HTN/Cardiovascular Patho Pt 2 Flashcards
Hypertension
=
When ___ or more Diastolic BP measurements are greater than __mmHg or
____ or more Systolic BP measurements are _____ (on separate visits)
A consistent elevation of systemic arterial blood pressure
2 or more DBP >90
3 or more SBP 140
No precise value for BP considered safe or pathological - Dependent on gender, size, etc
Classification of BP for Adults
- Optimal
- Prehypertension
-
Hypertension
- Stage 1 (mild)
- Stage 2 (moderate) aka severe, malignant HTN
- <120, <80
- 120-139, 80-89
- 140-159, 90-99
- _>_160, _>_100
Types of Hypertension
(2)
Primary Hypertension (95% of all HTN) - Essential or Idiopathic HTN (main problem, is the primary disease in question)
Secondary Hypertension (secondary complication to some other primary disease)
Secondary Hypertension Common Causes
- Renal Origin (2)
- Endocrine Origin (3)
- Hemodynamic/Cardiovascular (3)
- Neurologic (2)
- Chronic Renal Disease, Renal Artery Stenosis
- Adrenalcortical Hyperfunction, Hyperthyroid, Pregnancy induced
- Hypervolemia, Rigidity of the Aorta, Coarctation of the Aorta
- Increased ICP, Sleep Apnea
Secondary HTN Causes (Notes)
- Renal artery stenosis: _____ blood flow to kidneys -> renal _____ assumes BP is ___ since renal BP is low -> kidneys produce _____ amount of renin, ang II, aldosterone -> elevates BP
- Hyperfunction of adrenocorticotropic hormones: (2)
- Hypervolemia, rigidity/coarctation of aorta: affects function of _____ that are responsible for regulating BP
- Decreased -> baroreceptors assumes low BP -> excessive renin
- aldosterone/glucocorticoids
- baroreceptor function
Risk Factors with Primary HTN
- _____ History
- ___ age
- Gender: males ___, women ___
- Race:
- High dietary _____ intake
- D____
- S____
- O_____
- Heavy _____ consumption
- Low dietary/____deficiences (3)
- St____
- Family
- Old
- males <55, women>74
- African American
- sodium
- Diabetes
- Smoking
- Obesity
- Alcohol
- Mineral deficiences (K, Mg, Ca)
- Stress
Primary HTN (Notes)
- (1): Form of HTN very typical of old age that stems from widespread atherosclerosis causing a hardening of arteries (systolic elevated but diastolic not as elevated or normal)
Although we consider primary HTN as idiopathic bc no verifiable causes there are risk factors
-
Females: have protective reproductive ____ (estrogen/progesterone)
- Post menopause, womens risk tends to _____ with men
- AA: high risk mediated by?
- Sodium: high dietary sodium v common in what foods?
- Diabetic: chronic _____
- Smoking: ______ damage
- Low Ca, K, Mg: effects what?
-
Isolated Systolic HTN
- hormones, equalize after menopause
- Sodium sensitivity/Renin
- higher shelf-life, canned foods
- hyperglycemia
- epithelial
- effects excitability of smooth muscle in vasculature
Blood Pressure = CO x TPR
A whole host of factors contribute to a rise and fall of TPR and CO and can cause persistent, elevated BP
- CO effected by (2) Factors
- TPR effected by (3) Factors
- Blood Volume, Cardiac Factors
- Humoral Factors, Neural Factors, Local Factors
Hypothetical Scheme for the Pathogenesis of Essential Hypertension
______ Influence + ______ Factors
(3)
Genetic Influence + Environmental Factors
- Defects in Renal Sodium Homeostasis
- Functional Vasoconstriction
- Defects in Vascular Smooth Muscle Growth
Patho of Essential Hypertension
Genetic Predispositions to HTN (Notes)
- _____ handling, kidneys have a harder time _____ it than others
- Individuals who have vasculature that response more ____ to circulating ______
- Defective smooth ____ growth (when individuals are prone to _____ of vascular smooth muscle -> _____ lumens -> HTN)
Note: Genetic vulnerability does not _____ appearance of HTN, interaction with _____ promotes it more
- Sodium, excreting
- rapidly to vasoconstrictors
- muscle overgrowth -> narrows lumens -> HTN
Genetic does not guarantee, environment promotes it more
Genetic Predispositions to HTN (Notes)
-
_______/back and forth of Vascular wall _____ and Vascular _____
- As wall thickens -> greater vascular _____ to constrictors which will then cause smooth muscle to _____ by thickening more -> higher genetic _______
-
Sodium group
- Inadequacy of excretion -> net sodium and water _____ -> elevated _____/ECF -> increased ___ -> since BP = __x___ -> BP increases
- In addition, when plasma increases -> _____ receptors stimulated to release (1) that causes _______ -> increases ____ -> increased BP (interacts wtih wall thickness again)
-
Potentiation, thickening, reactivity
- reactivitiy, adapt, vulnerability
-
Sodium Group
- retention -> plasma -> CO -> COxTPR = BP
- stretch, atrial natriuretic peptide, vasoconstriction -> TPR -> increased BP
Other Patterns of Altered Blood Pressure
(3)
How to diagnose?
