecting cardiac output:
|
1. Chronotropy- Heart rate
2. Inotropy- Contractility 3. Preload - Intravascular volume 4. Afterload-Systemic vascular resistance |
|
what is the formula for cardiac output
|
Cardiac output (CO) = stroke volume (SV) x heart rate
|
|
Pressure = ___ x Resistance
|
Pressure = Flow x Resistance
|
|
MAP = CO x __
|
MAP = CO x systemic vascular resistance
|
|
Describe which type of heart failure (systolic or diastolic)
↓ Contractility leads to ↓ CO and ↓ SV Compensatory result: ↑ Afterload, ↑ Preload, ↑ Heart rate |
systolic dysfunction
|
|
Describe which type of heart failure (systolic or diastolic)
CO maintained @ resting heart rate Contractility and heart rate maintained ↓ Ventricular relaxation (remains stiff) decrease in Preload, +/- ↑ Afterload |
diastolic
|
|
what are the clinical effects of digoxin in HF pt
|
↑Contractility (inotropy)
↑ Stroke volume/Cardiac Output Weak inotrope There is mild systemic, coronary arterial, and venous vasoconstriction ( especially when given by intravenously) There is some diuretic effect as it inhibits reabsorption of Na+ at the kidneys. |
|
t/f the use of digoxin in HF has positive effects on long-term survival
|
false- use of digoxin has little to no effect on long-term survival
|
|
what is digoxin indicated for (2)
|
Congestive Heart Failure
Antidysrhythmic agent Used to slow the ventricular rate (< 100 bpm) in atrial flutter/fibrillation. |
|
Digoxin is know to cause- GI ,most common, AEs such as Nausea, vomiting, diarrhea, anorexia
What other AE is associated with Digoxin |
CNS
Confusion, visual disturbances (yellow halos around lights) |
|
list 5 drug interactions of digoxin
|
Sulfa, anatacids, diuretics, licorice, fiber, phenytoin, phenobarital
|
|
why is digoxin toxicity so common
|
Excretion is proportional to glomerular filtration rate (GFR)
Narrow therapeutic index: need to avoid toxicity T ½ = 1.5 days –2 days ( easy to build up blood levels) |
|
what are diuretics
|
drugs which increase the excretion of NaCl and NaHCO3 and thus increase the volume of urine,
in the absence of diuretics less than 1% filtered Na+ is excreted |
|
t/f thiazides are used in severe HTN with GFR < 30 cc/min
|
false- thiazides can be used in with mild to moderate HRN with normal renal and cardiac function
|
|
how do diuretics work
|
kidneys control the extracellular volume by altering NaCl and H2O
BP maintained at the expenes of extracellular fluid Na resorption is driven primarly by Na/K ATPase pump wihin the tubular epithelium primary goal of diuretics is to reduce edema by reducing extracelluarl volume diuretics prevent reabsorption of Na in the nephron |
|
what is the first line agent of diuretic for HTN and how does it work
|
1st line is thiazide
work by inhibiting NaCl transporters in loop of Henle and distal tubule thus increasing Na excretion causing diuresis. the reduction in plasma volume decrease cardiac output which decreases BP |
|
where does spironolactone work in kidney and give two other examples of drugs that work by this same mechanism
. in what pt population are they given to |
inhibits the Na reabsoption in the distal tubules and decreased K+ excretion
triamterene and amiloride work in same way Spironolactone used in pt with CHF, hepatic cirrhosis, ascites |
|
which class of diuretics inhibit the ability of the adrenal hormone, aldosterone, to stimulate Na+ reabsorption
|
potassium sparing diuretics like spinonolacton, amiloride, tramterene. blocking aldosterone's ability promotes K+ retention rather than loss into the luminal fluid
|
|
Definition
Chapter 31 any structural or functional abnormality of the ventricular myocardium |
cardiomyopathy
|
|
what are the 3 major types of cardiomyopathies
|
1. dilated
2. hypertrophic 3. restrictive/obliterative |
|
what are the 4 primary features of dilated cardiomyopathy
|
1. cardiomegaly
2. dilated ventricles 3. impaired systolic function 4. increased myocardial mass |
|
List 4 etiologies of dilated cardiomyopathies
|
1. Alcohol, arterial HTN
2. Beriberi, Babies( pregnancy) 3. Catecholamines (Pheo), Coxasackie, Cocaine, Chagas 4. Danorubicin, |
|
Describe the pathology of cardiomyopathy
|
1. cardiomegaly- hemodynamic changes due to failure as a pump since after time, heart will become stiff, leading to decreased cardiac output with decreased renal perfusion, which leads to increase sympathetic activity and activation of RAAS and increase peripheral resistance, leading to CHF
