CARDIAC PATHOPHYSIOLOGY Flashcards
what type of edema you may see in CHF
May see PULMONARY &/or SYSTEMIC EDEMA
a highly cardiac specific enzyme that is released into the blood during an MI
troponin
Atherosclerotic Heart Disease a.k.a.
Coronary Artery Disease
in myocardial ischemia…
Increased myocardial oxygen demand caused by?
Decreased myocardial oxygen supply caused by?
- Increased: exercise, mental stress, spontaneous fluctuations of HR or BP
- Decreased: decreased coronary blood flow (need 70% occlusion)
arteriography
- radiography of an artery, carried out after injection of a radio-opaque substance.
- preparation for surgery of peripheral artery aneuyrysm
Restrictive CM (RCM):
characteristics and causes
Type B aortic aneurysm
a aortic aneurysm anywhere but the ascending aorta
LDL:HDL ratio levels
- Provides a composite risk marker
- < or = 3:1 ratio is ↓ risk
- > or = 5:1 ratio is an ↑ risk
Pericarditis is commonly caused by
viral infection
MUSCULOSKELETAL Physiologic Consequences of CHF
- Muscle wasting & possible skeletal muscle myopathies and osteoporosis are possible due to inactivity or other co-morbidities and to vasculature’s impaired ability to vasodilate; leads to sedentary lifestyle.
- Inability in increase HR and SV
- Diastolic dysfunction is exacerbated with exercise
- EF correlates to exercise tolerance
normal LDL and HDL cholesterol levels
- Low Density Lipoprotein = <100 desirable, more than 190 very high
- High (healthy) Density Lipoprotein = >60 optimal, less than 40 low
📣
st wave elevation may be
transmural MI
Is there a difference between Coronary Heart Disease and Coronary Artery Disease?
- Terms used interchangeably
- CHD is actually caused by CAD
Surgical management of CHF
Transmural MI
- full thickness
- Q wave MI
Ventricular Remodeling in diastolic heart failure
hypertrophied heart
MI Classification:
(types of MI)
- Subendocardial = partial thickness = NSTEMI = Non-Qwave MI
- Transmural = full thickness = STEMI = Q wave MI
Pathogenic mechanism of plaque formation: the lipid hypothesis:
increased LDL in blood penetrates arterial wall → lipids accumulate in smooth muscle cells → hyperplasia of smooth muscle → endothelium tears and platelets aggregate → results in thrombus formation
‼️
Left ventricular hypertrophy results in ___________ dysfunction (impairs filling of
ventricles)
diastolic
Rapid ventricular emptying →may see high ejection fraction
Why is HDL cholesterol considered “good” cholesterol?
HDL cholesterol protects against CHD by taking LDLs out of the blood and keeping it from building up in arteries
Types of Aneurysms:
can be classified by shape and size and described as…
- Saccular: Usually spherical in shape and involve only a portion of the vessel wall
- Fusiform (“spindle-shaped”): often involve large portions of the ascending and transverse aortic arch, abdominal aorta, or less frequently the iliac arteries
- Mycotic: caused by the growth of fungi or bacteria within the vascular wall, usually following impaction of a septic embolus
- Dissecting: Resulting from hemorrhage that causes longitudinal splitting of the arterial wall, producing a tear in the intima and establishing communication with the lumen
HR protocol post MI
20-25 bpm of baseline (resting heart rate) in the first 6-8
Is felt as pulsatile mass on one or both sides of the thigh
may be femoral artery aneurysm
total cholesterol normal levels
less than 200 = desirable
more than 240 = high
endocarditis can cause ______ damage → CAN BE FATAL
valve
Pericarditis may progress to →
Pericardial effusion (excess fluid around the heart)
Leading to → Cardiac Tamponade ***EMERGENCY***
Type A aortic aneurysm
aortic dissection in the ascending aorta
____________ is the most common type of heart
disease, killing more than 370,000 people annually
Coronary heart disease
nodular deposits of fatty material that line the walls of the artery (plaques), and the vessel walls may also lose their elasticity and become sclerotic
Atherosclerotic Heart Disease a.k.a. Coronary Artery Disease
(“Hardening of the Arteries”)
Transports fatty acids and lipids
Cholesterol
Are cardiac tumors common?
no, generally very rare and many are curable with surgery
Inferior wall MI:
- RCA
- SA node
- Malignant cardiac tumors are usually classified as…
- which one is the most common?