White Coat Hypertension
Reverse White Coat Hypertension or “Masked Hypertension”
Alterations in Circadian Patterns of BP (“non-dipping” or a lack of night time drop in BP)
24 hr Ambulatory BP monitoring (takes BP Q20min)
White Coat Hypertension
=
False ______
Phenomenon where individuals who go into clinical settings (going to doctors), their BP elevates bc anxiety, goes back to normal when they leave
False Positive
Masked Hypertension
=
False ______
Reverse White Coat HTN, those that go through most of their days in HTN, but when in clinical settings it doesn’t measure in the HTN range (ie those with busy/hectic lives, in doctor’s office away from stressors, time to relax in waiting room)
False Negatives
Non-Dipping
=
- Graph of Normal Circadian Pattern
- ____ SBP on average is lower than _____ SBP: due to _____ release patterns (higher during _____ hours, peaks when you wake), cortisol contributes directly to elevation of BP bc increases _____ of vasculature
Pathological issue that leads to loss of night time dipping, v dangerous -> even someone with normal healthy BP who just has this condition -> increased risk for CV complications
- Sleeping SBP < Waking SBP, cortisol, waking, constriction
BP Treatment Algorithm (Notes)
- First Option =
- (3)
- In general, start with ____ med (diuretic, ARB, BB, CCB) if not working ____ dosing or _____ -keep playing with it till it works
- Barriers to Tx
- Most people aren’t given the ____ to be able to first manage with lifestyle modifications
- NOTORIOUSLY LOW _____ _______ why?
- Lifestyle Modifiications
- Exercise
- Low fat, low sodium, mediterranean diet
- Control Stress
- one med, increase or combine
- tools
- MEDICATION ADHERENCE - bc only sx in advanced disease “silent killer” -> soo when asymptomatic ppl are taking meds with SE and don’t like it
BP Treatment Algorithm
- Lifestyle Modifications
1. Not at goal pressure < ___/___ or < ___/___ for pts with (2) - Initial drug choices without compelling indications
- Stage 1 HTN (SBP 140-159 or DBP 90-99) =
- Stage 2 HTN (SBP > 160 or DBP > 100) =
- Initial drug choices with compelling indications: ____ antihypertensive drugs as needed (diuretics, ACEI, ARB, BB, CCB)
- If Not at goal BP =
- <140/90, <130/80 w DM, CKD
- Thiazide diuretic for most, may consider ACEI, ARB, BB, CCB or combination
- Two drug combo (usually thiazide + ACEI, ARB, BB, CCB)
- Other
- Optimize dosage or add additional until goal is achieved. Consider consultation w hypertension specialist.