2. dilated ventricles-biventricularly 3. impaired systolic function- and high end systolic volume and impaired emptying leading to intraventricular thrombi 4. increased myocardial mass- leading to huge heart on CXR |
|
what are the clinical manifestations of dilated cardiomyopathy
|
dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, decreased exercise tolerance
|
|
On physical exam list 4 findings of cardiomyopathy
|
1. tachycardia at rest
2. lateral displacement of cardiac impulses 3. JVD with hepatomegaly 4. S3 gallop |
|
which exam technique is used to differentiate between dilated cardiomyopathy and myocarditis
|
biopsy- not recommended as routine
|
|
atherosclerortic coronary heart disease leads to CHF and present similar to dilated cardiomyopathy, what can be used to "clinch the diagnosis" of atherosclerortic coronary heart disease
|
nuclear treadmilling and cardiac catherization
atherosclerortic coronary heart disease also presents with angina or preceding hx of MI |
|
hypertensive heart disease leads to CHF and present similar to dilated cardiomyopathy, what can be used to "clinch the diagnosis" of hypertensive heart disease
|
marked LVH on EKG and on Echo
CXR of LVH signs of target end organ damage elevated BP during episode of CHF |
|
t/f left ventricular dysfunction can be systolic or diastolic dysfunction
|
true
systolic dysfunction =impaired contractility diastolic dysfunction =impaired filling |
|
what are the treatments for dilated cardiomyopathy
|
1. Na and H20 restriction to avoid volume overload
2. diuretics to decrease preload 3. ACEI or ARBS to decrease afterload 4. Digoxin for refractory symptoms |
|
what is the abnormal physiology in hypertrophic cardiomyopathy (4)
|
1. decreased ventricular compliance leading to diastolic dysfunction
2. mitral regurg 3. systolic pressure gradient below the aortic valve in LV which creates obstruction outflow 4. systolic anterior motion of mitral valve may be due to Venturi effect |
|
what are 3 physical exam findings for hypertrophic cardiomyopathy
|
1. systolic murmur increased by standing up valsalva maneuver, murmur reduced by squatting an handgrip
2. arterial pulse abrupt, jerky and ill sustained 3. S3 and S4 |
|
t/f an echo is very specific for hypertrophic cardiomyopathy
|
false- very sensitive
|
|
t/f cardiac catherterization is very specific for hypertrophic cardiomyopathy
|
true
|
|
what is the sudden death in people with HOCM from
|
ventricular arrhythmias or a fib
|
|
what is the treatment for pt with HOCM
|
1. negative inotropes to reduce the gradient- beta blockers or Ca+2 blockers
2. treat dsyrrthmia- amiodarone |
|
t/f restrictive cardiomyopathy has diastolic dysfunction without systolic dysfunction
|
true- most common endomyocardial fibrosis and causes of death is CHF
|
|
what is endomyocardial fibrosis
|
travels's disease ( no ETEC like :-)
related to tropical environment fibrosis of ventricles and eosinophilia diastolic dysfunction and eventual obliteration of left ventricle- lead to death by CHF |
|
restrictive cardiomyopathy caused by amyloid would have which features on physical exam
|
1. kussmal's sign- JVD on inspiration!! supposed to have JVD on expiration
2. orthostatic hypotension reflecting autonomic nerve infiltration |
|
restrictive cardiomyopathy caused by amyloid would have which features on Echo, doppler, cxr, biopsy
|
"graunular sparkling"
doppler shows diastolic dysfunction cxr- cardiomegaly biopsy- definitive |
|
what causes the cardiac manifestation in pt with hemochromatosis and what is the classic tetrad of hemochromatosis
|
cardiac manifestation caused by Fe deposits in heart leading to arrhythmias, conduction problems and CHF bc ventricles dilate too much, leading to both diastolic and systolic dysfunction
tetrad- liver disease, heart disease, diabetes mellitus, and bronze skin pigmentation |
|
what is the effect of the following drugs on the heart
a. cyclophosphamide b. daunorubicin,doxorubicin c. amphetamine d. ETOH |
a. cyclophosphamide- myocarditis and myocardial necrosis
b. daunorubicin,doxorubicin- myocarditis and pericarditis c. amphetamine- cardiomyopathy d. ETOH- cardiomyopathy |
|
Chapter 31
what isthe most common virus implicated in myocarditis |
Coxsackie B
Echo could also be contributing |
|
Name 5 other infectious etiologies of myocarditis other than Coxsackie B virus and the vectors when appropriate
|
1. trapanasoma cruzi- Chagas' Reduuvi- lays indolent for 10-20 yrs!!