- usually classified as sarcomas
- Hemangiosarcomas (most common)
- Rhabdomyosarcoma
The Newest and Preferred Marker enzyme for the diagnosis of MI?
troponin
Localized dilatation and weakening of the wall of a blood vessel
Aneurysms
normal triglycerides levels
<150 normal
>500 very high (high risk)
NUTRITIONAL physiologic Consequences of CHF
May see anorexia that can lead to malnutrition & cachexia
SYMPATHETIC NS (SNS) Compensation for CHF
Decreased CO sensed by baroreceptors → Leads to increased SNS activity → Release of norepinephrine → increases HR, SV, myocardial contractility AND ↑systemic resistance and BP due to peripheral vasoconstriction that stimulates the kidneys to increase renin release
Classic Symptom Of Ischemia
Angina Pectoris (Angina)
Described as “pressure” or “heaviness”
Syndrome where the heart is unable to pump enough output to meet the body’s metabolic demands
Congestive Heart Failure (CHF)
Occurs almost exclusively at rest due to coronary artery spasm
Prinzmetal’s Angina (Variant or Atypical Angina)
Diverse group of diseases involving primary disorder of the myocardial cells with ultimate cardiac dysfunction (involve the myocardium) in which contraction, relaxation, or both of cardiac muscle are impaired
Cardiomyopathy (CM)
Dilated cardiomyopathy results in:
Prognosis?
- Decreased stroke volume
- Impaired ability to increase cardiac output with exercise
- Eventual development of left ventricular failure and right ventricular failure (less effective pump)
- Prognosis is good WITHOUT clinical heart failure
in Left Sided/Ventricular Failure: CHF may also see
– Also may see increased LVEDP (pressure)
– Also LV dilatation may stretch mitral valve
Compensated vs Decompensated CHF
Compensated: Mild/moderate symptoms & degree of volume overload
Decompensation: baseline abnormalities become further deranged
Clinical Manifestations of CHF, right ventricular failure:
- Dependent edema
- Hepatomegaly
- Ascites
- Fatigue
- Anorexia, nausea, bloating
- Right sided S3 or S4
- Accentuated P2 (heart sound—closure of pulmonic valve)
- Pulmonary or Tricuspid valve murmurs
- s/s: JVD, weight gain, RUQ (liver) pain, jaundice, cyanosis (nail bed), ↓urine output
The first symptom of hypertrophic CM my be
sudden collapse & possible death
Cardiac/Ventricular Remodeling
- Pathologic and physiologic changes in size, shape, structure and physiology of the heart after injury to the myocardium.
- Left ventricle may change from elliptical to spherical
- Apoptosis—programmed death of cells, is more severe with CHF
Response to MI
🚨
- 24h: inflammatory response to necrosis
- 2 - 4 days: visible necrosis, recovery begins
- 4 - 10 days: Debris cleared → matrix laid down
- 10 – 14 days: Formation of weak fibrotic scar
**The scar tissue is inelastic and is not able to contract and relax like healthy myocardial tissue
Right Sided/Ventricular Failure: Cor Pulmonale
Prolonged pulm HTN → Increased right ventricle afterload → Anatomical changes to right ventricle (dilatation → possible hypertrophy) → Right ventricular end-diastolic pressure (EDP) increases → Reflects back up to right atrium and venous system
Popliteal artery aneurysm use _______ to diagnose and measure diameter
ultrasound
Hormones Involved in CHF
what is the the most common cause of right CHF
left CHF
most common bening cardiac tumor
myxoma
Popliteal artery aneurysm Account for ____ of all peripheral artery aneurysms
~85%
the release of Natriuretic peptides (brain NP, atrial NP, endothelial C type NP) may reflect or indicate
acute and chronic volume pressure overload
what is the recommended LDL value for patients with DM or other CHD risk factors
less than 100
Cardiac Enzymes release after MI:
- Troponin (4-6 h): last several days
- Creatine kinase (4-8h): released when cells die, last 2-3 days
- Myoglobin (1-4 h): protein released with injury to the myocardium
Hypertrophic CM (HCM) characterized by
- Considerable increase in cardiac mass (hypertrophy)
- No cavity dilatation
- Normal or increased systolic function
- May demonstrate left ventricular outflow obstruction
(hypertrophic obstructive CM or IHSS)
Types of angina:
- Chronic stable angina: treat
- Unstable angina: don’t treat
Difference between ischemia and infarction
- Ischemia: decrease in blood flow
- Infarction: tissue death caused by ischemia
Causes of dilated cardiomyopathy
- Idiopathic (arises spontaneously or for which the cause is unknown)
- Heart disease and uncontrolled HTN (most common)
- Myocarditis
- Infectious or non-infectious inflammatory process
- Toxins (ex: ETOH, drugs, chemo)
- Pregnancy
- Metabolic disorder
- Hereditary disease (ex: muscular dystrophy)
Medical management of CHF
Treatment of CHF
Diagnosis of CHF:
difference between chronic stable angina and unstable angina
- Chronic Stable Angina: precipitated by exertion, emotional streess, heavy meals
- Unstable Angina: symptoms of angina without the demands that usually generate it
Treatment of Aneurysms
Surgical excision and grafting
– Endovascular (prefered) repair vs Open repair
Causes of MI:
👉🏻 Whatever leads to severe vasoconstriction
- Prolonged myocardial ischemia (atherosclerosis)
- Prolonged vasospasm
- Embolic occlusion
- Cocaine
- ➔ Leads to focal death of myocardial tissue in the area supplied by the involved coronary artery * Very often in the LV*
In Right Sided/Ventricular Failure: Cor Pulmonale, may also see what?