Other Strategies for BP Control
(3)
Home BP Monitoring
Paced Respiration
Screening for anxiety, panic, or other similar disorders
Alternative BP Strategies (Notes)
- Home BP Monitoring: results in _____ mechanism, unclear could be _____, unconscious/conscious small modifications
- Pace Respiration: guided reduction of ___ from 12-16 -> __-__, __-__ min per day (min ____ min per week) = effectiveness of ____ (one theory is that it enhances _____ reflex)
- Panic/Anxiety Disorder: subcategory of _____ HTN
- biofeedback, empowerment
- RR 6-10, 5-10 min/day, 40min/wk, meds, baroreceptor
- Secondary
Left Ventricular Hypertrophy (LVH)
Hypertensive Heart Disease
- Hypertension leads to LVH as a result of increased ______ imposed on the heart
- Wall Tension = LV __ X LV ___ / LV ___
- LVH leads to smaller (1) and increased (1)
- LVH increases risk of (4)
- workload
- LV SP x LV Radius/ LV Wall Thickness
- Smaller Radius, Increased End diastolic filling pressure
- Ventricular Arrhythmias, Sudden Cardiac Death, Death from MI, Chronic Heart Failure
LVH Notes
- LVH is an adaptation to a chronically elevated cardiac (1)
- Preload:
- Aterload:
- HTN increases ventricular afterload -> heart has to generate more ____ -> heart adapts by _____ of ventricular muscle
- afterload (Diastolic BP)
- Volume of ventricular filling (more filling, heart has to work harder to cause ejection)
- Any pressure that opposes ventricular ejection (usually aortic diastolic pressure)
- force -> hypertrophy
LVH Notes
- (1): The force needed to generate a particular ventricular pressure at a particular ventricular radius
- LVH: _____ change that _____ wall thickness and _____ radius -> pathologic effects of reduced __ and __
- AKA Structural Heart Disease
- Is an ____ adaptation to HTN
- Can measure using ___
- Increases risk for ventricular arrhythmias how? cardiac arrest, death from MI how?
- Increases progression to (1)
- Doesn’t take long for someone to develop LVH from elevated BP, but good thing is its _____ (quickley resolves once BP is under control)
- Wall Tension
-
Pathological, increases thickness, decrases radius -> SV and CO
- early
- US
- Structure of heart changes path of action potential, hypertrophy not proportional and leaves ventricle vulnerable to ischemia/hypoxic injury
- CHF
- reversible
Ischemic Heart Disease
LVH is type of Ischemic Heart Disease = imbalance of heart muscle (2)
Overall (1) of the heart determines (1)
- Supply (3)
- Demand (3)
imbalance of O2 demand and O2 supply
workload determines O2 demand
- Coronary Vessel Patency
- Ventricular Wall Compression
- Diastolic filling time (HR)
- Myocardial Contractility
- Heart Rate
- Wall stress (preload, afterload)
Coronary Circulation
Coronary arteries - branch off ______
Coronary veins - drain into ____ _____
Aorta
Vena Cava
Coronary Circulation (Notes)
Coronary Vessels Patency: heart can only extract __ from blood in _____ circulation
- During systole arteries are _______
- 2 main that branch off from aorta
- _____
-
_____
- _____
- _____
O2, Coronary
-
Compressed (clamped off)
- Right coronary artery (RCA)
-
Left coronary artery (LCA)
- Left Anterior Descending (LAD)
- Left Circumflex Branch: loops around to back of heart
Areas of Perfusion of Coronary Arteries
- Perfuses left lateral, posterior surface
- Perfuses much of inferior wall, loops around and perfuses much of posterior surface
- Perfuses much of anterior surface and most important part of heart: ventricular septum bc where bundles of His are located
- Left Circumflex Descending (LCD)
- Right Coronary Artery (RCA)
- Left Anterior Descending (LAD)
Coronary Artery Disease (Ischemic Heart Disease)
Ischemic Heart disease is an _____ between myocardial (1) and (1)
- Myocardial O2 demand determined by (4)
- Myocardial O2 supply determined by (3)
Imabance of O2 demand and O2 supply
- Demand
- Heart Rate
- Contractility
- Overall workload (preload/afterload)
-
Wall tension
- Tension proportional to = LV systolic pressure X LV radius / LV wall thickness
- Supply
- Diastolic Perfusion Pressure
- Coronary Vascular Resistance (F = *O2 Carrying Capacity
Blood Flow Reduced During Systole
- Blood flow in LCA plummates to ____ during ______
- Doesn’t fully recover until?
- zero during SYSTOLE
- beginning of diastole bc perfuses itself mainly in diastole
Coronary Vascular Resistance
- Extrinsic and Intrinsic Mechanisms
- Extrinsic:
- Intrinsic:
- Parasymphatic and sympathetic inervation
- Influence of local metabolites on endotheial releasing factors
Coronary Vascular Resistance (Notes)
- During Exercise, HR goes up, diastole time shortens -> less time to be perfused; Compensation of this =
- Not so healthy heart (Atherosclerosis) = Endothelial _____ so can’t release what?