2. Trichinella spiralis- pig 3. Echinococcosis- sheep 4. acute rheumatic fever- Step 5. Cory. diptheria- 6. clostridium perfingenes- gas gangrene |
|
chapter 33
definition: transient disturbance of mechanical, biochemical and electrical function of the myocardium due to inadequate oxygenation induced by coronary atherosclerosis |
ischemic heart disease
|
|
Defintion:
inadequate blood supply to the heart muscle usually caused by coronary atherosclerosis resulting in a relative deficiency of oxygen |
myocardial ischemia
|
|
Definition:
recurrent,prolonged episodes of severe ischemia caused by focal spasms of the epicardial coronary artery, usually occurs at rest may awaken pt from sleep |
prinzmetal angina
|
|
The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause is reduced coronary blood flow.
List 5 causes of reduced coronary blood flow to the heart |
1. atherosclerosis- most common
2. coronary vasospasm 3. bradyarrhythmias 4. hypotension 5. arterial thrombi |
|
The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause is decreased arterial oxygenation.
List 2 causes of decreased arterial oxygenation to the heart |
COPD
Cor pulmonale- RV hypertrophy and failure bc there is a disorder of the lung, pulmonary vessel and chest wall |
|
The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause isreduced O2 carrying capacity of the blood.
List 2 causes of reduced O2 carrying capacity of the blood |
anemia
carboxyhemoglobin- from tobacco smoking |
|
The pathophysiology of ischemic heart disease centers around myocardial O2 demand exceeding O2 supply. One such cause is reduced perfusion pressure (aortic pressure).
List 3 causes of reduced perfusion pressure (aortic pressure) |
hypotension
shock coronary steal syndrome |
|
What EKG finding suggest ischemia
|
T wave inversion
ST depression |
|
What EKG finding suggest myocardial infarction
|
hyperacute t wave
ST elevation Q waves |
|
Name 3 drugs used in the nuclear treadmilling test
|
dipyridamole, adenosine, dobutamine
|
|
which 2 management options are available for pt who need to have coronary revascularization
|
percutaneous transluminal coronary angioplasty PTCA, stents
aortocoronary bypass grafting |
|
what factors determine myocardial oxygen demand
|
1. Heart rate
2. contractility 3. preload- ventricular volume 4. afterload- LV pressure |
|
describe the pathogenesis of atherosclerosis
|
1. fatty streak from precursor lesions
2. intima thickening 3. fibrous plaque- can either be stable or unstable plaque if stable- can lead to coronary artery stenosis, reduced coronary artery blood flow or ischemia all of which could lead to silent ischemia or stable angina if unstable, plaque can rupture and cause a thrombus leading to a non-occlusive or occlusive thombus if non-occlusive can produce unstable angina, NSTEMI or sudden cardiac death if occlusive- Actue STEMI |
|
typical angina has which 3 clinical presentation
|
1. chest discomfort retrosternal
2. chest discomfort provoked by exertion or emotional stress 3. chest discomfort relieved by rest or nitroglycerin |
|
if the general appearance of pt is a follows, what do we think is wrong
respiratory distress, JVD, pink frothy sputum, rales, S3 gallop, hepatojugular reflex |
heart failure and pulmonary edema
|
|
Chapter 36
what is the drug therapy choice for stable angina |
single drug therapy
nitrates, or beta-blockers or Ca+2 blockers |
|
what is the drug therapy choice for prinzmetal angina
|
nitrates + Ca+2 blockers
|
|
what is the drug therapy choice for unstable angina
|
CCB, beta-blocker, nitrates, aspirin, IV heparin, antiplatelet drugs
|
|
t/f normally, coronary vasodilation due to release of NO by vascular endothelium predominates over vascular constriction by sympathetic
|
true
|
|
what time of day does a myocardial ischemic attack intensify