May see jugular venous distension (JVD), liver engorgement, ascites, and peripheral edema
when does troponin become elevated after an MI?
Elevated between 4-6 hours post MI
Peaks at 24 hours
Non-Drug Management of CHF
what is the recommended LDL value for patients with CHD or vessel disease?
less than 70
when does myocardial recovery begin s/p MI
2 - 4 days s/p MI
symptoms of angina
- Pain, pressure and heaviness over the heart (precordial), in the shoulder, arm, throat or jaw
- DOE (dyspnea on exertion)
- Fatigue
- Weakness
- Syncope
Occurs when myocardial oxygen demand is greater than the supply
Myocardial Ischemia
The earliest detectable atherosclerotic lesion is known as
the fatty streak (lipid foam cells)
Fatty streak → fibrous plaque
Diagnosis of MI, at Least 2/3 of the following symptoms must be present
-
Anginal Symptoms: Chest pressure, heaviness, pain, arm, jaw
- DOE
- Fatigue
- Syncope
- Belching
- EKG Changes
- Rise of Cardiac Enzymes
Dilated cardiomyopathy characterized by:
- Increased cardiac mass
- Dilatation of all 4 cardiac chambers
- With little or no wall thickening
- Systolic dysfunction
Cholesterol comes from 2 sources:
- 75% our bodies
- 25% from food sources (animal products only)
Chronic Stable Angina is relieved with
nitroglycerin (NTG)
(vasodilation)
Peripheral Artery Aneurysms occur almost exclusively in
men
Athero =
Sclerosis =
- gruel, soft deposit
- hardening
Systolic Heart Function Failure:
- Increased preload → lead to pump failure
- Increased afterload → leads to pump failure
- Decreased contractility of the myocardium → leads to pump failure; most common.
- Changes in rate of contraction (chronotropic) → (to slow or too fast) lead to pump failure.
3 main categories of cardiomyopathy
- Dilated Cardiomyopathy (DCM)
- Hypertrophic Cardiomyopathy
- Restrictive Cardiomyopathy
PANCREATIC physiologic Consequences of CHF
Possible impaired insulin secretion & subsequent glucose tolerance – May also be another source of a myocardial depressant factor
Pathogenic mechanism of plaque formation: chronic endothelial injury
Injury of the interior of the cell wall by macrophages causes platelets, monocytes, lipids & smooth muscle cells to migrate and aggregate from the media to the intima where they form a fibrous cap → platelets form clots & release proteins with tough fibers further hardening the artery → Can block blood flow or break off and throw a clot.
Inflammation of endocardium (usually due to microbial infection)
Endocarditis
Silent Myocardial Infarction
- No symptoms of angina
- Can occur in any patient but more common in those with DM and ETOH (alcohol) abuse
– Peripheral neuropathies may contribute to this - Must be ruled in by EKG changes and Cardiac Enzymes
Clinical Manifestations of CHF, left ventricular failure:
- Progressive Dyspnea (exertion→rest)
- Dyspnea & orthopnea PND (paroxysmal nocturnal dyspnea)
- Fatigue/weakness
- Pulmonary rales
- S1 heart gallop, S3
- Enlarged heart
- Functional MR, TR
- s/s: pulmonary edema, pallor, cyanosis, diaphoresis, tachypnea, anxiety, agitation, s/s of cerebral hypoxia
How is myocardial ischemia diagnosed?