- Ability of vessels endothelium to dilate (remember NO causes vasodilation) - happens normally in a healthy heart
- dysfunction -> can’t release Nitric Oxide and vasodilate when demand increased -> ischemia -> angina (nitrogylcerin replaces function of NO)
Local Metabolic Changes
O2, CO2, Acidity, Adenosine
- What causes Vasoconstriction?
- What is released?
- What causes Vasodilation?
- What is released?
- Increased O2, Decreased CO2, Acidity, Adenosine
- Endothelin
- Decreased O2, Increased CO2, Acidity, Adenosine
- Nitric Oxide (EDRF) Endothelial Relaxing Factor
Coronary Heart Disease Types
-
Chronic Ischemic Heart Disease
- _____ Angina
- ____ Angina
- _____ Myocardial Ischemia
-
Acute Coronary Syndrome
- _____ Elevation
- _____ Elevation
- _____ Angina
- Both can lead to?
-
Chronic Ischemica Heart Disease
- Stable
- Variant
- Silent
-
Acute Coronary Syndrome
- ST-segment (STEMI)
- Non-ST segment (NSTEMI)
- Unstable
- Acute MI
Coronary Heart Disease Types (Notes)
- Chronic Ischemic Heart Disease: has to do with _____ to increase oxygen ____ as oxygen ____ increase (so ischemia is _____ driven) -> _____ angina
- Acute Coronary Syndrome: abrupt change in blood _____ (usually asctd with _____ of atherosclerotic plaque) completely ____ vessel and causes death of tissue/___, if NOT occlusive -> _____ angina
- inability, supply, demand (demand driven) -> stable
- supply, rupture, OCCLUDES -> MI, NOT OCCLUSIVE -> unstable angina
Atheroslcerotic Plaques
- What type of plaque causes stable angina?
- That progresses to (1) disease, _____ loss or dysfunction
- What type of plaque causes acute coronary syndromes?
- Plaque rupture + non-occlusive clot =
- Plaque rupture + larger occlusive clot =
-
Stable fixed
- Chronic ischemic heart disease, Endothelial loss/dysfunction
-
Unstable
- Abrupt ischemia (unstable angina)
- Acute MI - ST elevation
Chronic Stable Ischemic Heart Disease
- Occult coronary disease is so prevalent among _____ countries that it is the ____ rather than the exception
- Most individuals with non-obstructive coronary disease are completely ______
- ______ is also very often asymptomatic but can also manifest as ischemic cardiac pain in the form of _____
Three Basic categories of Cardiac Ischemic Pain
- A diffuse _____ component
- A better defined ______ component conforming to a distribution of ______
- An interpretive component modulated by ______ factors
- industrialized, norm
- asymptomatic
- Ischemia, angina
- visceral
- somatic, dermatomes
- psychological
Cardiac Ischemic Pain (Notes)
Varies greatly depending on ______
- Diffuse Visceral Component: ischemia that stimulates (1) nerves in the heart -> awareness of signal is complicated (1)
- Somatic Component conforming to a distribution of dermatomes: AKA _____ Pain
- Interpretive component by pschological factors: We modulate our experience by?