|
during the morning surge of catecholamines and later afternoon peak
|
|
what is the major limiting factor of using nitrates or organic nitrates for pt with initial stable or unstable angina
|
rapid tolerance develops
|
|
t/f arteriolar dilation predominates over the venous dilation at the therapeutic doses of organic nitrates
|
false- venous dilates predominates over arteriolar
|
|
in which pt population are nitrates contraindicated
|
in pt taking viagra bc sildenafil is a phosphodiesterase inhibitor so pathway geared to cGMP which will dephosphorlyate the myosin light chain to myosin-LC and relax
that's toooo much vasodilation in one organ especially if add organic nitrates |
|
how does the therapeutic doses of nitrates work
|
reduce preload by dilating capacitance vessels-veins
|
|
t/f higher doses of nitrates reduce afterload on heart by dilating arterioles and reducing left ventricular volume
|
true
|
|
which drug causes coronary steal phenomenon
|
dypyridamole- or any drug that dilated coronary resistance vessels and will increase angina
|
|
t/f nitrates cause non-specific smooth muscle relaxation of bronchi, GI tract, but have no effect on cardiac or skeletal muscles
|
true
|
|
which has better bioavailability- isosobide mononitrate or isosobide dinitrate
|
isosobide mononitrate- no 1st pass metabolism and a longer duration of action, renal excretion after glucuronidation
|
|
what are the AE of nitrates
|
1. HA
2. postural hypotension 3. rash |
|
which drug can be given to produce methemglobin in treating cyanide poisoning
|
bitrates
|
|
what is the DOC for chronic stable angina
|
beta blocker or CCB (verapamil)
|
|
T/F CCB dilate coronary arteries and peripheral arterioles but not veins
|
true- increase vasodilation, and decrease afterload and myocardial O2 demand
|
|
why do CCB have little effect on skeletal muscle
|
bc skeletal muscle depends on intracellular Ca rather than on Ca+2 influx through membrane channels
|
|
what is the DOC for pt with chronic angina and HTN
|
beta blocker- nadolol
or if contraindicated use CCBs |
|
where are L-type Ca2 channels located
|
in sarcolemma of cardiac and smooth muscles
|
|
where are T-type Ca2 channels located
|
SA node and have role in automaticity
|
|
of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which one has the most vasodilatation effect
|
nifedipine
|
|
of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which one has the most depression on the cardiac contractility
|
verapamil
|
|
of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which one has the most effect on the depression of the automaticity of the SA node
|
verapamil
|
|
of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipinediltiazem and verapamil) which one has the most depression of the automaticity of the AV node
|
verapamil
|
|
of the following Ca+2 channel blocking drugs ( Nifedipine, nimodipine, diltiazem and verapamil) which does not cause bronchiolar constriction
|
nifedipine
|
|
of the following Ca+2 channel blocking drugs ( Nifedipine, diltiazem, nimodipine, verapamil) which one reduces morbidity following a subarachnoid hemorrhage
|
nimodipine
|
|
describe fetal circulation
|
|
|
what is the normal pressure in the right atrium of a child
|
about 0- 5 mm Hg
|
|
what is the normal pressure in the right ventricle of a child ( systolic and diastolic)
|
25/5 mmHg
|
|
what is the normal pressure in the pulmonary artery of a child ( systolic and diastolic)
|
25/10 mmHg
|
|
what is the normal pressure in the left atrium of a child ( systolic and diastolic)
|
10 mm Hg
|
|
what is the normal pressure in the left ventricle of a child ( systolic and diastolic)
|
100/5
|
|
what is the normal pressure in the aorta of a child ( systolic and diastolic)
|
120/80 mmHg
|
|
describe the blood flow in a child
|
|
|