- by exercise stress test
- arrhythmias and T wave inversion on an EKG → later becoming ST elevation
NEUROCHEMICAL Physiologic Consequences of CHF:
Increased sympathetic stimulation desensitizes heart to β1-adrenergic receptor stimulation → decreases heart’s inotropic effect (strength of the contraction)
Ventricular Remodeling in systolic heart failure
dialated heart
Types of thoracic aneurysms:
-
Infrarenal (90%): May be symptomatic/asymptomatic.
- Symptoms: chronic mid-abdominal &/or low back pain
-
Thoracic: Usually asymptomatic.
- May also be due to Marfan’s syndrome
Counter-regulatory Hormones in CHF
HEMATOLOGIC Physiologic Consequences of CHF
Possible anemia and hemostatic abnormalities
cardiac disease count for 1 in every ___ deaths
4
CARDIAVASCULAR Physiologic Consequences of CHF:
Decreased myocardial performance → try to increase venous return w/peripheral vascular constriction → increased peripheral vascular resistance (sympathetic ns contributes to this)
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What are the systems involved in compensating CHF?
- Autonomic Nervous system: ↑vasocontriction
- Renin-Angiotensin-Aldosterone system: ↑vasocontriction, ↑water retention
- Natiuretic peptide counter-regulatory system: ↑vasodilation, ↓filling pressures, improved myocardial relaxation, ↑ water excretion, suppression of AS and ANS activity
EKG Changes with MI
- Peaked T Waves
- ST Elevation (transmural)
- Q Wave Present
- T Wave Inversion
Sign of aneurysm:
pulsating swelling that produces blowing murmur on auscultation
In a multi-center study of 515 women who had an acute myocardial infarction (MI), the most frequently reported symptoms were:
- unusual fatigue,
- sleep disturbances
- shortness of breath,
- indigestion and anxiety
Symptoms of Prinzmetal’s Angina
- Often severe chest pain, awakening patient from sleep
- Often spasm responds to NTG (though not always)
types of aneurisms
- True aneurysm (3 layes involved)
- False or Pseudo-aneurysm: blood leaking confined by sourrounding tissues
Pressure in pulmonary vasculature where see pulmonary edema develop is ~___ mmHg
25
myocardial infarction
COMPLETE interruption of blood supply to an area of the myocardium
How are cardiac enzymes used in the diagnosis of MI/
Cardiac muscle cells become necrotic resulting in the diffusion of several cardiac markers into the blood
- Troponin
- Creatine kinase
- Myoglobin
Lateral wall MI:
Left Circumflex Artery
2 types of peripheral artery aneurysm in men:
- Popliteal artery aneurysm
- Femoral artery aneurysm
Decreased SV and CO (decreased EF) → Increased LVEDV → Decreased LV compliance → Increased left atrial dilatation → Increased pressure in pulmonary vessels → Transudation of fluid from pulmonary capillaries
Left Sided/Ventricular Failure: CHF
CHF may result from:
Any structural/functional cardiac disorder that impairs the filling or pumping ability of the ventricles
PULMONARY Physiologic Consequences of CHF:
Develop pulmonary edema due to increased filling pressures
Anterior Wall MI:
- Left Coronary Artery
- More severe effect: L ventricle
New York Heart Association of CHF
RENAL Physiologic Consequences of CHF
Due to decreased CO → decreased renal blood flow & glomerular filtration rate → sodium & fluid retention
{Heart failure also associated with increased circulating levels of arginine vasopressin (vasoconstrictor & inhibitor of water excretion)}
📣
ST wave depression may be
Subendocardial MI
HEPATIC physiologic Consequences of CHF
Possible cardiac cirrhosis due to hypoperfusion due to decreased CO or hepatic venous congestion
Subendocardial MI
- partial thickness
- Non Qwave MI
- May not have as significant EKG changes, but pt symptomatic and lab values indicate injury
“Build-up of plaque in the heart’s arteries that can cause a heart attack.”
Coronary Heart Disease (CHD)
Left Sided/Ventricular Failure aka
CHF
tissue zones of infarction: which area is recoverable?
- Zone of Infarct: cell death
- Zone of Injury: not cell death
- Zone of Ischemia: recoverable area
RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM Compensation for CHF
- systems that maintain BP when we have low volume in our bodies
- increases venous and atrial tone
- triggers the release of norepinephrine
- The release of RENIN (by the ANS) in the system → Angiotensin II: Powerful vasoconstrictor → Initially restores BP but can ultimately lead to decreased CO, renal perfusion, Contributes to remodeling and promotes the release of aldosterone (Acts on the kidneys increase resorption of water)
Is myocardial ischemia reversible?
yes, usually with rest