GENDER
- Afferent autonomic nerves -> ambiguous feeling of feeling not well, abdominal unease
- Referred Pain
- How much we expect it to hurt/fear (anticipatory feeling) - is not all in your head, there are descending inputs to this experience of pain that makes it worse
pic of referred pain
Chronic Stable Angina
Most patients with stable angina describe (2) rather than (1)
- Sometimes described (4) sensation
- Some discomfort located outside the chest (5)
- Some people experience ____, profound f____, w____, or s_____
Usually ischemic episodes are ____ (__-__ min) and are brought on by (1) or (1)
- _____ can be very _____ and can be lowered by exposure (3)
20% of patients experience “____ ___” angina
retro-sternal chest discomfort or distress rather than pain
- heaviness, burning, tightness, choking
- arms, shoulders, back, jaw, epigastrium
- dyspnea, fatigue, weakness, syncope
brief (3-5min), physical activity or emotional stress
- Threshold predictable (ie. after 10 steps), cold weather, smoking, ingesting a meal
Warm up: chest pain at onset of physical exercise but once warmed up that angina goes away (a form of stable chronic angina)
Areas most commonly associated with Referred Pain
Darker areas =
Only __% of Women present with chest pain, more often ____, ___ pain, etc
More severe
30% women present with chest pain, more often indigestion, back pain
Some Major Causes of Anginal Chest Pain
Coronary Artery Disease (2)
Other Cardiac Disorders (4)
- Fixed Obstructive coronary disease (most common)
- Coronary disease with dynamic flow (ie unstable angina)
- Aortic Stenosis: narrowing of aortic valve, greatly increases afterload, leads to LVH
- Hypertrophic Cardiomyopathy: congenital
- Hypertensive Heart Disease and LVH: asctd w HTN
- Mitral Valve Prolapse
Angina Classification
Ischemic heart disease is, in the majority of cases, a consequence of _____ of the ___ _____ and develops when BF is _______
The major EFFECTS of ischemic heat disease include ____ _____ (chest pain)
- Chronic Stable Angina
-
Activity evoking, Limits to normal activity
- Class I
- Class II
- Class III
- Class IV
- _____ Angina AKA?
- _____ ______
Atherosclerosis, Coronary Arteries, inadequate BF
Angina Pectoralis
-
Chronic Stable Angina
- Prolonged Exertion, None
- Walking > 2 blocks, Slight
- Walking < 2 blocks, Marked
- Minimal or rest, Severe
- Unstable Angina (Acute coronary syndrome)
- Myocardial Infarction
Ischemic Heart Disease and the ECG
There are predicable changes in the ECG that often happen with imbalances of myocardial O2 supply and demand
- ST segment depression =
- ST segment elevation =
- most commonly associated with “demand ischemia” (upon exertion, ie exercise testing)
- most commonly associated with “supply ischemia” (upon occlusion
ST Depression
Problem with ______
- Most commonly associated with?
- Exercise stress test helps to identify ______ the presence of?
DEMAND
- demand ischemia
- noninvasively, coronary artery disease/other cardiac syndrome thats causing ischemia
ST Elevation
Problem with ______
- Most commonly associated with ____ of myocardial tissue: caused by ______ problem, a _____ NOT by change in demand
SUPPLY
- death, supply, blockage
Acute Coronary Syndrome
Acute Coronary Syndrome describes a spectrum of clinical symptoms ranging from ______ to ____ to ____
The major pathophysiological mechanism for ACS is ____ or fissure of a plaque with a superimposed _____
____ ____ is a syndrome ______ between chronic stable angina and MI
- A clinical diagnosis based on a history of chest pain and _____ of MI by ___ and _____ testing for myocardial necrosis
- The chest pain will be (1) or (1)
- May also represent ______ symptoms of _____ stable angina
Unstable Angina, NSTEMI, STEMI
rupture, thrombus
Unstable Angina, intermediate
- exclusion by ECG, biomarkers
- prolonged at rest or new onset
- accelerating, previously stable angina
Acute Coronary Syndrome
- ECG -> (2)
-
Cardiac Markers
- Negative -> (1)
- Positive -> (1)
- ST elevation, No ST elevation
- Cardiac Markers
- Unstable Angina
- MI (STEMI or NSTEMI)
Classification of Unstable Angina
- What Severity Class I-III?