Name 3 types of ASD and in which gender they are more common
|
starting from the top of the atrium
1. sinus venosus 2. ostium secundum 3. ostium primum more common in girls |
|
1. in pts with ASD, what type of shunting is there (R to L or L to R) and why
2-4. what are the symptoms and signs of pts with ASD 5. how do we treat pts |
1. left to right shunting bc RV more compliant with volume changes than LV so no pulmonary edema
2. so pt have minimal cardiac symptoms the RV pressure is actually normal in pt with ASD 3. fixed split of S2 4. pulmonary ejection murmur 5. surgical closure or transcatheter closure |
|
what is the most common location for a VSD
|
perimembranous
others include: muscular and supracristal |
|
what are symptoms of a VSD
|
1. tachypnea
2. poor feeding 3. slow growth 4. irritability |
|
1. what type of shunting happens in VSD
2. does pulmonary venous congestion occur |
1. left to right shunting bc LV is poorly compliant and intolerant of volume overload but it can respond to pressure changes well
2. since LV poorly compliant there is pulmonary venous congestion leading to pulmonary edema, pulmonary HTN and LVH |
|
1. what type of shunting happens in VSD
2. does pulmonary venous congestion occur |
1. left to right shunting bc LV is poorly compliant and intolerant of volume overload but it can respond to pressure changes well
2. since LV poorly compliant there is pulmonary venous congestion leading to pulmonary edema, pulmonary HTN and LVH |
|
which type of overciruculatory lesion will pts have bounding pulses, continuous murmurs, and tachypnea, tachycardia, and growth failure
|
patent ductus arteriosus
|
|
name 3 cyanotic heart lesions
|
1. transposition of great vessels
2. tetrology of fallot 3. tricuspid atresia |
|
1. what is the hallmark of cyanotic heat lesions
2. what is the response to O2 in cyanotic lesions |
1. hallmark is cyanosis without tachypnea
2. little response to O2 |
|
Name 5 cyanotic lesion of children
|
1transposition of great vessels
2. tetrology of fallot 3. truncus arteriosus 4. tricuspid/ pulmonary atresia 5. total anomalous pulmonary venous |
|
Transposition of the great vessel
1. why is this considered a ductal dependent lesion 2. what is the management of this pt |
1. mixing at the level of the atrial septum and the ductus, while the RV is the systemic ventricle
2. mgt. is O2, prostglandin E1 to maintain patency of ductus, then need sugery |
|
what are the components of Tetrology
|
1. Pulmonary stensosis
2. RVH 3. Overriding aorta 4. VSD |
|
what is an obligate characteristic in this condition
and what medication is needed |
Tricuspid Atresia
1 ASD 2. VSD 3. PGE1 to keep ductus arteriosus opened |
|
list 6 congenital heart diseases that present with cardiogenic shock
|
1. hypoplastic left heart syndrome
2. severe coartation of the aorta 3. critical aortic stenosis 4. ebstein anomaly of tricuspid 5. large PDA 6. systemic AV malformation |
|
what is the clinical presentation of this pt and then the treatment
|
ashen, tachypnea, tachycardia, pulseless, hepatomegaly,
treatment: give PGE1 to keep ductus open, mechanically |
|
Define this condition
|
narrowing of the aorta resulting from localized thickening of the media protruding posteriorly into the lumen of the vessel causing obstruction
|
|
what type of murmur is heard and where on this pt
|
loud harsh systolic murmur at lower left sternal boarder
|
|
what type of hypertrophy (RVH or LVH)
|
right VH
|
|
what type of hypertrophy (RVH or LVH)
|
right VH
|
|
what type of hypertrophy is seen this pt
|
LVH possibly both
|
|
t/f this is the most commonly reported congenital heart disease
|
VSD is the most common
|
|
what is the clinical mgt
|
digoxin, diuretics- preload reduction and afterload reduction with hyralzaine or captopril
|
|