- Angina at rest within 48 hours (angina at rest, acute)
- New onset of severe angina, no pain at rest
- Angina at rest within past month but not within preceding 48 hours (angina at rest, subacute)
- Can also group patients on
- Presence of ____-cardiac condition, ____ MI, ____ for stable angina, presence of transient ___ changes during chest pain
- Severity Class
- Class III
- Class I
- Class II
- Group patients
- extra cardiac condition, previous, treatment, ST
Myocardial Infarction
Myocardial Infarction is a term used when there is evidence of myocardial _____ consistent with ischemia
The classic symptoms of MI
- intense, oppressive, durable, excrutiating chest ______ with an impending sense of ____ and radiation of pain to ___
- chest h____ or b_____, radiation to (5)
Also common is ____ skin, signficant ______ (may indicate extensive MI), and elevated ___
Other symptoms may be related to an intense ____ response: like (3)
necrosis
- chest pressure, impending doom, radiation to left arm
- heaviness, burning, radiation to jaw, neck, shoulder, back, both arms
pale, tachycardia, elevated BP
fear: nausea, vomiting, dyspnea
Elevated BP from stress response OR drop in BP bc of drop in CO (no matter how much stress hormone) - might hear crackles from backup of blood into lungs
Differential: Aortic dissection presents similarly
Myocardial Infarction
Myocardial infarction is a term used when there is evidence of myocardial Necrosis consistent with ischemia
Some signs include:
- Detection of _____ (especially ____)
- ____ Changes (3)
MIs can be classified in many ways including by
- _____ (microscopic, moderate, large…10%, 10-30%, >30% of LV myocardium respectively)
- ____ changes
- By _____ (anterior, posterior, inferior, lateral, etc)
signs
- Biomarkers (Troponin)
- ECG (ST elevation, exaggerated Q wave, T wave inversion)
classified
- Size
- EKG
- Location
Cardiac Enzyme Changes with MI
(3)
Which ones are not specific to cardiac - just shows any muscle injury?
Which one is cardiac specific, so we see a much greater, more rapid elevation?
Troponin
Creatine Kinase
Lactate Dehydrogenase
Lactate and Creatinine
Troponin
Q wave
What happens to the Q wave?
Q wave abnormalities is usually goes with what type of MI?
Too large of a Q wave
STEMI
T Wave Inversion
Is a sign of what?
Tends to be signs of a recent or active MI (a very early change in ECG)
Location of Obstruction and Major Subgroups of MI
Location of Obstruction and Major Subgroups of MI
-
Right Coronary Artery (RCA) Obstruction
- If proximal RCA is occluded:
- If distal RCA is occluded
-
Left Anterior Descending (LAD) Obstruction
- Proximal LAD occluded:
- Mid LAD
- Distal LAD (___ common)
-
Left Circumflex Artery Obstruction
- LCA occluded:
-
RCA
- Moderate to large inferior (posterior, lateral, right ventricular)
- Small inferior
-
LAD
- ”widow maker”: high mortality, occlusion is located proximal to the first septal perforator, compromised perfusion to purkinje conduction tissue**
- Mid LAD
- Distal LAD: less common
-
LCA
- Moderate to Largery Anterior and Posterior left infarctions
RCA obstruction: how proximal, close to the aorta is it? - the more proximal, the larger area of infarction bc artery descends
Mid and distal LAD better mortality but less common
Time is Muscle (Notes)
- Cardiac muscle DOES NOT _______
- What is the picture showing?
- Post MI: body goes through cardiac ______ (significant _____ and dead area is replaced by _____ tissue)
- Important to avoid (1)
- Cardiac remodeling is a form of _____ heart disease, why?
- Treatment?
- regenerate
- postmortem LAD dead tissue
- remodeling (inflammation -> fibrous scar tissue)
- Anti-inflammatory analgesics: interferes with healing process and most catastrophically can cause ventricular rupture
- Structural: bc fibrous/scar tissue does not expand, contract, or conduct action potential -> increased risk of arrhythmias, sudden cardiac death, death from subsequent MIs, progression to CHF
- Cardiac cath through femoral artery
Heart Failure (Acute v. Chronic)
Heart Failure: When the heart cannot generate enough ___ to match ____ needs
Acute Heart Failure (or Acute Decompensation)
- ____ Myocardial Infarction
- _____ Cardiac _____
- Due to cardiac arrhythmia or other manifestation of impaired ____ system
- Myocardial _____
- Acute _____ of ____ Heart Failure
- Generally either from severe acute (1) or (1)
CO, metabolic
- Fatal
- Sudden Cardiac Death
- conduction
- remodeling from healing from MI or LVH
- Decompensation of Chronic Heart Failure
- severe acute pulmonary edema or cardiorenal syndrome (poor response to diuretics) - usually happens with acute volume overload -> fluid backup to lungs
Chronic Heart Failure
Causes (4) General Categories
Abnormal Cardiac Muscle Function
Abnormal Left Ventricular Volume
Abnormal Left Ventricular Pressure
Abnormal Left Ventricular Filling
Chronic Heart Failure Causes
Abnormal Cardiac Muscle Function (2)
Abnormal Left Ventricular Volume (2)-(3)
- Myocardial Infarction
- Cardiomyopathies
- Valve insufficiency
- Blood volume expansion associated with high output states
- Chronic anemia
- Infusion of a large volume of IV fluids in a short period of time
- Pregnancy
Chronic Heart Failure Causes
Abnormal Left Ventricular Pressure (3)
Abnormal Left Ventricular Filling (3)
- Hypertension
- COPD
- Aortic or pulmonic valve stenosis
- Mitral valve stenosis
- Tricuspid valve stenosis
- AFib
Right Sided Heart Failure
Congestion of _____ Tissues
(3)
Peripheral Tissues
- Dependent edema and ascites
- GI tract congestion (anorexia, GI distress, weight loss)
- Liver congestion (signs related to impaired liver function)
Left Sided Heart Failure
- (1): ____ intolerance and signs of decreased tissue _____
-
(1)
- Impaired ____ exchange -> ____ and signs of _____
- Pulmonary ____
- ______
- Cough with ____ sputum
- Paroxysmal _____ dyspnea
- Decreased Cardiac Output: activity, perfusion
-
Pulmonary Congestion
- gas -> cyanosis, decreased tissue perfusion
- Edema
- Orthopnea
- Cough w Frothy sputum
- Nocturnal
Right Sided HF Notes
Can start on either side or other but will lead to failure of other side
- tends to hapen when the right side is forced to ____ hard (pulmonary __) at all bc it is normally not designed to generate high _____, is initially a ___ ___ system that generates just enough pressure to pump blood to pulmonary circulation
- Ex) ____: deoxygenation of blood in pulmonary circulation causes unique pulmonary vessels to _____ -> raises the pulmonary _____ -> increases right side ____ -> increased pressure right side of heart has to work against
- Leads to decreased __ on ___ side
- work (HTN), pressure, low pressure system normally
- COPD, vasoconstrict, pressure, afterload
- decreased CO on left side
Left Sided HF Notes
- might fail ____ due to elevated ____ pressure, left sided cardiac ___ not strong enough
- Effects: ____ CO, ____ congestion (imparied gas exchange), ____ intolerance
- Leads to increased pressure in _____ circulation and ___ sided failure
- first, arterial, muscle
- decreased CO, pulmonary congestion, activity intolerance
- pulmonary, right
Chronic Heart Failure
Makes up majority of HF cases
Progresses slowly but contains two important components that represent two phases (brings about all the clinical manifestations)
- Structural _____ of cardiac tissue as a result of cardiac tissue damage or death - causes a reduction in cardiac _____
- Multiple _____ events in response to decreased cardiac function makes up majority of _____ issues of CHF
- remodeling -> reduced function
- compensatory events -> pathological issues
Vicious Cycle of HF (Notes)
- Usually starts with (1)
- Body Compensates by: increased (4)
- Vicious Cycle: all of above increases _____ of the heart and if this heart is post MI, is going to lead to more ____ and more damage -> further decline in __ -> which responds with more _____ (body’s response is what causes a downward ____)
- Therefore, most treatments are designed to do what?
- decreased CO
- increases HR, SV (contractility), BP, blood volume
- workload, ischemia, further decline in CO -> more compnesation, spiral
- Limit body’s adaptation to decreased CO in order to preserve heart function
The pathophysiology of heart failure involves changes in
(2)
Cardiac Function
Neurohormonal Responses
Patho of HF
Cardiac Function
- (1): Relacement of healthy cardiac tissue with in-elastic fibrous tissue that has decreased contractile function and an altered inotropic function
- (1)
- Cardiac Remodeling
- Decreased CO
Patho of HF
Neurohormonal Responses (to decreased CO and SV)
- Activation of _____ nerves
- Activation of ____ system
- Increased release of (2)
The net effect of these neurohormonal responses is to
- Produces (1) (to help maintain arterial pressure)
- Produces (1) (increased venous pressure)
- Increases blood ______
- sympathetic
- RAAS
- ADH and Atrial natriuretic peptide (increases responsiveness of vascular smooth muscle)
- Arterial vasoconstriction
- Venous constriction
- volume
Patho of Chronic HF Chart
- Increased _____ Stimulation
- Effects
- Increased ___ and _____ -> increased O2 demand
- Increased __ -> increases afterload
- Effects
- Increased _____ System (dt decreased blood flow to kidneys)
- Effects
- Increased _______ which also causes constriction
- Increased ______ (sodium and water retention) to increase blood volume and more blood to heart -> increases _____
- Effects
- Sympathetic
- HR, Contractility
- BP
- RAAS
- Ang II
- Aldosterone -> preload
Alterations in the Frank Starling Mechanism with CHF
The greater the LV end diastolic pressure what happens to CO?