In which type of septal defect is pulmonary edema and pulmonary HTN noted
|
VSD
|
|
which congenital heart disease presents in more females and is associated with congenital rubella
|
PDA
|
|
t/f indomethacin must quickly be given to this pt
|
transpositon of great vessels, False- must give PGE1
|
|
how long does it take for the patent ductus to close
|
primary- 10-15 hrs
secondary 14-21 days |
|
what medication must be given within few hours and what are the AE of this medication
|
PGE1 to keep ductus open, causes apnea
|
|
what is a technique kids use to decrease hypercyanotic spells. what meds are given
|
TOF,
kids used knee chest to decrease blood back to heart given phenylephrine to raise Bp or ketamine |
|
what are the surgery options for this condition
|
1. Blalock taussig
2. gore-tex 3. potts 4. waterston 5. glenn |
|
this condition is most commonly associated with what else
|
bicuspid aortic valve
|
|
describe the pulses and BP
|
absent femoral pulses with BP differences
|
|
Chapter 38
what is the normal direction of depolarization of the myocardium |
endocardium ---> epicardium
|
|
what is the normal direction of repolarization of the myocardium
|
epicardium ----> endocardium
upright T wave |
|
what is the effect of myocardial ischemia reducing regional ATP
|
1. altered Na/K ATPase pump
2. decrease intracellular K 3. prolonging phase 3 4. epicardial repolarization delayed |
|
what is the direction of replorization of ischemia area
|
in epicardial region ischemia
endocardium---> epicardium, inverted T wave endocardial region of ischemia epicardium---> endocardium but hyperacute T waves |
|
what are the finding on EKG for myocardial injury
|
Altered ion transport across myocardial cell membrane
Reduced regional ATP produces Altered Na+-K+ ATPase pump ↓ Intracellular K+ Altered Phase 2 & Phase 3 of APD Results in ↑ ST segment |
|
what are the EKG finding of myocardial infarction
|
1. abnormal Q-wave- Duration > 0.04 sec
2. ST elevation 3. inverted T waves |
|
what is the difference between ischemia and infarction EKG
|
Ischemia
ST segment depression Inverted T-waves Infarction ST segment elevation T-wave inversion Q-waves |
|
how can you tell how old an infarct is on EKG
|
acute- ST segment elevation
subacute- inverted t waves old- q waves |
|
describe the changes that take place on EKG from a normal EKG to ischemic EKG
|
|
|
which lead repesent which part of the LV
|
Anterioseptal- V1-2
Anterior wall- V3-4 Lateral wall- V5-6 an I and AVL Inferior wall II, III, aVF Posterior wall- V1-2 but ST depression, upright T waves and R waver > S wave (so everything opposit) |
|
describe the EKG
|
AMI
|
|
describe the EKG
|
septal Ami
|
|
describe the ekg
|
inferior ekg
|
|
describe the EKG
|
|
|
what type of cardiac abnormality is this and in what population.
|
Ebstein's
Ebstein's anomaly is the downward displacement of a portion of the tricuspid valve with atrialization of a large part of the RV (see Figure 12). There is often an associated ostium secundum ASD. The atrialized portion of the ventricle hinders rather than helps the forward flow of blood and there is tricuspid regurgitation. Occasionally Ebstein's anomaly is asymptomatic, but it generally presents in childhood or early adulthood with dyspnea, fatigue, signs of tricuspid regurgitation, and right-sided cardiac failure. Patients with Ebstein's anomaly require prophylaxis for endocarditis. In pt of mothers who took lithium during preganancy |
|
name the condition:
name given to reversal in the direction of a cardiac shunt caused by the development of pulmonary hypertension. It applies regardless of whether the shunt is atrial or ventricular. Initial flow is always from high pressure (left) to low pressure (right), but pulmonary pressure can rise above systemic pressure and cause a reversal of flow. |
Eisenmenger's syndrome
|