As end diastolic pressure goes up, CO goes down
Stages of Heart Failure
- At ____ for Heart Failure
- STAGE A =
- STAGE B =
- ____ Heart Failure
- STAGE C =
- STAGE D =
- Risk for HF
- High risk for developing HF
- Asymptomatic LV dysfunction
- Has HF
- Past or Current Symptoms of HF
- End stage HF
Stage A HF
=
- E.g Patients with
- H_____
- Ath_____ disease
- D____
- _____ syndrome
- OR patients using ____ with HF or CM
- Therapy Goals
- Treat ____
- Encourage _____ cessation
- Treat ____ dissorders
- Encourage regular _____
- Discourage ____ intake, illicit ___ use
- Control ____ syndrome
- Drugs ___ or ____ in appropriate patients (see text) for vascular disease or diabetes
- high risk but without structural heart disease or sx of HF
- Patients with
- HTN
- Atherosclerosis
- Diabetes
- Metabolic
- cardiotoxins
- Therapy Goals
- HTN
- smoking
- lipid
- exercise
- alcohol, drug
- metabolic
- ACEI or ARBS
Stage B HF
=
- E.g Patients with
- previous __
- LV _____ including LVH and low EF
- Asymptomatic ____ disease
- Therapy Goals
- All measures under stage A
- Drugs (2)
- Devices in Selected Patients (1)
Structural heart disease w/o heart disease or sx of HF
- E.g patients with
- MI
- remodeling
- asx valvular disease
- Therapy Goals
- ACEI or ARB or BB in appropriate patients
- Implantable defibrillators
Stage C HF
=
- E.g Patients with
- Known _____ heart disease AND ___ or fatigue, reduced ____ tolerance
- Therapy Goals
- All measures under stages A and B
- Dietary ___- restriction, drugs for routine use
- _____ for fluid retention
- A___
- B___
- Drugs in Selected Patients
- Aldosterone ____
- A _ _ _
- D_____
- Hy____/ni_____
- Devices in Selected Patients
- Biventricular ______
- Implantable ______
Structural Heart disase WITH prior or current symptoms of HF
- E.g patients with
- Known structural heart disease AND SOB, reduced exercise tolerance
- Therapy goals
- salt restriction
- Diuretics
- ACEI
- BB
- Drugs
- antagonists
- ARBS
- Digitalis
- Hydralizine/nitrates
- Devices
- Pacing
- Defibrillators
Stage D HF
=
- Eg. Patients who have marked ____ at ____ despite maximal medical _____ (e.g those who are currently ____ or cannot be safely discharged from hospital without specialized interventions)
- Therapy Goals
- Appropriate measures under stages A, B, C
- Decision re appropriate lvl of care
- Options
- Compassionate (1) care/h____
- Extraordinary measures such as?
Refractory HF requiring specialized interventions
- symptoms, rest, therapy, hospitalized
- Options
- end of life care/hospice
- heart transplant, chronic inotropes, permanent mechanical support, experimental surgery or drugs
Medications (Notes)
(6)
Again, all meds are designed to minimize what?
Body’s natural response to drop in CO
ACE Inhibitors
Angiotensin Receptor Blockers
Aldosterone Antagonists
Beta Blockers
Digoxin
Diuretics
ACE Inhibitors
=
Reduces production of Angiotensin II -> will reduce vasoconstriction and volume overload
Angiotensin Receptor Blockers
=
Aldosterone Antagonists
=
Similar to ACEI but blocks the receptors to angiotensin
Specifically aimed at limiting sodium and water retention
Beta Blockers
=
Digoxin
=
Decreases HR -> reduces O2 demand on heart -> preserves heart function
Increases contractility of heart (given much later stages of HF (elderly))-> trying to maintain minimal heart function (is the outlier of these drugs)
Diuretics
=
+/- Sodium Restricted Diets
Limits Fluid Retention
